European Manual of Medicine
Vascular Surgery C. D. Liapis Chief Editor K. Balzer, F. Benedetti-Valentini, J. Fernandes e Fernandes Editors
Editors
C. D. Liapis, K. Balzer, F. Benedetti-Valentini, J. Fernandes e Fernandes
Vascular Surgery With 385 Figures and 58 Tables
123
Series Editors
Volume Editors
Wolfgang Arnold, MD HNO und Poliklinik Klinikum rechts der Isar München Germany
Christos D. Liapis, MD, FACS, FRCS Department of Vascular Surgery Athens University Medical School Attikon University Hospital Athens Greece
Uwe Ganzer, MD HNO und Poliklinik Heinrich-Heine-Universität Düsseldorf Germany
Klaus Balzer, MD Division of Vascular Surgery Evangelisches Krankenhaus Mülheim Germany Fabrizio Benedetti-Valentini, MD Department of Vascular Surgery University of Rome „La Sapienza“ Rome Italy José Fernandes e Fernandes, MD, PhD Chief of Service Department of Vascular Surgery Hospital Santa Maria and Faculty of Medicine Director Instituto Cardiovascular de Lisboa Lisbon Portugal
ISBN-10 3-540-30955-1 Springer Berlin Heidelberg NewYork ISBN-13 978-3-540-30955-0 Springer Berlin Heidelberg NewYork Library of Congress Control Number: 2006928312 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag. Violations are liable for prosecution under the German Copyright Law. Springer is a part of Springer Science + Business Media springer.com © Springer-Verlag Berlin Heidelberg 2007
The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Editor: Gabriele M. Schröder, Heidelberg, Germany Desk Editor: Waltraud Leuchtenberger, Heidelberg, Germany Production: LE-TeX Jelonek, Schmidt & Vöckler GbR, Leipzig, Germany Cover Design: Frido Steinen-Broo, eStudio Calamar, Spain Printed on acid-free paper 24/3100Wa 5 4 3 2 1 0
V
Acknowledgements
When the invitation came from Springer-Verlag to produce this first European manual of vascular surgery, it was accepted enthusiastically by the editors, albeit with some trepidation concerning the demands of such a venture. This concern was due to the diverse nature of the vascular system, which covers every part of the human body; therefore, diseases of the vascular system affect all organs and all parts of the human anatomy and in order to provide a thorough perspective on the discipline of vascular surgery, the manual would have to cover the full spectrum of vascular diseases. However, the pressing need to produce a long-overdue European manual on vascular surgery was the driving force that brought together several of the finest minds in Europe, who so generously accepted the task of imparting their expert knowledge by contributing chapters in their own specific areas. The diversity of the discipline, coupled with the differences in management of vascular diseases by authors originating from different European countries, required the work to be carefully formatted to render it an effective reference book, based on recommended European standards for professionals and trainees with a common goal: optimum care of the vascular patient. The editors are deeply grateful to the distinguished authors and all their associates involved in this compilation. Apart from these tremendous contributions, this project would not have been possible without the enormous assistance of my associate Dr. Yannis Kakisis and the invaluable cooperation of Ms. Gabriele Schroeder and Ms. Waltraud Leuchtenberger of Springer-Verlag, Patrick Waltemate of LE-TeX and my administrative assistant Ms. Vivienne Rose. We hope the readership will benefit from this first European Manual of Medicine: Vascular Surgery.
The editors Christos D. Liapis Klaus Balzer Fabrizio Benedetti-Valentini José Fernandes e Fernandes
VII
Foreword Gregory D. Skalkeas Professor Emeritus, Academician, President of the Foundation of Biomedical Research of the Academy of Athens
Vascular surgery has acquired a well-established identity throughout the European Union, where vascular diseases are still the leading cause (40%) of death and disability. Proper management of vascular diseases is dependent on public awareness and appropriate training of specialists. This stands true for every medical discipline. For vascular surgery it has an additional aspect because, besides the required above-average standard of technical dexterity, the vascular surgeon should also be well versed in a variety of subjects such as molecular biology, in the use of ultrasound and – with the introduction of endovascular techniques – a skilful operator of guidewires and laparoscopic instruments. All the accumulated know-how and skills required for proper management of the vascular patient demand a rapid change in the training of vascular surgeons and an indepth knowledge of the various manifestations of vascular diseases. The information necessary for the above is disseminated through books, journals and the internet. Most of the time, however, articles in journals reflect the experience and enthusiasm of the authors on the subject but not the level of knowledge of the medical community as a whole. Electronic information is fast and reliable but always gives the reader the impression of being short-lived. Books, on the other hand, allow a reflection of what has been written and a true interactive role for the reader. Multi-author books have the inherited handicap of not conveying a specific message by virtue of the diversity of thought; however, when the authors happen to be experts in their field and to represent most of the countries within the European Continent that is striving to prove its successful function as a union, then such a collaboration can indeed convey a message: the level of knowledge and the modus vivendi of vascular surgery in Europe. The editor and authors of this compilation are to be congratulated for such an endeavour, worthy of the European spirit of unity and collaboration.
IX
Preface Sir Peter Bell Professor of Surgery, University of Leicester
European Manual of Medicine: Vascular Surgery Vascular surgery has evolved and expanded in a spectacular fashion during the last 50 years. During this time previously untreatable conditions have become treatable and dealt with on a regular basis by vascular surgeons. Many of the pioneers of vascular surgery were from Europe, starting with Cid Dos Santos who invented angiography and made the whole field of vascular surgery possible. Jean Kunlin in 1949 was the first surgeon to use a reversed vein by-pass graft successfully. In the field of aortic surgery, Lerich and Matas were pioneers in this area and Felix Eastcott started the long and successful treatment of carotid artery stenosis by surgery. Successive generations of Europeans have continued to be involved in the evolution of vascular surgery, taking it to a new phase of activity. European surgeons continue to be at the forefront of changes in vascular practice and have made it possible for the new era of laparoscopic and endovascular surgery to progress and flourish. One might ask why we need yet another textbook of vascular surgery. This is a perfectly reasonably question and the answer is because no book exists that offers comprehensive knowledge, both theoretical and practical, to every level of vascular surgeon. Buying books is expensive and it is therefore important that such books are of use to all of those who may wish to read them. The aim of this book is to be as useful to the vascular trainee as to the established vascular consultant. To this end the editors have enlisted and given a clear brief to leading practitioners in the field. All of the topics that one would normally expect to see in such a book are included and the text is sufficiently referenced to make it authoritative. Pictures and figures are also used but not extensively and are not a major selling point of this volume. The theoretical and practical aspects of open surgery, endovascular procedures and laparoscopic surgery are all covered in detail and venous disease and lymphatic problems are not ignored. One question that might be asked is: why are all the contributing surgeons from Europe and none from other countries or continents? This is intentional and not xenophobic, but an attempt to show that the necessary expertise to cover all aspects of the practice of vascular surgery exists in the expanded European community. It is also to acknowledge the fact that vascular procedures and practice are not necessarily the same the world over. The approach to some problems is different in Europe than it is in other continents and these differences are reflected in this book. I am sure that those who buy and read this book will not be disappointed in its content or style. It will be extremely useful to all readers and be a signpost to the future of vascular surgery.
XI
Introduction Christos D. Liapis, John D. Kakisis
Vascular diseases are the most frequent cause of death and disability of Europeans. The aim of the present book, European Manual of Medicine: Vascular Surgery, is to give an indication of European standards for the diagnosis and therapy of vascular diseases. It is designed with the same format as other books in the series European Manuals of Medicine and focuses on the description of each clinical entity (definition, epidemiology, aetiology, symptoms and complications) and on the recommended European standard diagnostic and therapeutic steps. In contrast to other textbooks, most of the information is presented in bulleted listings instead of lengthy paragraphs. This is done in the hope of enabling the reader to retrieve information easily and quickly. The first chapters of this book refer to the pathogenesis of vascular diseases, including the development of atherosclerosis and the effect of dyslipidaemia, clotting disorders and emerging biochemical risk factors. Subsequent chapters present the noninvasive and invasive means of diagnosis, including latest developments such as computer-guided diagnosis of vascular diseases. The preoperative evaluation and optimization as well as the peri-operative care of the vascular patient are also discussed. The book includes a review of the history of vascular surgery in Europe and a chapter on the training of vascular surgeons for endovascular procedures in order to highlight the continuity and the progress of vascular surgery over the past century and the future perspectives. The chapters of the book cover the entire range of arterial, venous and lymphatic disorders with an emphasis on all recent developments including endovascular and laparoscopic surgery. The text is comprehensive since the book is intended not only for vascular specialists but also for students, residents in vascular surgery and other interested physicians. The chapters have been written mainly by national representatives on the newly established Section of Vascular Surgery of the European Union of Medical Specialists (UEMS), thus drawing upon the collective experience of vascular surgeons/specialists from the various European countries. The authors are experts in their field, providing the reader with a professional opinion reflecting what is generally considered to be the state-of-the-art in each area. We hope that the readers, especially the hard working trainees in vascular surgery to whom this book is dedicated, will find it useful.
XIII
Contents
Vascular Surgery and the Vascular Patient 1.1 1.1.1 1.1.2 1.1.3 1.1.3.1
1.1.3.2
1.1.3.3
1.1.4
1.1.5
The History of Vascular Surgery in Europe . . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . . The Origin and the Foundations of European Vascular Surgery . . . . . . . Europe, Cradle of the World’s Vascular Surgery . . . . . . . . . . . . . . . . . . . The Nursery of Vascular Surgery in Europe in the 1930s was the René Leriche School in Strasburg, France . . . . . . . . . . . . . . . . . . Reference to European Surgeons who Through their Pioneering Work Developed Vascular Surgery in their Continent with International Influence . . . . . . . . . . . . Medical and Interventional Vascular Contributions to the Development of Vascular Surgery in Europe and Worldwide . . European Vascular Surgical and Angiological Societies and Congresses . . . . . . . . . . . . . . . . . . . . . . . Epilogue . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgements . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . .
3 3
1.2.2.2
1.2.2.3 1.2.3
3 7
1.2.3.1 1.2.3.2 1.2.4
8
1.2.5 1.2.6
10
1.2.7 1.2.8
12
1.3
14 17 19 20
1.3.1 1.3.2 1.3.2.1 1.3.2.2 1.3.2.3
1.2 1.2.1 1.2.2 1.2.2.1
Development of Atherosclerosis for the Vascular Surgeon . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . Physiopathology of Atherosclerosis . . . . . . . . . . . . . . . . . . . Normal Blood Vessel Morphology . . . . . . . . . . . . . . . . . . . . . .
23 23
1.3.3
23
1.3.4
23 1.3.5
Initiation of Atherosclerosis and Role of Endothelial Dysfunction . . . . . . . . . . . . . . . . . . . . . . Evolution of the Atherosclerotic Plaque . . . . . . . . . . . . . . . . . . . . . . . . . . . Contributive Factors to Endothelial Dysfunction and Plaque Formation . . . . . . . . . . . . . Miscellaneous Factor . . . . . . . . . . . . . . The Oxidized LDL Hypothesis . . . . . . Plaque Instability and Complicated Plaques . . . . . . . . . . Classification of Atherosclerotic Plaques . . . . . . . . . . . . . . . . . . . . . . . . . . . Assessment and Evaluation of the Risk of an Atherosclerotic Plaque . . . . . . . . . . . . . . . . . . . . . . . . . . . General Therapeutic Measures . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . Lipids and Peripheral Arterial Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Effect of Lipid Lowering on PAD . . . Prevention of PAD . . . . . . . . . . . . . . . . Improvement of Symptoms Associated with PAD . . . . . . . . . . . . . Reduction of the Risk of Vascular Events Associated with PAD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Peripheral Vascular Surgery and Statins . . . . . . . . . . . . . . . . . . . . . . . . . . . Additional Potential Actions of Lipid-lowering Drugs that may Benefit PAD Patients . . . . . Are all Statins the Same? . . . . . . . . . . .
23 26
28 28 28 30 30
31 31 32 32
35 35 35 35 35
36 36
37 37
XIV
Contents
1.3.6
1.4
1.4.1 1.4.2 1.4.2.1 1.4.3 1.4.3.1 1.4.3.2 1.4.3.3 1.4.3.4
1.4.3.5
1.4.4
1.5 1.5.1 1.5.1.1 1.5.1.2 1.5.1.3 1.5.1.4 1.5.1.5 1.5.1.6 1.5.2 1.5.2.1 1.5.2.2 1.5.2.3 1.5.3 1.5.3.1 1.5.3.2 1.5.3.3 1.5.3.4
Concluding Comments . . . . . . . . . . . . 37 References . . . . . . . . . . . . . . . . . . . . . . . . 38 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Venous Thrombosis . . . . . . . . . . . . . . . Risk Factors . . . . . . . . . . . . . . . . . . . . . . What Should a Surgeon do when Faced with Hypercoagulation? . . . . . Should a Search for Thrombophilia be Undertaken? . . . . How Should the Search be Done? . . . . . . . . . . . . . . . . . . . . . . . . . Diagnosing Thrombotic Disease in Patients with Thrombophilia . . . . . Treating Thromboembolic Disease in Patients with Thrombophilia . . . . . . . . . . . . . . Specific Considerations in Treating Thromboembolic Disease Related to Thrombophilia . . Summary . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . Noninvasive Diagnosis of Vascular Diseases . . . . . . . . . . . . . . . Peripheral Arterial Disease . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Physical Examination . . . . . . . . . . . . . . Basic Haematological and Biochemical Tests . . . . . . . . . . . . . Special Investigations, Other Than Imaging . . . . . . . . . . . . . . . . . . . . . Imaging Techniques . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . Disease of Arteries Supplying the Brain . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Imaging Techniques . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . Diseases of the Venous Circulation . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Chronic Venous Insufficiency . . . . . . Deep Vein Thrombosis . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . .
41 41 41 41 45 45
1.6 1.6.1 1.6.2 1.6.3 1.6.3.1 1.6.3.2 1.6.3.3 1.6.3.4 1.6.3.5 1.6.3.6 1.6.4 1.6.4.1 1.6.4.2
45 46
1.7
46
1.7.1 1.7.2
46 47 47
51 51 51 51
1.7.2.1 1.7.2.2 1.7.2.3 1.7.2.4 1.7.2.5
1.7.3
Invasive Diagnosis of Vascular Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . History . . . . . . . . . . . . . . . . . . . . . . . . . . . Arteriography . . . . . . . . . . . . . . . . . . . . . Techniques . . . . . . . . . . . . . . . . . . . . . . . Pre-procedure Evaluation and Preparation . . . . . . . . . . . . . . . . . . . Technique . . . . . . . . . . . . . . . . . . . . . . . . Post-procedure Care . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . . . Direct Toxicity . . . . . . . . . . . . . . . . . . . Phlebography . . . . . . . . . . . . . . . . . . . . . Indications . . . . . . . . . . . . . . . . . . . . . . . Techniques . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . Computer-Aided Diagnosis of Vascular Disease . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . Computer-Aided Diagnosis in Vascular Imaging . . . . . . . . . . . . . . . Image Pre-processing . . . . . . . . . . . . . . Definition of Regions of Interest – Automatic Segmentation . . . . . . . . . Extraction and Selection of Characteristic Features . . . . . . . . . Classification . . . . . . . . . . . . . . . . . . . . . ANALYSIS: a Modular Software System to Support Diagnosis of Vascular Disease . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . .
65 65 65 68 68 69 69 70 70 71 72 72 72 74
77 77 77 78 78 78 80
81 82 82
51 1.8 51 54 55 56 56 56 59
1.8.1 1.8.2 1.8.2.1 1.8.2.2 1.8.2.3 1.8.3 1.8.3.1
59 59 59 61 61 62
1.8.3.3 1.8.3.4 1.8.3.5
Preoperative Evaluation of a Vascular Patient . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Systemic Evaluation . . . . . . . . . . . . . . . Cardiovascular System . . . . . . . . . . . . . Respiratory System . . . . . . . . . . . . . . . . Renal System . . . . . . . . . . . . . . . . . . . . . Evaluation of Specific Vascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . Aneurysmal Disease: Abdominal Aortic Aneurysm . . . . . . Peripheral Vascular Disease: Chronic Lower Limb Ischaemia . . . . Peripheral Vascular Disease: Acute Limb Ischaemia . . . . . . . . . . . . . Carotid Disease . . . . . . . . . . . . . . . . . . .
85 85 85 85 86 88 89 89 89 90 91
Contents
1.8.3.6
Venous Disease . . . . . . . . . . . . . . . . . . . 92 References . . . . . . . . . . . . . . . . . . . . . . . . 93
1.9
Peri-operative Care of the Vascular Patient . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . . . Preoperative Planning . . . . . . . . . . . . . Effects of Anaesthesia . . . . . . . . . . . . . . Peri-operative Monitoring . . . . . . . . . Monitoring for Cardiac Ischaemia . . . . . . . . . . . . . . . . . . . . . . . . Peri-operative Temperature Control . . . . . . . . . . . . . . . . . . . . . . . . . . Level of Hypnotic Depth . . . . . . . . . . . Prevention of Cardiac Ischaemia . . . Preoperative Revascularization . . . . . Good Peri-operative Haemodynamic Control . . . . . . . . . . . Anaemia . . . . . . . . . . . . . . . . . . . . . . . . . Adrenergic Tone . . . . . . . . . . . . . . . . . . Postoperative Ischaemia Prevention . . . . . . . . . . . . . . . . . . . . . . . Aneurysm Surgery . . . . . . . . . . . . . . . . Effects of Clamping and Declamping . . . . . . . . . . . . . . . . . . . . . . Prevention of Spinal Cord Ischaemia in Thoracic Aortic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . Autotransfusion During Surgery . . . . Heparin . . . . . . . . . . . . . . . . . . . . . . . . . . Peri-operative Heparin . . . . . . . . . . . . Prophylaxis of Deep Leg Vein Thrombosis . . . . . . . . . . . . . . . . . . . . . Peri-operative Monitoring after Arterial Reconstructions . . . . Prophylactic Antibiotic Administration . . . . . . . . . . . . . . . . . Postoperative Pain Treatment . . . . Pulmonary Complications, Prophylaxis and Treatment . . . . . . . Peri-operative Care and Endovascular Surgery . . . . . . . Intensive Care Ward is Needed Only for Selected Patients . . . . . . . . Pre- and Postoperative Gut Function and Nutrition . . . . . . . . . . Discharge Planning . . . . . . . . . . . . . . Summary . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
1.9.1 1.9.2 1.9.3 1.9.4 1.9.4.1 1.9.4.2 1.9.4.3 1.9.5 1.9.5.1 1.9.5.2 1.9.5.3 1.9.5.4 1.9.5.5 1.9.6 1.9.6.1 1.9.6.2
1.9.6.3 1.9.7 1.9.7.1 1.9.7.2 1.9.8 1.9.9 1.9.10 1.9.11 1.9.12 1.9.13 1.9.14 1.9.15 1.9.16
95 95 95 95 96 96 96 97 97 97 97 97 97 98 98 98
99 99 99 99 100 100 100 100 100 101 101 101 102 103 103
1.10
1.11
1.11.1 1.11.2 1.11.3 1.11.4 1.11.5 1.11.6 1.11.7 1.11.7.1 1.11.7.2 1.11.7.3 1.11.7.4 1.11.7.5 1.11.7.6 1.11.8
1.12 1.12.1 1.12.1.1 1.12.1.2 1.12.1.3 1.12.1.4 1.12.1.5 1.12.1.6 1.12.1.7 1.12.2 1.12.2.1 1.12.2.2 1.12.2.3 1.12.3 1.12.3.1 1.12.3.2 1.12.3.3 1.12.3.4 1.12.3.5
Training of the Vascular Surgeonfor Endovascular Procedures . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Peripheral Arterial Disease and Emerging Biochemical Vascular Risk Factors . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Homocysteine (Hcy) . . . . . . . . . . . . C-reactive Protein (CRP) . . . . . . . . Lipoprotein (a) [Lp(a)] . . . . . . . . . . Fibrinogen . . . . . . . . . . . . . . . . . . . . . . Endothelium . . . . . . . . . . . . . . . . . . . . PAD and Other Potentially Relevant Emerging Risk Factors . . Creatinine . . . . . . . . . . . . . . . . . . . . . . Urate . . . . . . . . . . . . . . . . . . . . . . . . . . Microalbuminuria . . . . . . . . . . . . . . Insulin Resistance and Metabolic Syndrome . . . . . . . . . . . . . . . . . . . . . . Platelets, Fibrinolysis and D-Dimers . . . . . . . . . . . . . . . . . . Other Markers of Inflammation . . Conclusions . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . Quality Control in Vascular Surgery . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Physical Examination . . . . . . . . . . . . Angiography . . . . . . . . . . . . . . . . . . . . Continuous Wave (CW) Doppler . . . . . . . . . . . . . . . . . . . . . . . . Duplex and Colour Duplex Scan . . Intravascular Ultrasonography (IVUS) . . . . . . . . . . . . . . . . . . . . . . . . . Angioscopy . . . . . . . . . . . . . . . . . . . . . Flowmetry . . . . . . . . . . . . . . . . . . . . . . Arteries of the Abdomen . . . . . . . . Abdominal Aorta . . . . . . . . . . . . . . . Visceral Arteries . . . . . . . . . . . . . . . . Renal Arteries . . . . . . . . . . . . . . . . . . Lower Extremity By-pass . . . . . . . . Angiography . . . . . . . . . . . . . . . . . . . . Ultrasound (CW Doppler, PW Doppler, Duplex, Colour Duplex) Angioscopy . . . . . . . . . . . . . . . . . . . . . Flowmetry . . . . . . . . . . . . . . . . . . . . . . Conclusions . . . . . . . . . . . . . . . . . . . .
107 110
111 111 111 111 112 112 113 113 113 113 114 114 114 114 114 115
117 117 117 117 117 118 118 118 119 119 119 119 120 120 121 122 123 124 124
XV
XVI
Contents
1.12.4
Carotid Arteries . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
124 127
2.2.5.3 2.2.6 2.2.6.1
Cerebrovascular Arteries 2.1
2.1.1 2.1.2 2.1.3 2.1.4 2.1.5 2.1.6
2.2 2.2.1 2.2.2 2.2.3 2.2.3.1 2.2.3.2 2.2.3.3 2.2.3.4 2.2.3.5 2.2.3.6 2.2.4 2.2.4.1 2.2.4.2 2.2.4.3 2.2.4.4 2.2.4.5 2.2.4.6 2.2.4.7 2.2.4.8 2.2.4.9 2.2.5 2.2.5.1 2.2.5.2
Haemodynamic Changes and Other Risk Factors for Complications During Carotid Procedures . . . . . . . . . . . . . . Cerebral Blood Flow . . . . . . . . . . . . . General Complications . . . . . . . . . . Cerebral Monitoring and Protection During CEA . . . . . . Cerebral Embolization during CEA and CAS . . . . . . . . . . . . . . . . . . Adjuvant Medical Therapy . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Extracranial Carotid Artery Disease . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Pathogenesis of Brain Ischaemia . . Clinical Manifestations . . . . . . . . . . Amaurosis fugax . . . . . . . . . . . . . . . . Transient/Reversible Cerebral Ischaemia . . . . . . . . . . . . . . . . . . . . . . Established Stroke . . . . . . . . . . . . . . . Stroke in Evolution (“Waving and Waning”) . . . . . . . . . . . . . . . . . . . Global Cerebral Ischaemia . . . . . . . Asymptomatic Carotid Disease . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Arteriography . . . . . . . . . . . . . . . . . . . Colour Flow Duplex Scan . . . . . . . High-resolution Ultrasonography . . . . . . . . . . . . . . . . Measuring the Degree of Stenosis . Transcranial Doppler Examination . . . . . . . . . . . . . . . . . . . Other Flow-imaging Techniques . . Indications for Arteriography . . . . Computerized Tomography and Magnetic Resonance Imaging Examination of the Retina . . . . . . . Selection, Treatment and Results . . Medical Treatment . . . . . . . . . . . . . . Surgical Treatment . . . . . . . . . . . . . .
131 131 131 132 133 133 134 134
137 137 138 140 140 140 140 140 140 141 141 141 141 143 143 144 144 144
2.3 2.3.1 2.3.2 2.3.3 2.3.4 2.3.5
2.4 2.4.1 2.4.1.1 2.4.1.2 2.4.1.3 2.4.1.4 2.4.1.5 2.4.1.6 2.4.2 2.4.2.1 2.4.2.2 2.4.2.3 2.4.2.4 2.4.2.5 2.4.2.6 2.4.2.7 2.4.2.8 2.4.2.9 2.4.2.10 2.4.2.11
2.5 2.5.1
144 144 145 145 145
2.5.2 2.5.2.1 2.5.2.2
Technique of Carotid Endarterectomy . . . . . . . . . . . . . . . . . Endovascular Treatment . . . . . . . . . What are the Established Indications for Endovascular Procedures in Extracranial Carotid Disease? . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
149 150
Eversion Carotid Endarterectomy Technique . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Technique . . . . . . . . . . . . . . . . . . . . . . Advantages . . . . . . . . . . . . . . . . . . . . . Disadvantages . . . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
155 155 155 159 159 159 159
Fibromuscular Dysplasia . . . . . . . . . Basics . . . . . . . . . . . . . . . . . . . . . . . . . . Anatomy . . . . . . . . . . . . . . . . . . . . . . . Physiology, Pathophysiology . . . . . Organ-related Questions . . . . . . . . . Principles of Clinical Examination . . . . . . . . . . . . . . . . . . . . Technical Diagnostic Procedures . . Organ-specific Radiology . . . . . . . . Organ-related Diseases . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Exemplary Surgical Procedures . . . Special Remarks . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Aneurysms of the Extracranial Carotid Arteries . . . . . . . . . . . . . . . . Definition and Historical Background . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Atherosclerosis Aneurysms . . . . . . Previous Surgery/POS Endarterectomy . . . . . . . . . . . . . . . . .
146 149
161 161 161 161 165 165 165 166 166 166 166 166 167 168 168 168 169 169 169 170 170
173 173 173 173 174
Contents
2.5.2.3 2.5.2.4 2.5.2.5 2.5.2.6 2.5.3 2.5.4 2.5.5 2.5.5.1
2.5.6 2.5.6.1 2.5.6.2
2.6 2.6.1 2.6.2 2.6.3 2.6.4 2.6.4.1
2.6.4.2 2.6.4.3 2.6.5 2.6.5.1 2.6.5.2 2.6.5.3 2.6.5.4 2.6.5.5 2.6.5.6 2.6.6 2.6.6.1
2.6.6.2
2.6.6.3 2.6.6.4 2.6.7 2.6.8
Trauma . . . . . . . . . . . . . . . . . . . . . . . . . Infection . . . . . . . . . . . . . . . . . . . . . . . Dissections . . . . . . . . . . . . . . . . . . . . . Other Possible Causes . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Conservative Treatment . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Endovascular Treatment of Carotid Stenosis . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Indications for Surgery – Indications for Angioplasty . . . . . Types of Stents . . . . . . . . . . . . . . . . . . Brain Protection Devices . . . . . . . . . Distal Occlusion Balloon (Theron’s System, PercuSurge GuardWire® Medtronic) (Fig. 2.6.5) . . . . . . . . . . . . . . . . . . . . . . Filters . . . . . . . . . . . . . . . . . . . . . . . . . . Proximal Occlusion System . . . . . . Preoperative Evaluation . . . . . . . . . . Neurological Examination . . . . . . . Special Imaging Examination . . . . Duplex Ultrasound . . . . . . . . . . . . . . Digital Subtraction Angiography (DSA) . . . . . . . . . . . . . . . . . . . . . . . . . . Magnetic Resonance Angiography (MRA) (Fig. 2.6.10) . . Brain Computed Tomography (CT) . . . . . . . . . . . . . . . . . . . . . . . . . . . Technique . . . . . . . . . . . . . . . . . . . . . . Step 1: Approach to the Common Carotid Artery Access Site . . . . . . . . . . . . . . . . . . . . . . . . . . . . Step 2: Cannulation of the Common Carotid Artery (Fig. 2.6.12) . . . . . . . . . . . . . . . . . . . . . Step 3: Angioplasty and Stenting . . Step 4: Control Angiography . . . . . Peri-operative Monitoring . . . . . . . Complications . . . . . . . . . . . . . . . . . .
174 174 174 174 175 175 175
2.6.8.1 2.6.8.2 2.6.8.3 2.6.8.4
175 176 176 177 179
2.6.9 2.6.10
181 181 181 183 184
2.6.8.5 2.6.8.6 2.6.8.7
2.7 2.7.1 2.7.2 2.7.3 2.7.4 2.7.5 2.7.6 2.7.6.1
2.7.6.2 184 184 186 187 188 188 188
2.7.7 2.7.7.1 2.7.7.2 2.7.8
2.8 188 189 189 190
190
2.8.1 2.8.2 2.8.2.1 2.8.2.2 2.8.3 2.8.4
191 192 193 193 193
2.8.4.1 2.8.4.2
Technical Failure . . . . . . . . . . . . . . . . Contrast Encephalopathy . . . . . . . . Access Site Complications . . . . . . . . Hyperperfusion Syndrome (Fig. 2.6.16) . . . . . . . . . . . . . . . . . . . . . Hypotension and Bradycardia . . . Embolic Complication . . . . . . . . . . . Complications Involving Brain Protection Devices . . . . . . . . . . . . . . Follow-up . . . . . . . . . . . . . . . . . . . . . . Carotid Angioplasty and Stenting (CAS): Present and Future References . . . . . . . . . . . . . . . . . . . . . . Carotid body tumour . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition of the Disease . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Additional Useful Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Conservative therapy . . . . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . Combined Treatment of Coronary Plus Other Arterial Pathologies: the Magnitude of the Polyatherosclerotic Patient . . . Introduction . . . . . . . . . . . . . . . . . . . . The Magnitude of Multifocal Arterial Disease . . . . . . . . . . . . . . . . . Material and Methods . . . . . . . . . . . Results . . . . . . . . . . . . . . . . . . . . . . . . . Multifocal Occlusive and Aneurysmal Arterial Disease . Multifocal Carotid and Coronary Occlusive Disease . . . . . Material and Methods . . . . . . . . . . . Results . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgements . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
193 193 193 193 194 194 195 195 196 197 201 201 201 201 202 202 203
203 205 206 206 206 208 208
209 209 209 209 209 211 212 213 214 214 214
XVII
XVIII
Contents
Upper Extremity Arteries 3.1 3.1.1 3.1.2 3.1.2.1 3.1.2.2 3.1.2.3 3.1.2.4 3.1.3 3.1.3.1 3.1.3.2 3.1.3.3 3.1.3.4 3.1.3.5 3.1.4 3.1.4.1 3.1.4.2 3.1.4.3 3.1.5 3.1.5.1 3.1.5.2 3.1.5.3 3.1.6 3.1.6.1 3.1.6.2 3.1.6.3 3.1.6.4 3.1.7 3.1.7.1 3.1.7.2 3.1.7.3 3.1.8 3.1.9
3.2 3.2.1 3.2.1.1 3.2.1.2 3.2.1.3 3.2.1.4 3.2.1.5 3.2.2 3.2.2.1
Upper Extremity Occlusive Disease . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Types of Upper Extremity Occlusive Disease . . . . . . . . . . . . . . . Acute and Chronic Ischaemia . . . . Raynaud’s Phenomenon . . . . . . . . . Trophic Lesions . . . . . . . . . . . . . . . . . Differential Diagnosis of Upper Extremity Occlusive Disease . . . . . Embolism . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Occlusive Arterial Disease . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Proximal Arterial Disease . . . . . . . . Distal Arterial Disease . . . . . . . . . . . Aneurysms . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Arteriovenous Fistulae . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Investigations . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Vascular Trauma . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Iatrogenic Aetiologies . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Vasospastic Disorders of the Upper Extremities . . . . . . . . . Raynaud’s Syndrome . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Hyperhidrosis . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . .
219 219 219 219 219 220 220 220 220 220 220 221 221 222 222 222 226 232 232 232 232 232 232 233 233 233 233 233 233 233 233 234 234
237 237 237 237 237 237 239 240 240
3.2.2.2 3.2.2.3 3.2.2.4 3.2.3 3.2.3.1 3.2.3.2 3.2.3.3 3.2.3.4 3.2.4 3.2.4.1 3.2.4.2 3.2.4.3 3.2.4.4 3.2.5 3.2.5.1 3.2.5.2 3.2.5.3 3.2.6 3.2.6.1 3.2.6.2 3.2.6.3 3.2.6.4 3.2.6.5
3.3 3.3.1 3.3.2 3.3.2.1 3.3.2.2 3.3.2.3 3.3.2.4 3.3.2.5 3.3.3
3.3.3.1 3.3.3.2 3.3.3.3 3.3.3.4 3.3.4
3.3.4.1 3.3.4.2 3.3.5
Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Acrocyanosis . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Livedo Reticularis . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Cold Hypersensitivity . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Complex Regional Pain Syndrome . . . . . . . . . . . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
240 240 241 242 242 242 242 243 243 243 243 243 243 243 243 244 244
Thoracic Outlet Syndrome . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Neurogenic Thoracic Outlet Compression Syndrome (N-TOCS) Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Clinical Examination . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Arterial Thoracic Outlet Compression Syndrome (A-TOCS) . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Investigations/Examination . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . A Case Apart: Primary Subclavian–Axillary Vein Thrombosis . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Primary SVT . . . . . . . . . . . . . . . . . . . Summary . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
247 247
245 245 245 245 245 245 246
247 247 247 247 248 248
251 251 251 251 251
254 254 254 256 256
Contents
3.4 3.4.1 3.4.2 3.4.2.1 3.4.2.2 3.4.3 3.4.3.1
3.4.4 3.4.4.1 3.4.4.2 3.4.4.3 3.4.5
Traumatic Injury of Upper Extremity Arteries . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Penetrating Trauma . . . . . . . . . . . . . Blunt Trauma . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Conservative Therapy . . . . . . . . . . . Endovascular Therapy . . . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
257 257 257 257 257 257
257 258 258 258 258 259 260
4.2.3.5 4.2.3.6 4.2.3.7 4.2.4 4.2.4.1 4.2.4.2 4.2.5 4.2.5.1 4.2.5.2 4.2.6 4.2.6.1
4.2.6.2 4.2.6.3 4.2.7
Thoracic Aorta 4.1 4.1.1 4.1.2 4.1.3 4.1.3.1 4.1.3.2 4.1.4 4.1.4.1 4.1.4.2 4.1.4.3 4.1.5 4.1.5.1 4.1.6 4.1.7
4.2 4.2.1 4.2.2 4.2.3 4.2.3.1 4.2.3.2
4.2.3.3 4.2.3.4
Thoracoabdominal Aneurysms . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Investigations . . . . . . . . . . . . . . . . . . . Imaging . . . . . . . . . . . . . . . . . . . . . . . . Additional Investigations . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Operative Repair . . . . . . . . . . . . . . . . Open Surgery: Operative Technique . . . . . . . . . . . . . . . . . . . . . . Open Surgery: Adjuvant Techniques . . . . . . . . . . . . . . . . . . . . . Endovascular Intervention . . . . . . . Visceral Hybrid Procedure . . . . . . . Outcome . . . . . . . . . . . . . . . . . . . . . . . Summary and Conclusions . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
265 265 265 266 266 266 267 267
Aortic Dissection . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Association with Atherosclerotic Disease . . . . . . . . . . . . . . . . . . . . . . . . . Association with Genetic Disease/Congenital Malformations . . . . . . . . . . . . . . . . . . Association with Trauma . . . . . . . . Other Associations . . . . . . . . . . . . . .
277 277 277 277
267 267 269 269 271 272 273
277
277 277 277
4.2.8 4.2.8.1 4.2.8.2
4.3 4.3.1 4.3.2 4.3.2.1 4.3.2.2 4.3.2.3 4.3.3 4.3.3.1 4.3.3.2 4.3.4 4.3.5 4.3.5.1
4.3.6 4.3.6.1 4.3.6.2
Localization . . . . . . . . . . . . . . . . . . . . Classification . . . . . . . . . . . . . . . . . . . Factors Determining Extension of Dissection . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Stanford Type A . . . . . . . . . . . . . . . . Stanford Type B . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Type A . . . . . . . . . . . . . . . . . . . . . . . . . Type B . . . . . . . . . . . . . . . . . . . . . . . . . Diagnosis/Investigation . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Additional Useful Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . . Clinical Judgement . . . . . . . . . . . . . . Prognosis of Acute or Subacute Aortic Dissection Without Treatment . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Treatment of Type A Aortic Dissection . . . . . . . . . . . . . . . . . . . . . . Treatment of Type B Aortic Dissection . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Trauma of the Thoracic Aorta . . . . Introduction . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Automobile-related Incidences . . . Blunt Thoracic Trauma . . . . . . . . . . Outcome . . . . . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Anatomy . . . . . . . . . . . . . . . . . . . . . . . Mechanism of Pathology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Endovascular Approach . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
278 278 279 282 282 282 283 283 283 285
285 285 285
289 289 289 290 296 299 299 299 299 299 300 300 300 301 301 302
302 306 306 309 312
XIX
XX
Contents
Abdominal Aorta and Iliac Arteries 5.1 5.1.1 5.1.2 5.1.3 5.1.3.1 5.1.3.2 5.1.3.3 5.1.3.4 5.1.3.5 5.1.4 5.1.4.1 5.1.4.2 5.1.4.3 5.1.5 5.1.5.1
5.1.5.2 5.1.6 5.1.6.1 5.1.6.2 5.1.6.3 5.1.6.4 5.1.7 5.1.8
5.2
5.2.1 5.2.2 5.2.2.1 5.2.3 5.2.3.1
5.3 5.3.1 5.3.2 5.3.3 5.3.4 5.3.4.1
Abdominal Aortic Aneurysm (AAA) . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Risk Factors . . . . . . . . . . . . . . . . . . . . Prevalence . . . . . . . . . . . . . . . . . . . . . . Incidence of AAA Rupture . . . . . . . Disease Progression . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Expanding Aneurysm . . . . . . . . . . . Inflammatory AAA . . . . . . . . . . . . . . Rupture . . . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Aspects on Screening . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Open Surgery . . . . . . . . . . . . . . . . . . . Endovascular Aortic Repair (EVAR) . . . . . . . . . . . . . . . . . . . . . . . . Rupture and Reconstruction . . . . . Outcome . . . . . . . . . . . . . . . . . . . . . . . Possible Complications of Surgery . . . . . . . . . . . . . . . . . . . . . . Practical Recommendations . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
317 317 317 317 318 318 319 319 320 320 320 320 320 321
5.3.4.2 5.3.4.3 5.3.5 5.3.5.1 5.3.5.2 5.3.6 5.3.6.1
5.3.7 5.3.7.1 5.3.7.2
5.4
5.4.1 5.4.2 321 321 322 322 322 322 323 323 323 323
Treatment Options for Abdominal Aortic Aneurysm (AAA) . . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Open Repair . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Endovascular Repair . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
325 325 325 327 327 328 329
Inflammatory Aneurysms of the Abdominal Aorta . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Extension of Inflammation . . . . . . .
331 331 331 332 333 333
5.4.2.1 5.4.2.2 5.4.3 5.4.3.1 5.4.3.2 5.4.3.3 5.4.3.4 5.4.4
5.5 5.5.1 5.5.2 5.5.3 5.5.3.1 5.5.4 5.5.5 5.5.6 5.5.6.1 5.5.6.2 5.5.7 5.5.7.1 5.5.7.2
Infection . . . . . . . . . . . . . . . . . . . . . . . Autoimmune Disease . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Literature . . . . . . . . . . . . . . . . . . . . . . . Rupture . . . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Endovascular Treatment . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Universally Challenging Situations . . . . . . . . . . . . . . . . . . . . . . Vascular Access Morphology . . . . . Aortic Aneurysm Configuration . . Special Challenging Situations . . . . The Case of Aortic Arch Aneurysm . . . . . . . . . . . . . . . . . . . . . . The Case of Aortic Dissection . . . . The Case of Aortic Bronchial and Enteric Fistula . . . . . . . . . . . . . . Other Challenging Cases for EVAR . . . . . . . . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Aortoiliac Occlusive Disease . . . . . Basics . . . . . . . . . . . . . . . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Morphological Features in the Chronic Forms . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Chronic AIOD . . . . . . . . . . . . . . . . . . Acute AIOD . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard . . . . . . . . . . . . . . . . . . . . . . . Additional/Useful Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . .
333 333 333 334 334 334
335 336 336 338 341
343 343 343 343 343 347 347 347 349 350 350 351 355 355 355 355 356 357 357 358 358 359 359 359 360
Contents
5.5.8 5.5.8.1 5.5.8.2 5.5.9 5.5.9.1 5.5.9.2 5.5.10 5.5.11 5.5.11.1 5.5.11.1 5.5.11.2 5.5.11.3
5.5.11.4 5.5.11.5 5.5.11.6 5.5.11.7 5.5.11.8 5.5.11.9 5.5.11.10 5.5.11.11 5.5.11.12
5.6
5.6.1 5.6.2 5.6.2.1
Treatment . . . . . . . . . . . . . . . . . . . . . . Conservative Treatment . . . . . . . . . Endovascular and Surgical Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . In the Case of Chronic AIOD . . . . In the Case of Acute AIOD . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Surgical and Endovascular Principle . . . . . . . . . . . . . . . . . . . . . . . Aortoiliac Angioplasty and Stenting . . . . . . . . . . . . . . . . . . . . . . . . Unilateral and Bilateral Aortofemoral By-pass . . . . . . . . . . . Unilateral or Bilateral Aortoiliac By-pass . . . . . . . . . . . . . . . . . . . . . . . . . Aortic Exclusion and Bilateral Aortoiliac or Bilateral Aortofemoral Prosthetic Reconstruction . . . . . . . . . . . . . . . . . Unilateral or Bilateral Thoracoiliofemoral By-pass . . . . . . Aortoiliac Endarterectomy . . . . . . . Iliofemoral By-pass . . . . . . . . . . . . . . Femoro-femoral Cross-over By-pass . . . . . . . . . . . . . . . . . . . . . . . . . Unilateral or Bilateral Axillofemoral By-pass . . . . . . . . . . . Retrograde Femoral Embolectomy . . . . . . . . . . . . . . . . . . . New Surgical Trends . . . . . . . . . . . . . Aortobifemoral Video-assisted By-pass with Hand-Port System . . Aortobifemoral Totally Laparoscopic By-pass with Coggia’s Technique . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Operative Procedures . . . . . . . . . . . . Laparoscopy-Assisted Operative Procedures with Vascular Suturing by the Minimally Invasive Route . . . . . . . . . . . . . . . . . .
360 360
5.6.3 5.6.3.1
361 363 363 363 363
5.6.3.2 5.6.3.3 5.6.3.4
364 364
5.6.4 5.6.4.1
365
5.6.4.2
366 5.6.5 5.6.5.1 5.6.5.2 367 367 368 368
5.6.6 5.6.7
5.7 368 369 369 370 371
372 373
5.7.1 5.7.2 5.7.3 5.7.4 5.7.5 5.7.6 5.7.7 5.7.8 5.7.9 5.7.10
375 375 375
Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Indications . . . . . . . . . . . . . . . . . . . . . Contraindications . . . . . . . . . . . . . . . Preoperative Management . . . . . . . Procedure . . . . . . . . . . . . . . . . . . . . . . Results and Complications . . . . . . . Patency of the Femoro-femoral Crossover By-pass . . . . . . . . . . . . . . Local Wound Complications, Graft Infection and Morbidity . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
377
377 379 380 380 381 381
381 382 382 382 383 384 384
387 387 387 387 388 388 388 389 390 391 395 395
Visceral Arteries 6.1
375
Totally Laparoscopic Operative Procedures . . . . . . . . . . . . . . . . . . . . . Retrocolic or Prerenal Transperitoneal Procedure as Described by Coggia [8, 11] . . . . . . Combined Transperitoneal and Retroperitoneal Procedures . . Retroperitoneal Operation . . . . . . . Direct Transperitoneal Procedure [7] . . . . . . . . . . . . . . . . . . . Instrumentation . . . . . . . . . . . . . . . . . Standard Laparoscopic Instruments . . . . . . . . . . . . . . . . . . . . Specific Laparoscopic Instruments for Vascular Laparoscopy . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Intraoperative Complications . . . . Early Postoperative Complications . . . . . . . . . . . . . . . . . . Current Indications and Results . . Conclusions . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
6.1.1 6.1.2 6.1.3
Occlusive Disease of the Coeliac and Superior Mesenteric Arteries . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . .
401 401 401 401
XXI
XXII
Contents
6.1.4 6.1.5 6.1.5.1
Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Additional Useful Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Angioplasty . . . . . . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
402 402
6.2 6.2.1 6.2.2 6.2.3 6.2.4 6.2.5 6.2.6 6.2.7 6.2.7.1 6.2.7.2 6.2.8
Visceral Artery Aneurysms . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Endovascular Therapy . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
411 411 411 411 412 412 413 413 413 414 414 415
6.3
Acute Ischaemia of the Visceral Arteries . . . . . . . . . . . . . . . . . . . . . . . . Acute Intestinal Ischaemia . . . . . . . Basics . . . . . . . . . . . . . . . . . . . . . . . . . . Acute Thrombotic or Embolic Arterial Occlusion . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Mesenteric Venous Thrombosis . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . Intestinal Ischaemia after Aortoiliac Surgery . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Acute Renal Ischaemia . . . . . . . . . . .
6.1.5.2 6.1.6 6.1.6.1 6.1.6.2 6.1.7
6.3.1 6.3.1.1 6.3.2 6.3.2.1 6.3.2.2 6.3.2.3 6.3.2.4 6.3.2.5 6.3.3 6.3.3.1 6.3.3.2 6.3.3.3 6.3.3.4 6.3.4 6.3.4.1 6.3.4.2 6.3.4.3 6.3.4.4 6.3.5
6.3.5.1 6.3.5.2
Thrombosis . . . . . . . . . . . . . . . . . . . . . Embolism . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
422 422 423
402
Lower Extremity Arteries 403 403 404 406 408 408
417 417 417 417 417 417 418 418 419 419 419 420 420 420 420 420 421 421 421 422
7.1 7.1.1 7.1.2 7.1.2.1 7.1.2.2 7.1.2.3 7.1.2.4 7.1.3
7.2 7.2.1 7.2.2 7.2.3 7.2.4 7.2.4.1 7.2.4.2 7.2.4.3 7.2.5 7.2.6 7.2.7 7.2.7.1 7.2.7.2 7.2.7.3
7.3 7.3.1 7.3.2 7.3.3 7.3.4 7.3.4.1 7.3.4.2 7.3.4.3 7.3.5 7.3.5.1 7.3.5.2 7.3.5.3 7.3.5.4
Lower Limb Arterial Recanalization . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Problems and Questions . . . . . . . . . Solved Problems . . . . . . . . . . . . . . . . Unsolved Problems . . . . . . . . . . . . . . Permanent Problems . . . . . . . . . . . . Arising Questions . . . . . . . . . . . . . . . Conclusions . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . .
427 427 427 428 428 430 430 432 433
Femorodistal By-pass Surgery . . . . Introduction . . . . . . . . . . . . . . . . . . . . General Considerations . . . . . . . . . . Operative Indications . . . . . . . . . . . . Technical Considerations . . . . . . . . Proximal Anastomotic Site . . . . . . . Graft Material . . . . . . . . . . . . . . . . . . . Distal Anastomotic Site (Fig. 7.2.3) . . . . . . . . . . . . . . . . . . . . . . Special Considerations . . . . . . . . . . . Graft Surveillance . . . . . . . . . . . . . . . Results . . . . . . . . . . . . . . . . . . . . . . . . . Survival . . . . . . . . . . . . . . . . . . . . . . . . Graft Patency and Limb Salvage . . Quality of Life . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
437 437 437 438 438 438 439 441 442 443 443 443 443 445 445
Acute Ischaemia of the Lower Extremities . . . . . . . . . . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Embolism . . . . . . . . . . . . . . . . . . . . . . Thrombosis . . . . . . . . . . . . . . . . . . . . . Trauma . . . . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . Paraesthesia . . . . . . . . . . . . . . . . . . . . Paralysis . . . . . . . . . . . . . . . . . . . . . . . . Pallor . . . . . . . . . . . . . . . . . . . . . . . . . .
449 449 449 449 449 449 450 451 451 451 451 451 452
Contents
7.3.5.5 7.3.6 7.3.7 7.3.7.1
7.3.7.2 7.3.8 7.3.8.1 7.3.8.2 7.3.8.3 7.3.9 7.3.10
7.4 7.4.1 7.4.2 7.4.2.1 7.4.2.2 7.4.2.3 7.4.2.4 7.4.2.5 7.4.2.6 7.4.2.7 7.4.3 7.4.3.1 7.4.3.2 7.4.3.3 7.4.3.4 7.4.3.5 7.4.3.6 7.4.4 7.4.4.1 7.4.4.2 7.4.4.3 7.4.4.4 7.4.4.5 7.4.4.6 7.4.5 7.4.5.1 7.4.5.2 7.4.5.3 7.4.5.4
Pulselessness . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Additional Useful Diagnostic Procedures . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Conservative Treatment . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Thrombolytic Therapy . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Lower Extremity Aneurysms . . . . . Basic Concepts . . . . . . . . . . . . . . . . . . Popliteal Aneurysms (PA) . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . Aneurysms of the Common Femoral Artery . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . Aneurysms of the Superficial Femoral Artery . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . Aneurysms of the Distal Branches . . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Clinical Symptoms . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . Therapy . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . .
452 452 452
452 453 453 453 453 455 457 457 457 459 459 459 460 460 460 460 460 461 462 462 462 462 463 464 464 466
7.5 7.5.1 7.5.2 7.5.3 7.5.4 7.5.5 7.5.6 7.5.6.1
7.5.7 7.5.7.1 7.5.7.2 7.5.7.3 7.5.7.4
7.6
7.6.1 7.6.2 7.6.3 7.6.4 7.6.4.1
7.6.5 7.6.5.1 7.6.6
7.7 466 466 467 467 467 467 467 468 468 468 468 468 468
7.7.1 7.7.1.1 7.7.1.2
7.7.2 7.7.2.1 7.7.2.2 7.7.2.3 7.7.3 7.7.3.1
Buerger’s Disease of the Lower Extremities . . . . . . . . . . . . . . . . . . . . . Synonym . . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Conservative Treatment . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Popliteal Artery Entrapment and Popliteal Adventitial Cystic Disease . . . . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Recommended European Standard Surgical Procedures . . . . Special Remarks . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Vascular Trauma of the Lower Limb . . . . . . . . . . . . . . . . . . . . . . . . . . . The Problem . . . . . . . . . . . . . . . . . . . . Encountering Vascular Injury . . . . How Can Ischaemia of the Lower Limb be Detected or Ruled Out Reliably? . . . . . . . . . . . Mechanisms of Injury . . . . . . . . . . . Sharp Injury . . . . . . . . . . . . . . . . . . . . Blunt injury . . . . . . . . . . . . . . . . . . . . . Iatrogenic . . . . . . . . . . . . . . . . . . . . . . Consequences of Arterial Injury of the Lower Limb . . . . . . . . . . . . . . Compartment Syndrome . . . . . . . .
471 471 471 471 471 472 473
473 476 476 476 477 477 477
479 479 479 479 480
480 481 481 483 484
485 485 486
486 488 488 488 490 493 493
XXIII
XXIV
Contents
7.7.3.2 7.7.4
7.7.5
False Aneurysms and ArterioVenous Fistulas . . . . . . . . . . . . . . . . . The Management of Vascular Trauma (With Special Reference to the Knee Joint) . . . . . . . . . . . . . . . Bulleted Summary . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
494
494 497 497
Diabetic Foot 8.1 8.1.1 8.1.2 8.1.2.1 8.1.2.2 8.1.2.3 8.1.3 8.1.3.1 8.1.3.2 8.1.4 8.1.4.1 8.1.4.2 8.1.4.3 8.1.4.4 8.1.5 8.1.5.1 8.1.5.2 8.1.5.3 8.1.5.4 8.1.6 8.1.7 8.1.7.1 8.1.7.2 8.1.7.3 8.1.7.4 8.1.7.5 8.1.7.6 8.1.7.7 8.1.8
Diabetic Foot . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Foot Ulcers . . . . . . . . . . . . . . . . . . . . . Amputation . . . . . . . . . . . . . . . . . . . . . Social and Economic Costs . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Pathogenesis of the Neuropathic Ulcer . . . . . . . . . . . . . . . . . . . . . . . . . . . Pathogenesis of the Ischaemic Ulcer . . . . . . . . . . . . . . . . . . . . . . . . . . . Complications: NeuroOsteoarthropathy . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Symptoms/Investigations/ Diagnosis/Treatment . . . . . . . . . . . . Diagnosis/Investigations . . . . . . . . . Clinical Examination . . . . . . . . . . . . Circulation . . . . . . . . . . . . . . . . . . . . . Paraclinical Evaluation . . . . . . . . . . Classification Systems . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Infections . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Pathophysiology . . . . . . . . . . . . . . . . Microbiology . . . . . . . . . . . . . . . . . . . Clinical Presentation . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Severity Classification . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Treatment of the Diabetic Ulcer . . References . . . . . . . . . . . . . . . . . . . . . .
9.1.1 9.1.1.1 9.1.2 9.1.3 9.1.3.1 9.1.3.2 9.1.4 9.1.4.1
501 501 501 501 501 502 503
9.1.4.2 9.1.5 9.1.6 9.1.6.1 9.1.6.2 9.1.6.3 9.1.6.4
503 505 506 506 506 507 507 507 507 508 509 509 509 510 510 511 512 512 513 514 515 517 518
9.1.6.5 9.1.6.6 9.1.6.7 9.1.7 9.1.8
Introduction . . . . . . . . . . . . . . . . . . . . Scope of the Problem . . . . . . . . . . . . Incidence and Morbidity of Amputation . . . . . . . . . . . . . . . . . . Classification and Indications . . . . Emergency Amputation . . . . . . . . . Elective Amputations . . . . . . . . . . . . Determination of Amputation Level . . . . . . . . . . . . . . . . . . . . . . . . . . . Transcutaneous Oxygen Tension (PtCO2) Measurement . . . . . . . . . . . Clearance of [133Xe] . . . . . . . . . . . . . Preoperative Management . . . . . . . Surgical Techniques of Amputation . . . . . . . . . . . . . . . . . . . . Toe Amputation . . . . . . . . . . . . . . . . . Ray Amputation . . . . . . . . . . . . . . . . Transmetatarsal Amputation . . . . . Syme’s Amputation (Ankle Disarticulation) . . . . . . . . . . Below-knee Amputation . . . . . . . . . Above-knee Amputation . . . . . . . . . Amputation of the Upper Extremity . . . . . . . . . . . . . . . . . . . . . . Postoperative Considerations and Rehabilitation . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
525 525 525 526 526 526 527 528 528 528 528 528 529 530 531 532 533 534 534 535 535
Venous Diseases 10.1 10.1.1 10.1.2 10.1.2.1 10.1.2.2 10.1.2.3 10.1.3 10.1.3.1 10.1.3.2 10.1.3.3 10.1.3.4 10.1.3.5 10.1.3.6
Chronic Venous Insufficiency . . . . Introduction . . . . . . . . . . . . . . . . . . . . Functional Anatomy and Physiology of the Venous System . . Superficial Veins . . . . . . . . . . . . . . . . Deep Veins . . . . . . . . . . . . . . . . . . . . . Perforating Veins . . . . . . . . . . . . . . . . Chronic Venous Insufficiency . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Conclusion . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
539 539 539 539 539 539 539 539 540 541 543 545 549 549
Deep Venous Thrombosis . . . . . . . . Epidemiology/Aetiology . . . . . . . . .
551 551
Amputations 9.1
Amputation of Extremities . . . . . . .
525
10.2 10.2.1
Contents
10.2.2 10.2.3 10.2.3.1 10.2.3.2 10.2.3.3 10.2.4 10.2.4.1 10.2.4.2 10.2.4.3 10.2.5 10.2.6
Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Clinical Signs . . . . . . . . . . . . . . . . . . . Laboratory Tests and Imaging . . . . Recommended European Standard . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Conservative Treatment of DVT . . Invasive Treatment of DVT . . . . . . Prevention of DVT . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
551 551 551 552 552 552 552 553 556 556 557 557
12.1.6 12.1.6.1 12.1.6.2 12.1.7 12.1.7.1 12.1.7.2 12.1.7.3 12.1.8
Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Examination . . . . . . . . . . . . . . . . . . . Laboratory Investigations and Imaging . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Treatment According to the Type of the Malformation . . . . . . . . . . . . . Conservative Treatment . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
580 580 580 581 581 582 583 583 583
Angioaccess Surgery Lymphatics 11.1 11.1.1 11.1.1.1 11.1.1.2 11.1.2 11.1.3 11.1.3.1 11.1.3.2 11.1.4 11.1.5 11.1.5.1 11.1.5.2 11.1.5.3 11.1.6 11.1.6.1 11.1.6.2
Lymphoedema . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Capillary Microcirculation . . . . . . . Capillary Circulation and Limb Oedema . . . . . . . . . . . . . . . . . . . . . . . . Definition of Lymphoedema . . . . . Aetiology/Epidemiology . . . . . . . . . Primary Lymphoedema . . . . . . . . . . Secondary Lymphoedema . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . History and Examination . . . . . . . . Laboratory Tests . . . . . . . . . . . . . . . . Imaging . . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Conservative Treatment . . . . . . . . . Surgery . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
13.1 561 561 561 562 563 563 563 565 566 566 566 567 567 568 568 568 570
Arteriovenous Malformations 12.1 12.1.1 12.1.2 12.1.2.1 12.1.3 12.1.3.1 12.1.4 12.1.4.1 12.1.5 12.1.5.1 12.1.5.2
Arteriovenous Malformations . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Terminology . . . . . . . . . . . . . . . . . . . . Epidemiology . . . . . . . . . . . . . . . . . . . Classification . . . . . . . . . . . . . . . . . . . Aetiology . . . . . . . . . . . . . . . . . . . . . . . Embryology and Anatomy . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Vascular Bone Syndrome . . . . . . . . Specific Vascular Malformations . .
573 573 573 573 573 573 575 575 576 576 577
13.1.1 13.1.2 13.1.2.1 13.1.2.2 13.1.2.3 13.1.2.4 13.1.3 13.1.3.1 13.1.3.2
Vascular Access to Patients in Haemodialysis . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Urgent (Acute) Haemodialysis . . . . External A–V Shunt . . . . . . . . . . . . . Subclavian Catheters . . . . . . . . . . . . Jugular Catheters . . . . . . . . . . . . . . . . Femoral Catheters . . . . . . . . . . . . . . . Chronic Haemodialysis . . . . . . . . . . Internal A–V Shunt (A–V Fistula) . . . . . . . . . . . . . . . . . . . . . . . . . Arteriovenous Grafts . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
587 587 587 587 588 588 589 589 589 591 594
Multidisciplinary Vascular Issues 14.1 14.1.1 14.1.2 14.1.2.1 14.1.2.2 14.1.2.3 14.1.3 14.1.4 14.1.5 14.1.6 14.1.6.1 14.1.6.2 14.1.6.3 14.1.6.4 14.1.7 14.1.7.1
Infections in Vascular Surgery . . . . Introduction . . . . . . . . . . . . . . . . . . . . Pathogenesis of Infection . . . . . . . . Pathogen Virulence . . . . . . . . . . . . . Host Response . . . . . . . . . . . . . . . . . . Device Factors . . . . . . . . . . . . . . . . . . Microbiology and Diagnosis . . . . . Imaging . . . . . . . . . . . . . . . . . . . . . . . . Antimicrobial Therapy . . . . . . . . . . . Prevention . . . . . . . . . . . . . . . . . . . . . . Primary Prophylaxis . . . . . . . . . . . . . Local Antibiotic Prophylaxis . . . . . Secondary Prophylaxis . . . . . . . . . . . Other Measures of Prevention . . . . Infections in Specific Vascular Implants . . . . . . . . . . . . . . . . . . . . . . . Prosthetic Graft Infections (PGI) . .
597 597 597 597 598 598 598 599 599 600 600 602 602 602 602 602
XXV
XXVI
Contents
14.1.7.2 14.1.7.3 14.1.7.4 14.1.7.5 14.1.7.6
14.2 14.2.1 14.2.2 14.2.2.1 14.2.2.2 14.2.3 14.2.3.1 14.2.3.2 14.2.4
14.3 14.3.1 14.3.2 14.3.2.1 14.3.3 14.3.3.1 14.3.3.2 14.3.3.3 14.3.4
14.4
Peripheral Vascular Stent Infections (PVSIs) . . . . . . . . . . . . . . . Prosthetic Carotid Patches Infections (PCPIs) . . . . . . . . . . . . . . Arterial Closure Devices Infections . . . . . . . . . . . . . . . . . . . . . . Venal Caval Filter Infections . . . . . Infections of Haemodialysis Prosthetic Grafts and Autologous Arteriovenous Fistulas (HPGFIs) . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Vascular Problems in Urological Surgery . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Vascular Lesions on Preoperative Evaluation . . . . . . Abdominal Aortic Aneurysm (AAA) . . . . . . . . . . . . . . . . . . . . . . . . . Renal Tumours Involving the Vena Cava . . . . . . . . . . . . . . . . . . Unexpected – Iatrogenic Vascular Injuries . . . . . . . . . . . . . . . . Venous Injuries . . . . . . . . . . . . . . . . . Arterial Injuries . . . . . . . . . . . . . . . . . Bulleted Summary . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Vascular Trauma in Orthopaedic Surgery . . . . . . . . . . . . . . . . . . . . . . . . Introduction . . . . . . . . . . . . . . . . . . . . Basic Principles in Microvascular Surgery . . . . . . . . Basic Microvascular Techniques . . Application of Microvascular Surgery to Trauma Orthopaedics . . Replantation . . . . . . . . . . . . . . . . . . . . Major Limb Revascularization and Replantation . . . . . . . . . . . . . . . . Open Fractures – Type IIIb and IIIc . . . . . . . . . . . . . . . . . . . . . . . . Vascular Complication in Orthopaedic Patients . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . Treatment of Aortic Arch Diseases . . . . . . . . . . . . . . . . . . . . . . . .
14.4.1 604 607 608 609
609 611
615 615 615 615 616 618 618 619 620 620
623 623 623 624 626 626 630 634 635 635
639
14.4.1.1 14.4.1.2 14.4.2 14.4.2.1 14.4.2.2 14.4.2.3 14.4.2.4 14.4.2.5 14.4.2.6 14.4.2.7 14.4.2.8 14.4.3 14.4.3.1 14.4.3.2 14.4.3.3 14.4.3.4 14.4.3.5 14.4.4 14.4.5 14.4.5.1 14.4.5.2 14.4.5.3 14.4.5.4 14.4.5.5 14.5.5.6 14.5.5.7 14.4.6 14.4.6.1 14.4.6.2 14.4.6.3 14.4.6.4 14.4.6.5 14.4.7
14.4.7.1 14.4.7.2 14.4.7.3 14.4.7.4 14.4.8 14.4.8.1 14.4.8.2 14.4.8.3 14.4.8.4 14.4.9
Aortic Arch Aneurysms in Coarctation of the Aorta . . . . . . Epidemiology/Aetiology . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Intramural Haematoma . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Obstructed Aortic Arch . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Recurrent Obstruction of the Aortic Arch . . . . . . . . . . . . . . . . . . . . Takayasu’s Arteritis . . . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Aortic Arch Atherosclerotic Aneurysm . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Atheromas and Penetrating Atherosclerotic Ulcerations of the Aortic Arch . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Aortic Arch Thrombosis . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Aortic Arch Trauma . . . . . . . . . . . . .
639 639 640 640 640 640 640 640 640 640 641 641 641 641 641 641 641 642 642 643 643 643 643 644 644 644 645 645 645 645 646 646 647
648 648 648 648 648 649 649 649 649 649 650
Contents
14.4.9.1 14.4.9.2 14.4.9.3 14.4.9.4 14.4.9.5 14.4.9.6 14.4.9.7 14.4.9.8 14.4.9.9 14.4.10 14.4.10.1 14.4.10.2 14.4.10.3 14.4.10.4 14.4.10.5 14.4.10.6 14.4.11 14.4.11.1 14.4.11.2 14.4.11.3 14.4.11.4 14.4.11.5 14.4.11.6
Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Ascending Aortic Dissection . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Marfan’s Syndrome . . . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . .
650 650 650 650 651 651 651 651 652 652 652 652 652 653 653 654 654 654 654 654 654 654 655
14.4.11.7 14.4.11.8 14.4.11.9 14.4.12 14.4.12.1 14.4.12.2 14.4.12.3 14.4.12.4 14.4.12.5 14.4.12.6 14.4.12.7 14.4.12.8 14.4.12.9 14.4.13 14.4.13.1 14.4.13.2 14.4.13.3 14.4.13.4 14.4.13.5 14.4.13.6 14.4.13.7 14.4.13.8
Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Ehlers–Danlos Syndrome . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . Prognosis . . . . . . . . . . . . . . . . . . . . . . . Noonan Syndrome . . . . . . . . . . . . . . Synonyms . . . . . . . . . . . . . . . . . . . . . . Definition . . . . . . . . . . . . . . . . . . . . . . Epidemiology/Aetiology . . . . . . . . . Symptoms . . . . . . . . . . . . . . . . . . . . . . Complications . . . . . . . . . . . . . . . . . . Diagnosis . . . . . . . . . . . . . . . . . . . . . . . Treatment . . . . . . . . . . . . . . . . . . . . . . Differential Diagnosis . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . .
655 655 655 655 655 656 656 656 656 656 656 656 656 656 656 656 656 656 657 657 657 657 657
XXVII
XXIX
List of Contributors
Acosta, Stefan, MD, PhD Department of Vascular Surgery Malmö General Hospital Malmö, Sweden (E-mail:
[email protected])
Barbas, Maria José, MD Hospital Garcia de Orta Servico de Angiologia e Cirurgia Vascular Almada, Portugal (E-mail:
[email protected])
Angelides, Nicos S., MD Cardiovascular and Thoracic Unit Nicosia General Hospital Nicosia, Cyprus (E-mail:
[email protected]
Bastounis, Elias A., MD, PhD First Department of Surgery Athens University Medical School Athens, Greece (E-mail:
[email protected])
Anagnostopoulos, Constantine E., MD, ScD Department of Cardiothoracic Surgery Athens University Medical School Athens, Greece and Columbia University St. Luke’s/Roosevelt Hospital New York New York, USA (E-mail:
[email protected])
Bell, Sir Peter, MD University of Leicester Department of Surgery Robert Kilpatrick Building Leicester Royal Infirmary Leicester, UK (E-mail:
[email protected])
Anagouras, Dimitrios C., MD, FETCS Department of Cardiothoracic Surgery University of Athens School of Medicine Attikon Hospital Center Athens, Greece (E-mail:
[email protected]) Balas, Panagiotis E., MD P. Psihico, Greece (E-mail:
[email protected]) Balzer, Klaus, MD Department of Vascular Surgery Evanglisches Krankenhaus Mülheim Mülheim/Ruhr, Germany (E-mail:
[email protected])
Benedetti-Valentini, Fabrizio, MD Department of Vascular Surgery University of Rome “La Sapienza” Rome, Italy (E-mail:
[email protected]) Berg, Patrick, MD Department of Vascular Surgery Centre Hospitalier Luxembourg (E-mail:
[email protected]) Bergqvist, David, MD, PhD, FRCS Department of Surgical Sciences Uppsala University, Hospital Uppsala, Sweden (E-mail:
[email protected])
XXX
Contributors
Biasi, Giorgio M., MCHiR, FACS, FRCS Department of Surgical Sciences and Intensive Care School of Medicine, University of Milan-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected])
Carmo, Michele, MD Division of Vascular Surgery Ospedale S. Carlo Borromeo University of Milan Milan, Italy (E-mail:
[email protected])
Björck, Martin, MD, PhD Department of Vascular Surgery Academic Hospital Uppsala Uppsala, Sweden (E-mail:
[email protected])
Cau, Jérôme, MD Vascular Surgery Service University Hospital Jean Bernard Poitiers, France (E-mail:
[email protected])
Black, Stephen A., MD Regional Vascular Unit St. Mary’s Hospital London, UK (E-mail:
[email protected])
Chamogeorgakis, Themistocles, MD Department of Cardiothoracic Surgery University of Athens School of Medicine Attikon Hospital Center Athens, Greece (E-mail:
[email protected])
van Bockel, J. Hajo, MD, PhD Department of Vascular Surgery Leiden University Medical Centre Leiden, The Netherlands (E-mail:
[email protected]) Brooks, Marcus J., MD Regional Vascular Unit St. Mary’s Hospital London, UK (E-mail:
[email protected]) Cairols, Marc, MD Servei d’Angiologia I Cirurgia Vascular Hospital Universitari de Bellvitge University of Barcelona Barcelona, Spain (E-mail:
[email protected]) Camesasca, Valter, MD School of Medicine University of Milan-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected])
Cormier, Jean-Michel, MD Division Vascular Surgery St. Joseph-Hospital Paris, France (E-mail:
[email protected]) Daenens, Kim, MD Department of Vascular Surgery University Hospital Gasthuisberg Leuven, Belgium (E-mail:
[email protected]) Dallatana, Raffaello, MD Division of Vascular Surgery Ospedale S. Carlo Borromeo Milan, Italy (E-mail:
[email protected]) Daskalopoulos, Marios E., MSC, DIC, MD Department of Vascular Surgery University of Athens Medical School Athens, Greece (E-mail:
[email protected])
Contributors
Daskalopoulou, Stella S., MsC, DIC, MD, FASA Department of Vascular Surgery University of Athens Medical School Athens, Greece and Department of Clinical Biochemistry and Surgery Royal Free Hospital London, UK (E-mail:
[email protected]) De Angelis, Gianni A. T., MD Division of Vascular Surgery Ospedale S. Carlo Borromeo University of Milan Milan, Italy (E-mail:
[email protected]) Defraigne, Jean-Olivier, MD Department of General and Human Biochemistry and Physiology, Centre Hospitalier Universitaire du Sart Tilman University of Liège, Belgium (E-mail
[email protected]) Deleo; Gaetano, MD School of Medicine University of Milan-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected]) Dimakakos, Panos B., MD Vascular Department-B Surgical Clinic Aretaeion Hospital University of Athens, Athens, Greece (E-mail:
[email protected]) Dzsinich, Csaba, MD, PhD Department of Cardiovascular Surgery Semmelweis University Budapest, Hungary (E-mail:
[email protected]) Farghadani, Hirad, MD Department of Vascular Surgery Centre Hospitalier Luxembourg (E-mail:
[email protected])
Febrer, Guillaume, MD Department of Vascular Surgery University Hospital Poitiers, France (E-mail:
[email protected]) Fernandes e Fernandes, José, MD Professor of Surgery and Chief of Service Department of Vascular Surgery Hospital Santa Maria and Faculty of Medicine Director Instituto Cardiovascular de Lisboa Lisbon, Portugal (E-mail:
[email protected];
[email protected]) Fourneau, Inge, MD Department of Vascular Surgery University Hospital Gasthuisberg Leuven, Belgium (E-mail:
[email protected]) Fraedrich, Gustav, MD Department of Vascular Surgery Medical University of Innsbruck Innsbruck, Austria (E-mail:
[email protected]) Froio, Alberto, MD Vascular Surgery Unit University of Milano-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected]) Geelkerken, Robert H., MD Medisch Spectrum Twente Enschede, The Netherlands (E-mail:
[email protected]) Georgopoulos, Sotiris E. First Department of Surgery Athens University Medical School Athens, Greece (E-mail:
[email protected])
XXXI
XXXII
Contributors
Gerasimidis, Thomas, MD Professor of Vascular Surgery Head of the Fifth Surgical Clinic Aristotle University of Thessaloniki Hippokrateio Hospital Thessaloniki, Greece (E-mail:
[email protected]) Giamarellou, Helen, MD, PhD 4th Department of Internal Medicine and Infectious Diseases Athens University Medical School University General Hospital “ATTIKON” Athens, Greece (E-mail:
[email protected]) Giannopoulos, Aris M., MD First Urology Department University of Athens Medical School, Laiko Hospital Athens, Greece (E-mail:
[email protected]) Golematti, Spyretta, MD, PhD Biomedical Simulations and Imaging Laboratory Faculty of Electrical and Computer Engineering National Technical University of Athens Athens, Greece (E-mail:
[email protected]) Gossetti, Bruno, MD Department of Vascular Surgery Policlinico Umberto 1° University of Rome “La Sapienza” Rome, Italy Goulao, J., MD Hospital Garcia de Orta Servico de Angiologia e Cirurgia Vascular Almada, Portugal (E-mail:
[email protected]) Guillou, Matthieu, MD Department of Vascular Surgery Hospital Jean Bernard Poitiers, France (E-mail:
[email protected])
Heikkinen, Maarit A., MD Division of Vascular Surgery Tampere University Hospital and Tampere University Tampere, Finland (E-mail:
[email protected]) Horrocks, Michael, MD Academic Department of Surgery Royal United Hospital Bath, UK (E-mail:
[email protected]) Horsch, Svante, MD Department of Vascular and Endovascular Surgery Krankenhaus Porz am Rhein Porz, Germany (E-mail:
[email protected]) Kakisis, John D., MD 3rd Department of Surgery Attikon Hospital Athens, Greece (E-mail:
[email protected]) Karamanos, Dimitrios Vascular Surgeon Fifth Surgical Clinic Aristotle University of Thessaloniki Hippokrateio Hospital Thessaloniki, Greece (E-mail:
[email protected]) Katsilambros, Nicholas, MD First Department of Propaedeutic Medicine Athens University Medical School Laiko University Hospital Athens, Greece (E-mail:
[email protected]) Kiskinis, Dimitrios A., MD, PhD Papageorgiou General Hospital Department of Vascular Surgery Aristotle University of Thessaloniki Thessaloniki, Greece (E-mail:
[email protected])
Contributors
Klocker, Josef, MD Department of Vascular Surgery Medical University of Innsbruck Innsbruck, Austria (E-mail:
[email protected])
Laurito, Antonella, MD Department of Vascular Surgery and Service of Nuclear Medicine Policlinico Umberto I, “La Sapienza” University Rome, Italy
Konstantinidis, Konstantinos Vascular Surgeon Fifth Surgical Clinic Aristotle University of Thessaloniki Hippokrateio Hospital Thessaloniki, Greece
Lecis, Alexandre, MD Department of Vascular Surgery University Hospital Jean Bernard Poitiers, France (E-mail:
[email protected])
Kostakis, Alkiviadis, MD Department of Surgery Athens University Medical School Laiko Peripheral General Hospital Athens, Greece (E-mail:
[email protected]) Kotsis, Thomas E., MD Vascular Department-B Surgical Clinic Aretaeion Hospital School of Medicine, University of Athens Athens, Greece (E-mail:
[email protected]) Ktenidis, Kiriakos, MD, PhD, EBSQ-VASC. Papageorgiou General Hospital Ass.Prof. Dr. K. Ktenidis Aristotle University of Thessaloniki 1st Department of Surgery-Vascular Surgery Thessaloniki, Greece (E-mail:
[email protected]) Lamont, Peter, MD, FRCS-EBSQ-VASC Consultant Vascular Surgeon Bristol Royal Infirmary Bristol, UK (E-mail:
[email protected]) Largiadèr, Jon, MD Universitätsspital Zurich Zurich, Switzerland (E-mail:
[email protected])
Lens, Vincent, MD Department of Radiology and Neuroradiology Centre Hospitalier Luxembourg (E-mail:
[email protected]) Liapis, Christos D., MD, FACS, FRCS Department of Vascular Surgery University of Athens Medical School Athens, Greece (E-mail:
[email protected]) Liloia, Angela, MD Department of Surgical Sciences and Intensive Care, School of Medicine University of Milan-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected]) Limet, Raymond R., MD Department of Cardiovascular Surgery University Hospital of Liège CHU Sart-Tilman Liège, Belgium (E-mail:
[email protected]) Lindahl, Anne-Karin, MD Sykehuset Asker og Baerum HF, Norway (E-mail:
[email protected]) Ljungman, Christer, MD, PhD Department of Surgical Sciences, Section Surgery Academic University Hospital Uppsala, Sweden (E-mail:
[email protected])
XXXIII
XXXIV
Contributors
Makrilakis, Constantinos, MD First Department of Propaedeutic Medicine Athens University Medical School Laiko University Hospital Athens, Greece (E-mail:
[email protected]) Mallios, Alexandros Resident in Surgery Fifth Surgical Clinic Aristotle University of Thessaloniki Hippokrateio Hospital Thessaloniki, Greece Mambrini, Simone, MD Unit of Vascular and Endovascular Surgery University Hospital “San Martino” Genoa, Italy (E-mail:
[email protected]) Mansilha, Armando, MD Porto, Portugal (E-mail:
[email protected]) Mantas, Dimitrios, MD Department of Surgery Athens University Medical School Laiko Peripheral General Hospital Athens, Greece (E-mail:
[email protected]) Marchand, Christophe, MD Vascular Surgery Service University Hospital Jean Bernard Poitiers, France (E-mail:
[email protected])
Mataigne, Frédéric, MD Department of Radiology and Neuroradiology Centre Hospitalier Luxembourg (E-mail:
[email protected] Melas, N., MD First Department of Surgery and Vascular Surgery Aristotle University of Thessaloniki Papageorgiou General Hospital Thessaloniki, Greece Menezes, J. Daniel, MD Servico de Angiologia e Cirurgia Vascular Hospital Garcia de Orta Almada, Portugal (E-mail:
[email protected]) Mercandalli, Giulio, MD Division of Vascular Surgery Ospedale S. Carlo Borromeo University of Milan Milan, Italy (E-mail:
[email protected]) Metcalfe, James, MD Academic Department of Surgery Royal United Hospital Bath, UK (E-mail:
[email protected]) Metz René, MD Department of Neurology Centre Hospitalier Luxembourg (E-mail:
[email protected])
Martinelli, Ombretta, MD Department of Vascular Surgery Policlinico Umberto I° University of Rome “La Sapienza” Rome, Italy
Mikhailidis, Dimitri P., MD, FASA, FFPM, FRCP, FRCPATH Department of Clinical Biochemistry (Vascular Disease Prevention Clinics) and Department of Surgery, Royal Free Hospital London, UK (E-mail:
[email protected])
Massa, Rita, MD Department of Vascular Surgery and Service of Nuclear Medicine, Policlinico Umberto I° University of Rome “La Sapienza” Rome, Italy (E-mail:
[email protected])
Mitropoulos, Fotios, MD, PhD Department of Cardiothoracic Surgery University of Athens School of Medicine Attikon Hospital Center Athens, Greece (E-mail:
[email protected])
Contributors
Moreno, Rosa M., MD Hospital Clinico Universitario San Carlos Madrid, Spain (E-mail:
[email protected]) Nachbur, Bernhard, MD, FMH Ittingen, Switzerland (E-mail:
[email protected]) Nevelsteen, Andre, MD, PhD, FRCS Department of Vascular Surgery University Hospital Gasthuisberg Leuven, Belgium (E-mail:
[email protected]) Nikita, Konstantina S., MD Biomedical Simulations and Imaging Laboratory Faculty of Electrical and Computer Engineering National Technical University of Athens Athens, Greece (E-mail:
[email protected]) Nyman, Rickard, MD, PhD Department Diagnostic Radiology Academic University Hospital Uppsala, Sweden (E-mail:
[email protected]) Palombo, Domenico, MD Unit of Vascular and Endovascular Surgery University Hospital “San Martino” Genoa, Italy (E-mail:
[email protected]) Parsson, Hakan N., MD Department of Surgery Uppsala University Helsingborgs Lasarett Helsingborg, Sweden (E-mail:
[email protected]) Pedro, Luis Mendes, MD Faculty of Medicine University of Lisbon Consultant in Vascular Surgery Hospital de Santa Maria Lisbon, Portugal (E-mail:
[email protected])
Piazzoni, Claudia, MD Department of Surgical Sciences and Intensive Care School of Medicine University of Milan-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected]) Poulakou, Garyphallia, MD 4th Department of Internal Medicine and Infectious Diseases, Athens University Medical School University General Hospital “ATTIKON” Athens, Greece (E-mail:
[email protected]) Pozzi, Grazia, MD Department of Surgical Sciences and Intensive Care, School of Medicine University of Milan-Bicocca San Gerardo Hospital Monza, Italy (E-mail:
[email protected]) Riera, S, MD Servei d’Angiologia I Cirurgia Vascular Hospital Universitari de Bellvitge Barcelona, Spain (E-mail:
[email protected]) Ricco, Jean-Baptiste, MD, PhD Vascular Surgery Service University Hospital Jean Bernard Poitiers, France (E-mail:
[email protected]) Rokkas, Chris K., MD Department of Cardiothoracic Surgery University of Athens School of Medicine Attikon Hospital Center Athens, Greece (E-Mail:
[email protected]) Saarinen, Jukka P., MD Division of Vascular Surgery Tampere University Hospital and Tampere University Medical School Tampere, Finland (E-mail:
[email protected])
XXXV
XXXVI
Contributors
Salenius, Juha-Pekka, MD Division of Vascular Surgery Tampere University Hospital and Tampere University Medical School Tampere, Finland (E-mail:
[email protected])
Skalkeas, Gregory D., Professor Emeritus, Academician President of the Foundation of Biomedical Research of the Academy of Athens Athens, Greece (E-mail:
[email protected])
Sampaio, Sérgio, MD Porto, Portugal (E-mail:
[email protected])
Sosa, Tomislav, MD (deceased) University Hospital Merkur Zagreb, Croatia
Saratzis, A., MD Department of Vascular Surgery Aristotle University of Thessaloniki Thessaloniki, Greece (E-mail:
[email protected])
Soucacos, Panayotis N., MD, FACS Department of Orthopaedic Surgery University of Athens, School of Medicine “K.A.T.” Accident Hospital Athens, Greece (E-mail:
[email protected])
Saratzis, Nikos A., MD Department of Vascular Surgery Aritstotle University of Thessaloniki Thessaloniki, Greece (E-mail:
[email protected]) Schmitz, Serge, MD Department of Vascular Surgery Centre Hospitalier Luxembourg (E-mail:
[email protected]) Schulte, Stefan, MD, PhD Department of Vascular Surgery Krankenhaus Porz am Rhein Porz, Germany (E-mail:
[email protected]) Sechas, Michael N., MD, FACS Athens, Greece (E-mail:
[email protected]) Sefranek, Vladimir, MD, PhD Slovak Institute of Cardiovascular Diseases Bratislava Bratislava, Slovakia (E-mail:
[email protected]) Settembrini, Piergiorgio G., MD Division of Vascular Surgery Ospedale S. Carlo Borromeo University of Milan Milan, Italy (E-mail:
[email protected])
Stamou, Sotiris, MD, PhD Department of Cardiothoracic Surgery Athens University Medical School Athens, Greece (E-mail:
[email protected]) Stravodimos, Konstantinos G., MD First Urology Department University of Athens, Medical School Laiko Hospital Athens, Greece (E-mail:
[email protected]) Stumpo, Regina, MD Department of Vascular Surgery Policlinico Umberto 1° University of Rome “La Sapienza” Rome, Italy Tentolouris, Nicholas, MD First Department of Propaedeutic Medicine Athens University Medical School Leiko University Hospital Athens, Greece (E-mail:
[email protected]) Toumpoulis, Ioannis K., MD Department of Cardiothoracic Surgery University of Athens School of Medicine Attikon Hospital Center Athens, Greece (Email:
[email protected])
Contributors
Tsapogas, Panagiotis, MD First Department of Propaedeutic Medicine Athens University Medical School Leiko University Hospital Athens, Greece (E-mail:
[email protected]) Vidjak, Vinko, MD University Hospital Merkur Zagreb, Croatia (E-mail:
[email protected])
Wanhainen, Anders, MD, PhD Department Diagnostic Radiology Academic Hospital Uppsala Uppsala, Sweden (E-mail:
[email protected]) Wolfe, John H. N., MD Regional Vascular Unit St. Mary’s Hospital London, UK (E-mail:
[email protected])
XXXVII
Vascular Surgery and the Vascular Patient
3
1.1 The History of Vascular Surgery in Europe Panagiotis E. Balas
To study the texts of the illustrious personalities of the past. GALEN
1.1.1 Introduction Writing the history of a medical specialty necessitates extensive historical and bibliographic research and the collection of data from various other sources such as information from medical people. The author must be experienced in collecting, evaluating and crosschecking the historical data in a scientific way to preserve objectivity. Undertaking this task of presenting the history of vascular surgery in Europe is difficult within the allotted time constraints, which necessarily are in conflict with being comprehensive and objective. My major concern however is that by studying and working exclusively in the field of angiology and vascular surgery for almost 40 years, by participating in the foundation of relevant scientific societies and by organizing congresses and other activities at home and abroad, I was part of the evolution of this medical field during the last half of the twentieth century and this could lead to a lack of objectivity. Therefore, my goal is to maintain the objectivity of this work while avoiding, as far as possible, any bias due to continental, national and personal scientific and professional preoccupations and interests. In this historical review, the development, evolution and recognition of the specialty of vascular surgery in Europe, including references to the associated medical specialties, will be presented, followed by an account of the various national contributions to this field.
1.1.2 The Origin and the Foundations of European Vascular Surgery The first interventions of Man on the blood vessels are lost in the depth of history, although some descriptions exist in ancient Indian and Greek texts. All the great
classical physicians, such as Hippocrates (fifth century b.c.), Aurelius Celsus (first century a.d.), Galen (second century a.d.) and Paulus Aegineta (sixth century a.d.), described various methods of treating varicose veins by ligation, cauterization and even stripping of the dilated long saphenous vein [14, 38]. The Greek Antyllus of the third century a.d., the most famous surgeon of antiquity, applied the well-known Antyllus’ method, an operation for aneurysm in which he applied two ligatures to the artery and cut between them. This was the accepted method of dealing with aneurysms until the work of Jon Hunter in the eighteenth century. Antyllus was the first to recognize two forms of aneurysm: the developmental, caused by dilatation, and the traumatic, following arterial trauma [38]. The famous surgeon-philosopher René Leriche (1879– 1955) credits four people who, with their ideas, practice and findings, influenced the development and evolution of knowledge in order to establish vascular surgery and to a certain extent its destination in Europe and the world all over. These four people were Ambroise Paré, William Harvey, Jean-Louis Petit and John Hunter [38].
Ambroise Paré
In 1546, Ambroise Paré performed the first arterial ligation during leg amputation in the midst of a combat and said “without having seen this attempt by any other person, nor heard or read but God advised me to tie the artery of the amputee”. He also introduced the first arterial forceps, the “bec de corbin”.
William Harvey
William Harvey (1578–1657), an Englishmen, went to the University of Padova, the most prestigious Institute at that time, and he studied under Hieronymus Fabricius. In 1603, Fabricius, an ardent anatomist, published the first
4
1.1 The History of Vascular Surgery in Europe
treatise on the valves of the heart and the great veins of the body, entitled De venarum ostiolis and observed the one-way valves in veins, but had not figured out exactly what their role was [10]. Harvey became Professor of Anatomy and Surgery at St. Bartholomew’s Hospital in London and, after 9 years of experimentation on living animals and cadavers, proved that the blood was circulating in a circuit system including the heart, arteries and veins. The connection between arteries and veins through the capillaries was discovered later by the Italian Marcello Malpighi, by using the microscope. He presented his findings in 1628 in his book Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus (An Anatomical Study on the Motion of the Heart and Blood in Animals) (Figs. 1.1.1 and 1.1.2). Thus 1300 years after the Greek physician Galen had concluded that the cardiovascular system carried blood and not air, Harvey disclosed the circulation [38].
The end of the eighteenth and the beginning of the nineteenth century marked a golden age in which many surgeons contributed to knowledge on vascular diseases and surgery. There follows a brief description of their contributions. Hallowel applied the first arterial suture, an idea proposed by Lambert around 1770. In 1774 Morel, a
John Hunter
John Hunter was born in 1728 in Scotland and at the age of 23 arrived at St. Bartholomew’s Hospital to work with Percivall Pott. He worked on comparative and human anatomy and described the exposition of the arteries in the human body. His books and publications had a profound impact on the medical and surgical practice of that time. He described, famously, the very proximal ligation of the femoral artery, for the preservation of the collateral branches, in the treatment of popliteal aneurysm. One such surgical specimen is exhibited at the renowned museum of the Royal College of Surgeons of England in London. In 1757, William Hunter, John’s older brother, described and properly analysed the development of arterio-venous aneurysms [38].
Jean-Louis Petit
Jean-Louis Petit (1731) was the first surgeon to study haemostasis [38]. The famous English surgeon Sir Astley Cooper, at Guy’s Hospital, made two important contributions: a successful ligation of the common carotid artery for aneurysm in 1805 and in 1817 his attempt to treat an aneurysm of the iliac artery by ligation, for the first time, of the aorta above the bifurcation. He was also the first to use the extraperitoneal approach to the abdominal aorta, which was reintroduced by C. Rob in 1963 [56].
Fig. 1.1.1 William Harvey, Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus [Anatomical Exercise on the Motion of the Heart and Blood in Animals]. Edition, Roterdami, A pud Arnoldum Leers A 1661. (From author’s personal collection)
1.1.2 The Origin and the Foundations of European Vascular Surgery
military surgeon, applied the haemostatic tourniquet to the extremities in the battlefield. During the eighteenth century 123 studies had been conducted on aneurysms and their treatment with arterial ligation and the discussion on this topic continued until the middle of the twentieth century [38]. The pathologist Rudolf Virchow, the “Pope of German medicine”, described in 1852 the existence of arterial embolism. He also coined the terms thrombosis and embolism and later described the aetiological triad of venous thrombosis known as Virchow’s triad. In 1859 Karl Hueter in Germany reported the first case of venous gangrene of the extremities [25].
The pioneer of vascular surgery in Russia was N. I. Pirogov who, in 1865, developed surgical approaches to the aorta and peripheral arteries, arguing against the dogmatic views that a vascular suture was not promising. P. Girsztowt of Warsaw recommended in 1868 the excision of the large varicose veins. Eugene Koeberle, a surgeon in Strasburg, invented a simple haemostatic clamp and applied it in surgery in 1868. It was the first operation actually ushering in our present technique of clamping and tying, which was carried out and popularized by J. Pean with a clamp he invented in 1869 [38]. N. V. Ekk, an outstanding Russian surgeon and physiologist in Pavlov’s laboratory in St. Petersburg, performed in
Fig. 1.1.2 This illustration depicts one of William Harvey’s experiments included in the book Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus. Harvey shows that venal blood flows only towards the heart. He ligatured an arm to make obvious the veins and their valves, then pressed blood away from the heart and showed that the vein would remain empty because it was blocked by the valve
5
6
1.1 The History of Vascular Surgery in Europe
1877 the first experimental vascular anastomosis between the portal vein and the inferior vena cava (Ekk’s fistula) [54]. Rudolf Matas, born in Louisiana USA and trained in the USA (with additional training in Paris and Barcelona), made history in 1888 by performing the first endoaneurysmorraphy for a traumatic aneurysm of the brachial artery [22]. In 1895 the Russian surgeon I. F. Sabaneyev made the first attempt in the world to remove an embolus from the femoral artery while the Russian R. R. Vreden performed in 1897 the first retrograde embolectomy of the aorta with limited success [54]. In 1896 the Lyon veterinarian M. Jaboulay proposed in the journal Lyon Medical an inverted suture of the arteries, known as the mattress-suture. Interestingly, this suture technique was clinically applied 50 years later by A. Blalock in Baltimore, USA [23]. In 1897 the Turkish Cemil Topuzlu Pacha, Pean’s pupil, repaired an axillary artery with five stitches [3]. Jaboulay’s technique was improved by one of his pupils, Alexis Carrel, who in 1902 published the technique of suturing the vessels in Lyon Medical. Also during this period Carrel performed outstanding research work in Lyon on arterial suturing and transplantation of arteries and organs. He successfully performed the first experimental cardiac homo-transplantation in the world, transplanting the heart of an animal to the neck of another by joining the carotid arteries (!). He published his work in the journal Lyon Medical in 1902 [24]. Carrel left Lyon in 1904 for Canada and the USA later, following political-religious turmoil due to his testimony of a miracle at Lourdes. In Chicago as Director of the Hull Laboratory of Physiology at the University of Chicago in collaboration with Charles C. Guthrie, he mastered his suturing techniques as the well-known Carrel’s Triangulation Techniques, and also the venous patch grafts made to enlarge the diameter of arteries. Later as Director of the Department of Experimental Surgery, at the Rockefeller Institute for Medical Research in New York, he worked on the preservation of arterial and venous segments for replacement of arteries and veins. He performed canine transections and end-to-end anastomosis of the descending aorta, or inserted a segment of preserved vena cava between the divided segments of the aorta. He also experimented with the insertion of a paraffined tube as an internal shunt within the aortic lumen in order to prolong the time of safe occlusion [24]. In addition to transplanting vessels and organs, Carrel worked on tissue cultures and organ preservation. The Norwegian R. Ingebrigtsen participated in this work and performed later interesting scientific work on arteriovenous fistulae in his country. In
1906, Carrel wrote the following instructions which are still valid a century later: “The vessels must be handled very gently and the endothelium must be protected…No dangerous metallic forceps are used. Great care is exercised to obtain accurate and smooth approximation of the endothelium of the vessel without invagination. Sutures should be made with very fine needles while the wall is somewhat stretched. Stenosis or occlusion only occurs as a result of faulty technique” [24]. Carrel received the Nobel Prize in Physiology and Medicine in 1912 for his spectacular experimental work [24]. During the ceremony of presentation of the Prize, the President of the Committee J. Ackerman among other things also said “To the great intelligence you have received from your mother country, France, to whom humanity owes so many great things, is united the energy and resolve of your adapted country. Your miraculous operations are the evident result of this happy collaboration…”. With his associate C. A. Lindbergh (famed for making the first solo airplane transatlantic flight in 1927) he developed in 1935 the first mechanical heart, a pump for circulating blood or fluids through preserved organs, namely the precursor of the extra-corporeal circulation which is in use today [24]. C. A. Lindbergh wrote in 1974 “medical scientists evaluating his work in the light of modern developments have said that he was fifty to a hundred years ahead of his time” [24]. In 1901, the Austrian Erwin Payr performed a vascular anastomosis with absorbable magnesium rings. Also arterial suturing was applied experimentally by Stich and Makkas (Germany) and many others [38]. In 1902 Tuffier attempted the resection of a syphilitic aneurysm of the ascending aorta but the patient died on the 13th day. Joe Goyanes of Madrid in 1929, after excision of a popliteal aneurysm, used an adjacent segment of popliteal vein to successfully bridge the defect (the first in situ vein graft) [27]. Six months later Erich Lexer at the University Hospital in Konigsberg, Germany performed excision of an axillary aneurysm and restored the arterial continuity by using a segment of the great saphenous vein [43]. This case was reported in the prestigious journal Archiv für Klinische Chirurgie which was read assiduously by prominent surgeons in Europe and in the United States. Among them was the American William S. Halsted, the famous first Professor of Surgery at the Johns Hopkins Medical School and Hospital, who had trained in Europe and, besides pioneering radical surgery of breast cancer, was also interested in vascular surgery, establishing a school of experimental vascular surgery. He studied various types of
1.1.3 Europe, Cradle of the World’s Vascular Surgery
arterial ligatures, among which was banding to achieve progressive arterial occlusion in order to reduce the size of distal aneurysms. In 1892 he successfully ligated the first part of the subclavian artery for the treatment of a huge distal aneurysm. Georges Labey, in 1911, performed the first successful arterial embolectomy of the extremities in the world [41], although there is information that in the same year the Hungarian surgeon J. Bakay performed a direct femoral embolectomy (D. Dzsinich, personal communication). In 1914 in Innsbruck, Austria, Hans von Haberer was the first surgeon to excise a false aneurysm of the carotid artery and to restore its continuity by an end-to-end anastomosis. He also published a monograph on “Kriegsaneurysmen” reporting on 72 operated cases of aneurysms [26]. During the First World War the pioneer Polish vascular surgeon Romuald Weglowski recommended the direct arterial reconstruction of arterial injuries, also using venous grafts for arterial bridging [57]. Vojislav Soubbotich, a pioneer vascular surgeon in Serbia during the Balkan wars (1912–14), performed repair, instead of ligation, of the injured vessels and of the post-traumatic aneurysms by using circular and lateral sutures, an experience commented on favourably by R. Matas [45, 59]. It is ironic that nearly 40 years passed before similar efforts were successful during the latter part of the Korean conflict [55]. Friedrich Trendelenburg, in Leipzig Germany, introduced an operation for varicose veins and in 1907 attempted a pulmonary embolectomy; however, he saw his pupil W. Kirchner perform a successful embolectomy in 1924, which was popularized later by many surgeons in Europe and the USA [40]. I was fortunate to attend the first pulmonary embolectomy under extra-corporeal circulation by Denton Cooley and A. Bell in 1960 at Saint Luke’s Hospital in Houston, Texas. The great breakthrough in the diagnosis of arterial diseases was the introduction of arteriography, namely the opacification of the arterial lumen, disclosing the abnormalities and even the occlusion of the artery, by intra-arterial injection of a liquid opacified by X-rays, which was first performed by J. Coapody in 1925 [13]. In Lisbon in 1926 Egaz Moniz, a Portuguese neurosurgeon, performed the first intra-carotid injection of thorium dioxide for the opacification of the carotid artery in a case of brain tumour [49]. Reynaldo dos Santos, a professor of urology in Lisbon, had performed the first translumbar aortography in 1929 [20] (Fig. 1.1.3). The first successful replacement of a semi-occluded femoral artery with a segment of the large saphenous
Fig. 1.1.3 A copy of the original aortograph performed by Reynaldo dos Santos in 1929, kindly given to the author by his son Joao Cid dos Santos in Lisbon in 1969
vein was performed by the Russian N. A. Bogoraz in 1935 (cited by A. N. Filatov) [54].
1.1.3 Europe, Cradle of the World’s Vascular Surgery European vascular surgery has been developed by the work of the above-mentioned pioneers and by European surgeons and medical angiologists since the 1930s and after the Second World War. During the second part of the twentieth century vascular surgeons were trained in Europe and many in the USA.
7
8
1.1 The History of Vascular Surgery in Europe
1.1.3.1 The Nursery of Vascular Surgery in Europe in the 1930s was the René Leriche School in Strasburg, France The identity of vascular surgery as a specialty in the major field of surgery, not only in Europe but also internationally, started emerging in the 1930s in the famous School of René Leriche in Strasburg. In this Clinic many young European surgeons and the American Michael E. DeBakey had their training and were indoctrinated with the impressive ideas and experience of Leriche concerning the pathophysiology and treatment of arterial diseases. Among Leriche’s pupils were Michael E. DeBakey (USA), Nicolas Christeas (Greece) (both were my teachers), Joao Cid dos Santos (Portugal) and the French René Fontaine, Jean Kunlin and others (Fig. 1.1.4). René Leriche, from Lyon, became director of a surgical clinic in Strasburg and later in Paris. He described
the occlusion of the terminal aorta, a condition which was coined Leriche syndrome [38]. For the treatment of occlusion of the abdominal aorta he performed lumbar sympathectomies with or without excision of the occluded aortic segment. Certainly he thought that the proper treatment should be resection of the occluded aorta and its replacement with an arterial substitute, as Carrel has done experimentally, but no arterial substitute for Man was available at the time [37]. He performed with R. Fontaine, his successor in Strasburg, stellate ganglion block for the release of arterial spasm in pulmonary embolism, in angina pectoris and in vasospastic conditions, such as Raynaud’s syndrome (Fig. 1.1.5). These methods were used for many years in our angiological practice [46]. In 1947 René Leriche proposed the establishment of the specialty of vascular surgery by stating “Arterial surgery is a special discipline of general surgery. The diagnostic investigation and the operations exist and the material is
Fig. 1.1.4 An historic picture of Leriche and his pupils in Strasburg in 1938. First row from left to right: (starting third from left) M. E. DeBakey (USA), René Leriche, N. Christeas (Greece), C. Eliades (Greece), J. Kunlin (France). Second row: from left to right: Joao Cid dos Santos (Portugal). (Picture from author’s personal collection)
1.1.3 Europe, Cradle of the World’s Vascular Surgery
abundant” [38]. His proposal was realized in the European Union countries after 57 years, in 2004 [42]. It is important to mention that many prominent American vascular surgeons had obtained their “portions” of training in Europe before the Second World War, e.g. Michael E. DeBakey, or after the war, e.g. Denton A. Cooley. The author owes a personal debt of gratitude to their two cardiovascular centres for the training he received. They are the Methodist Hospital-Texas Medical Center of Michael E. DeBakey and the St. Luke’s Hospital-Texas Heart Institute of Denton A. Cooley. A very large series of European surgeons was trained and many hundreds of European cardiovascular surgeons have visited these centres, obtaining experience in vascular and/or cardiac surgery, bringing it back to their home institutions. Most of these trainees and many other cardiovascular surgeons from all over the world became members of the M. E. DeBakey International Cardiovascular Society which I established in
Fig. 1.1.5 Leriche performing operation with Christeas on his left. Strasburg 1938. (Picture from author’s personal collection)
Fig. 1.1.6 Audience to the President of the Hellenic Republic, Professor Constantinos Tsatsos. From left to right : H. Eascott (UK), E. Malan (Italy), The President, M. E. DeBakey (USA), A. Senning (Switzerland), P. Balas (Greece)
9
10
1.1 The History of Vascular Surgery in Europe
Athens, Greece in 1976 (Fig. 1.1.6). Also, a similar Society of Denton A. Cooley was established. Many prominent American vascular surgeons were born in Europe and, after immigrating to the USA, developed leading vascular centres. Among them are the following: R. Linton born in Scotland, who was Director of Vascular Service in the Massachusetts General Hospital in Boston; Emeriick Szilagyi, born in Hungary, who was Director of Vascular Service in the Henry Ford Hospital, in Detroit; and Gega de Takats, also born in Hungary, who was Director of the Vascular Service in the University of Illinois, Chicago. Henry Haimovici from Tulcea Romania grew up and went to Medical School in Marseille, France. He moved to New York and became Head of Vascular Surgical Service Montefiore Hospital and Medical Center. It is very interesting that after his donation in 1976 the Rumanian Vascular Surgical Society was established. John Dormandy, born in Hungary, was Consultant Vascular Surgeon at St. George Hospital, London, UK. Peter Gloviczki, born in Hungary, is Professor and Chairman of the Department of Vascular Surgery, Mayo Clinic, Rochester, Minnesota, USA. Christopher K. Zarins, born in Latvia, is Director of Vascular Service in Stanford University Medical Center, Stanford, California. C. Rob moved from St. Mary’s Hospital in London, UK to the USA and became Chairman of the Department of Surgery at the Rochester University Medical School in Rochester, New York. In these centres many European surgeons were trained in vascular surgery, bringing about a reciprocal exchange of knowledge and experience among the surgeons and vascular surgical centres of Europe and the USA, starting from the old continent.
use of heparin for prevention of thrombosis, performed in 1947 the first successful thrombo-endarterectomy of the femoral artery with a silver ophthalmic spatula [40] (Fig. 1.1.7). During the next few years, open disobliteration was performed mainly by French surgeons, such as Bazy, Reboul and Huguier. Despite initial enthusiasm, it was apparent that the long-term results were not satisfactory. However, this technique revived following the introduction of patch graft angioplasty and extension of disobliteration of long occluded arterial segments by introducing the metallic ring strippers for semi-closed thrombo-endarterectomy. This was done first by the Americans Cannon and Baker and later by the Russian B. V. Petrovsky in 1959 [54] and in 1966 by the German J. Vollmar [61] using their own metallic ring strippers. Jean Kunlin, Leriche’s pupil, performed the first femoro-popliteal autologous saphenous venous by-pass in Paris in 1948 [36].
1.1.3.2 Reference to European Surgeons who Through their Pioneering Work Developed Vascular Surgery in their Continent with International Influence Clarence Crafοord, Director of Cardiovascular Surgery at the Karolinska Hospital in Stockholm, was a pioneer in performing pulmonary embolectomies and in 1944 performed the first successful correction of coarctation of the aorta. After the excision of the stenotic segment of the aorta he performed an end-to-end anastomosis, using Carrel’s triangulation technique [9]. In Russia V. F. Gudov, in 1945, designed and applied clinically the first vascular suturing apparatus [54]. Joao Cid dos Santos, taking advantage of the development of arteriography and the
Fig. 1.1.7 Jean Natali (France, left) and Joa Cid dos Santos (Portugal) in the early 1970s
1.1.3 Europe, Cradle of the World’s Vascular Surgery
In Paris Jacques Oudot performed experimental work in vascular surgery and the preservation of arterial homografts with the assistance of Jean Natali, who later became one of the leaders of French vascular surgery [50]. In 1950 Oudot was the first to replace the occluded abdominal aorta with a preserved aortic bifurcated homograft. Later on, due to occlusion of the right leg of the graft, he performed, also for the first time, a cross-over iliac–iliac by-pass with an arterial homograft [51, 53]. René Fontaine in 1951, established in Strasburg the first arterial bank in Europe, followed by similar banks in many European centres. The Russian N. I. Makhow performed in 1950 the world’s first implantation of femoral lymphatic channels into the femoral vein of a patient with secondary lymphoedema [54]. In 1951 Charles Dubost in Paris performed the monumental operation of excision of an abdominal aortic aneurysm and replacement with a 14-cm-long preserved segment of thoracic aorta [21]. In 1953 at St. Mary’s Hospital in London, UK, H. H. G. Eastcott together with Professor Charles Rob performed reconstruction of the occluded left carotid artery – the first time this had been done in Europe [23]; a similar procedure had been performed a few months earlier by M. E. DeBakey in Houston, Texas [18]. G. Arnulf in Lyon France published a book on carotid surgery [1]. In 1952, at St. Thomas’ Hospital in London, Sir John Kinmonth, who was a pioneer in the study and treatment of lymphatic diseases, introduced lymphangiography to image the lymphatic vessels of the extremities [35]. The Czech J. Dvorak and his collaborators were the first in Europe to manufacture cloth arterial prostheses of knitted terylene followed by other kinds of material [12]. These prostheses were first used in 1951 at New York’s
Fig. 1.1.8 B. V. Petrovsky, Russia
Columbia-Presbyterian Hospital, by Arthur Voorhees, who conceived the idea by chance on observing that silk sutures placed in a canine heart became completely covered with connective tissue. L. V. Lebedev and L. L. Plotkin in Leningrad in 1959 developed arterial prostheses from synthetic lavsan and later from fluorolon [54]. The most celebrated of Russian vascular surgeons Β. V. Petrovsky, Founder and Director until his mid-eighties of the All Union Research Center of Surgery (AURCS) in Moscow and past Minister of Public Health of the USSR, performed in 1947 the first successful resection of post-traumatic aneurysm in Europe [54] (Fig. 1.1.8). In 1959, the German pioneer in cardiovascular surgery Georg Heberer was the first in Europe to perform an intervention on a post-traumatic rupture of the thoracic aorta [5]. R. van Dongen, a prominent Dutch vascular surgeon and I. Boerema’s pupil, designed a specific table and used a special needle for aortography in the 1950s and later on published an impressive book with illustrations of vascular procedures [31, 60] (Fig. 1.1.9). In 1959 Karl Victor Hall, Professor of Surgery at the National Hospital of Oslo, applied in Europe, at about the same time as Cartier in Canada, in situ venous by-pass in the lower extremities. He later developed Hall’s valve stripper [30]. In 1962 A. V. Pokrovsky in Moscow was the first in the world to use retroperitoneal thoraco-abdomi-
Fig. 1.1.9 Presentation of a Diploma of Honorary Distinction of IUA, by P. Balas, Secretary of the Union (left), to R. J. A. M. van Dongen in Amsterdam in 1986 during the Eighth Course of Vascular Surgery organized by the honouree
11
12
1.1 The History of Vascular Surgery in Europe
nal access to the thoraco-abdominal aorta and visceral arteries [54]. In 1953 F. Cockett in London described the perforator veins in the leg as Cockett’s perforators [15] and also iliac compression syndrome in 1965 [16]. This syndrome was also described by R. May in Innsbruck [14]. Around 1954 the first vascular surgical clinics of England were set up in London, one by C. Rob and F. Eascott at St. Mary’s Hospital and the other by F. Cockett and J. Kinmonth at St. Thomas’ Hospital; another was established in Manchester by Michael Boyd (F. B. Cockett, communication by correspondence, 2004). A famous Polish vascular surgeon Jan Nielubowicz, in co-operation with Waldemar Olszewski, introduced in 1967 the surgical lymphatico-venous shunt in patients with secondary lymphoedema [52]. Later a Scandinavian plastic surgeon T. Ipsen and colleagues performed, with the use of a microscope, a lymph–venous anastomosis [32]. After the introduction of microvascular surgery in the USA by Julius Jacobson II in 1960 [33], this field was extended in Europe by the work of Victor Krylov in the early 1970s at AURCS in Moscow [2] and by M. Gazi Yasargil in Switzerland [19]. E. Malan, Director of a Cardiovascular Institute in Milan, proposed a “classification of the vascular malformations” and established in the 1970s and 1980s an important centre of vascular surgery in Italy. In 1967 in Athens, Greece, P. Balas performed the first replantation of a completely amputated upper extremity in Europe, which is functioning satisfactorily up to the present date [11]; this was followed by a successful case carried out by the Swiss Bruno Vogt in 1979. Jorg Vollmar in Germany developed a rigid endoscope in 1969 to inspect the luminal surface after closed arterial endarterectomy [61]. The Czech V. Michal in 1973–78 developed procedures for vasculogenic impotence (femoro-pudendal by-pass, internal iliac thrombo-endarterectomy and direct arterial anastomosis to the cavernous body) [48].
1.1.3.3 Medical and Interventional Vascular Contributions to the Development of Vascular Surgery in Europe and Worldwide Christian Doppler was a mathematician born in Salzburg, Austria. In 1842 he wrote a paper entitled “Concerning the colored light of double stars”, the substance of which is now known as the Doppler effect. He hypothesized that the pitch of a sound would change if the source of the
sound was moving. This hypothesis was tested in 1845. The Japanese Shige and Satomiga applied the Doppler effect to the diagnostic investigation of the cardiovascular system using ultrasound techniques. The resulting valuable tools for the study of the cardiovascular system include Doppler ultrasonography, which uses audio and graphic measurements to hear and measure blood flow, and duplex ultrasonography, with or without colour imaging. In the early 1950s, Swedish physicians, following the work of the Swede Gunnar Bauer in 1940, developed both ascending and descending phlebography and they also started the use of heparin for the treatment of venous thrombosis [4]. Sven Ivar Seldinger, a radiologist at the Karolinska Hospital in Stockholm, applied in 1952 a technique for peripheral arteriography; the procedure is now coined with his name [56] and is used at present for all endovascular procedures. In the 1960s the Swedes Carl Arnodi, Knut Haeger, Goran Nylander and others contributed to the study of venous disorders of the lower extremities (G. Hagmueller, communication by correspondence 2004). James S. T. Yao, working as research fellow at the vascular laboratory W. T. Irving at St. Mary’s Hospital in London in 1968, did pioneering work in the study of peripheral arterial circulation by using strain gauge plethysmography and ultrasound Doppler and developed the ankle/brachial blood pressure index (ABI), which has been and still is used extensively [62]. In the 1960s I. Boerema, father of modern hyperbaric medicine, applied hyperbaric oxygen therapy in cases of critical limb ischaemia and gangrene and in anaerobic infections of the extremities, and he also performed minor procedures in the hyperbaric facility in the University Hospital in Amsterdam [7] (Fig. 1.1.10). However, the largest and very impressive hyperbaric medical facility in Europe, and probably the world, was established in AURCS in Moscow in 1975, where Victor Krylov performed carotid endarterectomy and B. A. Konstantinov and others performed cardiac operations in 1998. In 1998 I visited this centre, which was under the direction of a senior professor specializing in hyperbaric medicine and included many sections such as surgical, obstetrics, gynaecology and others [2] (Fig. 1.1.11). In the early 1970s in London V. V. Kakkar made a breakthrough in the prevention of venous thromboembolism by introducing the subcutaneous injection of a low dose of heparin for the prophylaxis of deep vein thrombosis (DVT) [34].
1.1.3 Europe, Cradle of the World’s Vascular Surgery
Fig. 1.1.10 Hyperbaric Chamber, University Hospital of Amsterdam
A. Nikolaides contributed through original works to the study of venous diseases [6]. S. I. Seldinger, a radiologist at the Karolinska hospital in Stockholm, applied in 1952 a technique for periph-
Fig. 1.1.11 Performance of minor surgery in the chamber
eral arteriography; the procedure is now coined with his name [58]. In 1971 E. Zeitler, a German radiologist, started popularizing in Europe the American Charles Dotter’s technique of transcutaneous arterial disoblitaration. Andreas Gruntzig of the Angiological Clinic of Alfred Bollinger in Zurich, Switzerland, after his work with Zeitler, developed in 1974 the monumental method of arterial dilatation by using a balloon catheter for dilatation of the peripheral and coronary arteries, introducing percutaneous transluminal angioplasty (PTA) [28]. In 1976 Gruntzig performed the first PTA on the coronary arteries with the back-up of cardiac surgeons [28]. In 1977 Felix Mahler from the Department of Angiology of the University of Berne was the first to perform PTA of the renal arteries, for renovascular hypertension, with the back-up of vascular surgeons. The application of Gruntzig’s method (PTA) was one of the greatest breakthroughs in the treatment of cardiovascular diseases in the twentieth century. The radiologist I. K. Rabkin at AURCS in Moscow performed the first transcatheter intravascular procedure in
13
14
1.1 The History of Vascular Surgery in Europe
the USSR and was the first in the world to perform, in 1984, dilatation and endovascular prosthetic grafting of an external iliac artery [54]. N. L. Volodos was the world pioneer in devising and clinically applying endoprostheses in the aorta and iliac arteries in the Ukraine in 1985, before J. Parodi [54]. Claude Mialhe from France was a world pioneer, performing in 1995 endovascular abdominal aortic aneurysm repair by using a modular stent graft [47], followed immediately by Wolf J. Stelter in Frankfurt, Germany (personal communication, 1964). The Leicester group under Sir Peter Bell and the radiologist A. Bolia contributed to the advancement of endoluminal treatment by applying subintimal angioplasty to the lower extremities [8]. In the 1970s Herbert Ehringer in Vienna introduced intravenous thrombolysis for arterial occlusions. The German angiologist Hans Hess in Munich in the early 1980s introduced intra-arterial thrombolysis in peripheral arterial occlusive disease, followed by the Swede D. D. Do (1987).
1.1.4 European Vascular Surgical and Angiological Societies and Congresses Since the 1970s the following events have played an essential role in the development of European vascular surgery. The European Society of Vascular Surgery (ESVS) was founded by leading vascular surgeons R. Greenhalgh, Sir Peter Bell (UK), P. Fiorani (Italy), H. Mhyre (Norway), H. Van Urk (The Netherlands) and others. The inaugural meeting of the Society was held in May 1987, with the first President being Hans Myhre, during the International Symposium of the Charing Cross Hospital in London; it was organized by Greenhalgh, who had written the first constitution of the Society. Preceding the formation of the Society, the European Journal of Vascular Surgery was started by a European Editorial Board chaired by Greenhalgh and became the official journal of the Society [44] (Fig. 1.1.12). Concerning the establishment of vascular surgery as an independent specialty in the European Union (EU), credit has to be given, among others, to Domenico Palombo, an Italian vascular surgeon who organized a meeting of a working group of representatives of vascular surgical societies of the 12 EU countries at that time, in St. Vincent (Aosta-Italy) on March 1991, to discuss the perspectives of European vascular surgery. Through many meetings of representatives of European vascular surgical societ-
Fig. 1.1.12 Presentation by P. Balas, President of the ESVS, of a Diploma of Honorary Member of the Society to Roger Greenhalgh (UK) during the Congress of the Society in Berlin in 1993
ies, who formed the Council of Vascular Surgeons in the EU (Aosta group), a statute was attested by a notary and was drawn, defining the specialty of vascular surgery and the objectives of the Council, signed by the following: M. D’Addato (Italy), P. C. Maurer (Germany), H. G. Nicaise (France), R. Vanmaele (Belgium), J. Barbosa (Portugal), J. Buth (The Netherlands), P. L. Harris (UK), M. A. Cairols (Spain), P. Balas (Greece) and W. P. Paaske (Denmark). The Council approached the European Union of Medical Specialists (UEMS) and after long discussions, together with the help of the ESVS, a Division of Vascular Surgery in the Section of General Surgery of the UEMS was established in 1992 in Edinburgh. The Division organized a European Board of Vascular Surgical Qualification (EBSQ-VASC) to provide a European certification in vascular surgery for the vascular surgeons of the countries of the EU, following proper assessment. The first assessment took place in Venice in 1966 and subsequently each year in conjunction with the annual meeting of the ESVS. Following successful examinations a diploma is provided with the title Fellow of the European Board of Vascular Surgery [44]. On 15 October 2004 vascular surgery was recognized by the UEMS as an independent specialty in the EU (Fig. 1.1.13). People who over the years contributed to the recognition of the specialty were R. Greenhalgh (UK), P. Harris (UK), J. Buth (The Netherlands), W. P. Paaske (Denmark), C. Liapis (Greece), F. Benedetti-Val-
1.1.4 European Vascular Surgical and Angiological Societies and Congresses
Fig. 1.1.13 Creation of Section of Vascular Surgery, 15 October 2004. From left: F. Benedetti-Valentini, President UEMS Section of Vascular Surgery; R. Greenhalgh, President European Board of Surgery and UEMS Representative, Surgical Specialties; H. Halila, President UEMS; and C. Liapis, President ESVS
entini (Italy), J. Fernandes e Fernandes (Portugal), J. Wolfe (UK), G. Biasi (Italy), D. Bergqvist (Sweden) and others [44]. A crucial factor in the development and evolution of the field of endovascular therapies for peripheral arterial diseases in Europe was the establishment in 1992 in Bordeaux, France, of the International Society of Endovascular Surgery. Among the eight founders members of the Society four were Europeans: P. Balas (Greece), P. Bergeron (France), J. Busques (France) and J. Bleyn (Belgium) [17]. During the Congress of the European Society for Vascular Surgery (ESVS 1992), which I had organized in Athens (Fig. 1.1.14), we organized with Edwards Dietrich, from the Arizona Heart Institute, a spectacular satellite, live broadcast of endovascular procedures from his Institute to the Athens Hilton Hotel, an event that I am convinced was decisive for the decision of the European Society of Vascular Surgery and its journal to change their names to include the endovascular component [2]. European angiology played a pivotal role in the development of world angiological disciplines, among which was vascular surgery. The promotion of European and international angiology has been achieved by the International Union of Angiology (IUA) and its journal International Angiology, which started in 1982 with P. Balas as Editor-in-Chief, and essential to this process has been the co-operation of prominent European angiologists and vascular surgeons such as F. Pratesi, A. Strano and G.
Fig. 1.1.14 P. Balas, President of the Congress of the ESVS in Athens in 1992 and P. Fiorani (Italy), President of ESVS and Mrs P. Fiorani
Biasi (Italy), P. Maurer (Germany), H. Boccalon, L. Castellani (France), D. Clement (Belgium), A. Nicolaides (UK), L. Norgren (Sweden) and others. In 1988 The Mediterranean League of Angiology and Vascular Surgery (MLAVS) was established by P. Balas (Greece), A. Strano, G. Biasi (Italy), L. Castellani (France), A. Angelides (Cyprus), E. Hussein (Egypt), J. Fernandes e Fernandes (Portugal) and representatives from other European countries, under the patronage of the IUA, for the promotion of angiology in the Mediterranean countries [2]. The contribution of the angiological schools of Fernando Martorell (Barcelona, Spain), J. Merlen (Lille, France), C. Olivier (Paris), Franco Pratesi (Florence), A. Strano (Palermo-Rome, Italy), Alfred Bollinger (Zurich) and Bent Fagrell (Stockholm) should also be emphasized. In 1959 Max Ratschow, an outstanding German angiologist in Heidelberg, published an important book Angiologie. Among Ratschow’s pupils were outstanding German angiologists Hans Hess and W. Schoop and the Swiss Leo Widmer (Basel). All these contributed to the development of the major field of angiology in Europe, paving the way for the development of vascular surgery.
15
16
1.1 The History of Vascular Surgery in Europe
The following leading European cardiovascular surgeons George Arnulf (France), J. Kinmonth (UK), Edmondo Malan (Italy), R. Fontaine, Jean Natali (France), J. C. Dos Santos (Portugal), Jean Van Der Stricht (Belgium) and others were the founders of The European Chapter of the International Society for Cardiovascular Surgery in 1951 and of its official journal Journal of International Cardiovascular Surgery in the 1960s, playing a crucial role in the development of cardiovascular surgery in Europe [29]. Since the 1960s many international, European and national congresses, conferences, work-shops and other scientific activities have been organized in Europe, contributing significantly to the continuing education of trainees
in angiology-vascular surgery and of the vascular surgeons. Among them were the 25 annual Charing Cross Symposia in London, the annual congresses of the ESVS in various European countries since 1988 and the international and the European congresses of the IUA [2]. In Fig. 1.1.15, during the 15th World Congress of Angiology in Rome in 1989 are depicted the past, present and the future presidents of the IUA. From left to right: P. Balas (Greece), D. Clement (Belgium), P. Glovinczki (USA), P. Maurer (Germany), Cs. Dzsinich (Hungary), A. Strano (Italy), President of the Congress, L. Castellani (France), H. Boccalon (France), A. Schirger (USA) and G. Parulkar (India). Fourteen Annual Mediterranean
Fig. 1.1.15 The Presidents of the IUA, during the 15th World Congress of Angiology, Rome, 1989
1.1.5 Epilogue
Congresses have been organized so far. Also, 14 Annual Congresses of the MLAVS have also been organized (Fig. 1.1.16). Tables 1.1.1 and 1.1.2 present various national data concerning vascular surgery in various European countries. It was possible to collect these through personal communications with leading vascular surgeons and/or from publications. Some omissions are due to lack of information.
1.1.5 Epilogue This historical review is a tribute to the personalities who contributed to some extent to the progress of vascular surgery in Europe, both those who are among us at present and those who are fondly remembered (Fig. 1.1.17). However, from this short historical account many important persons and their work have not been mentioned due to limited space, but the interested reader can find them in other more extensive historical treatises.
Table 1.1.1 National data concerning vascular surgery in Europe. (A The existence of the independent speciality of vascular surgery and date of establishment, B the existence of vascular surgical clinics and date of establishment, B1 number of state clinics, B2 number of university clinics, B3 total number, C date of establishment of a vascular surgical society and/or angiological society, D the publication of vascular surgical and/or angiological journals, E the publication of books on vascular surgery and/or angiology, + existence, – existence, ? no information available) Country
A
B B1
B2
C
D
E
–
+
–
B3
Austria
+ (1983)
1 (1972)
4
–
Bulgaria
+ (1994)
1 (1964)
–
7
Croatia
?
9 (1964)
13
19
Cyprus
+ (1987)
–
–
–
–
+
–
+ (1996)
–
?
–
–
–
Czech Republic
+ (1986)
3
1
4
?
+
+
Denmark
+ (2004)
4
5
9
–
–
–
Germany
+ (1978)
?
?
100
+ (1984)
+
+
Greece
+ (1989)
2
4
6
+ (1982)
+
+
Hungary
+
?
?
?
+
+
+
Iceland
–
1 (1994)
–
–
–
–
–
Ireland
–
1 (Late 50s)
–
–
+ (With UK)
–
–
Italy
+ (1974)
28
79
107
+
?
+
Norway
+ (1986)
–
–
–
+ (1990)
+
–
Poland
+ (2001)
–
–
–
+ (2001)
+
+
Serbia
+ (1992)
1 (1989)
–
–
–
–
–
Slovak Republic
+ (1988)
1 (1978)
–
–
–
–
–
Spain
+ (1978)
1 (1963)
–
42
?
+
+
Switzerland
+ (2002)
–
–
–
+ (1989, 2000)
+
+
The Netherlands
–
–
–
–
+ (1981)
–
–
Turkey
–
1 (1961)
–
–
+ (1982)
+
+
UK
+ (1966)
?
?
?
+
–
+
Ukraine
–
1 (1972)
?
?
+ (2001)
+
+
17
?
?
1961
1966
?
1968
1966
1958
1957
1956
1953
Turkey
1957
Switzerland
? 1967
The Netherlands Yes
? 1962
?
Serbia
Spain
1947
Russia
Slovak Republic
1979 ?
Poland
?
Ireland
Norway
1954 ?
Iceland
Early 70s 1958
Greece
Hungary
Early 60s Early 60s ?
Czech Republic
1978
?
?
?
?
?
?
?
?
?
?
?
?
1964
?
?
1988
?
1960
Cyprus
?
Bulgaria
?
A3
?
A2
Austria
A1
A
?
Yes
?
1963
1961
1965
?
1963
1958
1956
1973
1969
1963
Early 60s
1981
1962
1962
B
?
?
?
?
1953
?
?
1958
1955
?
?
1949
Early 70s
Early 60s
?
?
?
C
?
Yes
?
?
1964
1966
1959
?
?
1959
1960
1967
1963
?
?
?
1958
D
?
1962
?
E2
?
?
?
1959
?
1956
?
Late 50s
?
?
?
1951
1962
?
?
?
?
1960
?
?
Late 50s
?
1954
?
?
1961
Middle 50s 1958
?
?
1952
E1
E
?
?
?
?
1981
1970
1999
1992
?
?
?
1986
?
1979
?
1974
?
F
?
?
?
?
G3
?
?
?
?
?
?
?
?
Early 2000 1997
?
?
?
?
G2
?
1994
?
?
?
?
?
?
?
?
?
?
?
?
?
?
?
?
?
?
?
Last years Last years ?
1995
?
?
1997
1996
1994
2000
?
?
G1
G
Table 1.1.2 Dates that various vascular surgical procedures started. (A Excision of aneurysms, A1 thoracic, A2 abdominal, A3 peripheral, B carotid endarterectomy, C arterial endarterectomy, D aortic by-pass, E femoro-popliteal by-pass, E1 with vein, E2 with plastic arterial prosthesis. F venous reconstruction, G endovascular aneurysm repair, G1 abdominal, G2 thoracic, G3 peripheral, ? no information available). The dates indicate the first performed operation
18 1.1 The History of Vascular Surgery in Europe
1.1.5 Epilogue
I trust that the new generations of vascular surgeons, inspired by the achievements of the important and leading personalities in angiology and vascular surgery of the past, will continue to carry the torch of progress of vascular surgery with enthusiasm and vision, to pioneer scientific work and carry out excellent medical practice for the benefit of our fellow humans afflicted by vascular diseases.
Fig. 1.1.16 The President of the MLAVS, P. Balas, presenting a Diploma of Honorary Member to G. Biasi (Italy), former Secretary of the League
Fig. 1.1.17 Galene’s Dictum in Greek (To study the texts of the illustrious personalities of the past)
Acknowledgements I greatly appreciate the following colleagues for providing important historical data concerning the development and evolution of vascular surgery in their countries: • V. Anastasov, Plovdiv, Bulgaria • Nicos Angelides, Nicosia, Cyprus • Sir Peter Bell, Leicester, UK • Patrice Bergeron, Marseille, France • David Bergqvist, Uppsala, Sweden • Giorgio Biasi, Milan, Italy • Andrea Brunner, Nuremberg, Germany • Murat Byazit, Turkey • Josep M. Capdevila, Barcelona, Spain • Lazar B. Davidovic, Belgrade, Serbia • R. J. A. M. van Dongen, Amsterdam, The Netherlands • Csaba Dzsinich, Budapest, Hungary • H. H. G. Eastcott, London, UK • Bert Eiklboom, Utrecht, The Netherlands • Georg Hagmueller, Vienna, Austria • William P. Hederman, Dublin, Ireland • A. V. Gavrilenko, Moscow, Russia • Roman Jaworski, Wroclaw, Poland • Kiriaki Kalligianni, Athens, Greece • Milan Krajicek, Praha, Czech Republic • William MacGowan, Dublin, Ireland. • Zygmunt Mackiewicz, Bydgoszcz, Poland • Nikolay Muz, Ukraine • Hans O. Myhre, Trondheim, Norway • Bernhard Nachbur, Ittigen, Switzerland • Jean Natali, Paris, France • Anatoly Pokrovsky, Moscow, Russia • V. Riambou, Barcelona, Spain • Einar Stranden, Oslo, Norway • Vladislav Treska, Plezen, Czech Republic • James Yao, Chicago, USA • F. Zernovicky, Bratislava, Slovak Republic I would also like to thank my friends Professor Julius Jacobson, II, New York, N. Y., USA and Mr. L. H. Brown, Athens, Greece, for their editorial assistance.
19
20
1.1 The History of Vascular Surgery in Europe
References 1. Arnulf G (1957) Pathologie et chirurgie des carotids. Masson et Cie, Paris 2. Balas P (2003) Memoirs of an angiologist and vascular surgeon. Zita, Athens 3. Batirel HF, Yuksel M (1997) Our surgical heritage. Ann Thorac Surg 64:1201–1203 4. Bauer G (1940) Venographic study of thromboembolic problems. Acta Chir Scand 84 (Suppl) 61:1–75 5. Becker HM (2000) In memoriam Prof. Dr. Georg Heberer. Gefasschirurgie 5:4–5 6. Bergqvist D, Comerota JA, Nicolaides A, Scurr JH (1994) Prevention of venous thromboembolism. Med-Orion, London 7. Boerema I (1961) An operating room for high oxygen pressure. Surgery 47:291–298 8. Bolia A, Miles KA, Brennan J, Bell PRF (1990) Percutaneous transluminal angioplasty of occlusions of the femoral and popliteal arteries by subintimal dissection. Cardiovasc Intervent Radiol 13:357 9. Bjork VO (1984) Clarence Crafoord (1900–1984) The leading European thoracic surgeon died. J Cardiovasc Surg 25:473 10. Caggiati M, Rippa M, Bonati A, Pieri A, Riva A (2004) Four centuries of valves. Eur J Vasc Endovasc Surg 28:439–441 11. Christeas N, Balas P, Giannikas A (1969) Replantation of amputated extremities. Report of two successful cases. Am J Surg 118:68–73 12. Chvapil M, Krajicek N (1963) Principle and construction of a highly-porous collagen-fabric vascular graft. J Surg Res 5:358–364 13. Coapody J (1925) Arterienphotographien vermittels, Lipiodol. Klin Wehnschr 4:2327 14. Cockett FB (1990) A historical outline of varicose vein surgery up to the present day. Flebolinfologia 1:3–5 15. Cockett FB, Jones DE (1953) The ankle blow-out syndrome. A new approach to the varicose ulcer problem. Lancet [Jan 3] 1:17–23 16. Cockett FB, Thomas ML (1965) The iliac compression syndrome. Br J Surg 52:816–821 17. Criado F (1998) ISES: the first five years 1992–1997. J Endovasc Surg 5:XXI–XXII 18. DeBakey ME (1975) Successful carotid endarterectomy for cerebrovascular insufficiency. J Am Med Assoc 233:1083–1085 19. Donaghy RMP, Yasargil MG (1967) Micro-vascular surgery. Mosby, St Louis; Georg Thieme, Stuttgart
20. Dos Santos R, Lamas A, Pereirgi CJ (1929) L’arteriographie des members de l’aorte et ses branches abdominal. Bull Soc Nat Chir 55:587 21. Dubost C, Allary M, Oeconomos N (1951) A propos du traitement des aneurysmes de l’aorte. Ablation de l’aneurysme, retablissment de la continuité par greffe de l’aorte humaine conservée. Mem Acad Chir 77:381 22. Eascott HHG (1969) Arterial surgery. Lippincott, Philadelphia 23. Eascott HHG, Pickering GW, Rob CG (1954) Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet ii:994–996 24. Edwards WS (1974) Alexis Carrel. Visionary surgeon. Charles C Thomas, Springfield 25. Encyclopaedia Britannica On line. Virchow (12/9/2004) www.britannica.com. 26. Fraedrich G (2004) From Hippocrates to Palmaz-Schatz. The history of carotid surgery. Eur J Vasc Endovasc Surg 28:455 27. Goyanes J (1929) Nuenos trabajos de cirugia vascular. Substitucion plastica de las arterias por las venas, o atrerioplastica venosa, applicada como nuevo metodo, al tratamiento de los aneurismas. El Siglo Med Sept pp 346–561 28. Gruntzig A, Holff H (1974) Perkutaene rekanalisation chronischer arterieller verschluess mit einem neuen dilatationskatheter. Dtsch Med Wochenschr 99:2502 29. Haimovici H (1977) The history of the International Cardiovascular Society. J Cardiovasc Surg 18:207–240 30. Hall KV (1962) The great saphenous vein used in situ as an arterial shunt after extirpation of the vein valves. Surgery 51:492–495 31. Heberer G, van Dongen RJAM (1989) Vascular surgery. Springer, Berlin Heidelberg New York 32. Ipsen T, Pless J, Fredriksen PB (1990) Experience with microlymphaticovenous anastomoses for the treatment of obstructive lymphedema. Plast Reconstr Surg 85:562–571 33. Jacobson J, II, Suarez EL (1960) Microsurgery in anastomosis of small vessels. Surgical Forum XI:243 34. Kakkar VV, Spindler J, Flute PT et al (1972) Efficacy of the low doses of heparin in prevention of deep venous thrombosis in blind randomized trail. Lancet 2:101 35. Kinmonth JB (1952) Lymphangiography in man; a method of outlining lymphatic trunks at operation. Clin Sci 11:13–20 36. Kunlin J et al (1951) Le traitement de l’ischémie artéritique par la greffe veineuse longue. Rev Chir 15:206–235 37. Landry P (1999) Biographies, William Harvey. www.blupete.com/Literature/Biographies/Science/Harvey.htm
References
38. Leriché R (1923) Des oblitérations artérielles hautes (obliteration de la terminaison de l’aorte) comme causes des insuffisances circulatoires des membres inferieurs. Bull Mem Soc Chir Paris 49:401–404 39. Leriche R (1940) De la resection du carefour aorto-iliaque avec double sympathectomie lombaire pour thrombose arteritique de l’aorte: le syndrome de l’obliteration terminoaortique par arterite. Presse Med 48:601 40. Leriche R (1943) Physiologie pathologique et chirurgie des artères des membres. Masson et Cie, Paris 41. Leriche R (1947) Les embolectomies de l’artere pulmonaire et des artères des membres. Masson Cie, Paris 42. Leriche R (1947) Rapport. Sur la desobstraction des thromboses artérielles anciennes, par M. Jean Cid dos Santos (de Lisbone). Mem Acad Chir 73:409–411 43. Lexer E (1907) Die ideale operation des arteriellen und des arteriell-venosen aneurysma. Arch Klin Chir 83:459 44. Liapis CD, Paaske WP (2004) Status of vascular surgery in Europe. Elsevier, Amsterdam 45. Matas R (1903) An operation for the radical cure of aneurism based upon arteriography. Ann Surg 37:161–196 46. Mellière D (2000) Petite histoire du traitement des maladies artérielles et de ses pionniers. Europeene D’ Editions, Paris 47. Mialhe C, Amicabile C (1995) Traitement endovasculaire des aneurysmes de l’aotre sous-renal par endoprothese Stentor, Serie preliminaire. J Mal Vasc 20:290–295 48. Michal V, Kramar R, Pospichal J (1974) Femoro-pudendal by-pass, internal iliac thromboendarterectomy and direct arterial anastomosis to the cavernous body in the treatment of impotence. Bull Soc Int Chir 33:343–350 49. Moniz E (1934) L’angiographie cerebrale. Masson et Cie, Paris
50. Natali J (1992) L’apport de Jacques Oudot a la chirurgie de la bifurcation aortique. Ann Chir Vasc 6:185–192 51. Natali J (2002) The Lèriche Memorial Lecture. In: The 50th International Congress of the European Society for Cardiovascular Surgery, June 20–23, 2001, Budapest, Hungary. Endocardiovascular WEB Magazine 6:7–17 52. Nielubowicz J, Olszewski W (1968) Surgical lymphatico-venous shunts in patients with secondary lymphoedema. Br J Surg 55(6):440 53. Oudot J (1951) La greffe vasculaire dans les thromboses du carrefour aortique. Presse Med 59:234 54. Pokrovsky A, Bogatov YP ( 2000) Vascular surgery in Russia. J Angiol Vasc Surg 6(3):8–20 55. Rich NM, Clagett PG, Salander JM, Piscevic S (1983) The Matas/Soubbotitch connection. Surgery 93:17–19 56. Rob C (1963) Extraperitoneal approach to the abdominal aorta. Surgery 53:87–89 57. Schumacker HB (1987) Romuald Weglowski: neglected pioneer in vascular surgery. J Vasc Surg 6:95–97 58. Seldinger SI (1953) Catheter replacement of the needle in percutaneous arteriography. A new technique. Acta Radiol 39:368–376 59. Soubbotitch V (1913) Military experience of traumatic aneurysms. Lancet 2:720 60. Van Dongen RJAM (1970) Photographic atlas of reconstructive arterial surgery. Stenfert Kroesse, Leiden 61. Vollmar J, Storz L (1974) Vascular endoscopy: possibilities and limits of its clinical application. Surg Clin North Am 54:111–122 62. Yao JST, Hobbs JT, IrvineWT (1968) Ankle pressure measurement in arterial diseases of the lower extremities. Br J Surg 55:859–860
21
23
1.2 Development of Atherosclerosis for the Vascular Surgeon Jean-Olivier Defraigne
1.2.1 Introduction Atherosclerosis is a complex disease involving various vascular segments and blood vessels such as the aorta, carotid, coronary and/or peripheral arteries. Taken together, the thrombotic or thromboembolic complications arising from this systemic process (stroke, myocardial infarction and gangrene) are the leading causes of morbidity and mortality in United States, Europe and also Asia. A high plasma cholesterol level is known to be a major risk factor for the development of atherosclerotic lesions. As a consequence, atherosclerosis is too often considered as a simple overload of lipids within the intimal layer of blood vessels [3]. Nevertheless, a revolution in the concept of atherosclerosis occurred after the recognition that the intrinsic vascular wall cells are not merely passive responders to inflammatory stimuli but can elaborate various mediators implicated in the initiation of an inflammatory process [41, 42]. Thus, although it is clear that the accumulation of lipids in macrophages and smooth muscle cells is a prominent aspect of the disease, numerous sequential cellular events leading to an inflammatory disease of the blood vessels play a central role in atherogenesis. Untreated or poorly treated atherosclerosis has significant medical consequences. So, better knowledge of both the atherosclerotic disease course and of factors favouring the onset of complications will help in improving not only medical treatment but also the selection, indications and adequacy of surgical interventions.
1.2.2 Physiopathology of Atherosclerosis
and adventitia. Endothelial cells (EC) lineate the intima and are in contact with the blood flow. Smooth muscle cells (SMC) are encountered in the media. Based on their fibre content and on cell composition, two main types of arteries are distinguished. Besides collagen fibres, elastic arteries contain a high proportion of elastic fibres in the media. Located proximally to the heart, these arteries store energy within their wall during the heart systole. Thereafter, during the diastole period, they recoil and reinstate this energy, thus transforming pulsatile flow into a continuous one. In contrast, more distal arteries exhibit a larger amount of SMC in the media. These latter arteries provide the resistive properties to the arterial tree, thus contributing to vascular tone [14]. Molecular signals and complex interactions between EC and SMC are implicated in the preservation of normal blood flow and vascular patency [42]. Regarding its total surface and its metabolic activities, the endothelium may be considered as a whole organ [7]. EC indeed produce and release several mediators implicated in the local control and regulation of vascular tone, blood flow, vessel patency and SMC activities (Table 1.2.1). By expressing cell adhesion molecules, EC also regulate cell traffic through the vascular wall. ECs are implicated in blood coagulation, notably by acting on platelet aggregation. For example, in response to local thrombotic events, EC secrete vasodilating substances such as prostacyclin (PGI2), prostaglandin E2 (PGE2), nitric oxide (NO) and endothelial-dependent relaxing factor (EDRF). In addition, as listed in Table 1.2.1, EC are also implicated in matrix product elaboration, as well as immunological and growth regulatory functions.
1.2.2.2 Initiation of Atherosclerosis and Role of Endothelial Dysfunction
1.2.2.1 Normal Blood Vessel Morphology From the lumen to the external side, normal arteries are made up of three concentric layers named intima, media
Atherosclerotic lesions develop progressively with a succession of events leading to the constitution of mature lesions named atheromatous plaques (Fig. 1.2.1). These lat-
24
1.2 Development of Atherosclerosis for the Vascular Surgeon
Table 1.2.1 Products released by endothelial cells Function
Products secreted
Elaboration of matrix components
Fibronectin, laminin, collagen (type I, II, III, IV), proteoglycans
Control of vascular tonus
NO, prostacyclin (PGI2), prostaglandin E2 (PGE2), angiotensin-converting enzyme (ACE), thromboxane (TXA2), leukotrienes, endothelin-1
Control of cell proliferation
Platelet-derived growth factor (PDGF), endothelial-derived growth factor (EDGF), fibroblast growth factor (FGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-β (TGF-β), granulocyte-monocyte-colony stimulating factor (GM-CSF)
Control of coagulation
Von Willebrand factor (vWF), thromboplastin, platelet activating factor (PAF), plasminogen activator inhibitor 1 and 2 (PAI-1 and PAI-2), high molecular weight kininogen (HMWK), thombomodulin, antithrombin III, heparan sulfate, adenosine diphosphatase, tissue plasminogen activator, protein C
Control of inflammatory processes and immunological function
Interleukins-1, -6, -8, leukotrienes B4, C4, D4, E4, cell adhesion molecules (CAM), major histocompatibility complex II (MHC II)
Fig. 1.2.1 Steps and processes observed during atheromatous plaque formation and maturation
1.2.2 Physiopathology of Atherosclerosis
ter are composed mainly of: (1) cells (monocyte-derived macrophages, T lymphocytes and SMC); (2) connective tissue and extracellular matrix (collagen, proteoglycans, fibronectin and elastic fibres); and (3) lipid deposits (crystalline cholesterol, cholesteryl esters and phospholipids). Due to varying proportions of these components, a spectrum of lesions may be observed, giving rise to stable, fibrous or vulnerable plaques. The fatty streak forming yellow streaks on the luminal surfaces of blood vessels is often considered to be a lesion preceding the development of a more advanced plaque [46]. Aside from SMC and T lymphocytes, monocyte-derived macrophages are a major component of this highly cellular lesion that represents a primitive inflammatory response. Nevertheless, the relationship between fatty streaks and the ultimate development of atherosclerosis is not completely elucidated. For examples, fatty streaks may be observed in fetuses and in children and may regress spontaneously. In addition, they are more frequent in females whereas atherosclerosis is more frequent in males.
To explain the process of developing atherosclerosis, several theories have been proposed. For example, the plaque cluster could result from the monoclonal proliferation of modified SMC originating from a single progenitor (monoclonal theory) [2]. Another theory considers the role of a small accumulation of SMC, which acts as a primordial stage of stem cells prone to playing a role in the development of atherosclerosis (intimal cell hypothesis) [49]. Although some isolated cases are perhaps relevant, none of these theories is able to completely explain all the aspects of ongoing atherosclerosis. This suggests that the eventual onset of atherosclerosis is also determined by superimposed extrinsic factors such as increased cholesterol levels, smoking, etc. Whereas, as mentioned previously, EC normally express anticoagulant and vasodilatative properties, in some circumstances (ischaemia, stimulation by humoral factors, influence of various pathological processes), EC may modify their activities and exhibit procoagulant and vasoconstrictive properties (Fig. 1.2.2). In this latter per-
Fig. 1.2.2 Consequences of endothelial dysfunction. Normal endothelium displays antiaggregant, anticoagulant and vasodilatative properties, along with inhibition of cell proliferation. After exposure to various agents causing endothelial dysfunction, these functions are modified toward procoagulant and vasoconstrictive activities together with stimulation of cell recruitment and proliferation. (LDL Low density lipoprotein, PAF platelet activating factor, PAI-1 plasminogen activator inhibitor-1, PGI2 prostacylin, TXA2 thromboxane A2, SMCs smooth muscle cells)
25
26
1.2 Development of Atherosclerosis for the Vascular Surgeon
spective, numerous observations of animal models and in clinical situations led to the concept of the responseto-injury hypothesis, which takes into account the different steps involved in atherosclerosis. A first version of this hypothesis proposed that endothelial denudation or abrasion was the initial event. At the present time, rather than endothelial denudation, endothelial dysfunction is considered a keystone in the triggering and progression of the atherosclerotic process [41, 42]. So, injury to the endothelium layer and to underlying SMC initiate a protective compensatory response, ultimately altering the normal homeostatic properties of endothelium. During these compensatory responses, aside the release of growth factors and cytokines, expression of adhesion molecules on the endothelial surface is simultaneously increased, resulting in increased adhesiveness for leukocytes and platelets. So increased vascular permeability, altered control of the vascular tone and altered balance between pro- and antithrombotic factors follow EC dysfunction. Finally, a chronic inflammatory response is installed, leading to healing or to a fibroproliferative response and eventually to an advanced, complicated lesion.
1.2.2.3 Evolution of the Atherosclerotic Plaque Adhesion and Migration of White Blood Cells Cellular adhesion molecules (CAMs) are implicated in the interactions between EC and circulating leukocytes, monocytes or T lymphocytes. After injury, the adhesiveness of the EC increases progressively and several adhesion molecules are sequentially expressed on the luminal surfaces of EC, such as members of the immunoglobulin super family VCAM-1 (vascular cell adhesion molecule-1), ICAM-1 (intercellular adhesion molecule-1) or membrane glycoprotein E-selectin [11, 42]. VCAM-1 is the ligand for VLA-4 (very-late forming antigen-4) and ICAM-1 binds to LFA-1 or Mac-1. The latter are integrins present at the surface of different kinds leukocytes. E-selectin is involved in interaction with leukocytes and platelets, since E-selectin binds P-selectin and to L-selectin, expressed by platelets and leukocytes, respectively [7]. The pattern of expression of each CAM (onset after injury, time course and duration, and degradation) is variable, thus conferring a specific role to each of them and providing an insight into the understanding of their specific role in leukocyte adhesion. For example, E-selectin is
the first to be expressed after stimulation and initiates the process of leukocyte rolling. In a second step, ICAM-1 and probably VCAM-1 are expressed, thus contributing to stronger and permanent adhesion. These latter interactions precede the leukocyte infiltration of the intima, starting the atherosclerotic process. Adhesion of circulating monocytes to the surface of the EC is effectively an early event in the development of an atherosclerotic plaque. In response to a chemoattractant (monocyte chemoattractant protein-1, MCP-1, produced by EC), monocytes adhere to, and insinuate themselves between, the tight junctions of the EC, to enter the subendothelial space [33, 40]. Inside the intima, they transform and differentiate into a phagocyte state (macrophages). They ingest modified lipids [primarily oxidized lipids coming from low-density lipoprotein (LDL), see below] and attempt to remove these lipids from the intima. As their lipid content increases, these macrophages take on a foamy appearance (“foam cells”) and accumulate locally. The process of “scavenging” lipoproteins by macrophages also leads to the release of cytokines, which stimulate smooth muscle migration and proliferation (see below). Immune mechanisms also appear to play a role in the process. Albeit in small numbers in human plaques, T lymphocytes (implicated in the cell-mediated immune response) are present in both young and advanced fibrous lesions. A suggested role for T lymphocytes during atherogenesis is help in mobilizing macrophages, which is similar to their role in immune responses [14, 26].
Influence of Haemodynamic Factors Haemodynamic forces imposed on the endothelium influence its biological response. High shear stress (tangential drag force) appears to reduce the incidence of early intimal lesions by affecting the migration, proliferation and biological functions of ECs [31, 51]. For example, it has been shown that cultured ECs submitted to a flow still present an alignment parallel to the direction of flow. When high shear stress is applied, change in the endothelial cytoskeleton is observed and the actin microfilament bundles are aligned. In contrast, the latter remain dense and nonaligned in areas where shear stress is low and the flow nonlaminar and turbulent. In addition, high shear stress increases the production of vasodilating and anti-aggregating prostacyclin (PGI2). These findings imply a mechanism that may contribute to increased atherogenicity in areas of low shear stress. Moreover, mitotic
1.2.2 Physiopathology of Atherosclerosis
division of EC is more frequent in areas of turbulent flow than in contiguous areas [50]. At atherosclerotic lesion-prone sites of the circulatory system, the expression of VCAM on the endothelium can be altered by abrupt changes in the direction and force of local blood flow. An element responsive to shear stress has been identified in the regulatory region of several genes (one coding for platelet-derived growth factor, PDGF) and promotes the expression of adhesion molecules as well as other molecular factors that participate in atherogenesis. It is supposed that a transcription factor produced in response to abnormal shear forces can induce the expression of genes contributing to the development of atherosclerosis. As a consequence, intimal lesions preferably develop in areas of low levels of shear stress. If one considers laminar flow in a straight, un-branching segment of a vessel, the flow velocity is greatest at the centre of the vessel and, because of friction, is least at the blood–endothelium interface. Depending on fluid viscosity, mean velocity and blood vessel diameter, bifurcations and other geometric changes result in turbulent flow, with random and erratic flow profiles. The velocity vector of blood flow in these areas becomes nonlinear. These changes in haemodynamic factors that occur at bifurcations account for the topographical distribution of atherosclerosis [14, 58]. So in the vessels particularly prone to atherosclerosis (coronary arteries, major branches of the aortic arch, abdominal aorta, major visceral and lower extremity branches), the plaque localizations are not strictly randomly determined. In the carotid territory for example, plaque formation occurs frequently at the origin of the proximal internal carotid artery. The area of the carotid sinus opposite the flow divider between the external and internal carotid arteries exhibits lower shear stress and is thus subjected to changes in haemodynamic forces that promote atherosclerosis. Maximal intimal thickness occurs on the side opposite the flow divider and intimal thickening is minimal on the inner wall while flow remains laminar. Such data may be transposed to other vascular territories.
factor (HB-EGF), vascular endothelial cell growth factor (VGEF)]. All of these have been detected in atherosclerotic plaques [29, 42, 43]. In response to these chemoattractants, SMC migrate from the media to the intima. Migrating SMC are morphologically different from the native SMC found in the media and their growth and proliferation are stimulated. Where denudation of endothelium is noted, other factors are also implicated. Coagulation factors and other products released by platelets forming micro-thrombi also contribute to the evolution of the plaque [39]. Simultaneously, neo microvascularization originating from the vasa vasorum develops within the plaque and the vessel wall, and allows local delivery of substances contributing to the evolution of the atheroma. Like PDGF, thrombin released by focal haemorrhages in the plaque area is a modulator of SMC activity [24]. So whereas EC dysfunction is the key factor initiating the plaque, SMC are implicated in its progression [43]. Nevertheless, the rate of SMC proliferation within the plaques is not uniform and slow progression may be observed for a long period of time, interspersed with transient bouts of increased cell proliferation. Within the plaques, local cytostatic mediators such as transforming growth factor-β (TGF-β) and interferon-γ (IFN-γ) may be implicated in the regulation of cell proliferation [32]. As the plaque matures, SMC display high secreting activities, producing various constituents of the extracellular
The Role of Smooth Muscle Cells (SMC) Leukocytes and ECs produce and release numerous cytokines and potent mitogens [interleukin-1 (IL-1), tumour necrosis factor-α (TNF-α), macrophage-colony stimulating factor (M-CSF)] or growth factors [fibroblast growth factor (FGF), heparin-binding epidermal growth
Fig. 1.2.3 Atherosclerotic plaque. This mature plaque is characterized by a fibrous cap and by the presence of cholesterol clefts in the vessel wall
27
28
1.2 Development of Atherosclerosis for the Vascular Surgeon
matrix (such as type I and type III collagen, elastin and proteoglycans). As a consequence, more mature plaques are characterized by increased fibrous and less cellular architecture [42, 58] (Fig. 1.2.3).
1.2.3 Contributive Factors to Endothelial Dysfunction and Plaque Formation Several potential factors leading to endothelial dysfunction have been identified and include smoking, diabetes mellitus, hypertension, increased plasma level of oxidized modified lipoprotein (LDL, low density lipoprotein), hyper homocysteinemia, infectious microorganisms (Herpes virus or Chlamydia pneumoniae), or combinations of these or other factors.
pounds. Besides effects on lipid metabolism (stimulation of lipolysis and increase in LDL levels), nicotine contributes to the conversion of SMC from a contractile to a synthetic phenotype. Increased levels of fibrinogen, increased platelet activity and blood viscosity together with decreased prostacyclin levels also contribute to altering the vascular wall. Homocysteinemia is an autosomal recessive disease that is the consequence of a deficiency of the enzyme cystathione β-synthase [5]. Elevated levels of homocysteine are correlated with an increased risk of coronary heart disease, stroke and peripheral vascular disease [52]. Homocysteine causes EC dysfunction, SMC proliferation and collagen production. Increased LDL oxidation and inhibition of endogenous anticoagulant activity are associated features of the disease.
1.2.3.2 The Oxidized LDL Hypothesis 1.2.3.1 Miscellaneous Factor Hypertension is associated with increased vascular permeability resulting in enhanced migration of lipoproteins and macromolecules into the intima. In the presence of hypertension, cyclic strain and pulsatile stretching of the vessel wall are increased, which lead to repetitive, circumferential, pulsatile pressure distension being conferred to the vascular wall [57]. In response to cyclic strains, signal transduction pathways in ECs are activated with resulting changes in morphology and proliferation. As mentioned previously, expression of cellular adhesion molecules (ICAM-1 for example) is increased. In addition, production of toxic oxygen species (hydrogen peroxide, superoxide anion, hydroxyl radical) is increased by hypertension, with reduction of endothelial nitric oxide release resulting in increased peripheral resistance [9]. Cyclic strains also affect the arterial sub endothelium, with changes in SMC shape, orientation and proliferation and the secretion of extracellular matrix contributing to the development of atherosclerotic lesions. Notably, collagen production is increased when SMC are submitted to cyclic strains. Finally, angiotensin II promotes SMC hypertrophy and its levels are frequently elevated during hypertension. Smoking is damaging for the vascular wall, resulting in swelling and luminal surface projections of ECs [53]. Cigarette smoke contains several potentially toxic compounds including nicotine, aromatic hydrocarbons, sterols, aldehydes, nitriles, cyclic ethers and sulfur com-
Low density lipoproteins (LDL) are plasma particles that contain in association with protein several types of lipids with a predominance of phospholipids, free and esterified cholesterol, for a total of about 1200 unsaturated fatty acid chains. In the presence of high levels of LDL – a well-recognized risk factor for developing atherosclerosis – influx of cholesterol and LDL into the intima is increased. In addition to binding to connective tissue elements (such as proteoglycans), accumulated LDL is progressively oxidized [36–38, 56] (Fig. 1.2.4). This increased oxidation gives rise to the production of several toxic products. For example, free radicals chain reaction within the lipid chains form hydroperoxides that easily break down, generating aldehydes (malonaldehyde, 4-hydroxynonenal) and other toxic substances that can react with lysine moieties in the B-apoprotein part of the LDLs. Other toxic products include for example 7-β-hydroperoxycholesterol, 7-ketocholesterol, lysophosphatidylcholine, oxidized fatty acid and epoxy sterols [18]. Native (nonoxidized) LDLs are collected by the extremely specific LDL receptors, and then cleared by a nonatherogenous process. In contrast, the oxidatively modified LDLs are not recognized by these receptors. They are metabolized in an unregulated way by scavenger receptors expressed by the macrophages present in the vascular wall and derived from the circulating monocytes, as mentioned previously [48]. Removal and sequestration of modified LDLs by macrophages may be considered a protective role minimizing the effects of modified
1.2.3 Contributive Factors to Endothelial Dysfunction and Plaque Formation
Fig. 1.2.4 Role of LDL oxidation in atheromatous plaque formation. After oxidation, LDLs exert toxic effects on endothelial cells with resultant expression of cell adhesion molecules and release of growth factors. Oxidized LDL also stimulates smooth muscle cell proliferation. After endocytosis of oxidized LDL, macrophages transform into foam cells. (E-selectin Endothelial selectin, GM-CSF granulocyte-monocyte-colony stimulating factor, ICAM-1 intercellular adhesion molecule-1, LDL low density lipoprotein, Lyso-PC lysophosphatidylcholine, MCP-1 monocyte chemoattractant protein-1, ox-chol oxidized cholesterol VCAM-1 vascular cell adhesion molecule)
LDL. Nevertheless, this route is atherogenous, since the internalization of LDL by macrophages leads to the formation of lipid peroxides and facilitates the transformation of macrophages into foam cells [60]. Vitamins C and E protect LDLs against oxidation and protective effects of vitamin E supplementation have been suggested in some reports [17]. In addition to their ability to injure macrophages, oxidized LDLs contribute to the perpetuation of the inflammatory reaction and to progression of the plaque, mainly for two reasons [35]. First, oxidized LDLs are implicated in the recruitment and proliferation of monocytes and lymphocytes, notably via upregulation of gene expression for MCP-1 and for M-CSF. This inflammatory response
increases the inward movement of lipoprotein within the artery, leading to a positive feedback. This induces a vicious cycle favouring development and progression of the plaque. Second, autoantibodies directed toward modified LDLs are produced. Along with scavenging of LDL, immune complexes taken up by macrophages stimulate the release of cytokines and growth factors by macrophages, thus contributing to stimulation of SMC migration and proliferation. Diabetes is often associated with an accelerated course and a diffuse character of atherosclerosis, especially in peripheral arteries, with devastating cardiovascular complications. In this case, the nonenzymatic glycosylation process of LDL impairs binding of LDL to its receptor and
29
30
1.2 Development of Atherosclerosis for the Vascular Surgeon
increases the formation of foam cells [22]. This process is facilitated since vascular permeability is increased subsequent to alteration of the components of the extracellular matrix and to thickening of the basement membrane [54].
1.2.4 Plaque Instability and Complicated Plaques Generally, atherosclerotic plaques remains asymptomatic because of the development of a collateral circulation heralded by chronic or subacute episodes of hypoxia and because of a compensatory enlargement of the blood vessel, thus trying to maintain adequate blood flow and constant lumen diameter (vascular remodelling) [23]. Increasing the vessel size is effective until the narrowing is approximately less than 40% of the normal lumen [59]. However, during its maturation process the plaque may become vulnerable and predisposed to ulceration and/or rupture [12, 19]. Once a plaque becomes ulcerated and disrupted, the coagulation cascade is initiated, with formation of platelet-rich white thrombi, that differ from the red thrombi formed in regions of stasis or low flow. Despite simultaneous endogenous thrombolysis, the initial small mural thrombus may evolve to a major, near-occlusive thrombus. It may also embolize, resulting in distal small vessel occlusion leading eventually to massive arterial occlusion. In these circumstances, acute clinical conditions may occur, with the onset of a wide range of symptoms including rapidly installing unstable angor pectoris, myocardial infarction, transient ischaemic attack, or toe gangrene. Several factors influencing plaque stability have been identified, such as the extent of the lipid core, the fibrous cap and its thickness, and the amount of inflammation within the cap. Thin or ruptured fibrous caps with lack of SMC-mediated healing, a large lipidic core (with a predominance of cholesterol esters) and intense cell infiltration with inflammatory activity render the plaque more vulnerable [6]. In other words, dense and uniform fibrous caps are generally associated with stable plaques. Usually, erosion and thinning of the plaque are uneven and rupture frequently occurs at the shoulder of the lesion where the fibrous cap is the thinnest and more susceptible to physical forces causing rupture [21]. In the areas of rupture, the plaque is also massively infiltrated by macrophage-derived foam cells and SMC proliferation seems impaired, with a high frequency of apoptosis of
these latter cells [4]. Once immunologically activated by T lymphocytes, these macrophages massively release matrix metalloproteases (such as collagenases, elastases and stromelysins) [16]. Although metalloproteases probably exert a regulatory action by breaking down extracellular matrix formation during the early stage of plaque formation, these serine and cysteine proteases degrade the various components of the extracellular matrix, further destabilizing the plaques [15, 27, 44]. Simultaneously, production of tissue-factor procoagulant and other haemostatic factors further increase the possibility of thrombosis. Along with intrinsic factors, extrinsic factors also influence the plaque stability. Low or oscillatory shear stress promotes plaque complication. Cyclic blood pressure changes may cause circumferential bending of eccentric soft plaques, which may weaken them. In addition, large deposits of calcium found on atheromatous plaques can be directly mediated by interaction with collagen. This massive calcification of the plaque alters the elastic properties and has significant haemodynamic consequences.
1.2.5 Classification of Atherosclerotic Plaques The American Heart Association Committee on Vascular Lesions has proposed a classification of atherosclerotic plaques [46, 47]. This classification is based on the plaque’s evolution and maturation stages. Phase I lesions correspond to early arterial changes that will progress in a stable fashion for several years. Phase II lesions are lipid-rich plaques that are prone to rupture. Phase III and phase IV lesions refer to acutely complicated plaques with formation of a nonocclusive (phase III) or an occlusive (phase IV) thrombus. Phase V lesions consist of an organized and fibrotic thrombus. From a histological perspective and according to their cell and lipid contents, different types (I, II and III) are distinguished in phase II lesions. The vulnerable type IV (lesion with intermixed lipids and fibrous tissue) and Va (lesion with an increased lipid core covered by a thin fibrous cap) lesions are the most relevant to acute ischaemic lesions. Disruption of a type IV or type Va lesion leads to the formation of a thrombus or “complicated” type VI lesion. Type VI lesions consist of confluent cellular lesions with a great deal of extracellular lipid intermixed with fibrous tissue covered by a fibrous cap. The complicated type VI is reserved for phase III and IV lesions causing acute syndromes. These lesions are more the consequence
1.2.7 General Therapeutic Measures
of an occlusive thrombus rather than being characterized by a small mural thrombus.
1.2.6 Assessment and Evaluation of the Risk of an Atherosclerotic Plaque As shown above, the sequence of events characterizing atherosclerosis is associated with an active inflammation process. This explains the elevation of plasma concentrations of various markers, such as fibrinogen, C-reactive protein and E-selectin, which may indicate ongoing atherosclerosis. Elevated levels of circulating metalloproteases have also been found in patients with unstable and complicated carotid plaques [42]. Description of the various technical methods available to evaluate an atherosclerotic patient presenting with clinical symptoms is outside the scope of this chapter and is reported elsewhere. Nevertheless, when considering atherosclerosis development and complications, an essential goal is to identify or recognize a vulnerable or unstable plaque prone to thrombosis and rupture. This is essential if one is to eventually decrease the complication rate of atherosclerosis and to prevent acute complications. Several invasive (e.g. X-ray angiography, intravascular ultrasound and angioscopy) and noninvasive (surface Bmode ultrasound and ultrafast computed tomography) imaging techniques may provide information on morphological characteristics of the disease, such as lumen diameter, degree of stenosis or wall thickness [8, 34]. Nevertheless, some of these techniques are limited in the evaluation of the evolutionary tendency of atherosclerosis. For example, measurement of luminal stenosis from digital subtraction techniques does not adequately reflect disease burden in carotid atherosclerosis. Vessel wall remodelling may produce normal luminal measurements despite a large atheromatous plaque in situ. Moreover, although an assessment of the relative risk associated with the atherosclerotic disease may be obtained with some techniques, these techniques do not give information on the composition of the plaque and are therefore incapable of identifying unstable plaques. In this context, noninvasive high-resolution magnetic resonance imaging (MRI) is an alternative for atherosclerotic plaque characterization, as shown by animal and human studies [30]. MRI differentiates plaque components on the basis of biophysical and biochemical parameters such as chemical composition and concentration, water content, physical state, molecular motion, or diffusion…
Initial studies were performed ex vivo and focused on lipid assessment with nuclear magnetic resonance spectroscopy and chemical shift imaging [45]. With the improvement of the MRI techniques, high resolution and contrast imaging became possible and therefore allowed the in vivo study of different plaque components [10]. As shown in vivo on human carotid, coronary and peripheral arteries, MRI allows characterization of the plaque components, such as lipid core, neovascularization, fibrous cap, necrotic cores, intraplaque haemorrhage and thrombus, with very high overall sensitivity and specificity [28]. Correlation is excellent with histopathology in grading the lesion shape and type. The concentration of serum markers of inflammation also correlates with MR markers of atherosclerosis, as shown in patients presenting with plaques in the aorta and common carotid artery [55]. The patients with MRI markers of unstable plaques have higher values of IL-6, C-reactive protein and VCAM-1 than those without MRI markers. Finally, in the thoracic aorta, MRI and trans-oesophageal echocardiography cross-sectional aortic images show a strong correlation for estimation of the plaque composition and of the mean maximum plaque thickness [20]. Along with monitoring of basic studies of atherosclerotic disease, MRI may thus be used to follow the progression of atherosclerosis in a given patient (hypercholesterolemic patient for example) or to detect atherosclerosis prospectively and its location in a given population. For example, an MRI study of asymptomatic patients from the Framingham Heart Study (FHS) showed that atherosclerotic disease prevalence and burden (i.e. plaque volume/aortic volume) significantly increased with age and was higher in the abdominal aorta compared with the thoracic aorta. So, in vivo, high-resolution, multi-contrast MR imaging is a promising method for imaging vulnerable plaques, characterizing plaques in term of lipid and fibrous content, and identifying the presence of thrombus or calcium in all arteries including the coronary arteries. MRI also allows serial evaluation assessment of the progression and/or regression of atherosclerosis over time.
1.2.7 General Therapeutic Measures Since atherosclerosis is a systemic disease frequently associated with several risk factors, hygieno-dietetic measures must be recommended in addition to drug therapies. Smoking must be discontinued with the help
31
32
1.2 Development of Atherosclerosis for the Vascular Surgeon
of smoking cessation programmes and antidepressant therapy, if necessary. Lipid-lowering drugs are especially indicated, with the use of HMG-CoA reductase inhibitors. Statins not only decrease cholesterol levels but also exert pleiotropic effects on the vascular wall limiting the inflammatory process within the plaques [1, 13]. Plaque regression with lipid-lowering therapy has been reported in both the aorta and carotids. An LDL cholesterol level less than 100 mg/dl should be attained. The incidence of cardiac event may be minimized by appropriate control of heart rate and blood pressure. Diabetic patients should be adequately treated and monitored. Haemoglobin A1c should be less than 7%. Dietary supplementation of vitamin B12 and folic acid should be prescribed, especially in patients with hyperhomocysteinemia [25]. Exercise decreases LDL cholesterol and all patients should maintain a regular exercise regimen. Lastly, the use of anti-platelet drugs may reduce the risk of fatal and nonfatal ischaemic events in patients with vascular disease. Several drugs are available and aspirin and clopidogrel are quite effective.
1.2.8 Conclusion Knowledge about atherosclerosis has increased dramatically over the last 20 years. Despite significant improvements in medical and surgical treatment, atherosclerosis remains a serious disabling and sometimes life-threatening disease. Perhaps in the future the development of gene therapy will provide a new mode of therapy able to modify not only the initiation but also the progression of the plaque. Nevertheless, at the present time, general therapeutic, preventive and adjunctive measures are the only way to limit the progression and consequences of atherosclerosis. In addition, a screening programme is also useful in order to detect the unstable plaques prone to rupture and to complications. References 1. Bellosta S, Via D, Canavesi M (1998) HMG-CoA reductase inhibitors reduce MMP-9 secretion by macrophages. Arterisocler Thromb Vasc Biol 18:1671–1678 2. Benditt EP, Benditt JM (1973) Evidence for a monoclonal origin of human atherosclerotic plaque. Proc Natl Acad Sci USA 70:1753–1756 3. Berliner JA, Navab M, Fogelman AM, Frank JS, Demer LL, Edwards PA, Watson AD, Lusis AJ (1995) Atherosclerosis: basic mechanisms: oxidation, inflammation and genetics. Circulation 91:2488–2496
4. Bjorkerud S, Bjorkerud B (1996) Apoptosis is abundant in atherosclerotic lesions, especially in inflammatory cells (macrophages and T-cells), and may contribute to the accumulation of gruel and plaque instability. Am J Pathol 149:367–380 5. Boushey CJ, Beresdorf SA (1995) A quantitative assessment of plasma homocysteine as a risk factor for vascular disease: probable benefits of increased folic acide intakes. J Am Med Assoc 274:1049–1057 6. Boyle JJ (1997) Association of plaque rupture and atherosclerotic inflammation. J Pathol 181:93–99 7. Burrig KF (1991) The endothelium of advanced arteriosclerotic plaques in humans. Arterio Thromb 11:1678–1689 8. Celermajer DS (1998) Noninvasive detection of atherosclerosis. N Engl J Med 339:2014–2015 9. Chobanian AV (1983) The influence of hypertension and other hemodynamic factors in atherogenesis. Cardiovasc Dis 26:177–196 10. Choi CJ, Kramer CM (2002) MR imaging of atherosclerotic plaque. Radiol Clin North Am 40:887–898 11. Davies MJ, Wollf N (1993) Atherosclerosis: what is it and why does it occur? Br Heart J 69 (Suppl):S3–S11 12. Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J (1993) Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J 69:377–381 13. Davignon J, Mabile L (2002) Mécanismes d’action des statines et leurs effets pléiotropiques. Ann Endocrinol 62:101–112 14. De Palma RG, Gallagher GL (1997) In: Sidawy AN, Sumpio BE (eds) The basic science of cardiovascular disease. Futura, Armonk, N.Y., pp 151–186 15. Defawe O, Colige A, Lambert C, Munaut C, Delvenne P, Nusgens B, Lapière C, Limet R, Sakalihasan N (2003) TIMP2 and PAI-I mRNA levels are lower in aneurysmal as compared to atheroocclusive abdominal aortas. Cardiovasc Res 60:205–213 16. Dollery CM, McEwan JR, Henney AM (1995) Matrix metalloproteinases and cardiovascular disease. Circ Res 77:863–868 17. Esterbauer H, Rotheneder M, Striegl G, Waeg G, Ashy A, Sattler W, Jurgens G (1989) Vitamin E and other lipophilic antioxidants protect LDL against oxidation. Fat Sci Technol 91:316–324 18. Esterbauer H, Dieber-Rotheneder M, Waeg G, Striegl G, Jurgens G (1990) Biochemical structural and functional properties of oxidized low density lipoprotein. Chem Res Toxicol 3:77–92 19. Falk E (1992) Why do plaques rupture? Circulation 86 (Suppl III):III30–III42
References
20. Fayad ZA, Tamana N, Badimon JJ, Goldman M, Weinberger J, Fallon JT, Aguinaldo G, Shinnar M, Chesebro JH, Fuster V (1998) In vivo MR characterization of plaques in the thoracic aorta. Circulation 98:I515 21. Fuster V (1999) Plaque stabilization: present and future trends. In: Fuster V (ed) The vulnerable atherosclerotic plaque: understanding, identification and modification. American Heart Association, Armonk, N.Y., pp 393–412 22. Ginsberg HN (1991) Lipoprotein physiology in non-diabetic and diabetic states: relationship to atherosclerosis. Diabetes Care 14:839–845 23. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ (1987) Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 316:1371–1375 24. Heldin CH, Westermark B (1990) Platelet-derived growth factor: mechanism of action and possible in vivo function. Cell Regul 1:555–556 25. Jacques PF, Selhub J et al (1999) The effect of folic acid fortification on plasma folate and total homocysteine concentration. N Engl J Med 340:1449–1454 26. Jonasson L, Holm J, Skalli O, Bjonders G, Hansson GK (1986) Regional accumulations of T cells, macrophages and smooth muscle cells in the human atherosclerotic plaque. Arteriosclerosis 6:131–138 27. Konx JB, Sukhova GK, Whittemore AD, Libby P (1995) Evidence for altered balance between matrix metalloproteinases and their inhibitors in human aortic diseases. Circulation 95:205–212 28. Kramer CM, Cerilli LA, Hagspiel K, DiMaria JM, Epstein FH, Kern JA (2004) Magnetic resonance imaging identifies the fibrous cap in atherosclerotic abdominal aortic aneurysm. Circulation 109:1016–1021 29. Libby P, Ross R (1996) Cytokines and growth regulatory molecules. In: Fuster V, Ross R, Topol E (eds) Atherosclerosis and coronary artery disease. Lippincott-Raven, Philadelphia, pp 585–594 30. Martin AJ, Gotlieb AI, Henkelman RM (1995) High-resolution imaging of human arteries. J Magn Reson Imaging 5:93–100 31. Matsushita H, Lee KH, Tsao PS (2001) Cyclic strain induces reactive oxygen species production via an endothelial NAD(P)H oxidase. J Cell Biochem 36 (Suppl):99–106 32. Moses HL, Yang EY, Pietenpol JA (1990) TGF-beta stimulation and inhibition of cell proliferation: new mechanistic insights. Cell 63:245–247 33. Nelken N, Coughlin S, Gordon D ( 1991) Monocyte chemoattractant protein-1 in human atherosclerotic plaques. J Clin Invest 88:1121–1127
34. Nissen SE, DeFranco AC, Tuzcu EM, Moliterno DJ (1995) Coronary intravascular ultrasound: diagnostic and interventional applications. Coron Artery Dis 6:355–367 35. Parthasarathy S, Steinberg D, Witzum JL (1992) The role of oxidized low-density lipoprotein in the pathogenesis of atherosclerosis. Annu Rev Med 43:219–255 36. Pincemail J, Defraigne J-O, Limet R (1996) Oxidative stress in clinical situations: fact or fiction? Eur J Anaesthiol 13:219–234 37. Pincemail J, Lecomte J, Castiau JP, Collard E, Vasankari T, Cheramy-Bien J-P, Limet R, Defraigne J-O (2000) Evaluation of autoantibodies against oxidized LDL and antioxidant status in top soccer and basketball players after four months of competition. Free Radic Biol Med 28:559–565 38. Pincemail J, Bovy JC, Chapelle JP, Gielen J, Defraigne J-O, Rorive G (2001) Markers of oxidative stress linked to increased risk of cardiovascular diseases in chronic hemodialysis patients. Free Radic Biol Med (Suppl 1) 31(A345) 39. Rauch U, Osende JI (2001) Thrombus formation on atherosclerotic plaques in humans. Ann Intern Med 134:224–238 40. Rollins BJ, Yoshimura T, Leonard EJ (1990) Cytokine-activated human endothelial cells synthesize and secrete a monocyte chemoattractant, MCP-1/JE. Am J Pathol 136:1229–1233 41. Ross R (1993) The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 362:801–809 42. Ross R (1999) Atherosclerosis – an inflammatory disease. N Engl J Med 340:115–126 43. Ross R, Glomset JA (1973) Atherosclerosis and the arterial smooth muscle cell: proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. Science 180:1332–1339 44. Shah PK, Falk E, Badimon JJ, Fernandez-Ortiz A, Mailhac A, Villareal-Levy G, Fallon JT, Regnstrom J, Fuster V (1995) Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic fibrous caps. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture. Circulation 92(6):1565–1569 45. Shinnar M, Fallon JT, Wehrli S, Levin M, Dalmacy D, Fayad ZA, Badimon JJ, Harrington E, Fuster V (1999) The diagnostic accuracy of ex vivo magnetic resonance imaging for human atherosclerotic plaque characterization. Arterioscler Throm Vasc Biol 19:2756–2761 46. Stary HC, Chandler AB, Glagov S, Guyton JR, Insull W, Ronsefeld ME, Schaffer SA, Schwartz CJ, Wagner WD, Wissler RW (1994) A definition of initial, fatty streak, and intermediate lesions of atherosclerosis: a report from the Committee on Vascular Lesions of the Council of Arteriosclerosis, American Heart Association. Circulation 89:2462–2478
33
34
1.2 Development of Atherosclerosis for the Vascular Surgeon
47. Stary HC, Chandler AB, Dinsmore RE, Fuster V, Glagov S, Insull W, Ronsefeld ME, Schwartz CJ, Wagner WD, Wissler RW (1995) A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on a Arteriosclerosis, American Heart Association. Circulation 92:1355–1374 48. Steinberg D, Parthasarathy S et al (1989) Modification of low-density lipoprotein that increases its atherogenicity. N Engl J Med 320:915 49. Strong JP (1993) Natural history of aortic and coronary atherosclerotic lesions in youth: findings from the PDAY study. Arterio Thromb 13:1291–1298 50. Sumpio BE (1989) Mechanical stress ands cell growth. J Vasc Surg 10:570–571 51. Sumpio BE (1993) In: Sumpio BE (ed) Hemodynamic and vascular cell biology. RG Landes, Austin 52. Tsai JC, Perella MA (1994) Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis. Proc Natl Acad Sci USA 91:6369–6373 53. Villablanca AC, McDonald JM, Rutledge JC (2000) Smoking and cardiovascular disease. Clin Chest Med 21:159–172
54. Vlassara H, Bucal R, Stiker L (1994) Pathogenesis effect of advanced glycosylation: biochemical and biologic implication for diabetes and aging. Lab Invest 70:138–151 55. Weiss CR, Arai AE, Bui MN (2002) Arterial wall MRI characteristics are associated with elevated serum markers of inflammation in humans. J Magn Reson Imaging 2001:698–704 56. Witzum JL, Berliner JA (1998) Oxidized phospholipids and isoprostanes in atherosclerosis. Curr Opin Lipidol 9:441–442 57. Xu C, Lee S et al (2001) Molecular mechanisms of aortic wall remodeling in response to hypertension. J Vasc Surg 33:570–578 58. Zarins CK, Glagov S (1982) Aneurysms and obstructive plaques: differing local responses to atherosclerosis. In: Bergan JJ, Yao JS (eds) Aneurysms. Diagnosis and treatment. Grune and Stratton, New York, p 61 59. Zarins CK, Weisenberg E, Glagov S (1988) Differential enlargement of artery segments in response to enlarging atherosclerotic plaques. J Vasc Surg 7:386–394 60. Zhang H, Basra HJK, Steinbrecher UP (1990) Effects of oxidatively modified LDL on cholesterol esterification in cultured macrophages. J Lipid Res 31:1361–1369
35
1.3 Lipids and Peripheral Arterial Disease Stella S. Daskalopoulou, Marios E. Daskalopoulos, Christos D. Liapis, Dimitri P. Mikhailidis
1.3.1 Introduction Peripheral arterial disease (PAD) is associated with a high risk of vascular events [1, 2, 14, 18, 19, 31, 32]. This is true whether PAD is symptomatic or asymptomatic. This risk is so high that PAD is considered as a coronary heart disease (CHD) equivalent [5, 13]. It follows that these patients need to have their modifiable vascular risk factors controlled. Dyslipidaemia, a modifiable vascular risk factor, should be treated aggressively with lipid-lowering drugs, according to international guidelines [5, 13, 16, 37]. The earlier low density lipoprotein-cholesterol (LDL-C) targets {European LDL-C target <96 mg/dl (2.5 mmol/l) [5] and National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III [13] LDL-C target <100 mg/dl (2.6 mmol/l)} have been revised recently. Thus, the UK guidelines set the LDL-C goal to ≤2.0 mmol/l (77 mg/dl) for high-risk patients (March 2004) [37]. Furthermore, the revised NCEP ATP III guidelines proposed the optional target of ≤70 mg/dl (1.8 mmol/l) for very highrisk patients (July 2004) [16]. Other lipid variables, such as high density lipoproteincholesterol and triglycerides, are also important and they have recently attracted more attention [11]. However, the guidelines still focus on LDL-C levels as the main target for treatment [5, 13, 16, 37]. In this review, we consider the evidence showing the effect of lipid-lowering drugs on: • Prevention of PAD • Improvement of symptoms associated with PAD • Reduction of the risk of vascular events [e.g. myocardial infarction (MI), stoke or revascularization] associated with PAD.
1.3.2 Effect of Lipid Lowering on PAD 1.3.2.1 Prevention of PAD A post-hoc analysis of the Scandinavian Simvastatin Survival Study (4S) found that new or worsening intermittent claudication was significantly (p = 0.008) reduced (by 38%) in those taking the statin when compared with the group assigned to placebo [30]. All the patients (n = 4444) participating in this trial had CHD and were followed-up for a median of 5.4 years. In the Program on the Surgical Control of Hyperlipidemias (POSCH) [9] the effect of cholesterol-lowering induced by partial ileal by-pass in patients (n = 838) with a previous MI and hyperlipidaemia was assessed. The incidence of new cases of claudication was significantly lower [relative risk (RR): 0.66, 95% confidence interval (CI): 0.20–0.90; p = 0.009] in the intervention group when compared with the control (nonintervention) group 4 years after the closure of the trial.
1.3.2.2 Improvement of Symptoms Associated with PAD As mentioned above, new or worsening intermittent claudication was significantly (p = 0.008) reduced (by 38%) in the active treatment group of the 4S trial [30]. In another study [24] patients (n = 354) with intermittent claudication were assigned to placebo or active treatment with atorvastatin 10 mg or 80 mg daily. Maximal walking time after 12 months of treatment did not change significantly. However, there was a significant (p = 0.025) improvement in pain-free walking time in the 80 mg group compared with placebo. A physical activity questionnaire showed improvement (p = 0.011) in ambulatory ability for the 10 and 80 mg groups, whereas two quality of life questionnaires did not show significant changes.
36
1.3 Lipids and Peripheral Arterial Disease
Another study [21] included 392 patients with an ankle brachial pressure index (ABPI) <0.90 and 249 with ABPI 0.90–1.50. After adjusting for age, sex, ABPI, co-morbidities, cholesterol and other confounders, those taking statins had significantly better walk performance indices than participants not taking statins. Positive associations were slightly attenuated after additional adjustment for C-reactive protein (CRP) level but remained statistically significant for walking velocity and the summary performance score. These findings suggest that both the cholesterol-lowering and non-cholesterol-lowering actions of statins may favourably influence functioning in persons with and without PAD. The effect of short-term therapy with simvastatin on walking performance was assessed in hypercholesterolaemic (>220 mg/dl; 5.7 mmol/l) patients (n = 86) with PAD [25]. The patients were assigned either to simvastatin 40 mg (n = 43) or to a placebo (n = 43). At 6 months, the mean pain-free walking distance increased by 90 m (95% CI: 64–116; p < 0.005) more in the simvastatin group than in the placebo group. Similar results were seen for the mean total walking distance (increased by 126 m; 95% CI: 101–151; p < 0.001). The ABPI at rest increased by 0.09 (95% CI: 0.06–0.12; p < 0.01) and after exercise by 0.19 (95% CI: 0.14–0.24; p < 0.005) in those taking simvastatin. There was also a greater improvement in claudication symptoms among patients treated with simvastatin. In the Lower Extremity Arterial Disease Event Reduction (LEADER) trial [22], bezafibrate 400 mg daily (n = 783 men) or placebo (n = 785 men) were compared (median follow-up of 4.6 years). Bezafibrate reduced the severity of intermittent claudication for up to 3 years. The changes in symptoms may be related to the angiographic improvement documented in several studies.
1.3.2.3 Reduction of the Risk of Vascular Events Associated with PAD The Heart Protection Study (HPS) [17] confirmed that statin treatment reduces the risk of death and adverse cardiovascular events in patients with coronary and noncoronary atherosclerosis, including patients with PAD but without diagnosed CHD (n = 2701). There was a significant reduction (approximately 25%) in the first major vascular event (major coronary event, stroke or revascularization) among patients with PAD, with or without prior CHD (both p < 0.0001). In HPS there was a significant 16% [standard error (SE) 6.0, 95% CI: 5.0–26.0)] propor-
tional reduction in the rate of noncoronary revascularization (4.4% versus 5.2%; p = 0.006). Half of that difference involved a definite reduction in carotid endarterectomy or angioplasty (0.4% versus 0.8%; p = 0.0003). In the Mohler et al. study [24], mentioned above, there was a significant (p = 0.003) reduction in vascular events after 12 months. There were 3 events in the 240 patients (1.3%) assigned to atorvastatin (10 and 80 mg/day) and 9 events in the 114 patients (7.9%) assigned to placebo. Statin use has also been shown to decrease the risk of vascular events in diabetics with and without prior MI [2]. In a comparison of 318 PAD patients treated with statins versus 342 patients not on lipid-lowering drugs there were significant changes in the event rates after a mean follow-up of 39 months [1]. Sudden coronary death, fatal MI and new coronary events were all significantly reduced (p = 0.0005, p = 0.007 and p < 0.0001, respectively). In the LEADER trial [22], bezafibrate had no effect on the incidence of CHD and of stroke combined. However, the incidence of nonfatal coronary events was reduced (RR: 0.60, 95% CI: 0.36–0.99; p = 0.05), particularly in those aged <65 years at entry, in whom all coronary events may also be reduced (RR: 0.38, 95% CI: 0.20–0.72). In this trial plasma fibrinogen levels fell by 13% (p < 0.0001) in the bezafibrate group. It is well established that elevated plasma levels of this coagulation factor contribute to whole-blood viscosity and to an increased risk of vascular events in patients with PAD.
1.3.3 Peripheral Vascular Surgery and Statins Graft patency and limb salvage were improved in patients taking statins before infra-inguinal by-pass surgery [18]. Aggressive lipid lowering may reduce the high mortality and morbidity (mainly from coronary events) associated with vascular surgery in PAD and other patients [14, 29]. Coronary events are the most important cause of long-term morbidity and mortality after peripheral vascular surgery [12, 14]. Even PAD patients without overt CHD are at significant risk of long-term cardiac events. The effect of atorvastatin compared with placebo on the occurrence of a composite of cardiovascular events after vascular surgery was assessed [12]. Patients (n = 100) were randomly assigned to atorvastatin 20 mg once daily (n = 50) or placebo (n = 50) for 45 days, irrespective of
1.3.6 Concluding Comments
their serum cholesterol concentration. Vascular surgery was performed on average 30 days after randomization. During the 6-month follow-up, the incidence of cardiac events was higher in the placebo compared with the atorvastatin group [13 (26.0%) versus 4 (8.0%); p = 0.031]. In a case-control study, among patients (n = 2816) who underwent major vascular surgery, 160 (5.7%) died during their hospital stay [32]. After adjustments, statin therapy was significantly less common in the patients who died than in controls (8% versus 25%; p < 0.001). The adjusted OR for peri-operative mortality among statin users as compared with nonusers was 0.22 (95% CI = 0.10–0.47).
1.3.4 Additional Potential Actions of Lipid-lowering Drugs that may Benefit PAD Patients Statins exert pleiotropic effects, which may be independent of LDL-C lowering. These effects may appear even before a change in lipid level occurs [26, 35]. Statins increase nitric oxide (NO) production and improve endothelial function (e.g. increased flow-mediated dilatation). They have antioxidant properties and they inhibit the migration of macrophages and smooth muscle cell proliferation, leading to an antiproliferative effect and the stabilization of atherosclerotic plaques. Statins have anti-inflammatory effects including a reduction in the circulating levels of CRP, inflammatory and proinflammatory cytokines [e.g. interleukin-6 (IL-6), IL8], adhesion molecules [e.g. intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1)] and other acute phase proteins. They reduce tissue factor expression and platelet activity, whereas fibrinolysis can be enhanced. Statins improve microalbuminuria, renal function, hypertension and arterial wall stiffness. A significant reduction of the carotid and femoral intima-media thickness was also reported early after statin treatment. In the GREACE trial, the effect [3, 4] of atorvastatin on serum creatinine and uric acid in patients with CHD was rapid and it was reversed equally rapidly if patients happened to discontinue atorvastatin. The fall in creatinine was greater in both those with higher baseline serum levels of this indicator of the glomerular filtration rate and at the higher doses of atorvastatin. Simvastatin can also significantly reduce serum creatinine and serum
uric acid (p < 0.0001) in patients with PAD treated for 3–4 months [38]. The difference in the creatinine levels was more pronounced in the tertile of patients with the highest baseline creatinine levels. Statins can reduce circulating CRP levels [6, 20]. Other lipid-lowering drugs (e.g. ciprofibrate [33], fenofibrate [36] and ezetimibe [7, 34]) can also decrease circulating CRP levels. However, the potential relevance of lowering CRP levels to a greater or lesser extent remains unclear. Furthermore, recent evidence suggests that circulating CRP levels may only be a moderate predictor of CHD risk. Patients with the metabolic syndrome have a clustering of many risk factors, such as hypertension, insulin resistance/type 2 diabetes mellitus, dyslipidaemia and obesity [11]. Therefore, it not surprising that these patients are at increased risk of developing PAD [15, 28]. The prevalence of the metabolic syndrome in PAD patients in a crosssectional survey [15] was 58%.
1.3.5 Are all Statins the Same? Statins are of proven efficacy in secondary prevention in high-risk groups such as PAD patients. However, we do not know if all statins are equally effective. This question can only be answered by “head to head” comparison trials that incorporate clinical endpoints. Potential differences between statins can conveniently be considered in the context of: • LDL-C lowering potency, and • Pleiotropic actions. So far, “head to head” comparisons clearly show that some statins are considerably more potent, in terms of LDL-C lowering, than others [10, 27]. However, potency must not be considered in the decision-making process at the expense of safety and event-based evidence. What is less clear is whether statins differ in properties that may not be exclusively due to variations in their LDL-C-lowering capacity, the so-called pleiotropic actions [8].
1.3.6 Concluding Comments Trial-based evidence shows that lipid-lowering treatment is beneficial in patients with PAD. However, these
37
38
1.3 Lipids and Peripheral Arterial Disease
patients are often under-treated despite their high risk for vascular events [19, 23]. It is also not widely appreciated that lipid lowering can improve PAD-related symptoms. The time has come for those looking after PAD patients to use aggressive preventive treatment. Although statins can improve both clinical outcomes and symptoms in PAD, it is possible that further benefit can be obtained if LDL-C levels are lowered beyond the “older” targets for high-risk patients [from 96–100 mg/ dl (2.5–2.6 mmol/l) to 70–77 mg/dl (1.8–2.0 mmol/l)]. However, we do not know if these “new” LDL-C targets provide further symptomatic improvement or a more effective prevention of events in PAD. These issues need to be resolved by appropriately designed trials. References 1. Aronow WS, Ahn C (2002) Frequency of new coronary events in older persons with peripheral arterial disease and serum low-density lipoprotein cholesterol ≥125 mg/dl treated with statins versus no lipid-lowering drug. Am J Cardiol 90:789–791 2. Aronow WS, Ahn C (2003) Elderly diabetics with peripheral arterial disease and no coronary artery disease have a higher incidence of new coronary events than elderly nondiabetics with peripheral arterial disease and prior myocardial infarction treated with statins and with no lipid-lowering drug. J Gerontol A Biol Sci Med Sci 58:573–575 3. Athyros VG, Mikhailidis DP, Papageorgiou AA, Symeonidis AN, Pehlivanidis AN,Bouloukos VI, Elisaf M (2004a) The effect of statins versus untreated dyslipidaemia on renal function in patients with coronary heart disease: a subgroup analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) Study. J Clin Pathol 57:728–734 4. Athyros VG, Elisaf M, Papageorgiou AA, Symeonidis AN, Pehlivanidis AN, Bouloukos VI, Milionis HJ, Mikhailidis DP; GREACE Study Collaborative Group (2004b) Effect of statins versus untreated dyslipidemia on serum uric acid levels in patients with coronary heart disease: a subgroup analysis of the GREek Atorvastatin and Coronary-heartdisease Evaluation (GREACE) study. Am J Kidney Dis 43:589–599 5. De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, Dallongeville J, Ebrahim S, Faergeman O, Graham I, Mancia G, Manger Cats V, Orth-Gomer K, Perk J, Pyorala K, Rodicio JL, Sans S, Sansoy V, Sechtem U, Silber S, Thomsen T, Wood D: Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (2003) European guidelines on cardiovascular disease prevention in clinical practice. Eur Heart J 24:1601–1610
6. Balk EM, Lau J, Goudas LC, Jordan HS, Kupelnick B, Kim LU, Karas RH (2003) Effects of statins on nonlipid serum markers associated with cardiovascular disease: a systematic review. Ann Intern Med 139:670–682 7. Ballantyne CM, Houri J, Notarbartolo A, Melani L, Lipka LJ, Suresh R, Sun S, LeBeaut AP, Sager PT, Veltri EP; Ezetimibe Study Group (2003) Effect of ezetimibe coadministered with atorvastatin in 628 patients with primary hypercholesterolemia: a prospective, randomized, double-blind trial. Circulation 107:2409–2415 8. Bonetti PO, Lerman LO, Napoli C, Lerman A (2003) Statin effects beyond lipid lowering – are they clinically relevant? Eur Heart J 24:225–248 9. Buchwald H, Bourdages HR, Campos CT, Nguyen P, Williams SE, Boen JR (1996) Impact of cholesterol reduction on peripheral arterial disease in the program on the surgical control of the hyperlipidemias (POSCH). Surgery 120:672–679 10. Cannon CP, Braunwald E, McCabe CH, Rader DJ, Rouleau JL, Belder R, Joyal SV, Hill KA, Pfeffer MA, Skene AM; Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators (2004) Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med 350:1495–1504 11. Daskalopoulou SS, Mikhailidis DP, Elisaf M (2004) Prevention and treatment of the metabolic syndrome. Angiology 55:589–612 12. Durazzo AE, Machado FS, Ikeoka DT, De Bernoche C, Monachini MC, Puech-Leao P, Caramelli B (2004) Reduction in cardiovascular events after vascular surgery with atorvastatin: a randomized trial. J Vasc Surg 39:967–975 13. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (2001) Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). J Am Med Assoc 285:2486–2497 14. Farkouh ME, Rihal CS, Gersh BJ, Rooke TW, Hallett JW Jr, O’Fallon WM, Ballard DJ (1994) Influence of coronary heart disease on morbidity and mortality after lower extremity revascularization surgery: a population-based study in Olmsted County, Minnesota (1970-1987). J Am Coll Cardiol 24:1290–1296
References
15. Gorter PM, Olijhoek JK, van der Graaf Y, Algra A, Rabelink TJ, Visseren FL; For the SMART Study Group (2004) Prevalence of the metabolic syndrome in patients with coronary heart disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm. Atherosclerosis 173:361–367 16. Grundy SM, Cleeman JI, Merz CN, Brewer HB Jr, Clark LT, Hunninghake DB, Pasternak RC, Smith SC Jr, Stone NJ; National Heart, Lung, and Blood Institute; American College of Cardiology Foundation; American Heart Association (2004) Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation 110:227–239 17. Heart Protection Study Collaborative Group (2002) MRC/ BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 360:7–22 18. Henke PK, Blackburn S, Proctor MC, Stevens J, Mukherjee D, Rajagopalin S, Upchurch GR Jr, Stanley JC, Eagle KA (2004) Patients undergoing infrainguinal bypass to treat atherosclerotic vascular disease are underprescribed cardioprotective medications: effect on graft patency, limb salvage, and mortality. J Vasc Surg 39:357–365 19. Hirsch AT, Gotto AM Jr (2002) Undertreatment of dyslipidemia in peripheral arterial disease and other high-risk populations: an opportunity for cardiovascular disease reduction. Vasc Med 7:323–331 20. Kinlay S, Schwartz GG, Olsson AG, Rifai N, Leslie SJ, Sasiela WJ, Szarek M, Libby P, Ganz P; Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering Study Investigators (2003) High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation 108:1560–1566 21. McDermott MM, Guralnik JM, Greenland P, Pearce WH, Criqui MH, Liu K, Taylor L, Chan C, Sharma L, Schneider JR, Ridker PM, Green D, Quann M (2003) Statin use and leg functioning in patients with and without lower-extremity peripheral arterial disease. Circulation 107:757–761 22. Meade T, Zuhrie R, Cook C, Cooper J (2002) Bezafibrate in men with lower extremity arterial disease: randomised controlled trial. Br Med J 325:1139–1141 23. Meijer WT, Grobbee DE, Hunink MG, Hofman A, Hoes AW (2000) Determinants of peripheral arterial disease in the elderly: the Rotterdam study. Arch Intern Med 160:2934–2938 24. Mohler ER, Hiatt WR, Creager MA (2003) Cholesterol reduction with atorvastatin improves walking distance in patients with peripheral arterial disease. Circulation 108:1481–1486
25. Mondillo S, Ballo P, Barbati R, Guerrini F, Ammaturo T, Agricola E, Pastore M, Borrello F, Belcastro M, Picchi A, Nami R (2003) Effects of simvastatin on walking performance and symptoms of intermittent claudication in hypercholesterolemic patients with peripheral vascular disease. Am J Med 114:359–364 26. Napoli C, Sica V (2004) Statin treatment and the natural history of atherosclerotic-related diseases: pathogenic mechanisms and the risk-benefit profile. Curr Pharm Des 10:425–432 27. Nissen SE, Tuzcu EM, Schoenhagen P, Brown BG, Ganz P, Vogel RA, Crowe T, Howard G, Cooper CJ, Brodie B, Grines CL, DeMaria AN; REVERSAL Investigators (2004) Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. J Am Med Assoc 291:1071–1080 28. Olijhoek JK, van der Graaf Y, Banga JD, Algra A, Rabelink TJ, Visseren FL; the SMART Study Group (2004) The metabolic syndrome is associated with advanced vascular damage in patients with coronary heart disease, stroke, peripheral arterial disease or abdominal aortic aneurysm. Eur Heart J 25:342–348 29. Pasceri V, Patti G, Nusca A, Pristipino C, Richichi G, Di Sciascio G; ARMYDA Investigators (2004) Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study. Circulation 110:674–678 30. Pedersen TR, Kjekshus J, Pyorala K, Olsson AG, Cook TJ, Musliner TA, Tobert JA, Haghfelt T (1998) Effect of simvastatin on ischemic signs and symptoms in the Scandinavian simvastatin survival study (4S). Am J Cardiol 81:333–335 31. Peripheral Arterial Diseases Antiplatelet Consensus Group (2003) Antiplatelet therapy in peripheral arterial disease. Consensus statement. Eur J Vasc Endovasc Surg 26:1–16 32. Poldermans D, Bax JJ, Kertai MD, Krenning B, Westerhout CM, Schinkel AF, Thomson IR, Lansberg PJ, Fleisher LA, Klein J, van Urk H, Roelandt JR, Boersma E (2003) Statins are associated with a reduced incidence of perioperative mortality in patients undergoing major noncardiac vascular surgery. Circulation 107:1848–1851 33. Rizos E, Bairaktari E, Kostoula A, Hasiotis G, Achimastos A, Ganotakis E, Elisaf M, Mikhailidis DP (2002) Effect of ciprofibrate on lipoproteins, fibrinogen, renal function, and hepatic enzymes. J Cardiovasc Pharmacol Ther 7:219–226 34. Sager PT, Melani L, Lipka L, Strony J, Yang B, Suresh R, Veltri E; Ezetimibe Study Group (2003) Effect of coadministration of ezetimibe and simvastatin on high-sensitivity C-reactive protein. Am J Cardiol 92:1414–1418
39
40
1.3 Lipids and Peripheral Arterial Disease
35. Tsiara S, Elisaf M, Mikhailidis DP (2003) Early vascular benefits of statin therapy. Curr Med Res Opin 19:540–556 36. Tsimihodimos V, Kostoula A, Kakafika A, Bairaktari E, Tselepis AD, Mikhailidis DP, Elisaf M (2004) Effect of fenofibrate on serum inflammatory markers in patients with high triglyceride values. J Cardiovasc Pharmacol Ther 9:27–33
37. Williams B, Poulter NR, Brown MJ, Davis M, McInnes GT, Potter JF, Sever PS, Thom SM; BHS guidelines working party, for the British Hypertension Society (2004) British Hypertension Society guidelines for hypertension management 2004 (BHS-IV): summary. Br Med J 328:634–640 38. Youssef F, Gupta P, Seifalian AM, Myint F, Mikhailidis DP, Hamilton G (2004) The effect of short-term treatment with simvastatin on renal function in patients with peripheral arterial disease. Angiology 55:53–62
41
1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? Rosa M. Moreno
1.4.1 Introduction In daily clinical practice, the vascular surgeon frequently has to evaluate and manage patients who present with venous thrombosis. Identifying the cause of this disease along with its risk factors has several interesting implications, which are reviewed in this chapter concerned with abnormalities in the blood clotting mechanism that generates hypercoagulation states.
1.4.2 Venous Thrombosis Venous thrombosis is a significant cause of morbidity and mortality in western countries, and is estimated to affect between 1 and 3 persons per 1000 each year [36]. A hypercoagulation, or hypercoagulable, state is defined as an abnormal situation of the circulating blood, in which a smaller stimulus is required to induce the onset of thrombosis compared to the normal coagulation state. It most commonly manifests as thromboembolic disease, deep vein thrombosis (DVT), pulmonary thromboembolism (PTE) or post thrombotic syndrome. However, venous thrombosis can affect any body site such as the retina, veins of the arm, or the mesenteric, hepatic or cerebral veins. Venous thrombosis seems to be age-related, since rates during childhood according to some authors are as low as 1 per 100,000 annually, while the incidence could reach 1% per year in elderly subjects [38]. The thrombotic state is produced by an upset in the normal balance of procoagulant, anticoagulant and fibrinolytic factors. An inherited tendency for thrombosis, irrespective of the causative factor, has been denoted primary or hereditary thrombophilia. Situations in which thrombosis is acquired are known as secondary hypercoagulable states. In
these cases, thrombosis is the final consequence of several factors making the precise definition of its physiopathological basis extremely difficult.
1.4.2.1 Risk Factors Acquired risk factors and predisposing conditions for the development of DVT have been described by an ad hoc team on behalf of The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter [42] (Table 1.4.1). The factors classically defined are: a previous history of DVT, immobilization, the postoperative state, age, heart disease, trauma to the lower limbs, a concurrent malignancy, hormone therapy, pregnancy, the postpartum period and obesity. Familial thrombophilia, a genetic risk factor, has been known since 1965 when Egeberg [10] identified an inherited tendency for thrombosis caused by an antithrombin III deficiency in a Norwegian family. It was not until almost two decades later that protein C [16] and protein S [44] deficiencies were identified, and anomalies such as factor V Leiden thrombophilia, mutation of the prothrombin gene or dysfibrinogenemia have been only recently described.
Acquired or Environmental Risk Factors Previous History of DVT
A previous episode of DVT in the lower limb is the most significant risk factor for developing a subsequent DVT episode. Specific phlebographic findings or the results of noninvasive tests are considered sufficient to confirm a previous DVT episode. A patient with post thrombotic syndrome yet no history of DVT should be suspected of having undergone a previous episode.
42
1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases?
Table 1.4.1 Risk factors for venous thrombosis Acquired
Congenital
Mixed
Previous thrombosis
Antithrombin III deficiency
Hyperhomocysteinaemia
Immobilization
Protein C deficiency
High factor VIII levels
Postoperative period
Protein S deficiency
High factor IX levels
Age
Factor V Leiden
High factor XI levels
Heart disease
Prothrombin gene mutation
Acquired PC resistance
Lower limb trauma
Blood group
Dysfibrinogenemia
Malignant tumour
Methylenetetrahydrofolate reductase
Hormone treatment
Dysfibrinogenemia
Pregnancy/postpartum Obesity Antiphospholipid syndrome
Immobilization
All situations affecting the action of the calf muscular pump are associated with DVT. Several situations are related to immobilization, such as bed rest, in turn produced by conditions such as acute myocardial infarction, cardiac insufficiency, respiratory insufficiency, paralysis or trauma, or even prolonged periods of sitting when travelling long distances. The duration and cause of immobilization affect the risk of DVT [37]. Since 1954, when Homans [18] reported the first case of DVT after a long commercial flight, this subject has generated much interest among both the medical and general population, with the so-called tourist class syndrome frequently appearing in the general press. Several publications reflect the interest in this topic [27, 43]. Some have reported findings such as sudden death being more common in airport arrivals than departure lounges [43]. Attention has also been paid to the possible influence that the length of the flight might have. Hence, the risk of DVT is 50 times higher in flights of distance longer than 10,000 km compared to flights covering a distance of 5000 km [27]. Other studies, some controlled, find no conclusive data regarding the size of possible risks, and attribute travel-related DVT to a multifactorial predisposition [11, 26]. In 2002, the World Health Organization launched its WRIGHT study (WHO Research into Global Hazards of Travel) to try to more precisely define these concepts. This investigation aims to establish the mechanisms through which thrombosis is induced and identify the roles of hypoxia and hypobaria. These
factors appear to act as triggers for coagulation, although these results have not yet been published.
The Postoperative State
The duration of surgery and the type of anaesthesia are related to the postoperative onset of DVT. These risks are particularly high in patients undergoing orthopaedic procedures [6, 19] at the level of the pelvis, hip or legs, with risks estimated at 30% to 50%. Further variables considered risk factors are neurosurgery procedures, any intraabdominal procedure, and gynaecological and urological surgery, especially radical prostatectomy [29].
Age
The risk of thrombosis increases with age. This may be explained by a combination of factors such as reduced mobility, diminished muscle tone, increased morbidity and the deterioration of the venous system itself. The age effect is considerable and should always be considered before making any clinical decision. When this risk is weighed up against the undesirable effects of treatment, the cost of screening or the disadvantages of not prescribing treatment, the management option selected can vary tremendously depending on the patient age group.
1.4.2 Venous Thrombosis
Heart Disease
The severity of a heart condition seems to increase the risk of developing DVT and, according to the New York Heart Association (NYHA) functional class, a correlative risk score is assigned [37, 42].
Trauma to the Lower Limbs
Major trauma is an important risk factor for thrombosis, which occurs in 50% to 60% of patients with cranial, or spinal cord trauma and fractures of the pelvis, femur or tibia [13].
A Concurrent Malignancy
DVT is more common in patients with a malignant tumour, an observation made for the first time by Trousseau [47] in 1865. DVT can be the first sign of cancer and is taken as a warning sign for malignant disease. The thrombogenic effect of cancer arises from the production of humoral factors (procoagulants), mechanical factors (vein compression or local infiltration) and general factors indicated by the presence and increased levels of acute phase reactants [5]. Indirectly, thrombosis may also be induced by reduced patient mobility and diminished uptake of vitamins such as folates. Finally, thrombosis may be promoted by the treatment received by the patient including radiotherapy and chemotherapy [31, 49], and may also be triggered by postsurgery fibrosis. The prevalence of cancer in patients with DVT has been estimated at 3% to 18% by different studies. In a Swedish population study [34], 19% of patients with DVT already had a diagnosis of cancer and 1 year later this proportion had increased by 5%. The type of tissue affected may also be related to the development of DVT [37], adenocarcinoma (especially mucinous) and cerebral malignant glioma being associated with the greatest risk.
Hormone Therapy
Several publications [50] have reported that oral contraceptives (OC), including those containing mini hormone doses, are linked to an increased risk of thrombosis of about fourfold. Most OC contain an oestrogen and progesterone. Over the years, the amount of oestrogen has been steadily reduced until the present dose of 30 μg or even less of ethinyloestradiol. However, there is still no convincing evidence that this dose reduction has managed to decrease the risk of thrombosis. Both early and
recent studies have shown a 4% to 8% increased risk of thrombosis among women using OC, yet comparisons between OC containing 30 μg and 50 μg have not yielded conclusive results [14]. Progestagens are also thought to affect the risk of thrombosis. Third-generation progestagens (desogestrel and gestodene) have been related to a risk of thrombosis of up to two times that of preparations containing second-generation progestagens [22, 51]. Hormone replacement therapies (HRT) based exclusively on oestrogens increase the risk of endometrial cancer, to the extent that there is a tendency to prescribe oestrogen and progesterone HRT except in hysterectomized women. There are reports indicating a two- to fourfold increased risk of DVT in women on HRT [9, 15]; this should be taken into account when evaluating menopausal women. It should also be kept in mind that a large number of epidemiological studies conclude that Asian women, because of their diet rich in soy, reach the menopause in better condition than Occidental women and have a lower incidence of undesirable effects. Moreover, and despite the large number of published reports focusing on isoflavones (a Medline search of the term isoflavones yields over 7500 citations), there is no mention in the literature of an increased risk of thrombosis linked to the uptake of these components of soy.
Pregnancy and the Postpartum Period
It has been estimated that 1 in 2000 women develop thrombosis during pregnancy. This risk increases 10 times when compared with nonpregnant women of the same age [23, 30]. This risk also goes up in the postpartum period. Pregnancy leads to increased levels of the blood clotting factors I, VII, VIII, IX, X, XI and XII, an increased platelet count and reduced protein S and antithrombin concentrations. Further, the fibrinolytic pathway may be blocked by the increased levels of activated plasminogen inhibitors 1 and 2, produced in the placenta. These factors, combined with the venous stasis produced by compression by the uterus of draining leg veins, can increase the risk of thrombosis during the prepartum period by up to 20 times. Some 2 months after childbirth, fibrinolytic and coagulation systems return to their normal state.
Obesity
Severe obesity can be an independent risk factor for developing thrombosis, especially if 175% of the ideal weight is surpassed [37].
43
44
1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases?
Genetic Risk Factors
risk of thrombosis by 3- to 8-fold in heterozygous carriers and by 50- to 80-fold in homozygous carriers [24].
Antithrombin III Deficiency
This condition is produced by point mutations in the antithrombin III (AT-III) gene and shows an autosomal dominant transmission pattern. AT-III is an α2 globulin that inhibits factors XIIa, XIa, IXa, Xa, IIa and plasmin. Its prevalence is less than 1 in 1000 people [45]. The homozygous state is incompatible with life. Heterozygotes show 40% to 60% the normal functional activity of AT-III. An acquired AT-III deficiency may occur in cases of its reduced production (in liver disorders or following the administration of OC), enhanced excretion (nephrotic syndrome, protein-losing enteropathy), excessive consumption, or disseminated intravascular coagulation (DIC).
Prothrombin Gene Mutation 20210A
This anomaly described in 1996 is caused by a mutation in nucleotide 20210 of the prothrombin gene (guanine replaced by adenine). The heterozygous state occurs in 1% to 4% of the general population and in up to 6% to 10% of subjects with venous thrombosis. The risk of thrombosis increases 2–3 times with respect to the population at large, and seems to be mediated by increased prothrombin levels [35]. It has even been suggested that prothrombin gene and factor V Leiden mutations occur in 63% of families with thrombophilia [3].
Blood Group Protein C Deficiency
Protein C is vitamin K dependent. It acts by inactivating factors Va and VIIIa and requires the presence of protein S as a cofactor, activated by thrombin and thrombomodulin. Protein C deficiency is a hereditary disorder of autosomal dominant transmission. The prevalence [39, 46] of an asymptomatic heterozygous deficiency is low at 1/300–500, with 1/16,000–36,000 showing clinical signs. A homozygous protein C deficiency manifests as neonatal purpura fulminans progressing with thrombosis in the microcirculation and DIC.
Protein S Deficiency
Protein S is a vitamin-K-dependent glycoprotein that acts as a cofactor to protein C in the degradation of factors Va and VIIIa. Its pattern of transmission is autosomal dominant. Its prevalence is similar to those of protein C and AT-III deficiencies.
Resistance to Activated Protein C
This anomaly is the consequence of the substitution of the amino acid arginine 506 by glutamine in the factor V molecule. This mutated factor V, designated factor V Leiden, is resistant to the catalytic action of activated protein C. This disorder, first described in 1993 by Dahlbäck [8], has an autosomal dominant pattern of transmission and is the most common deficiency in the general Caucasian population linked to thrombosis. Its prevalence [4, 41] is high at 5% to 15%, yet it is relatively uncommon in populations of other races. Factor V Leiden increases the
Non-O blood groups are associated with a 2- to 4-fold increased risk of venous thrombosis [21].
Methylenetetrahydrofolate Reductase 677T
A variation in the gene coding for methylenetetrahydrofolate reductase (MTHFR), an enzyme involved in homocysteine metabolism, has been associated with slightly elevated homocysteine levels in the blood [12], increasing the risk of thrombosis.
Other Plasma Anomalies Related to the Risk of Thrombosis Hyperhomocysteinemia
Homocysteine is an amino acid that metabolizes cysteine (with vitamin B6 acting as cofactor) or methionine (with vitamin B12 as cofactor). Its blood levels can rise as the result of either a congenital deficiency in one of the enzymes involved in these processes or a nutritional deficiency of folate, vitamin B6 or vitamin B12. High blood homocysteine levels induce endothelial damage and are associated with an increase in tissue factor, and the enhanced activity of factors V and XII, and protein C. Homocysteine levels above 18 μmol/l are linked to an increased risk of thrombosis [32]. Patients with hyperhomocysteinemia have a 3.5 times higher risk of presenting with thrombosis. This risk increases by over 20-fold if the patient also has factor V Leiden. Treatment with folate and vitamins B6 and B12 reduces homocysteine concentrations.
1.4.3 What Should a Surgeon do when Faced with Hypercoagulation?
Antiphospholipid Antibodies
Antiphospholipid syndrome (APS) is a commonly acquired cause of hypercoagulation. It appears in 1% to 15% of the population, this rate increasing with age (to 50% in patients over the age of 80 years) [28]. APS affects patients with lupus anticoagulant or anticardiolipin antibodies. These antibodies react with endothelial cells, platelets and phospholipids. Recurrent venous thrombosis is one of its clinical manifestations [20]. Thrombotic complications, estimated to be as high as 50%, have also been reported after vascular reconstruction procedures [1]. A further common manifestation of APS is miscarriage. Its diagnosis should include the identification of lupus anticoagulant and anticardiolipin antibodies. Treatment consists of eliminating risks such as avoiding pregnancy and taking OC. If venous thrombosis has already been provoked, heparin or urokinase should be immediately given followed by oral anticoagulation with warfarin adjusted to maintain the international normalized ratio (INR) between 2 and 3. Patients with a history of DVT or miscarriage who are pregnant should be treated with heparin throughout pregnancy and switched to oral anticoagulation after giving birth.
High Coagulation Factor Levels
Augmented levels of prothrombin (factor II), factor VIII, factor IX, or factor XI have been linked to a high risk of thrombosis [25]. Although little is known about the aetiology of these abnormalities, they have been described as a combination of congenital and acquired alterations.
1.4.3 What Should a Surgeon do when Faced with Hypercoagulation? When confronted with an episode of DVT, several uncertainties immediately come to mind. First, should we search for evidence of thrombophilia? How should this be done and when? Also important to the vascular surgeon is the question of whether to consider special therapeutic options in patients who are carriers of thrombophilia.
1.4.3.1 Should a Search for Thrombophilia be Undertaken? All acquired risk factors can be controlled to a certain extent whether at the level of prophylaxis or treatment. The major worry is evaluating a genetic hypercoagulable state because its presence can be well demonstrated but its treatment not yet well defined. There are several arguments in favour of embarking on a search for thrombophilia. Its discovery could benefit relatives. Prophylaxis may be started in situations of added risk. It is well known that both pregnancy and OC are associated with factor V Leiden or a mutation in prothrombin gene 20210A, increasing the risk of thrombosis by 4–8 times. A similar situation arises owing to the link with HRT or treatment with tamoxifen. In contrast, if, in an elderly patient presenting an idiopathic venous thrombosis, thrombophilia is discovered, this will avoid worry and an exhaustive, sometimes unforthcoming, search for neoplastic disease.
Defects in the Fibrinolytic System
A drop in fibrinolytic activity and a predisposition to thrombosis may be secondary to diminished plasminogen levels, to reduced activity of plasminogen activator or to the increased action of the plasminogen inhibitor. Reduced fibrinolytic activity occurs in acquired disease states (myocardial infarction, generalized arteriosclerosis, diabetes, scleroderma, thrombocytopenic purpura, ulcerative colitis, Crohn’s disease) [7]. Congenital plasminogen deficiency is transmitted in an autosomal dominant manner. Thrombotic events usually occur when plasminogen levels fall below 40% of those related to normal biological activity [17]. This disorder is extremely rare with reports of only a few isolated cases [33].
1.4.3.2 How Should the Search be Done? As mentioned previously, the most recently discovered deficiencies (factor V Leiden and prothrombin gene mutation 20210A) are highly prevalent, thus generating an increased number of patients whose venous thrombosis could be attributed to an inherited thrombophilia. The first step of diagnosis will involve drawing up a careful clinical record, a meticulous physical examination and a basic laboratory routine check to characterize the severity of the thrombotic process, and determine the presence of any of the causes of hypercoagulability. Obviously, an objective test for the diagnosis of venous thrombosis will also have to be conducted. The second step will be to screen for the causes of hereditary thrombophilia, which if identified will mean
45
46
1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases?
adopting a specific management plan. Screening should be performed, especially if DVT appears before the age of 50 years in cases of DVT recurrence and if there is a family history of DVT. If one or more of these conditions are met, a complete evaluation will be needed to rule out thrombophilia.
1.4.3.3 Diagnosing Thrombotic Disease in Patients with Thrombophilia All patients presenting juvenile, idiopathic, recurrent thrombosis with a family history of thrombosis should be assessed for possible deficiencies. Once a suspicion of thrombophilia has been established, the following factors may be determined during the episode of thrombosis: anticardiolipin antibodies, homocysteine, factor V Leiden and prothrombin gene mutation. Other factors may be consumed during the coagulation process or be reduced by anticoagulant therapy, or because of hepatic insufficiency or sepsis. For this reason, the clinician should wait until the end of the 6-month treatment period and then leave a further treatment-free interval (proposed by some as ideally 2 months), before determining the presence of the remaining possible deficiencies (protein C, protein S, antithrombin III).
1.4.3.4 Treating Thromboembolic Disease in Patients with Thrombophilia The treatment regime for a patient with DVT and pulmonary thromboembolism is usually heparin initially and oral anticoagulant for 3–6 months, adjusted to keep the INR between 2 and 3. According to several randomized trials, after a first episode, the incidence of recurrent venous thromboembolism is between 5% and 15% in the first year and from 20% to 30% at 4 years [2]. At the same time, it should be taken into account that the risk of haemorrhage is estimated at 2% to 3% per year. This yearly risk in young patients, with no added risks for the haemorrhage, is unimportant but may give rise to a series of contraindications for treatment in patients with multiple associated diseases and an advanced age. In general there is scarce information on thrombotic recurrence in nonselected patients. Most studies have been based on select populations with generally very high recurrence rates. For the most prevalent abnormalities, factor V Leiden and prothrombin mutation 20210A, the available data fail to indicate a higher recurrence after
a first episode [38]. The current consensus is that there is no need to prolong treatment in the presence of these anomalies. However, the risk of recurrence is probably high in the heterozygous population simultaneously having both anomalies. It is also important to keep in mind that interaction between an acquired and a congenital risk factor can substantially increase the risk threshold. A clear example is the increased relative risk produced when the use of OC is added to the presence of factor V Leiden [48] (RR increases from 6 to 35), or if HRT is added to this factor (RR increases from 4 to 15) [40]. When these anomalies are detected in asymptomatic carriers (relatives of the patient), in the presence of additional risk factors, these subjects might benefit from a selective prophylaxis regimen. These subjects could be rejected by insurance companies. Indefinite anticoagulation is only considered appropriate for patients categorized as high risk, meaning two or more events; a spontaneous (without another DVT risk factor) severe event; or a patient with a spontaneous event and documented antiphospholipid antibodies. When patients are categorized as having moderate risk, i.e. in the absence of symptoms or if the stimulus for a thrombotic event has been identified, prophylaxis would only be given in a risk situation.
1.4.3.5 Specific Considerations in Treating Thromboembolic Disease Related to Thrombophilia Antithrombin III Deficiency The treatment of this deficiency consists of infusions of fresh plasma or preferably antithrombin concentrate. Long-term treatment involves oral anticoagulation provided there have been past thrombotic episodes. Heparin is given during pregnancy or in other risk situations (e.g. surgery, trauma, sepsis).
Protein C Deficiency Intravenous infusion of fresh plasma can restore functional levels of protein C. Heparin prophylaxis (during pregnancy) or treatment should be given in risk situations such as after surgery, trauma or sepsis. Lifetime oral anticoagulation is required for recurrent or life-threatening thrombosis.
References
Protein S Deficiency The management of this deficiency is the same as for protein C deficiency.
Activated Protein C Resistance Heparin prophylaxis is given in high-risk situations for thrombosis. Lifetime anticoagulation therapy is required for recurrent or life-threatening thrombosis.
Prothrombin Gene Mutation The treatment for this condition remains to be clearly defined. Long-term oral anticoagulation therapy is also recommended in patients with recurrent thrombosis.
1.4.4 Summary • The occurrence of venous thrombosis is the result of interaction between both genetic and acquired factors. • Screening should be based on characterizing patients according to their clinical history. • Tests should be undertaken 2 months after the end of anticoagulation therapy. • Asymptomatic carriers do not require treatment yet should undergo prophylaxis in situations of risk. • Treatment of a first episode of DVT with proven thrombophilia is the same as for the general population. • There is a need for greater insight into all possible risk factors and in particular the interactions produced among several risk factors, since this will synergistically potentiate the risks involved. • Future data will enable the physician to gauge this risk in each individual patient and design the tools needed to prevent the thromboembolic state. References 1. Ahn SS, Kalunian K, Rosove M, Moore WS (1988) Postoperative thrombotic complications in patients with the lupus anticoagulant: increased risk after vascular procedures. J Vasc Surg 7:745–756
2. Anderson FA, Wheeler HB, Goldberg RJ et al (1991) A population based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT study. Arch Intern Med 151:933–938 3. Bertina RM (1997) Factor V Leiden and other coagulation factor mutations affecting thrombotic risk. Clin Chem 43:1678–1683 4. Bertina RM, Koeleman RPC, Koster T et al (1994) Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 369 (117):750–753 5. Bick RL (1992) Coagulation abnormalities in malignancy: a review. Semin Thromb Hemost 18:353–369 6. Cohen SH, Ehrlich GE, Kaufman MS, Cope C (1973) Thrombophlebitis following knee surgery. J Bone Surg 55:106–111 7. Colleen D, Juhan-Vaghe I (1988) Fibrinolysis and atherosclerosis. Semin Thromb Hemost 14:180–183 8. Dahlbäck B, Carlsson M, Svensson PJ (1993) Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C. Proc Natl Acad Sci USA 90:1004–1008 9. Daly E, Vessey MP, Hawkins MM, Carson JL, Gough P, Marsh S (1996) Risk of venous thromboembolism in users of hormone replacement therapy. Lancet 348:977–980 10. Egeberg O (1965) Inherited antithrombin deficiency causing thrombophilia. Thromb Diath Hemorrh 13:516–530 11. Ferrari E, Cevallier T, Chapelier A, Baudouy M (1999) Travel as a study. Chest 115:440–444 12. Frosst P, Bloom HJ, Milos R et al (1995) A candidate genetic risk factor for vascular disease a common mutation in methylenetetrahydrofolate reductase. Nat Genet 10:111–113 13. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP (1944) A prospective study of venous thromboembolism after major trauma. N Engl J Med 331:1601–1606 14. Gertsman BB, Piper JM, Tomita DK, Ferguson WJ, Stadel BV, Laundin FE (1991) Oral contraceptive estrogen dose and the risk of deep venous thromboembolic disease. Am J Epidemiol 133:32–37 15. Grady D, Furberg C (1997) Venous thromboembolic events associated with hormone replacement therapy. J Am Med Assoc 278:477 16. Griffin JH, Evatt B, Zimmerman TS, Kleiss AJ, Wideman C (1981) Deficiency of protein C in congenital thrombotic disease. J Clin Invest 68:1370–1373 17. Hasegawa DH, Tyler BJ, Edson JR (1982) Thrombotic disease in three families with inherited plasminogen deficiency. Blood 60:213–217 18. Homans J (1954) Thrombosis of the leg veins due to prolonged sitting. N Engl J Med 250:148–149
47
48
1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases?
19. Hull RD, Raskob GE (1986) Prophylaxis of venous thromboembolic disease following hip and knee surgery. J Bone Surg 68:146–150 20. Insko EK, Haskal ZJ (1997) Antiphospholipid syndrome: patterns of life-threatening and severe recurrent vascular complications. Radiology 202:319–326 21. Jick H. Slone D, Westernholm B et al (1969) Venous thromboembolic disease and ABO blood type. Lancet i:539–542 22. Kemmeren JM, Algra A, Grobee DE (1995) Third generation oral contraceptives with differing progression components. Lancet 346:1589–1593 23. Kierkegaard A (1983) Incidence and diagnosis of deep vein thrombosis associated with pregnancy. Acta Obstet Gynecol Scand 62:239–243 24. Koster T, Rosendaal FR, De Ronde H, Briët E, Vandenbroucke JP, Bertina RM (1993) Venous thrombosis due to a poor anticoagulant response to activated protein C: Leiden Thrombophilia Study. Lancet. 342:1503–1506 25. Koster T, Blann AD, Riét E, Vandenbroucke JP, Rosendaal FR (1995) Role of clotting factor VIII in effect of von Willebrand factor on occurrence of deep-vein thrombosis. Lancet 345:152–155 26. Kraaijenhaghen RA, HaverKamp D, Koopman MM, Prandoni P, Piovella F, Büller HR (2000) Travel and risk of venous thrombosis. Lancet 356:1492–1493 27. Lapostolle F, Surget V, Borron SW et al (2001) Severe pulmonary embolism associated with air travel. N Engl Med 345:779–783 28. Manoussakis MN, Tzioufas AG, Silis MP, Pange PJ, Goudevenos J, Moutsopoulos HM (1987) High prevalence of anticardiolipin and other autoantibodies in a healthy elderly population. Clin Exp Inmunol 69:557–565 29. Mayo M, Halil T, Browse NL (1971) The incidence of deep vein thrombosis after prostatectomy. Br J Urol 43:738–742 30. McColl MD, Ramsay JE, Tait RC et al (1997) Risk factors for pregnancy associated venous thrombosis. Thromb Hemost 78:1183–1188 31. Meier CR, Jic H (1998) Tamoxifen and risk of idiopathic venous thromboembolism. Br J Clin Pharmacol 45:608–612 32. Mudd SH, Skovby F, Levy HL et al (1985) The natural history of homocystinuria due to cystathionine beta-synthetase deficiency. Am J Hum Genet 37:1–31 33. Nilsson IM, Tengborn LA (1984) A family with thrombosis associated with high level of tissue plasminogen activator inhibitor. Haemostasis 14:24–27 34. Nordstrom M, Lindblad B, Anderson H, Bergqv D, Kjellströ T (1994) Deep venous thrombosis and occult malignancy: an epidemiological study. BMJ 308:891–894
35. Poort SR, Rosendaal FR, Reitsma PH, Bertina RM (1996) A common genetic variation in the 3’-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood 88:3698–3703 36. Porter JM, Moneta GL (1995) Classification and grading of chronic venous disease. A consensus statement. J Vasc Surg 21:635–645 37. Porter JM, Moneta JL (1995) Reporting standards in venous disease: an update. J Vasc Surg 21:635–645 38. Rosendal FR (1997) Thrombosis in the young: epidemiology and risk factors, a focus in venous thrombosis. Thromb Hemost 78:1–6 39. Rosendaal FR, Koster T Vandenbroucke JP, Reitsma PH (1995) High risk of thrombosis in patients homozygous for factor V Leiden (activated protein C resistance). Blood 85:1504–1508 40. Rosendal FR, Vessey M, Rumley A et al (2002) Hormonal replacement therapy, prothrombotic mutations and the risk of venous thrombosis. Br J Haematol 116:851–854 41. Rees DC, Cox M, Clegg JB (1995) World distribution of factor V Leiden. Lancet 346:1133–1134 42. Rutherford RB, Clagett GP, Cranley JJ, O’Donell TF, Raju S, Zierler RE, Browse N, Nicolaides A (1988) Reporting standards in venous disease. J Vasc Surg 8:172–181 43. Savesvaan R (1986) Sudden natural deaths associated with commercial air travel. Med Sci Law 26:35–38 44. Schwarz HP, Fischer M, Hopmeier P, Batard MA, Griffin JH (1984) Plasma protein S deficiency in familial thrombotic disease. Blood 64:1297–1300 45. Tait RC, Walker ID, Perry DJ et al (1994) Prevalence of antithrombin deficiency in the healthy population. Br J Haematol 87:106–112 46. Tait RC, Walker ID, Reitsma PH et al (1995) Prevalence of protein C deficiency in the healthy population. Thromb Haemost 73:87–93 47. Trousseau A, Phegmasia Alba Dolens (1865) Clinique Médicale de l‘Hötel-Dieu de Paris. Vol. 3.Ballière, Paris, pp 652–695 48. Vandenbroucke JP, Koster T, Briët E, Reitsma PH, Bertina RM, Rosendaal FR (1994) Increased risk of venous thrombosis in oral contraceptives users who are carriers of factor V Leiden mutation. Lancet 344:1453–1457 49. Weijl NL, Rutten MF, Zwinderman AH et al (2000) Thromboembolic events during chemotherapy for germ cell cancer: a cohort study and review of the literature. J Clin Oncol 18:2169–2178
References
50. World Health Organization (1995) Venous thromboembolic disease and combined oral contraceptives: results of international multicentre case control study. World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Lancet 346:1575–1582
51. World Health Organization (1995) Effect of different progestagens in low estrogen oral contraceptives on venous thromboembolic disease. World Health Organization Collaborative Study of Cardiovascular and Steroid Hormone Contraception. Lancet 346:1582–1588
49
51
1.5 Noninvasive Diagnosis of Vascular Diseases P. Berg, H. Farghadani, V. Lens, R. Metz, F. Mataigne, S. Schmitz
Noninvasive vascular laboratory findings remain important in the diagnosis of peripheral arterial disease (PAD). In many circumstances they are as accurate as invasive imaging and have the advantage of being quick and inexpensive. The two basic modalities of evaluation are the indirect methods (ankle brachial pressure index, Doppler wave forms, treadmill exercise) that provide location and functional severity of disease, and the direct method of evaluation, colour duplex imaging (CDI), which provides more specific anatomical and physiological information.
• Platelet count: changes may precipitate or aggravate the symptoms of PAD. Associated haematological disease may influence treatment. • Blood glucose or haemoglobin HbA1c, urea, creatinine: diabetes and chronic renal insufficiency are important risk factors in PAD, for interpretations of results and for further treatment. • Lipid profile: elevated low-density lipoprotein (LDL), triglycerides and low high-density lipoprotein (HDL) represent major risk factors for PAD and have to be treated. Lipid modification can be associated with stabilization or regression of femoral atherosclerosis. • Hypercoagulability screen and homocysteine levels should be performed selectively in patients with a family history or atypical events.
1.5.1.2 Physical Examination
1.5.1.4 Special Investigations, Other Than Imaging
In the majority of patients, diagnosis can usually be made on the basis of the history. Chronic arterial insufficiency of the lower extremity causes two very characteristic types of pain: intermittent claudication and ischaemic rest pain. Information may be obtained in the case of sudden worsening of limb perfusion in acute limb ischaemia. Physical examination should include: • Palpable pulses. • Audible bruits. • Changes in colour and temperature. • Presence of ulcers or gangrene.
Pressure and Volume Measurements
1.5.1 Peripheral Arterial Disease 1.5.1.1 Introduction
1.5.1.3 Basic Haematological and Biochemical Tests The following blood tests are most frequently used and are those that should be performed for all new patients presenting with PAD: • Complete blood count (haemoglobin, haematocrit, white cell count).
Ankle Brachial Pressure Index (ABPI)
• The ABPI serves as a baseline for comparing the patient with him or herself at different times. • Widely standard in the evaluation of patients with PAD. • It is calculated for each extremity by dividing the highest ankle pressure by the highest arm pressure. The ABPI provides important basic information; the following indices are consistent with the following clinical diagnoses: • 1.0–1.2: normal. • 0.5–0.9: claudication. • <0.5: markedly decreased (often to less than 0.30). Seen in patients with rest pain, ischaemic ulcer or gangrene [11, 29, 33]. • >1.3: abnormally high. Secondary to noncompressible vessels due to medial calcification.
52
1.5 Noninvasive Diagnosis of Vascular Diseases
• For calcified arteries, the use of digital pressures or flow velocity recording in the pedal arteries is needed to supplement pressure recordings. • Specificity of this index is 100% for all reports. • Sensitivity is 92–94% [39].
Segmental Limb Systolic Pressure Measurements (SLP)
• Routinely used because of accurate haemodynamically significant detection of occlusive lesions between the heart and the measuring point. • The cuffs are placed in standard locations: high-thigh, low-thigh, below the knee, ankle and metatarsal. • Direct measurement is obtained by placing a Doppler probe over the artery just below the inflated cuff, or the probe can be placed over one of the pedal arteries giving a pressure gradient between the different cuffs. • A gradient greater than 20 mmHg suggests occlusive disease between the two cuffs.
Digital Pressure Measurement and Toe Brachial Index
• Digital pressures are useful in arterial occlusive disease within the foot or hand and in instances of falsely elevated ankle pressures secondary to medial calcification. • Using a small cuff (2.0 or 2.5 cm) and a photo electrode placed on the finger or toe as the pulse sensor, the digital pressure is obtained in the same way as for the ankle pressure. • The normal toe brachial index is 0.8–0.9. • An index of 0.35 ± 0.15 is consistent with claudication. • An index of 0.11 ± 0.10 is consistent with ischaemic rest pain [27]. • For absolute pressure, it is generally considered that a toe pressure less than 30 mmHg is indicative of severe ischaemia. • There is no difference between the mean values for diabetic and nondiabetic patients.
Segmental Plethysmography or Pulse Volume Recording (PVR)
• Any instrument measuring the change in volume of the limb during each cardiac cycle by a plethysmographic sensor may be used; for example, sphygmomanometer, mercury-in-silastic tube strain gauge or impedance captors.
• The pulse volume recording is obtained by a plethysmograph connected to these devices placed at selected locations of the limb [26]. • In addition a brachial cuff reflects the undampened cardiac contribution to arterial pulsatility. • Comparing each PVR reveals an eventual significant occlusive lesion. • The accuracy of each SLP and PVR alone is reported to be 85%. • These two measurements used together have an accuracy of over 95%. • This combination could help to recognize diabetic patients.
Doppler Velocity Waveform (VWF)
• Arterial VWF is recorded by a continuous-wave Doppler over the femoral, popliteal, posterior tibial and dorsalis pedis arteries. • Qualitative differences of the VWF between two adjacent recording points identify the presence of an occlusive lesion in the intervening arterial segment. • In normal individuals the VWF is triphasic, with reverse flow seen. • When atherosclerotic changes are present in the arteries, turbulence may be seen at the high-frequency peak or on the descending phase of the forward flow. • Dampened reverse flow suggests the presence of stenosis and with severe stenosis or occlusion the reverse flow is absent. In addition, the systolic acceleration of the forward flow becomes flattened. • In severe ischaemia the waveform becomes continuous and nonpulsatile. • In a patent but dilated artery, the flow waveform shows a widening of the systolic forward flow. • Visual inspection of these waveforms recorded over the different arteries described can detect and localize arterial occlusive disease in most cases. • These tests are painless, inexpensive, quick and accurate enough. VWF is more accurate than SLP alone. It has been reported [20] that VWF was 97% accurate (75% for SLP alone) in detecting superficial femoral artery lesions with over 50% luminal narrowing and 91% accurate (54% for SLP alone) in detecting similar lesions in the popliteal artery.
1.5.1 Peripheral Arterial Disease
Functional Testing Treadmill Exercise (TE)
• At rest, variation of flow in the lower limb requires an 80% stenosis, which is due to low flow and high resistance of its circulation. • Despite that, during exercise, a 20% stenosis is enough for significant haemodynamic changes because of high flow and low resistance of the circulation. • For practical reasons only brachial and ankle cuffs are routinely used. • The standard usually used is walking at 3.5 km/h on a 12% incline for 5 min. The ABPI is measured before exercise, at 1 or 2 min, at 5 min and then every minute until back to initial values. • Thus, the onset of claudication, the maximum walking distance, the percentage decrease in pressure and its absolute value during the post-exercise period (10–15 min) and recovery time are obtained. • In patients with multiple occlusions, the ankle pressure is often decreased to zero, with longer recovery time than patients with a single occlusion.
•
•
•
•
•
• Inducing Limb Hyperaemia (ILH)
• For the ILH, the pressure cuff is placed on the lower thigh and inflated to a level of 50 mmHg above the systolic pressure for 3–5 min. • Reactive hyperaemia occurs after the pressure cuff is abruptly deflated. • Ankle systolic pressure (AP) is then recorded at 1-min intervals until it returns to the resting level. • The decrease in AP 30 s after cuff deflation is equivalent to that observed 1 min after walking to the point of claudication on a treadmill [10, 14, 38]. • It is reported elsewhere [23] that ABPI and the treadmill test are widely superior to this test; nevertheless, ILH can be proposed if the treadmill is not possible. • Unfortunately, many patients do not tolerate the discomfort associated with this degree and duration of cuff inflation.
Microcirculatory Investigations Transcutaneous Oxygen Measurements (TcpO₂)
• TcpO2 provides valuable metabolic data which may be used to supplement the haemodynamic data provided
• • •
•
by other noninvasive tests. It provides a measure of the adequacy of the arterial oxygen supply to the tissues. An oxygen-sensing electrode is placed on the skin, which contains a small heating unit that warms the skin to a temperature of 44°C, conducive to efficient oxygen diffusion. The quantity of oxygen available for diffusion to the skin is a function of the arterial flow to the area and the amount of oxygen extracted from the blood to meet the metabolic requirements of the tissues. When arterial occlusive disease is severe, the tissue perfusion becomes marginal and capillary oxygen perfusion decreases as the proportion of oxygen extraction must increase to meet the metabolic demands of the tissue. TcpO2 is usually measured at the dorsum of the foot, medial aspect of the calf, and the thigh, with a reference electrode placed in the infraclavicular region. Comparing the values obtained at the lower extremity and the chest yields an index that can be compared to the normal value with regard to the patient’s age, cardiac output and arterial oxygen tension. The measurement should be done in a supine and in a sitting position; the difference between both values provides information about the microcirculatory reserve supply. The results are expressed in mmHg. There are important variations, essentially in older patients and in concomitant cardiopulmonary disease. In general, a TcpO2 <30 mmHg suggests ischaemia and nonhealing. As there is an admitted error range of ±10 mmHg, it is admitted that if TcpO2 <20 mmHg, healing will not occur and if TcpO2 >40 mmHg healing will be probable. There is a high positive predictive value (77–87%) [6, 34–37].
Laser Doppler Fluxmetry (LDF), Capillary Microscopy (CM)
• CM enables visualization of the nailfold capillaries of the big toe in the sitting position and provides information about capillary morphology, density and velocity. • LDF measurements on the pulp of the big toe give information about total skin perfusion, including capillaries, deeper vessels and arteriovenous anastomoses, which are mainly involved in thermoregulation.
53
54
1.5 Noninvasive Diagnosis of Vascular Diseases
• The reactive hyperaemia response after a 3-min arterial occlusion can be measured to assess the reserve capacity of skin blood supply. • In a Dutch multicentre study, clinical and Doppler systolic pressure parameters were found to be inadequate for predicting imminent amputation, because all patients met these criteria but only 44% of them underwent amputation.
• Enhancement of vascular structure requires high contrast flow rates of 3–5 ml/s of 300–350 mg/ml iodic contrast with a total amount of 120–150 ml. • Irradiation is inevitable and particular precautions have to be taken to reduce the irradiation dose as much as possible.
Aorta Conclusion
The combination of all three techniques – TcpO2, LDF and CM – showed the highest specificity (87%), but a rather low sensitivity (46%). The conclusion is that TcpO2 measures provide microcirculatory classification and are the easiest measurement to perform [36].
1.5.1.5 Imaging Techniques Duplex Scanning • Colour duplex imaging incorporates real-time B-mode imaging, and pulsed and colour Doppler. • Duplex scanning can provide most of the essential anatomical information plus some functional information; for instance, velocity gradients across stenoses. • The arterial tree of the lower extremities can be visualized, with the extent and degree of occlusive lesions accurately assessed and arterial velocities measured. • It can characterize specific lesions in regard to their suitability for endovascular treatment. Arterial reconstructive surgery can be performed on the basis of duplex scanning alone in some cases. • Real-time B-mode imaging is the best mode for determining the anatomical detail of a vessel (e.g. plaque characterization, intimal flap, mural thrombus, diameter measurements).
• Applications for evaluation of the aorta with CTA are: dissection, aneurysm, traumatic injury, atherosclerotic pathology and other inflammatory and congenital diseases. • Abdominal aneurysm disease, including diagnosis and post-operative follow-up, is well explored by CTA, providing information about the extent of the aneurysm formation and other extraluminal pathology. • Thoraco-abdominal aortic exploration can be achieved with CTA with the new multirow scanner in a single exploration of 20 s. • Due to its fast access, high availability and short examination time, CTA is the preferred method for diagnosis of aortic dissection and traumatic aortic injury. CTA gives direct visualization of the aortic traumatism.
Renal Arteries
• CTA is routinely used for the evaluation of renal artery stenosis, and evaluation of renal transplant donors. • Excellent information regarding renal lesions and renal arteries can be provided with appropriate exploration (section thickness of 0.625–1.25 mm).
Lower Limb CTA
• New MDCT allows study of the arterial system of the lower extremity with only one examination.
Multiple Detector Computer Tomography (MDCT)
Studies Comparing MDCT and CT Angiography
• Recent advances in CT scanner technology, mainly multiple detector rows and high gantry rotation speed, as well as developments in reformatting technique allow the CT scan to be used as a noninvasive method to explore the “deep” arterial system (including aorta and visceral arteries) as well as the lower limb arteries. • CTA is a “noninvasive” imaging modality, but it still requires injection of contrast media.
• Particular attention should be paid to the study of the axial native images including all the diagnostic information. • 3D reconstruction and post-processing images are highly operator dependent. • Inadvertent 3D manipulations could “create” or “ignore” pathological conditions.
1.5.1 Peripheral Arterial Disease
Fig. 1.5.1. Male 65 years, 76-mm-diameter infrarenal abdominal aortic aneurysm (AAA), stenosis of right common iliac artery. Postoperative CTA after endovascular aneurysm repair (EVAR)
Magnetic Resonance Angiography • MRA is a noninvasive and nonirradiating technique. • Its limitation is mainly due to the electromagnetic field, which creates the images but prohibits the use of this methodology on patients wearing pacemakers and other ferromagnetic foreign bodies. • As in ultrasound, “flow images” can be acquired without the use of contrast medium. • Use of non nephrotoxic intravenous contrast agent (gadolinium) enhances the MRA result. The bolus injection is done at a rate of 1.5–2 ml/s. • Enhanced MRA results in reduction of flow artefacts and enhanced image resolution. • Gadolinium-enhanced MRA has a reported sensitivity that ranges from 75% to 100% for assessment of extracranial carotid stenosis compared to conventional angiography. • MRA is used to image preoperative evaluation of endovascular aortic repair.
• The main limiting factor is low image resolution compared to CT. • MRA is used for imaging vessels of the lower extremity and visceral aortic branches (renal, mesenteric arteries). • For renal arteries MRA with contrast enhancement has a reported sensitivity of 96%. • With regard to the lower extremity vessel, MRA is a preoperative noninvasive tool mainly useful in planning peripheral intervention or surgery.
1.5.1.6 Conclusion Colour duplex imaging associated either with CT angiography or MR angiography allows, in most cases, conventional angiography to be avoided, which should be reserved for when there is a discrepancy between noninvasive imaging techniques or when an endovascular treatment is likely to be performed during the session.
55
56
1.5 Noninvasive Diagnosis of Vascular Diseases
Fig. 1.5.2. Female 71 years, occlusion of a left femoro-popliteal by-pass, patency of a stent of the right superficial femoral artery (SFA)
1.5.2 Disease of Arteries Supplying the Brain 1.5.2.1 Introduction • Stroke represents the third leading cause of death in industrialized countries today. • Macro-angiopathies are responsible for nearly onethird of all ischaemic strokes. • In extracranial disease, the correct diagnosis of the degree of carotid stenosis in combination with clinical findings is the key to deciding whether patients require carotid endarterectomy. • Digital subtraction intra-arterial angiography (DSA) is mostly considered to be the gold standard but different noninvasive methods are giving quite comparable results [24].
1.5.2.2 Imaging Techniques • Visualizing the intracerebral circulation is also more and more accurately done by noninvasive techniques. • Three noninvasive approaches for visualizing the brain-supplying arteries will de discussed: the first based on Doppler ultrasound, the second based on magnetic resonance and finally the third based on computer tomography.
Doppler Ultrasound • High-resolution ultrasound combined with colourcoded Doppler flow analysis (Duplex sonography) has become a clinical tool of great value permitting bedside noninvasive diagnosis of the extracranial and intracranial vessel pathology.
1.5.2 Disease of Arteries Supplying the Brain
Fig. 1.5.3. Male 74 years, asymptomatic stenosis of the right internal carotid artery (ICA). Velocity criteria correspond to a stenosis of 70–80%
• The accuracy of the description of the degree of carotid stenosis has been demonstrated in several studies. • Each neurosonology laboratory uses several standardized criteria which are refined according to the technical advances in Doppler ultrasound techniques combined with regular auto-evaluation. • Velocity criteria [2], pre- and post-stenotic Doppler spectrum and collateral flow allow the best evaluation of the degree of stenosis. • The detection of a floating thrombus and some characterization of the atheromatous plaque consistency is also used in evaluating the degree of instability of the arterial lesion. • Microembolic signals (HITS) in the post-stenotic flow also permit the prediction of stroke risk in high-grade stenosis.
• Recently, echocontrast agents have been shown to improve Doppler ultrasound image quality, permitting a better diagnosis of pseudo-occlusions and intracranial vessel disease [8]. • Doppler ultrasound techniques have the advantage that they can be repeated easily and even allow continuous monitoring of the acute stroke patient [7]. • Transcranial Doppler can also be applied during carotid surgery to help decide whether a shunt should be placed and verify its patency.
Magnetic Resonance Angiography • The first MR angiographic images were 2D and 3D time-of-flight (TOF) and had a low accuracy because of the tendency to often overestimate the lesion.
57
58
1.5 Noninvasive Diagnosis of Vascular Diseases
Fig. 1.5.4. MR angiography of the same patient as in Fig. 1.5.2. Eighty percent stenosis of the ostium of the right ICA. Reconstruction of the Circle of Willis demonstrating an absence of the segment A1 of the left anterior cerebral artery
• More recently, 3D contrast-enhanced MR angiography increased confidence in MRA and shows a good correlation with conventional DSA for extracranial and intracranial vessels. • MR imaging also permits the brain parenchyma to be visualized and thus shows the extent of the associated vascular lesions. • MR diffusion imaging techniques are a unique window to see, very early after stroke, the cytotoxic oedema provoked by an ischaemic injury. • MRA combined with MR diffusion and MR perfusion imaging has the advantage of giving the clinician a comprehensive analysis of the stroke in evolution and hints at its aetiology.
Computed Tomographic Angiography • Spiral CT angiography has demonstrated its clinical effectiveness in the assessment of narrowing of the lumen of the extracranial carotid artery bifurcation and is even more accurate than conventional CT angiography. • CT also permits extra- and intracranial vessels to be analysed as well as the brain parenchyma. Perfusion mapping is feasible and allows one to accurately determine the brain tissue at risk in acute stroke. • The practical advantages of CT imaging are the short scanning times with fewer motion artefacts, the easier handling of agitated and unstable stroke patients and the wide availability of CT machines.
1.5.3 Diseases of the Venous Circulation
Fig. 1.5.5. CT angiography of the same patient. Confirmation of a high-grade calcified stenosis of the right ICA
1.5.2.3 Conclusion • Doppler ultrasound, MRA and CTA all show similar accuracy in the diagnosis of occlusive diseases of the brain-supplying arteries [21]. • No noninvasive technique on its own is accurate enough to replace DSA. Especially in carotid stenosis, the combination of two techniques, with the addition of a third if the first two disagree, appears to be the best approach. Thus, invasive DSA before carotid endarterectomy can be avoided in the majority of patients. • For intracranial imaging, combined MRA and CTA is equal to the accuracy of DSA in most cases [12]. • Transcranial Doppler ultrasound is a bedside procedure, is easy to perform, and allows monitoring of brain haemodynamics, detection of microemboli as well as evaluation of collateral flow and may even enhance vessel reopening during thrombolysis [1].
1.5.3 Diseases of the Venous Circulation 1.5.3.1 Introduction • Venous problems are common. • They include chronic venous insufficiency and acute deep venous thrombosis. • Chronic venous insufficiency refers to both superficial varicosities and postphlebitic syndrome.
1.5.3.2 Chronic Venous Insufficiency Investigations When special tests with instruments have not satisfactorily explained the nature of the venous disorder, the following techniques for studying the vein can be used.
59
60
1.5 Noninvasive Diagnosis of Vascular Diseases
Fig. 1.5.6. Female 21 years, symptomatic chronic venous insufficiency of the left leg. Duplex ultrasound demonstrates normal respiratory movements on the right side and absence of reflux after blocking respiration. Normal photoplethysmography (red curve). On the left side, prolonged reflux after Valsalva, short venous filling time
Photoplethysmography
• By this method the number of red cells is estimated in the skin capillary bed using a photoelectrical transducer. • The signals are recorded as a line tracing on a chart recorder or a computerized display. • It has been shown that the degree of congestion of red cells in skin capillaries bears a close relationship to the venous pressure in the limb, and thus the signal from the photoplethysmograph closely parallels the venous pressure changes. • With exercise, in an upright position, the venous pressure within the limb generally falls, and it takes at least 20 s before the original pressure is regained (venous refilling time: VRT). • In states of superficial or deep vein valvular incompetence the refilling time may be decisively shortened by reflux of venous blood down the limb.
• A diminished refilling time demonstrates incompetent venous valves, but cannot differentiate whether this incompetence is within the superficial or deep venous system. Two successive recordings may be done, with and without saphenous occlusion, by finger or cuff pressure. • If RFT is corrected after saphenous occlusion, this means that incompetence is due to the superficial system. Placing the cuff successively over the thigh and the calf may make the same comparison. This differentiates between incompetence of the short and long saphenous veins.
Volume Plethysmography
• The limb volume closely parallels the venous pressure so that when the patient is standing still it is maximal but afterwards, when blood has been expelled from the limb, both venous pressure and limb volume will fall.
1.5.3 Diseases of the Venous Circulation
• The time taken for the volume to return to its original value is a good indication of valve competence. With fully competent valves, this will be at least 20 s, but when superficial or deep vein incompetence is present this will be shortened according to the severity of condition.
predictive values. Even if ascending venography has been described as the gold standard for the diagnosis of DVT, Duplex ultrasonography has become the method of choice, combined with plasma D-dimer assay.
Investigations Doppler Flowmeter
Duplex Scanning
• According to the direction and speed of movement of red cells, there is a Doppler shift in the phase of the signal which is recognized by the machine and made apparent. • Only speed and direction are represented by the signal, not the volume. • Abnormal flow in direction indicates that the valves are incompetent or absent. • The probe is placed over the vein to be examined while the patient is standing and the response to coughing, to calf compression, to exercise and to an occluded saphenous (long or short) vein is studied.
• Duplex scanning is a practical method of assessing blood flow in veins and valve cusp movements. • It can differentiate between acute and chronic thrombosis. • All the major deep veins of the lower limb can be assessed. • The technique is less accurate for the small veins of the calf and cannot demonstrate the presence of thrombi in these small veins. However, in many cases this depends on the ability and the experience of the technician. • The vein is scanned in transverse and sagittal planes. • The presence of thrombosis is evaluated by the compressibility of the vein. • In addition, a vein without thrombus should show Doppler evidence of flow, variation with respiration and increase when distal veins are compressed. • Recent thrombi tend to be anechoic and only later will show characteristic internal echoes.
Ultrasonography
• Ultrasonography provides a much more sophisticated demonstration by giving an image of veins and their valves on a display screen. It will show the movement in these structures and also the direction and speed of blood flow within them. • The vein walls and lumen can be outlined and studied, clot may be recognized by absence of flow and immobile vein walls, and the structure of valves and their competence can be scrutinized. • The anatomy of veins can be visualized preoperatively. Individual deep veins and their branches can be distinguished and their flow pattern displayed, so that, for instance, incompetence in gastrocnemius vein can be recognized and the reflux within it estimated to assess its significance. In the popliteal vein this will indicate the effectiveness of the musculovenous pump below the knee or, conversely, the severity of reflux in the deep veins at that level.
Volume Plethysmography
• Pulse volume recorders are used to assess venous outflow. • Two components of the curves are used: first, the circumference changes after the inflation of the cuff; second, the downslope of the curve after immediate deflation. • In the case of thrombosis, the downslope will be slow. • For calculation, two values are used: the maximum increase in calf volume and the maximum venous outflow during the first second after deflation of the cuff. • Both of these values are decreased in patients with DVT [4].
1.5.3.3 Deep Vein Thrombosis 1.5.3.4 Conclusion • The clinical diagnosis of deep vein thrombosis (DVT) is unreliable in more than 50% of cases, and, in recent years, plasma D-dimer assays have been used to predict the presence of DVT with high sensitivity and negative
Duplex scanning of the superficial and deep veins is the preferred imaging technique to asses venous disorders of the legs.
61
62
1.5 Noninvasive Diagnosis of Vascular Diseases
References 1. Alexandrov AV, Molina CA, Grotta JC, Garami Z, Ford SR, Alvarez-Sabin J, Montaner J, Saqqur M, Demchuk AM, Moyé LA, Hill MD, Wojner AW, the CLOTBUST Investigators (2004) Ultrasound-enhanced systemic thrombolysis for acute ischemic stroke. N Engl J Med 351:2170–2178 2. Archie JP Jr, Ranke C, Trappe H-J, Creutzig A, Becker H (1999) Standardization of carotid ultrasound. Stroke 30:402–406 3. Baker JD, Dix DE (1981) Variability of Doppler ankle pressures with arterial occlusive disease: an evaluation of ankle index and brachial-ankle pressure gradient. Surgery 89:134–137 4. Barnes RW, Collicot RE, Mozerski DI et al (1973) Noninvasive quantitation of venous reflux in postphlebitic syndrome. Surg Gynecol Obstet 136:769–773 5. Bunt TJ, Holloway GA (1996) TcPO2 as an accurate predictor of therapy in limb salvage. Ann Vasc Surg 10:224–227 6. Cassilas JM, Becker F, Roux J, Raup JC, Didier JP (1985) TCPO2 et viabilité du moignon d’amputaion. J Mal Vasc 10:71–72 7. Chernyshev OY, Garami Z, Calleja S, Soon J, Campbell MS, Noser EA, Shaltoni H, Chen C-I, Iguchi Y, Grotta JC, Alexandrov AV (2005) Yield and accuracy of urgent combined carotid/transcranial ultrasound testing in acute cerebral ischemia. Stroke 36:32–37 8. Droste DW, Metz RJ (2004) Clinical utility of echocontrast agents in neurosonology. Neurol Res 26:754–759 9. Feigelson HS, Criqui MH, Fronek A, Langer RD, Molgaard CA (1994) Screening for peripheral arterial disease: the sensitivity, specificity, and predictive value of noninvasive tests in a defined population. Am J Epidemiol 140:526–534 10. Fox MJ, Tripolitis A, Kirby S (1977) A comparison of reactive hyperemic test with a standard exercise test in the evaluation of peripheral vascular disease. Br J Surg 64:290 11. Gahtan V (1998) The noninvasive vascular laboratory. Surg Clin North Am 78:507–518 12. Hirai T, Korogi Y, Ono K, Nagano M, Maruoka K, Uemura S, Takahashi M (2002) Prospective evaluation of suspected stenoocclusive disease of the intracranial artery: combined MR angiography and CT angiography compared with digital subtraction angiography. Am J Neuroradiol 23:93–101 13. Jamieson CW (1982) The definition of critical limb ischaemia of the limb. Br J Surg 69 [Suppl]:S1 14. Johnson WC (1975) Doppler ankle pressure and reactive hyperemia in the diagnosis of arterial insufficiency. J Surg Res 18:177–180
15. Kohler TR, Nance DR, Cramer MM, Vandenburghe N, Strandness DE Jr (1987) Duplex scanning for diagnosis of aortoiliac and femoropopliteal disease: a prospective study. Circulation 6:460–469 16. Kohler TR, Nicholls SC, Zierler RE, Beach KW, Schubart PJ, Strandness DE Jr (1987) Assessment of pressure gradient by Doppler ultrasound: experimental and clinical observations. J Vasc Surg 6:460–469 17. Kohler TR, Andros G, Porter JM et al (1990) Can duplex scanning replace arteriography for lower extremity arterial disease? Ann Vasc Surg 4:280–287 18. Langsfeld M, Nepute J, Hershey FB et al (1988) The use of deep duplex scanning to predict hemodynamically significant aortoiliac stenoses. J Vasc Surg 7:395–399 19. Lezack JD, Carter SA (1970) Systolic pressures in the extremities of man with special reference to the toes. Can J Physiol Pharmacol 48:469–474 20. Moneta GL, Yeager RA, Antonovic R, Hall LD, Caster JD, Cummings CD et al (1992) Accuracy of arterial duplex mapping. J Vasc Surg 15:275–284 21. Nonent M, Serfaty J-M, Nighoghossian N, Rouhart F, Derex L, Rotaru C, Chirossel P, Guias B, Heautot J-F, Gouny P, Langella B, Buthion V, Jars I, Pachai C, Veyret C, Gauvrit JY, Lamure M, Douek PC for the CARMEDAS Study Group (2004) Concordance rate differences of 3 noninvasive imaging techniques to measure carotid stenosis in clinical routine practice: results of the CARMEDAS multicenter study. Stroke 35:682–686 22. Olsson AG, Ruhn G, Erikson U (1990) The effect of serum lipid regulation on the development of femoral atherosclerosis in hyperlipidaemia: a non-randomized controlled study. J Int Med 227:381–390 23. Ouriel K, McDonnell AE, Metz CE, Zarins CK (1982) Critical evaluation of stress testing in the diagnosis of peripheral vascular disease. Surgery 91:686–693 24. Patel SG, Collie DA, Wardlaw JM, Lewis SC, Wright AR, Gibson RJ, Sellar RJ (2002) Outcome, observer reliability, and patient preferences if CTA, MRA, or Doppler ultrasound were used, individually or together, instead of digital subtraction angiography before carotid endarterectomy. J Neurol Neurosurg Psychiatry 73:21–28 25. Pourcelot L (1982) L’examen doppler des vaisseaux périphériques. ACD Productions, Paris 26. Raines JK (1993) The pulse volume recorder in peripheral arterial disease. In: Bernstein EF (ed) Non-invasive diagnostic techniques in vascular disease. Mosby, St Louis, pp 534–543
References
27. Ramsey DE, Manke DA, Sumner DS (1983) Toe blood pressure. A valuable adjunct to ankle pressure measurement for assessing peripheral arterial disease. J Cardiovasc Surg (Torino) 24:43–48 28. Rittenhouse EA, Maixner W, Burr JW, Barnes RW et al (1976) Directional arterial flow velocity: a sensitive index of changes in peripheral vascular resistance. Surgery 79:350–355 29. Rutherford RB (1986) Suggested standards for reports dealing with lower extremity ischemia. Prepared by the Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery/North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg 4:80–94 30. Rutherford RB (1997) Recommended standards for reports dealing with lower extremity ischemia: revised version. Prepared by the Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery/North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg 26:517–538 31. Rutherford RB, Lowenstein DH, Klein MF (1979) Combining segmental systolic pressures and plethysmography to diagnose arterial disease of the legs. Am J Surg 138:211–218 32. Strandness DE Jr, Bell JW (1965) Peripheral vascular disease: diagnosis and objective evaluation using a mercury strain gauge. Ann Surg Suppl 161::3–35
33. TransAtlantic Inter-Society Consensus (TASC) (2000) Management of peripheral arterial disease (PAD), investigation of patients with intermittent claudication. J Vasc Surg 31(Part 2):S62–S72 34. TransAtlantic Inter-Society Consensus (TASC) (2000) Management of peripheral arterial disease (PAD), investigations for critical limb ischemia. J Vasc Surg 31(Part 2):S178–S183 35. Ubbink DT, Tulevski II, den Hartog D, Koelemay MJ, Legemate DA, Jacobs MJ (1997) The value of non-invasive techniques for the assessment of critical limb ischaemia. Eur J Vasc Endovasc Surg 13:296–300 36. Ubbink DT, Spincemaille GH, Reneman RS, Jacobs MJ (1999) Prediction of imminent amputation in patients with non-reconstructible leg ischemia by means of microcirculatory investigations. J Vasc Surg 30:114–121 37. Ubbink DT, Gersbach PA, Berg P, Amann W, Gamain J (2003) The best TcpO2 parameters to predict the efficacy of spinal cord stimulation to improve limb salvage in patients with inoperable critical limb ischemia. Int Angiol 22:356–363 38. Wilbur BG, Olcott C (1978) A comparison of three modes of stress on Doppler ankle pressures. In: Dietrich EB (ed) Non-invasive cardiovascular diagnosis: current concepts. University Park Press, Baltimore 39. Yao JS, Flinn WR, Bergan JJ (1984) Noninvasive vascular diagnostic testing: techniques and clinical applications. Prog Cardiovasc Dis 26:459–494
63
65
1.6 Invasive Diagnosis of Vascular Diseases Luís Mendes Pedro and José Fernandes e Fernandes
1.6.1 Introduction Angiography is the most used invasive technique to study vascular disorders. It consists of the introduction of iodinated contrast material into the vascular system, through percutaneous direct injection or catheterization of the vessels, allowing its visualization by X-rays. It followed the discovery by Roentgen of the capability of using radiation to visualize the bodily structures. The first “in vivo” angiogram was obtained in 1927 by the Portuguese neurologist Egas Moniz (Fig. 1.6.1a), through direct injection following surgical exposure of the common carotid artery. The original discovery was immediately adapted by Reynaldo dos Santos (Fig. 1.6.1b) to study the peripheral arterial circulation by direct injection into the abdominal aorta [22]. Major technical developments since the 1950s have improved the safety and utilization of this technique for the entire vasculature, such that angiography is now the gold standard method for studying vascular diseases and planning conventional surgical treatment, and is the basic and fundamental tool for new endovascular interventions. Arteriography comprises visualization of the arterial system and, despite the development of new noninvasive technologies for diagnosis of arterial diseases, it continues to be used not only for confirmation of the diagnosis, but as the first step of modern therapeutic intervention. The visualization of the venous system is called phlebography, and it was also initiated in Lisbon in 1933, by João Cid dos Santos (Fig. 1.6.1c); following the introduction of new noninvasive imaging technologies its use became very selective and new interest in it was regained with the introduction of new modalities of endovascular treatment for some venous disorders [4]. Lymphography was started in Porto in 1931 by Hernâni Monteiro, an anatomist, to study the lymphatic system “in vivo”, but it was the contribution of Kinmonth [14], with direct injection of a liposoluble radio-opaque
contrast, that promoted its clinical utilization to study lymphatic disorders. Its practical use declined and is restricted to the study and treatment of lymphoedemas in selected centres.
1.6.2 History The first ex vivo angiogram was obtained in 1896 by Haschek and Lindenthal [10] by injecting contrast in the arteries of an amputated upper limb. In 1923 Berberich and Hirsch [1] reported the first experimental in vivo human angiograms using radio-opaque contrast and in the following year Barney Brooks [2] conceived a potential clinical use for this procedure to determine the amputation level by injecting the lower limb arteries with sodium iodinated contrast. The discovery of angiography of the entire vascular system and the demonstration of its clinical relevance represents a major contribution made by Portugal to the medical sciences. The early experiences with X-rays to visualize the vessels stimulated Egas Moniz, a neurologist facing the clinical problem of diagnosing cerebral tumours, to conceive a technique of visualizing the arteries in the brain that would be displaced by a tumour, thus providing an objective method for its diagnosis. The first in vivo cerebral angiogram was performed in 1927 [19] by surgical exposure of the common carotid artery and intra-arterial injection of a sodium iodinated contrast. Its value as a major diagnostic tool to be used in several clinical settings was immediately recognized by Moniz and co-workers, who reported the first cases of in vivo internal carotid occlusion in patients with strokes [20]. The initial technique carried a higher incidence of contrast-related complications (2.6% of the 302 cases performed between 1927 and 1931) [29], leading to the use of torotrast as a radiological marker.
66
1.6 Invasive Diagnosis of Vascular Diseases
Fig. 1.6.1a–c a First cerebral angiograph. b First translumbar aortograph. c João Cid dos Santos and the first phlebography
1.6.2 History
Fig. 1.6.2 Translumbar aortography
Modifications of the original technique were introduced and in 1936 Loman and Myerson [21] demonstrated the feasibility of cerebral arteriography by direct percutaneous injection into the common carotid artery. Demonstration of occlusive lesions in the cervical arteries by arteriography was a major development in the understanding of the importance of these lesions in both intra- and extracranial vessels in the pathogenesis of stroke. Reynaldo dos Santos in 1929 conceived the application of the Moniz technique to the study of lower limb arterial circulation by direct injection into the abdominal aorta via the translumbar approach, starting a new era for the comprehension of the role of occlusive lesions in the arterial system of the lower limbs in the pathogenesis of gangrene [22] (Fig. 1.6.1b). Modern arteriography followed the development of new methods for distant contrast injection as proposed
by Loman and Myerson (1936), Fariñas (1941) and Radner (1948). These contributions led to the method of percutaneous retrograde catheterization described by Sven-Ivar Seldinger [27] in 1953, through the common femoral artery, which became the standard arteriographic technique. Other arteries were used as entry points into the arterial system, such as the axillary, brachial and popliteal arteries. The association of computer technology with angiographic equipment enabled new digital subtraction techniques, leading to great improvements in image quality and safety of the procedure. Visualization of the veins in a cadaveric arm was first reported by Berberich and Hirsch [1] in 1923, but the first in vivo phlebogram was obtained by J. Cid dos Santos in 1933, by direct exposure and injection of the long saphenous vein (Fig. 1.6.1c). The technique was modified subsequently with percutaneous vein puncture to inject the
67
68
1.6 Invasive Diagnosis of Vascular Diseases
contrast material, and several techniques were described using direct free-flow ascending visualization and descending techniques with retrograde filling of the venous system to study valvular function [16, 27].
garded in modern vascular practice as the first step of surgical or interventional treatment. • Therefore, arteriography should only be indicated when aggressive treatment is planned or if there is disagreement between clinical and noninvasive evaluation.
1.6.3 Arteriography Translumbar Aortography 1.6.3.1 Techniques Arteriography • Arteriography provides detailed visualization of the arterial segments and is an essential tool for planning revascularization by conventional or endovascular techniques. • Noninvasive technology combining new vascular imaging modalities with flow assessment has reduced the diagnostic importance of arteriography, which is re-
Fig. 1.6.3 Lower limb arteriography by direct femoral access
• Translumbar aortography (Fig. 1.6.2) was the first technique available. It is performed with the patient lying ventrally. • Under local anaesthesia percutaneous insertion of a long needle is performed aimed at the second or third lumbar vertebra and then shifted anteriorly to enter the lateral aspect of the aorta. • It provided good visualization of the aorto-iliac segment. • For the femoral and crural arteries successive pictures were obtained during a 50–70 ml injection of contrast. • Visualization of the distal arteries was poor, and required a complementary study by femoral percutaneous injection to obtain adequate information, particularly in patients with critical limb ischaemia and diabetes, where patency of crural and foot vessels may be of paramount importance to promote a limb-saving revascularization (Fig. 1.6.3). • The limitations of translumbar aortography related mainly to the discomfort of the patient, failure to obtain a clear visualization of the visceral vessels (which required more proximal puncture of the aorta with increased risk of iatrogenic lesions), risk of aortic and/or visceral arterial dissection (a rare but serious complication) and retroperitoneal haematoma, usually selfcontained and limited. • Popliteal arteriography can also be obtained by percutaneous puncture in the popliteal fossa under Duplex-scan guidance or contrast visualization obtained by injection elsewhere in the arterial system using a mobile radiological table. • Arteriography can still be required for the study of tumour vascularization and adequate planning of surgical resection. • Pain and moderate discomfort can be associated with contrast injection, but the new nonionic agents are much better tolerated, allowing the performance of arteriography under local anaesthesia and sedation.
1.6.3 Arteriography
• The major contraindications for arteriography are a history of previous severe allergic reaction to contrast media, pulmonary insufficiency and severe renal function impairment. • New low osmolarity contrasts are better tolerated with fewer gastrointestinal side-effects (nausea and vomiting) and cause fewer allergic reactions (although the risk of serious reactions may always be present). • Proper hydration of the patients and new pharmacological agents such as acetylcysteine seem to reduce the renal risk associated with arteriography.
• Interruption of anticoagulant treatment with warfarin at least for 48 h and normalization of INR. • Evaluation of renal and coagulation function. • Adequate control of arterial hypertension. • Absence of oral intake for 4 h before the exam. • Insertion of venous access. • Adequate hydration of the patient to promote maintained diuresis and reduce the risk of renal impairment. • Light sedation with benzodiazepines. • Correct selection of entry point according to pulse amplitude, presence of arterial disease and previous arteriograms.
Contrast Media [3, 8, 9] • The contrast media that are in use contain iodine; they vary according to the quantity of iodine and its osmolarity. • They are divided into two main groups: high osmolarity (ionic contrasts) and low osmolarity (ionic or nonionic contrasts). The amount of iodine is a major contributor to its global osmolarity. • Low osmolarity contrasts are better tolerated, with less severe gastrointestinal reactions (nausea and vomiting) and fewer allergic reactions. However, they are more expensive. • On the other hand, nonionic contrasts are less painful when injected in the peripheral circulation, being the preferred choice for limb arteriography. • Usually, the use of low osmolarity contrast media in cerebral arteriography is recommended during endovascular procedures in patients with a previous history of allergies and/or asthma, heart failure, pulmonary hypertension or a previous history of allergy to the contrast media, as well as in old patients and in those with known renal dysfunction.
1.6.3.2 Pre-procedure Evaluation and Preparation The indications for arteriography should be carefully evaluated and previous imaging studies should be reviewed. Medical history of the patient should also be complete, including history of allergic reactions and coagulation disorders. Proper management before arteriography requires the following steps: • Discontinuation of oral antidiabetic treatment replaced by rapid action insulin, until resumption of oral feeding.
1.6.3.3 Technique Vascular Access The choice of the site for access to the arterial system is an essential step for a successful arteriogram. It should facilitate good access to the area under study and ideally the arterial pulse should be normal, to exclude significant proximal occlusive disease. The most common access site is the femoral artery but in selected cases a brachial, radial, popliteal or even translumbar technique must be used. With the exception of the translumbar approach, arterial access is based on the Seldinger technique.
Seldinger Technique
• The skin and perivascular tissues are infiltrated with a local anaesthetic (10 ml lidocaine 20%) and a small (1 mm) incision is performed. • A needle is inserted at an angle of 45° until the blood comes out and an introduction guidewire is passed and the needle removed. • The introducer sheath and dilator is then inserted over the guidewire. • Finally, the dilator and the guidewire are removed and the sheath is flushed with heparinized solution. • This procedure should be performed meticulously to avoid dissection of the proximal arterial segment, which can lead to thrombosis. An alternative method to enter the artery is by transfixation puncture, access being obtained by the retrograde movement of the needle. This technique is associated with
69
70
1.6 Invasive Diagnosis of Vascular Diseases
a higher rate of haemorrhagic complications, because of a double (anterior and posterior) arterial orifice. This method provides retrograde access to the arterial system using the femoral artery as the entry point, and, through selective catheterization of different arteries, allows adequate visualization of the iliac system, aorta, visceral abdominal aortic branches, supra-aortic trunks, upper limb and cerebrovascular arteries. Access to the arteries of the contralateral lower limb can be achieved by a cross-over technique at the aortic bifurcation (antegrade access in the contralateral limb) and is usually adequate to carry out interventional procedures.
have used this approach to monitor intra-sac pressure following endovascular treatment of abdominal aortic aneurysms and to identify type II endoleaks [7].
Upper Limb Access
When the femoral route cannot be used, access from the upper extremity, using the brachial or less frequently the radial artery, can be adequate. This approach can also be helpful for retrograde endovascular treatment of proximal subclavian stenosis.
Catheters Antegrade Femoral Access
• The antegrade femoral technique through the ipsilateral common or superficial femoral artery provides access, for diagnostic or endovascular purposes, to the femoro-popliteal and tibio-peroneal arterial segments. • It is obtained through an antegrade, flow-directed percutaneous approach proximal to the femoral pulse with orientation of the needle appropriate for entry into the common femoral artery. • Care should be taken to avoid dissection and to orientate the guidewire in the proper direction to the femoro-popliteal segment.
Translumbar Aortic Access
In selected cases of complete aortic occlusion or bilateral iliac occlusion and when upper limb access cannot be used, arteriography can be obtained through a direct aortic puncture using a suitable needle. • The patient has to be in ventral decubitus. • After skin infiltration with a local anaesthetic and a small incision is made, the needle is inserted with an angulation of 45° in a point located in the left dorsal region 7–10 cm lateral to the midline and 2–3 cm below the 12th rib. • The needle is advanced tangential to the vertebral body, the transmission of the aortic pulsation can be felt, and the aorta usually entered through its lateral wall. Translumbar aortography is rarely used, except for extensive occlusive disease when retrograde catheterization is either impossible or difficult. However, some authors
• The choice of the appropriate angiographic catheter is essential and it depends on the artery that has to be studied and the type of angiographic examination. • A large number of different catheters are available and the main differences are related to their length, calibre, tip configuration and location of distal holes (single terminal or multiple lateral).
1.6.3.4 Post-procedure Care After removal of the angiographic sheath it is important to follow some essential steps in order to prevent the occurrence of complications: 1. Adequate manual compression at the puncture site should be maintained until there is a clear haemostasis. 2. The patient should maintain bed rest for 4 h in the case of a 4F or 5F introducer sheath and for a longer period (8–12 h) if a larger introducer sheath had been used. 3. Close surveillance of the puncture site should be maintained. 4. Surveillance of vital signs and peripheral pulses. 5. Maintenance of adequate hydration usually using the intravenous access.
1.6.3.5 Complications • Complications related to angiography occur in 5–8% of cases but only 1–2% require treatment [11]. However, angiography can be associated with potential life-threatening complications in 0.05–0.1% of instances [6].
1.6.3 Arteriography
• Angiography-related complications may arise from arterial lesions at the access site and allergic (pseudoallergic?) reactions or may be related to direct toxicity of the contrast agent.
Access Site Complications • Complications related to the access site may occur in about 1.7% of cases when the femoral artery is used and in about 7% when the entry point is the brachial artery. • The most common complications are the formation of a haematoma or even a pseudo-aneurysm that can become apparent only days after the procedure. Haematomas are usually treated conservatively; small pseudo-aneurysms may thrombose spontaneously but frequently require surgical or ultrasound-guided compression with associated thrombin injection. • The insertion of the introducer sheath can cause local dissection of the arterial wall which can lead to arterial thrombosis or distal embolization. • The incidence of access site complications is higher in an endovascular intervention setting than in diagnostic procedures, because there is a need to use larger diameters for the introducers and guiding sheaths. • The incidence of complication is also higher when anticoagulant, antiplatelet and thrombolytic drugs are used during the procedure. • The prevention of haematoma and pseudo-aneurysm formation includes a strict control of arterial hypertension during and after the procedure, careful access site compression and bed rest for 4–6 h in diagnostic procedures and 8–12 h when larger sheaths have been used. • The use of access site occlusion devices seems to be associated with fewer complications and needs less resting time after the procedure. • The prevention of arterial dissection includes the utilization of strictly correct technical principles and fluoroscopic control during sheath, guidewire and catheter introduction.
Pseudo-Allergic Reactions • Anaphylactoid reactions are also called pseudo-allergic because they are histamine mediated and not related to antigen–antibody reactions [24].
• They are common and range from simple urticaria or bronchospasm to severe laryngeal oedema or shock. • They are independent of the dose of contrast used and are more common in patients with a history of asthma and previous contrast reactions. • In patients at risk prophylactic medication with antihistamine drugs and corticosteroids is indicated to reduce the frequency and severity of these allergic complications.
1.6.3.6 Direct Toxicity Gastrointestinal Reactions • The most common gastrointestinal reactions are nausea and vomiting, related to osmolarity, and seem to be less frequent when low osmolar contrasts are used.
Renal Function Impairment Impairment of renal function after contrast injection is not common after diagnostic angiography. It can be relevant if previously there has been any degree of renal failure, in aged or diabetic patients and when high volumes of contrast are used [13, 23, 25]. The occurrence or worsening of renal dysfunction after angiography can be prevented or limited by some measures that must be taken into account in every patient, with special emphasis in those at risk: 1. Adequate hydration of the patient. 2. Use of low osmolarity contrast. 3. Limitation of the amount of contrast used. 4. Active maintenance of diuresis during and after the procedure. 5. Oral administration of acetylcysteine 400–600 mg b.d. 2 days before the procedure [13].
Pain During Injection • Burning pain after arterial injection of contrast is common during aortic and lower limb angiographic procedures. • It involves gluteal and thigh regions in aortic injections and the leg and foot in femoral injections, where it is usually more severe.
71
72
1.6 Invasive Diagnosis of Vascular Diseases
• The use of nonionic contrasts is associated with better tolerance and less pain during arteriography.
1.6.4 Phlebography • This became the most accurate method for evaluating lower limb veins and has been applied to patients with deep venous obstruction, post-thrombotic syndrome, superficial vein insufficiency as well as chronic deep venous reflux [15]. • The use of the new noninvasive imaging and flow assessment methods for the study of vascular diseases introduced in the 1980s provided adequate and reliable information for the diagnosis of venous disorders, reducing the scope of phlebography as a major diagnostic tool. • Its pitfalls were recognized, i.e. its invasive nature, the need to use contrast material and radiation exposure, and the publication of several reports of acute deep vein thrombosis associated with the contrast injection particularly in the lower limb veins. • As phlebography requires injection of iodinated material, the contrast-related complications are the same as described previously for arteriography. The same preventive measures should also be taken before the examination. • These reasons have led to a reduction in the number of phlebograms performed and its clinical indications have been reduced and limited to certain clinical situations where noninvasive information is inadequate, or in the presence of discrepancy between clinical and noninvasive evaluations, and prior to surgical or interventional treatment of the deep venous system.
1.6.4.1 Indications Current indications for the clinical use of phlebography are the following: • Atypical varicose veins the origin of which is not well documented by colour-flow Duplex scan. • Recurrent varicose veins without clear evidence of the sites of reflux by colour-flow Duplex scan. • Discrepancy between the clinical examination and the results of colour-flow Duplex scan. • Deep venous thrombosis with extension to the inferior vena cava when placement of a filter or other endovascular interventions may be considered.
• High clinical suspicion of deep venous thrombosis when noninvasive evaluation is doubtful or negative. • Planning of direct deep venous reconstructions such as venous crossover by-pass, venous valve transplantation or repair.
1.6.4.2 Techniques Ascending or Free-flow Phlebography • Ascending or free-flow phlebography is performed with the patient in the supine position; access is usually obtained through a dorsal vein of the foot and a tourniquet is applied at the ankle to block the superficial system thus directing the flow of contrast into the deep venous system. • An injection of 80 ml is often necessary to obtain adequate visualization of the entire deep venous system of the lower limbs, and its progression along the limb followed by fluoroscopy. • This allows the assessment of partial or complete obstruction of the deep venous system and the identification of sites of incompetence at different levels in the leg and thigh, and visualization of incompetent perforators.
Descending or Retrograde Phlebography • The main objective of this technique is the study of venous valve function and evaluation of venous reflux in both the deep and superficial venous system, and for detailed study of insufficiency at the sapheno-femoral and sapheno-popliteal junctions. • The initial technique of descending phlebography was through puncture of the femoral vein with the patient standing; it was developed subsequently by Cid dos Santos [18] to study sapheno-femoral incompetence and abnormal patterns of venous reflux in complex recurrent varicose veins. • It is performed with the patient in a 60° upright position using a tilting radiological table or with the patient in the standing position supported by a rigid frame. • The access is made by puncture of the common femoral vein, followed by cannulation using a standard Seldinger technique and a multiple side hole catheter inserted in the external iliac vein, to allow the injection of 40 ml iodinated contrast.
1.6.4 Phlebography
• Reflux of contrast is stimulated by a Valsalva manoeuvre in order to test the valve function and to diagnose deep system valvular incompetence and also deep to superficial reflux. • The extension of reflux into the deep system was classified according to its extension to the thigh and leg veins [26] and its clinical relevance seems to be associated with the involvement of popliteal and crural veins, the popliteal valve playing an essential protective role [28]. • Abnormal patterns of reflux in complex recurrences were clearly demonstrated by descending phlebography (Fig. 1.6.4) and this technique may be useful in pre-operative evaluation of varicose vein recurrences.
Popliteal phlebography was an additional descending technique promoted by Cid dos Santos and co-workers [5] to study the sapheno-popliteal junction and to diagnose abnormal patterns of reflux into the saphenous system. • With the patient standing, and supported by a frame, local anaesthesia was applied in the popliteal fossae and direct puncture of the popliteal vein obtained. • Injection of contrast initially during free-flow provided visualization of the superficial and common femoral vein; then, a Valsalva manoeuvre was performed to promote venous reflux and successive anterior and lateral pictures were obtained to visualize the popliteal and leg veins and assess the presence of abnormal venous reflux.
Fig. 1.6.4 Different phlebographic aspects of popliteal reflux (adapted from [30])
73
74
1.6 Invasive Diagnosis of Vascular Diseases
• Initial clarification of the variability of the anatomy of the short saphenous vein and its junction in the deep system were achieved by this technique. • Incompetence of the gastrocnemius vein as a cause of varicose veins in the leg was recognized [17] and insufficiency of the Giacomini vein associated with short saphenous incompetence as a source of reflux into the long saphenous vein was clearly demonstrated. Popliteal and femoral descending phlebography provided the anatomical basis for the understanding of venous physiology and the “road-map” for the subsequent use of noninvasive imaging modalities such as colour-flow Duplex-scan evaluation. Its use in modern practice is very limited to the study of deep valvular incompetence to plan reconstructive venous surgery and for difficult situations of recurrence where the colour-flow Duplex scan has not provided clear demonstration of the source of reflux. Popliteal phlebography may still play a role in clarifying recurrences following short saphenous surgery to facilitate surgical planning. Its main goal was to determine the exact location of the sapheno-popliteal junction before surgery, an objective that can be obtained by carefully performed Duplex-scan evaluation or more easily and directly by table phlebography and direct injection of the short saphenous vein [12]. References 1. Berberich J, Hirsh S (1923) Roentgenography of blood vessels. Klin Wochenschr 2:2226–2228 2. Brooks B (1924) Intra-arterial injection of sodium iodide. J Am Med Assoc 82:1016–1019 3. Bush WH, Swanson DP (1991) Acute reactions to intravascular contrast media: types, risk factors, recognition, and specific treatment. AJR Am J Roentgenol 157:1153–1161 4. Cid dos Santos J (1938) La phlebographie directe. Conception technique, premiers resultats. J Int Chir 35:625–669 5. Cid dos Santos J (1973) Introduction anatome-phisiopathologique à la technique phlébographique. Phlebologie 26:359–360 6. Coley BD, Roberts AC, Fellmeth BD, Valji K, Bookstein JJ, Hye RJ (1995) Postangiographic femoral artery pseudoaneurysms: further experience with US-guided compression repair. Radiology 194:307–311 7. Dias NV, Ivancev K, Malina M, Hinnen JW, Visser M, Lindblad B, Sonesson B (2004) Direct intra-aneurysm sac pressure measurement using tip-pressure sensors: in vivo and in vitro evaluation. J Vasc Surg 40:711–716
8. Gomes AS, Lois JF, Baker JD, McGlade CT, Bunnell DH, Hartzman S (1989) Acute renal dysfunction in high-risk patients after angiography: comparison of ionic and nonionic contrast media. Radiology 170:65–68 9. Greenberger PA, Patterson R, Tapio CM (1985) Prophylaxis against repeated radiocontrast media reactions in 857 cases. Adverse experience with cimetidine and safety of beta-adrenergic antagonists. Arch Intern Med 145:2197–2200 10. Haschek E, Lindenthal O (1896) A contribution to the practical use of the photography according to Roentgen. Wien Klin 9:63–64 11. Hessel SJ, Adams DF, Abrams HL (1981) Complications of angiography. Radiology 138:273–281 12. Hobbs J (1980) Per-operative venography to ensure accurate sapheno-popliteal vein ligation. Br Med J 2:1578 13. Kay J, Chow WH, Chan TM, Lo SK, Kwok OH, Yip A, Fan K, Lee CH, Lam WF (2003) Acetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention: a randomized controlled trial. J Am Med Assoc 289:553–558 14. Kinmonth JB (1952) Lymphangiography in man; a method of outlining lymphatic trunks at operation. Clin Sci (Lond) 11:13–20 15. Kistner RL, Kamida CB (1995) Update on phlebography and varicography. Dermatol Surg 21:71–76 16. Lea Thomas M, Treweeke PS (1987) The assessment of deep vein valve incompetence by ascending phlebography with a Valsalva manoeuvre: a comparison with descending phlebography. Vasa 16:274–277 17. Marques JS (1975) Varices of long saphenous system due to valvular insufficiency of short saphena’s cross. Folia Angiologica XXIII:135–144 18. Marques JS, Cid dos Santos J, Coito A (1970) Flebografia vertical directa. Progressos técnicos da prova popliteia. J Med 1406:5–19 19. Moniz E (1927) L’éncephalographie artérielle: son importance dans la localization des tumeurs cérébrales. Rev Neurol 2:172 20. Moniz E, Lima A, Lacerda R (1937) Hemiplegies par thrombose de la carotide interne. Presse Med 45:977 21. Pedro LM (2003) A window to atherosclerosis: high definition ultrasonography in the study of the arterial wall. University of Lisbon, Lisbon 22. Reynaldo dos Santos, Lamas A, Caldas JP (1931) L’arteriographie des membres et de láorte abdominale. Masson, Paris
References
23. Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ, Singh M, Bell MR, Barsness GW, Mathew V, Garratt KN, Holmes DR Jr (2002) Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 105:2259–2264 24. Routh WD (1995) Contrast angiography. In: Dean RH, Yao JS (eds) Current diagnosis and treatment in vascular surgery. Lange, Stamford 25. Rudnick MR, Berns JS, Cohen RM, Goldfarb S (1997) Contrast media-associated nephrotoxicity. Semin Nephrol 17:15–26 26. Rutherford RB, Padberg FT Jr, Comerota AJ, Kistner RL, Meissner MH, Moneta GL (2000) Venous severity scoring: an adjunct to venous outcome assessment. J Vasc Surg 31:1307–1312
27. Seldinger SI (1953) Catheter replacement of the needle in percutaneous arteriography. Acta Radiol 39:368–376 28. Shull KC, Nicolaides AN, Fernandes JF et al (1979) Significance of popliteal reflux in relation to ambulatory venous pressure and ulceration. Arch Surg 114:1304 29. Wickbom I (1948) Angiography of the carotid artery. Acta Radiol Supl LXXII:1–90 30. Diniz LT, Marques JS, Coito A, Pinto FO, Korn M (1979) A doença venosa dos membros inferiores. Bial, Porto
75
77
1.7 Computer-Aided Diagnosis of Vascular Disease Spyretta Golemati, Konstantina S. Nikita
1.7.1 Introduction To diagnose vascular disease, physicians usually base their decision on clinical history and physical examination of the patient, as well as visual inspection of medical images. In some cases, confirmation of the diagnosis is particularly difficult because it requires specialization and experience, or even the application of interventional methodologies (e.g. arteriography). While advances in medical imaging technology have greatly contributed to early detection and diagnosis of vascular disease, the selection of patients to whom surgery is offered remains one of the most challenging tasks in the management of vascular disease. In medical imaging, the accurate diagnosis and/or assessment of a disease depends on both image acquisition and image interpretation. Modern imaging devices based on fundamental concepts in physical science (e.g. X-ray, magnetic resonance, nuclear physics and acoustics) and incorporating the latest innovations in computer technology and data processing techniques have proved extremely useful for early diagnosis of vascular disease. More recent advances in imaging technology include advanced imaging possibilities (3D reconstruction, functional imaging, magnetic resonance angiography, elastography), novel imaging techniques (e.g. virtual angioscopy) and registration of images obtained with different modalities. The image interpretation process, however, has only recently begun to benefit from computer technology. Interpretation of medical images, usually performed by radiologists, is often limited due to the nonsystematic search patterns of humans, the presence of structure noise (camouflaging normal anatomical background) in the image, and the presentation of complex disease states requiring the integration of vast amounts of image data and clinical information. Computer-aided diagnosis (CAD) – defined as a diagnosis made by a physician who uses the output from a computerized analysis of medical data as a “second opinion” in detecting lesions, assess-
ing disease severity and making diagnostic decisions – is expected to enhance the diagnostic capabilities of physicians and reduce the time required for accurate diagnosis. With CAD, the final diagnosis is made by the physician. Thus, the computer output needs to be at a sufficient level of sensitivity and specificity, and in addition the output must be displayed in a user-friendly format for effective and efficient use by the clinician. This chapter reviews the field of CAD in vascular imaging, including aspects of image processing and presents an example of an in-house-developed CAD system.
1.7.2 Computer-Aided Diagnosis in Vascular Imaging The main steps in the diagnosis process include lesion detection, characterization and assessment. Lesion detection refers to the definition of possible pathological structures from image data. Lesion characterization involves the assessment of the status of the lesion, e.g. the likelihood that the lesion, such as a plaque, is malignant (symptomatic). Features that characterize normal and pathological tissue may be extracted from medical images. These include measurements of the size and shape of regions of interest (ROIs) within the tissue, texture features [20] and elasticity indices estimated from sequences of images [15]. In the case of vascular disease, the location and size of the lesion, namely the atheromatous plaque, need to be determined in order to estimate the degree of stenosis. Additional plaque characteristics, including texture and motion features, are important to assess disease severity. Lesion assessment refers to assigning a lesion to a class of a predefined set of classes. Symptomatic or asymptomatic plaques would be candidate classes in the case of arterial wall disease. Currently, CAD systems are being developed to detect, characterize and potentially diagnose lesions on vascular images. Such systems may take the digital image data as
78
1.7 Computer-Aided Diagnosis of Vascular Disease
input, process the data using computer vision and artificial intelligence techniques, and then output clinically relevant information, including locations of suspect lesions, characterizations of suspect lesions, estimates of the probabilities of malignancy of suspect lesions and/or numerical indices of risk of clinical symptoms. The typical structure of a CAD system includes the following procedures: • image pre-processing, • definition of regions of interest (ROIs), • extraction and selection of characteristic features, • classification.
1.7.2.1 Image Pre-processing To improve image quality, linear or nonlinear filters can be applied to the image. Image filtering is particularly important in the case of noisy images, such as ultrasound images. Histogram equalization is often used to enhance the appearance of ultrasound images. Histogram equalization modifies the dynamic range and contrast of an image by altering that image such that its intensity histogram has a desired shape [14].
development of computer vision methods requires a priori knowledge of the physical imaging properties of the digital image acquisition system and morphological information concerning the abnormal (e.g. atheromatous plaque) and normal tissue. Computer vision techniques usually include image processing (e.g. texture analysis, motion analysis) and feature extraction.
Texture Analysis Image texture may be defined as a function of the spatial variations in pixel intensity (grey values), which are generally due to some underlying physical variation in the sample. In medical image analysis, automatic extraction of texture features can be used for a variety of classification tasks, such as distinguishing normal from abnormal tissue or classifying different types of abnormal tissues. The most frequently used texture analysis techniques in medical imaging include: • First-order statistics • Second-order statistics • Neighbourhood grey tone difference matrix • Grey level difference statistics • Laws’ texture energy • Fractal dimension.
1.7.2.2 Definition of Regions of Interest – Automatic Segmentation First-order Statistics
Regions corresponding to suspect lesions (e.g. plaques) can be detected from medical images using either (1) manual and semi-automatic methodologies where the user interacts with the system in order to define a possible pathological region or (2) fully automated methodologies where suspect regions are detected with appropriate digital image processing techniques [4]. Several techniques for segmentation of arterial wall and plaques from images of various modalities have evolved recently. Examples include the segmentation of coronary plaques from intravascular ultrasound (IVUS) images [29], and the segmentation of carotid plaques from B-mode ultrasound using active contour models [24].
First-order statistics measure the likelihood of observing a grey value at a randomly chosen location in the image. First-order statistics can be computed from the histogram of pixel intensities in the image. These depend only on individual pixel values and not on the interaction or co-occurrence of neighbouring pixel values. A total of 16 first-order statistical features can be estimated from the normalized grey-level histogram of the selected region of the image, including minimal grey level, maximal grey level, median grey level, mean grey level, standard deviation of grey levels, coefficient of variation, grey level skewness, grey level kurtosis, grey level energy, grey level entropy, 10th percentile, 25th percentile, 50th percentile, 75th percentile, 90th percentile and histogram width.
1.7.2.3 Extraction and Selection of Characteristic Features
Second-order Statistics
Automatic extraction of features, which may or may not be visible to the human observer, from digital images is possible with the use of computer vision methods. The
Second-order statistics are defined as the likelihood of observing a pair of grey values occurring at endpoints of a dipole (or needle) of random length placed in the image at a random location and orientation. These are properties
1.7.2 Computer-Aided Diagnosis in Vascular Imaging
of pairs of pixels. Second-order statistics are derived from angular nearest-neighbour spatial-dependence matrices, also known as co-occurrence matrices [16]. The relative frequencies P(i, j, d, θ) with which two neighbouring pixels with grey levels i and j at a given distance d and orientation θ occur on the image are used to construct the cooccurrence matrices. A total of 14 textural measures can be estimated from the co-occurrence matrix, including angular second moment, contrast, correlation, variance, inverse difference moment, sum average, sum variance, sum entropy, entropy, difference variance, difference entropy, information measures of correlation (two features) and maximum correlation coefficient.
Neighbourhood Grey Tone Difference Matrix
For each ROI, information about spatial changes in intensity can be obtained by looking at the difference between each pixel and the grey tones of its surrounding neighbours. A one-dimensional (1D) matrix can be estimated for each ROI, in which the ith entry corresponds to the summation of the differences between the grey level of all pixels with grey level i, and the average grey level of their surrounding neighbours. The size of the neighbourhood depends on the selected distance, i.e. a distance equal to 1 results in a 3×3 neighbourhood. Five features are derived from this 1D matrix, namely coarseness, busyness, contrast, complexity and texture strength.
Grey Level Difference Statistics
First-order statistics of the local property values can be obtained using the grey level difference statistics method [32]. The computation of the local properties is based on the absolute difference between pairs of grey levels or of the average grey levels. For any given displacement δ=(Δx, Δy) the following four texture measures can be estimated: contrast, angular second moment, entropy and mean.
Laws’ Texture Energy
Laws’ texture energy measures [23] are derived from three simple vectors of length 3, L3 − − (1, 2, 1), E3 − − (–1, 0, 1) and S3 − (–1, 2, –1), which represent the 1D operations of centre-weighted local averaging, symmetric first differencing for edge detection, and second differencing for spot detection. If these vectors are convolved with themselves or with each other, five vectors of length 5 are obtained, L5 − − (1, 4, 6, 4, 1), S5 − − (–1, 0, 2, 2, –1), R5 − − (1, –4, 6, –4, 1), E5 − (–1, –2, 0, 2, 1) and W5 − (–1, 2, 0, –2, 1). If the col-
umn vectors of length 5 are multiplied by row vectors of the same length, then Laws’ 5×5 masks are obtained. To describe texture in an image using the obtained masks, the masks are convolved with the image and statistics (e.g. energy) of the results are used as texture properties.
Fractal Dimension
Many natural surfaces have a statistical quality of roughness and self-similarity at different scales. Fractals, first proposed by Mandelbrot [25], are very useful in modelling these properties in image processing. The definition of the fractal dimension is based on the concept of selfsimilarity. Given a bounded set A in a Euclidean n-space, the set A is said to be self-similar when A is the union of N distinct (nonoverlapping) copies of itself, each of which has been scaled down by a ratio of r. The fractal dimension D is related to the number N and the ratio r as follows: D = log N / log (1/r). The fractal dimension gives a measure of the roughness of a surface. For an image, the fractal dimension is a noninteger number between 2 and 3. Intuitively, the larger the fractal dimension, the rougher the texture. Image texture has been widely used to characterize biological tissue. In computer-aided diagnosis of vascular disease, the grey scale median (GSM), estimated from Bmode ultrasound images, was found to be significantly lower for symptomatic plaques [9, 30] and for high degrees of stenosis [9]. Echogenic plaques, defined as plaques with GSM > 50, were associated with a 9% incidence of ipsilateral brain CT infarction, whereas echolucent plaques, defined as plaques with GSM < 50, were associated with a 40% incidence of ipsilateral brain CT infarction [5]. The GSM was found to be lower for soft material (blood, lipid) and higher for fibrous tissue and calcific deposits [10, 22]. Furthermore, the mean pixel value (MPV) was found to decrease as the soft (fat and blood) content of the plaque increased, and to increase as the fibrocalcific tissue content increased [1, 26]. First-order statistics have been used to characterize texture in various areas of a typical B-mode ultrasound image of a diseased carotid artery (e.g. atheromatous plaque, blood and surrounding tissue) and were found to be significantly different for different areas [13]. Furthermore, symptomatic and asymptomatic atheromatous plaques have been characterized using the previously described texture analysis techniques [2, 8, 33]. In addition to this, analysis of image texture has been used to characterize coronary plaques from intravascular ultrasound images [31, 35]. These studies have shown
79
80
1.7 Computer-Aided Diagnosis of Vascular Disease
that quantitative information extracted from ultrasound images can be useful in the diagnosis of atherosclerosis and enable decision-making about disease management. Estimates of tissue texture may be used in a number of studies, including: (1) modelling of the mechanical behaviour of normal and abnormal tissue, and (2) drug assessment. In combination with estimates of tissue strain obtained from motion analysis, texture information may be used to estimate the stresses exerted on tissue [34]. In studies of drug treatment assessment, it is assumed that texture may change after treatment with specific drugs [7], and thus, texture estimates may be used to evaluate the performance of drug treatment.
Motion Analysis Motion analysis from sequences of images allows the estimation of mechanical strain experienced by the tissue. In the case of arterial walls, strain is due to stresses caused by blood pressure, blood flow and tethering to surrounding tissue. To estimate motion, temporal sequences of images need to be recorded at high frame rates. The estimation of motion patterns of biological tissue may provide useful insight into the mechanical properties of different types of tissue. In particular, in the case of atherosclerosis, the analysis of plaque motion may provide new insight into plaque modelling as well as into mechanisms of plaque rupture with subsequent embolism. The following techniques can be used to analyse arterial wall and plaque motion from sequences of images: • Region tracking and block matching • Optical flow.
Region Tracking and Block Matching
The method is described in detail elsewhere [12]. Briefly, a ROI can be selected in the first frame of the sequence and its position is automatically tracked in subsequent frames. Automatic tracking is based on matching ROI pixel intensities in each frame with those in the first frame. Rectangular ROIs can be tracked if their co-ordinates and dimensions are given by the user or can be defined using the mouse. The result of the motion analysis consists of waveforms showing radial and axial displacements, velocities and accelerations of the selected ROIs as well as correlation coefficients. The difference waveforms for the radial and axial displacement can be used to analyse relative motion between selected sites. The vectors of
maximum displacements for each ROI can be displayed superimposed on the B-mode image.
Optical Flow
The calculation of the apparent velocity field, i.e. optical flow, relies on the estimation of the spatiotemporal changes in pixel intensities throughout an image sequence. An implementation of a validated motion estimation algorithm [17], using a minimization of sum-of-squared differences between images, was used in this work to estimate optical flow. Results of motion estimation between consecutive frames are propagated, i.e. vector end points are used as starting co-ordinates for the next frame evaluation. The final result is a dense vector map where each pixel is represented by a vector corresponding to its velocity between two frames. Motion of the carotid artery wall has been estimated from sequences of two-dimensional B-mode ultrasound images [12] as well as from ultrasound radiofrequency images [3]. Image speckle patterns were tracked between successive frames using the correlation coefficient as the matching criterion. The results showed expected cyclical motion in the radial direction and some axial movement of the arterial wall. Meairs and Hennerici [27] studied carotid plaque motion using 4D ultrasonography and optical flow. They expressed plaque surface motion in terms of two parameters: (1) maximal surface velocity (MSV) and (2) maximal discrepant surface velocity (MDSV), defined as the maximum of differences between maximal and minimal surface velocities of successive 3D frame volumes. Asymptomatic plaques showed a homogeneous orientation and magnitude of computed velocity vectors corresponding to a global pattern of arterial motion without evidence of inherent plaque movement. Symptomatic plaques showed signs of inherent plaque motion, irrespective of arterial wall motion.
1.7.2.4 Classification Classification is possible through artificial intelligence techniques, which can be used to merge the mathematical descriptors of the image features into a diagnostic output. The process is similar to the decision-making task of a physician who weighs up different aspects of vascular imaging findings. Many computer analysis methods involve the use of classifiers to distinguish between actual lesions and false-positive detections, or between malignant and benign lesions, including rule-based methods, discrimi-
1.7.2 Computer-Aided Diagnosis in Vascular Imaging
nant analysis, Bayesian methods, artificial neural networks and fuzzy logic [19]. The features for input to these classifiers are selected using a variety of computer techniques such as stepwise methods and genetic algorithms [21].
1.7.2.5 ANALYSIS: a Modular Software System to Support Diagnosis of Vascular Disease ANALYSIS is a CAD system designed and developed in the Biomedical Simulations and Imaging Laboratory, School of Electrical and Computer Engineering, National Technical University of Athens, Greece. The system incorporates the main parts of a typical CAD system and has been used to support the diagnosis of vascular disease (carotid atherosclerosis). ANALYSIS can be installed
Fig. 1.7.1 User interface of ANALYSIS
on PC-based platforms operating under the Microsoft Windows operating system. Minimum requirements in processor speed and RAM are 600 MHz and 256 MB, respectively. Using these minimum requirements, motion analysis of two ROIs using block-matching takes 20 min. The main user interface of ANALYSIS is shown in Fig. 1.7.1. The two main windows of the interface are designed to support motion and texture analysis. Tool buttons and menu bars allow the user to select the parameters of the analysis, e.g. the number of investigated ROIs, the size and shape of ROIs, the inter-pixel distance for the calculation of second-order statistics and neighbourhood grey tone difference matrix, etc. The system includes a friendly wizard for importing results files, which can be subsequently analysed using ANOVA statistics and clustered into predefined groups using fuzzy c-means.
81
82
1.7 Computer-Aided Diagnosis of Vascular Disease
An important feature of ANALYSIS is the possibility of on-line tele-collaboration between health care professionals under a secure framework. The continuous advances in telecommunications allow exchange of information not only throughout but also beyond the hospital as well as real-time collaboration between remote users [6]. Thus, with the introduction of computer-aided diagnosis, a wide area of possible telematics applications for vascular disease can be identified. These include support of the diagnosis procedure [11, 28] and continuous medical education in arterial wall disease [28]. The collaborative environment of ANALYSIS extends the capabilities of the stand-alone CAD system, giving local and remote health care professionals the opportunity to co-operate for the delineation and image analysis of ROIs in ultrasound images. The implementation is based on a pointto-point communication scheme following the “What You See Is What I See” (WYSIWIS) paradigm. To support the collaborative environment, both asynchronous (off-line transfer of data sets) and synchronous (on-line collaboration) data exchange schemes are employed. The term “off-line” indicates the absence of user’s interaction with ANALYSIS and involves the transfer of large datasets. A sequence of B-mode ultrasound images after lossless compression requires 5–20 MB of storage depending on the number of images.
1.7.3 Conclusion CAD systems are expected to be useful tools in the diagnosis of vascular disease, because they can assist the interpretation of vascular images through a user-friendly interface. Their ultimate acceptance in clinical practice will depend not only on the performance of the computerized method alone, but also on how well the clinician performs the task when the computer output is used as an aid and on the ability to integrate the computerized analysis method into routine clinical practice [18]. Issues such as a friendly user-interface, a short system response time and low cost are critical for the daily routine use of CAD systems. References 1. Aly S, Bishop CC (2000) An objective characterization of atherosclerotic lesion. Stroke 31:1921–1924
2. Asvestas P, Golemati S, Matsopoulos GK, Nikita KS, Nicolaides AN (2002) Fractal dimension estimation of carotid atherosclerotic plaques from B-mode ultrasound: a pilot study. Ultrasound Med Biol 28:1129–1136 3. Bang J, Dahl T, Bruinsma A, Kaspersen JH, Hernes TAN, Myhre HO (2003) A new method for analysis of motion of carotid plaques from rf ultrasound images. Ultrasound Med Biol 29:967–976 4. Bankman I (2000) Handbook of medical imaging: processing and analysis. Academic Press, San Diego 5. Biasi GM, Sampaolo A, Mingazzini P, De Amicis P, El-Barghouty N, Nicolaides AN (1999) Computer analysis of ultrasonic plaque echolucency in identifying high risk carotid bifurcation lesions. Eur J Vasc Endovasc Surg 17:476–479 6. Caramella D, Reponen J, Fabbrini F, Bartolozzi C (2000) Teleradiology in Europe. Eur J Radiol 33:2–7 7. Cesarone MR, Belcaro G, Nicolaides AN, Geroulakos G, Bucci M, Dugall M, DeSanctis MT, Incandela L, Griffin M, Sabetai M (2001) Increase in echogenicity of echolucent carotid plaques after treatment with total triterpenic fraction of Centella asiatica: a prospective, placebo-controlled, randomized trial. Angiology 52 [Suppl 2]:S19–S25 8. Christodoulou CI, Pattichis CS, Pantziaris M, Nicolaides A (2003) Texture-based classification of atherosclerotic carotid plaques. IEEE Trans Med Imaging 22:902–912 9. Elatrozy T, Nicolaides A, Tegos T, Griffin M (1998) The objective characterisation of ultrasonic carotid plaque features. Eur J Vasc Endovasc Surg 16:223–230 10. El-Barghouty NM, Levine T, Ladva S, Flanagan A, Nicolaides AN (1996) Histological verification of computerized carotid plaque characterization. Eur J Vasc Endovasc Surg 11:414–416 11. Endean ED, Mallon LI, Minion DJ, Kwolek CJ, Schwarcz TH (2001) Telemedicine in vascular surgery: does it work? Am Surg 67:334–340 12. Golemati S, Sassano A, Lever MJ, Bharath AA, Dhanjil S, Nicolaides AN (2003) Carotid artery wall motion estimated from B-mode ultrasound using region tracking and blockmatching. Ultrasound Med Biol 29:387–399 13. Golemati S, Tegos TJ, Sassano A, Nikita KS, Nicolaides AN (2004) Echogenicity of b-mode sonographic images of the carotid artery – work-in-progress. J Ultrasound Med 23:659–669 14. Gonzalez RC, Woods RE (1993) Digital image processing. Addison-Wesley, New York 15. Greenleaf JF, Fatemi M, Insana M (2003) Selected methods for imaging elastic properties of biological tissues. Annu Rev Biomed Eng 5:57–78
References
16. Haralick RM, Shanmugam K, Dinstein I (1973) Textural features for image classification. IEEE Trans Syst Man Cybern SMC:610–621 17. Horn BKP, Schunck BG (1981) Determining optical flow. Artificial Intelligence 17:185–203 18. Hunt D, Haynes RB, Hanna S, Smith K (1998) Effects of computer-based clinical decision support systems on physician performance and patient outcomes. J Am Med Assoc 280:1339–1346 19. Jain AK, Duin RPW, Jianchang M (2000) Statistical pattern recognition: a review. IEEE Trans Pattern Anal Machine Intell 22:4–37 20. Kerut EK, Given M, Giles TD (2003) Review of methods for texture analysis of myocardium from echocardiographic images: a means of tissue characterization. Echocardiography 20:727–736 21. Kupinski MA, Giger ML (1999) Feature selection with limited datasets. Med Phys 26:2176–2182 22. Lal BK, Hobson RW, Pappas PJ et al (2002) Pixel distribution analysis of B-mode ultrasound scan images predicts histologic features of atherosclerotic carotid plaques. J Vasc Surg 35:1210–1217 23. Laws KI (1980) Rapid texture identification. Proc SPIE Conf Missile Guidance 238:376–380 24. Loizou CP, Pattichis CS, Istepanian RSH, Pantziaris M, Nicolaides AN (2004) Atherosclerotic carotid plaque segmentation. In: Proceedings of the 26th Annual International Conference of the IEEE EMBS, pp 1403–1406 25. Mandelbrot BB, Van Ness JW (1968) Fractional Brownian motion, fractional noises and applications. SIAM Rev 10:422–438 26. Mazzone AM, Urbani MP, Picano E et al (1995) In vivo ultrasonic parametric imaging of carotid atherosclerotic plaque by videodensitometric technique. Angiology 46:663–672
27. Meairs S, Hennerici M (1999) Four-dimensional ultrasonographic characterization of plaque surface motion in patients with symptomatic and asymptomatic carotid artery stenosis. Stroke 30:1807–1813 28. Ricci MA, Knight SJ, Nutter B, Callas PW (1998) Desktop telemedicine in vascular surgery: some preliminary findings. Telemed J 4:279–285 29. Sonka M, McKay CR, von Birgelen C (1997) Computer analysis of intravascular ultrasound images. In: Leondes CT (ed.) Medical imaging techniques and applications. Gordon and Breach, Amsterdam, pp 183–226 30. Tegos TJ, Stavropoulos P, Sabetai MM, Khodabakhsh P, Sassano A, Nicolaides AN (2001) Determinants of carotid plaque instability: echoicity versus heterogeneity. Eur J Vasc Endovasc Surg 22:22–30 31. Vince DG, Dixon KJ, Cothren RM, Cornhill JF (2000) Comparison of texture analysis methods for the characterization of coronary plaques in intravascular ultrasound images. Comput Med Imag Grap 24:221–229 32. Weszka JS, Dyer CR, Rosenfeld A (1976) A comparative study of texture measures for terrain classification. IEEE Trans Syst Man Cyber SMC 6:269–285 33. Wilhjelm JE, Grønholdt MLM, Wiebe B, Jespersen SK, Hansen LK, Sillesen H (1998) Quantitative analysis of ultrasound B-mode images of carotid atherosclerotic plaque: correlation with visual classification and histological examination. IEEE Trans Med Imaging 17:910–922 34. Zhao SZ, Xu XY, Collins MW (1998) The numerical analysis of fluid-solid interactions for blood flow in arterial structures. Part 1: A review of models for arterial wall behaviour. Proc Inst Mech Eng [H] 212:229–240 35. Zhang X, McKay CR, Sonka M (1998) Tissue characterization in intravascular ultrasound images. IEEE Trans Med Imaging 17:889–899
83
85
1.8 Preoperative Evaluation of a Vascular Patient Michael Horrocks, James Metcalfe
1.8.1 Introduction The purpose of preoperative evaluation is to identify and, if necessary, implement measures to prepare higher risk patients for surgery. Preoperative evaluation can decrease the length of hospital stay as well as minimize postponed or cancelled surgeries [4]. With the high likelihood of underlying coronary artery disease and the high degree of haemodynamic cardiac stress with profound alteration in heart rate, blood pressure, vascular volume, bleeding and clotting tendencies, vascular surgery represents an intermediate (1–5%) to high (>5%) mortality risk. Surgical morbidity and mortality generally falls into one of three categories: cardiac, respiratory and infectious complications. A good history and physical examination, focusing on risk factors for cardiac, pulmonary and infectious complications, and determination of a patient’s functional capacity are essential in the general evaluation process. With respect to the type of surgery, urgent and emergency procedures constitute higher risk situations than elective, nonurgent surgery and present a limited opportunity for preoperative evaluation and treatment.
daemia) are also risk factors for coronary artery disease (CAD). The incidence of CAD in patients with peripheral vascular disease is around 60%. The usual symptomatic presentation in this group of patients may be obscured by exercise limitations due to advanced age or intermittent claudication.
Risk Stratification The goal of risk stratification is to reduce overall morbidity and mortality associated with the surgical procedure. The information gathered from the history and examination will help to stratify the patient as at high, intermediate, or low risk for peri-operative cardiac complications. Consideration of further testing is based on the risk category at which the patient is placed. An example of risk stratification is shown in Table 1.8.1. For patients who have undergone coronary artery bypass grafting within the last 5 years, and whose clinical status has remained stable without recurrent symptoms or sign of ischaemia, further cardiac testing is not necessary. If a patient has had adequate coronary evaluation in the last 2 years and the findings were favourable, it is not usually necessary to repeat the tests unless there are new symptoms.
1.8.2 Systemic Evaluation Diagnostic Procedures A thorough systemic evaluation is appropriate in all patients undergoing vascular surgery. Specific areas of importance are discussed here.
Recommended European Standard Low Risk
• Electrocardiography (ECG) • Plain chest radiograph. 1.8.2.1 Cardiovascular System Intermediate Risk and High Risk
Cardiac complications are the leading cause of morbidity and death in patients undergoing vascular surgery [1]. Many of the risk factors contributing to peripheral vascular disease (diabetes mellitus, smoking, dyslipi-
• Exercise electrocardiography – in most ambulatory patients the test of choice is exercise electrocardiography, which provides an estimate of functional capacity and can detect myocardial ischaemia.
86
1.8 Preoperative Evaluation of a Vascular Patient
Table 1.8.1 A guide to risk stratification Low Risk
Intermediate Risk
High Risk
Advanced age
Prior myocardial infarction
Recent myocardial infarction
Abnormal electrocardiogram
Diabetes mellitus
Unstable or severe angina
Rhythm other than sinus
Compensated or prior congestive heart failure
Decompensated congestive heart failure
Low functional capacity
Mild angina pectoris
Severe valvular disease
History of stroke
Significant arrhythmias in the presence of underlying heart disease
Uncontrolled hypertension
Supraventricular arrhythmias with uncontrolled ventricular rate
Advanced age
• Stress echocardiography – useful in patients with a major abnormality or uninterpretable ECG, or patients who cannot meet the physical requirements of the exercise portion of an exercise ECG. Patients with positive results have an 8–38% risk of cardiac death or myocardial infarction (MI) within 30 days after surgery.
Treatment Recommended European Standard Low Risk
• β-Blockade – the ability of β-blockers to reduce the peri-operative risk of cardiac complications has been extensively documented [2]. Atenolol is often administered intravenously or orally beginning 2 days preoperatively and continuing for 7 days postoperatively; this intervention reduced the incidence of peri- and postoperative myocardial ischaemia by 30–50% in randomized controlled trials [7]. In the absence of contraindications all patients undergoing major vascular surgery should benefit from β-blockade. Intermediate and High Risk
Therapy in these groups should be based upon the results of noninvasive testing: • If negative – β-blockade only. • If positive – consider cardiac catheterization, the results of which may lead to either percutaneous coronary angioplasty (PTCA) or coronary artery by-pass grafting (CABG).
Useful Additional Therapeutic Strategies
For the small percentage of patients who are at high risk and have symptoms of unstable angina or residual angina after recent MI it may be appropriate to proceed directly to coronary angiography rather than noninvasive studies. PTCA or CABG should only be performed in patients who meet the criteria for the respective procedures independent of the proposed vascular surgery. The benefit of prophylactic coronary revascularization has never been proven in a randomized controlled trial (RCT); however, several retrospective studies have shown that patients who have undergone CABG have the same morbidity and mortality from cardiac complications as those with no clinical signs of coronary artery disease [3]. Figure 1.8.1 shows an algorithm for cardiac evaluation and management of vascular surgical patients.
1.8.2.2 Respiratory System The major pulmonary complications in the peri-operative period are atelectasis, pneumonia and bronchitis. Predisposing risk factors include cough, dyspnoea, smoking, a history of lung disease and obesity. Vascular surgery of the abdomen or chest has a far higher rate of pulmonary complications compared to vascular surgery in places other than the abdomen.
1.8.2 Systemic Evaluation
Vascular Surgical Patient
Risk Stratify
Intermediate / High Risk
<1yrs Since Favorable Evaluation of Coronary Arteries and Asymptomatic
Low Risk
Non Invasive Testing
Positive
Negative
Cardiac Catherterisation
Left Main Stem or Three Vessel Disease
1 or 2 Vessel Disease
CABG
PTCA
Negative
Peri-operative β Blockade
Vascular Procedure
Fig. 1.8.1 Algorithm for cardiac evaluation and management of vascular surgical patients
Coronary Revascularisation Within 5 yrs and Asymptomatic
Emergency Presentation
87
88
1.8 Preoperative Evaluation of a Vascular Patient
Diagnostic Procedures Recommended European Standard
• Plain chest radiograph – appropriate for patients with signs or symptoms of chest disease who have not had a chest radiograph in the previous year. • There is no RCT evidence that more complex respiratory function testing leads to changes in the management of patients with pre-existing respiratory disease.
Treatment Recommended European Standard
• Pharmacological – patients with respiratory disease may benefit from peri-operative use of bronchodilators or steroids. • Physiotherapy – patients at increased risk of pulmonary complications should receive instruction in deep breathing exercises or incentive spirometry.
Useful Additional Diagnostic Strategies
• Duplex ultrasound – 98% sensitivity and specificity of diagnosing significant RAS, however is dependent on a skilled user. Should be carried out in all patients where there is clinical suspicion of RAS. • Arteriography – the obvious advantages of conventional angiography are its ability to determine the clinical importance of suggestive lesions and the ability to concurrently perform endovascular therapy. However, specialists should weigh these advantages against the higher cost and greater morbidity of conventional angiography, and the risks of nephrotoxic contrast agents. • Magnetic resonance angiography (MRA) – the slightly inferior variability of MRA in diagnostic interpretation further supports the use of this technique as potentially the most appropriate tool for screening patients strongly suggested to have atherosclerotic renovascular disease.
Treatment Useful Additional Therapeutic Strategies
• Smoking cessation – the patient should cease smoking 8 weeks or more before surgery to minimize the surgical risk associated with smoking. This interval allows the mucociliary transport mechanism to recover, the secretions to decrease and the carbon monoxide levels in the blood to drop.
1.8.2.3 Renal System Patients with vascular disease have a high prevalence of renal dysfunction secondary to atherosclerotic renal artery stenosis (RAS). Early diagnosis of RAS is important in ensuring successful correction of any dysfunction.
Diagnostic Procedures Recommended European Standard
• Creatinine clearance – estimation of creatinine clearance should be performed to evaluate renal function in all patients undergoing vascular surgery, especially in the presence of co-existing hypertension.
All patients with bilateral stenoses and stenosis in a solitary functioning kidney are candidates for revascularization, regardless of whether they have renal insufficiency. When renal insufficiency is present, patients with unilateral stenosis are also possible candidates for revascularization prior to other major vascular surgery being performed. Table 1.8.2 Aneurysm screening Size
Aneurysm screening
<4 cm
Yearly USS
4–5.5 cm
Six-monthly USS
>5.5 cm
Elective repair
Rapidly expanding >1 cm/ Urgent elective surgery year or symptoms of tenderness
1.8.3 Evaluation of Specific Vascular Disease
1.8.3 Evaluation of Specific Vascular Disease 1.8.3.1 Aneurysmal Disease: Abdominal Aortic Aneurysm The decision to perform elective abdominal aortic aneurysm (AAA) repair is made on the balance of the operative risk of morbidity and mortality versus the risk of rupture and death associated with conservative treatment. The UK Small Aneurysm Trial showed no benefit from early surgery of asymptomatic infrarenal AAA between 4 cm and 5.5 cm when compared to regular ultrasound screening surveillance [5, 6].
Diagnostic Procedures Recommended European Standard
• Duplex ultrasound – rapid, cheap, noninvasive test, good for diagnosis and an important screening tool. Its may be difficult to interpret in obese patients or those with lots of bowel gas. It cannot easily diagnose rupture. • CTA and MRA – give excellent detail on size and configuration of the aneurysms necessary for surgical and endovascular treatment. • Intra-arterial digital subtraction angiography (IADSA) – limited role with improvement in MRA and CTA.
Treatment Recommended European Standard
• Open surgical repair – overall mortality from open repair should be less than 5% (nearer 2% in some centres). Inflammatory aneurysms increase risk of mortality to 3–20%. • Endoluminal repair – 70% of infrarenal AAA can be managed endovascularly. This type of repair minimizes haemodynamic insult but may increase the risk of distal embolization. Subject of many ongoing large multicentre studies – EUROSTAR, EVAR, RETA. Initial reports have suggested a problem with high re-intervention rates. At present it is to be considered for inflammatory aneurysms and patients unfit for open surgery.
Useful Additional Therapeutic Strategies
• Laparoscopic AAA repair – aims to reduce the complications associated with a large surgical incision; little RCT evidence to show proven benefit.
Aneurysmal Disease: Ruptured Abdominal Aortic Aneurysm A ruptured AAA should be suspected in anyone over the age of 50 years presenting as an emergency with sudden onset of severe pain in the abdomen, back or flank. This pain may be associated with collapse and shock. • Avoid palpating the abdomen more than necessary. • Note the presence or absence of distal pulses for future reference. • Do not waste time on investigations. • If the diagnosis is in doubt, and the situation is less acute and the patient is haemodynamically stable, computerized tomography should be performed straight away. • During the resuscitation of a suspected ruptured AAA you should avoid attempts to bring the blood pressure up as it may precipitate rupture and add to worsening anaemia and coagulopathy through haemodilution.
1.8.3.3 Peripheral Vascular Disease: Chronic Lower Limb Ischaemia Lower limb ischaemia is by far the most common form of symptomatic peripheral vascular disease. Most lower limb ischaemia is chronic due to atherosclerosis of the abdominal aorta, the iliac vessels and the lower limb vessels. Other causes include vasculitides, such as Buerger’s disease; haematological disorders and collagen diseases. When assessing an ischaemic limb it is important to identify both the severity and site(s) of the arterial tree that is affected. It is also important to exclude other causes of leg pain such as lumbar sacral nerve root compression, osteoarthritis and venous claudication of the post thrombotic limb. Diabetics are at greatly increased risk of limb ischaemia, with increased limb loss and mortality. Affected arteries can be heavily calcified making reconstruction difficult. Tibio-peroneal disease with occlusions at multiple levels is usually seen in these cases and is difficult to manage.
89
90
1.8 Preoperative Evaluation of a Vascular Patient
Diagnostic Procedures
• Endarterectomy • By-pass surgery.
Recommended European Standard
• Ankle brachial pressure index – maybe falsely elevated in diabetic patients due to medial sclerosis of the vessels. • Resting and post exercise Doppler pressures – exercise Doppler pressures are measured before and after a treadmill test using a standard protocol. A fall in Doppler pressure of >15 mmHg suggests that the cause is due to arterial insufficiency. • Duplex USS – noninvasive, inexpensive and repeatable and good at evaluating stenosis. • IADSA – allows intervention if required but carries the risk of arterial puncture.
Useful Additional Diagnostic Strategies
• CTA and MRA – can be used in patients with femoral artery occlusion. • Vein mapping – identification of a suitable autogenous vein graft is appropriate where surgical reconstruction is being considered.
Treatment Recommended European Standard
Conservative treatment for nondisabling claudication would include: • Smoking cessation • Correct/control • Cholesterol/triglyceride abnormality • Hypertension • Diabetes mellitus • Weight control • Exercise – to encourage collateral circulation development.
Useful Additional Therapeutic Strategies
In up to 20% of patients, arterial reconstruction is not feasible. Other treatments of critical limb ischaemia include: • Lumbar sympathectomy • Epidural spinal cord stimulation • Drug therapies such as prostanoids treatment. Results from these treatments are often disappointing and there is little proven overall benefit; amputation may still be required.
1.8.3.4 Peripheral Vascular Disease: Acute Limb Ischaemia Acute limb ischaemia is a surgical emergency. Prompt, accurate evaluation and management are important to reduce mortality and limb loss. Acute ischaemia is usually caused by either thrombosis on an atherosclerotic plaque or embolism. A embolic cause should be suspected where there is a history is a sudden onset of pain in the affected limb without any previous claudicant symptoms. Specifically a history of palpitations or known atrial fibrillation should be sought or whether the patient has had a recent MI. Examining the affected limb may not help to distinguish between an acute embolic and an acute on chronic condition. Examining the other limb for signs of chronic ischaemia is more useful. The popliteal fossa, femoral region and abdomen should be examined for evidence of aneurysmal disease.
Diagnostic Procedures The prognosis is that about 65% of patients will respond to conservative management; other progress and require more aggressive treatment. Surgery is indicated for disabling claudication or critical limb ischaemia. The procedure undertaken will depend on the state of the arterial tree as assessed by arteriography, which aims to identify the level and character of occlusion, and the quality of the proximal and distal arterial tree. Options for reconstruction include: • Balloon angioplasty ± intravascular stenting
Eighty to ninety percent of all emboli are of cardiac origin, secondary to atrial fibrillation, post MI mural thrombosis, prosthetic or diseased heart valves.
Recommended European Standard
• ECG – to identify arrhythmias • Urgent echocardiography – to identify mural thrombosis or valvular disease
1.8.3 Evaluation of Specific Vascular Disease
• Urgent abdominal USS – to exclude a AAA. • Urgent arteriography to localize stenosis, embolus and assess for reconstruction or thrombolysis.
Treatment Recommended European Standard
• Aspirin • Intravenous heparin • If embolus is suspected: • Embolectomy • If thrombosis suspected: • Limb viable: thrombolysis and treatment of the underlying lesions. Thrombolysis usually takes 4–24 h to dissolve the thrombus, therefore a limb which is unlikely to remain viable for this long is not appropriate for this therapy. • Limb threatened: urgent surgical thrombectomy ± reconstruction.
Useful Additional Therapeutic Strategies
Revascularization of an advanced acutely ischaemic limb is hazardous with a 30-day mortality of 15%. Late presentation (over 24 h) indicates a high risk and amputation may be safer in these circumstances. Signs of advanced ischaemia include: anaesthesia, muscle tenderness and swelling. The level of amputation should be considered carefully, below knee or above knee are most commonly performed with unreconstructable disease or advanced ischaemia. In a mobile patient preservation of the knee joint improves the use of the prosthesis and subsequent mobility. In patients who are unlikely to walk again an above-knee amputation may be more suitable.
Diagnostic Procedures Clinical examination may reveal nothing, and a carotid bruit is an unreliable sign of disease severity. Neurological and eye signs may be transient. Examination of the visual fields may reveal defects and fundoscopy may reveal evidence of previous emboli. Any residual paraesthesia or weakness will be on the opposite side to the carotid lesion.
Recommended European Standard
• Duplex ultrasound – to confirm carotid artery disease, bilateral colour Doppler ultrasound imaging (Duplex) of the carotid arteries should be performed. This is a very accurate method of diagnosing carotid artery stenosis. Its limitation is in the differentiation of a very tight stenosis and an occlusion of the artery where operation is contraindicated. • CT or MRI of the brain – to exclude neoplastic and other serious pathology. • IADSA – give additional information to that found on Duplex scanning, but there is a 1% stroke rate when the carotid is directly accessed.
Useful Additional Diagnostic Strategies
• MRA or CTA – indicated where the diagnosis of occlusion is uncertain on ultrasound. MRA and CTA can give information on the carotid disease at the same time as assessing for brain pathology.
Treatment Recommended European Standard
1.8.3.5 Carotid Disease Carotid surgery started in the 1950s and is of proven benefit to those with symptomatic disease of the internal carotid artery. The symptoms are usually caused by the atherosclerotic plaque usually located at the bifurcation of the common carotid artery undergoing ulceration, thrombus formation and distal embolization resulting in a transient ischaemic attack (TIA) or a stroke.
All patients should undergo risk factor modification to decrease the risk of disease progression. Asymptomatic Patients
• Stenosis of 70%, treat with low-dose aspirin. • Stenosis of 70–99%, most clinicians would treat conservatively although there are ongoing clinical trials to determine whether surgery would be beneficial. Patients with History of TIA
• Less than 20% stenosis, treat with anti-platelet drugs. • 20–69%, most surgeons would treat conservatively with anti-platelet drugs.
91
92
1.8 Preoperative Evaluation of a Vascular Patient
• 70–99%,defined benefit for surgery. • 100% occlusion, surgery contraindicated. Carotid Endarterectomy
• Can be performed under general or loco-regional anaesthesia. • The GALA trial is currently looking for differences in the morbidity, mortality and patient experience following either local or general anaesthesia.
• Exclusion of pelvic pathology – venous obstruction with secondary varicose veins can be the first sign of a pelvic malignancy, therefore clinical history and examination should take this into account, including internal examination.
The decision over which is the most appropriate treatment to use depends on local experience with surgical and radiological procedures.
There are many rudimentary methods for eliciting the site of incompetence, including cough impulses, percussive tests, calf squeezes and tourniquet tests. It is the authors’ opinion that the results from these tests should not be used as a guide to choice of surgical procedure. Often perforators or communicating veins can complicate clinical diagnosis and therefore where possible all patients undergoing varicose vein surgery should undergo a Duplex USS. This will identify unusual anatomy, such as Duplex long saphenous vein, thigh and calf perforators. It will also show competence and patency of the deep venous system. Where there is a history of previous deep vein thrombosis Duplex studies must be performed to confirm the status of the deep veins prior to any surgery.
1.8.3.6 Venous Disease
Treatment
The commonest vascular surgical procedure is varicose veins treatment: 1 in 1000 people undergo surgery for varicose veins every year in the western world.
The management of varicose veins depends mainly on the symptoms and the presence or absence of complications.
Carotid Stenting
• There has been a recent trend of performing balloon angioplasty of the internal carotid artery usually with the placement of a stent. However, there is a lack of RCT evidence on the benefit of this technique, unlike endarterectomy.
Diagnostic Procedures The clinician’s task is to determine if the patient’s symptoms are due to the varicosities and to determine the site of reflux from the deep to the superficial system. Preoperative evaluation of the status of the venous system in the affected leg is the key to reducing recurrence and avoiding unnecessary surgery.
Recommended European Standard Conservative Treatment
Advised if the varices are not severe or if intervention is contraindicated. Losing weight, skin care and graduated compression hosiery are the mainstay of conservative treatment. Compression hosiery has proven benefit, although patient compliance with this treatment, especially in the summer months, is poor. Surgical Treatment
Recommended European Standard
Patients should always be examined standing where possible. • Skin changes – the skin can reveal signs of lipodermatosclerosis or haemosiderin deposition, eczema and ulceration. • Varicose distribution – examination of the anterior and posterior aspects of the thigh and leg will review the distribution of dilated veins. • Peripheral pulses should be palpated.
The indications for intervention are severe disfiguring varices, aching or pain, the presence of skin changes or ulceration. Intervention may be contraindicated if there is any evidence of deep venous occlusion. • Historically stripping of the clinically incompetent vein with phlebectomies for dilated varicosities was the gold standard. This procedure however has always had a significant morbidity and recurrence rate. It may be more appropriate where bilateral treatment is required to operate on one limb at a time to encourage postoperative mobilization.
References
Useful Additional Therapeutic Strategies
• Endovenous thermal techniques can be easily performed under local anaesthesia in an office or daycase setting. They reduce the morbidity attached to stripping of the vein whilst reporting successful treatment in approximately 90% of patients at 2–5 years. Recently some evidence has been presented to suggest that new varicose formation occurs in approximately 30% of cases treated endovascularly at 5 years, similar to traditional surgery. • Recently endovenous foam sclerotherapy is gaining popularity, however there is little randomized controlled evidence of its efficacy or safety, although case series suggest a favourable outcome. • Subfascial endoscopic perforator surgery (SEPS) can be utilized where multiple calf perforators are the cause of reflux, especially in patients with overlying ulceration making direct access undesirable.
Authors Note Since this chapter was written there has been continuing debate on the appropriateness of peri-operative use of β-Blockade in patients undergoing surgery. The most significant development in this area is the POISE trial(1), a blinded, randomised, and controlled trial of controlled release metoprolol versus placebo in 10,000 patients at risk for a peri-operative cardiovascular event who are undergoing non-cardiac surgery. This trial has so far recruited more than 6300 patients of which 42% underwent vascular surgery, and should provide level one evidence. A recent 2006 Guidance update from the ACC and AHA (2) continues to recommend the use of peri-operative β Blockade in high risk surgical patients, a group to which most arterial patients belong. The author stands by the treatment algorithms presented in this chapter based upon a consensus of expert opinion in this field.
1. (2006) Rationale, design, and organisation of the Peri-Operative Ischemic Evaluation (POISE) Trial: A randomised controlled trial of metoprolol versus placebo in patients undergoing non-cardiac surgery. Am Heart J 152(2):223-230 2. Fleisher LA (2006) ACC/AHA 2006 Guideline Update on Peri-operative Cardiovascular Evaluation for Non-cardiac Surgery: Focused Update on Peri-operative β-Blocker Therapy. A Report of the American College of Cardiology / American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 47(11):2343-2355
References 1. Abir F, Kakisis I, Sumpio B (2003) Do vascular surgery patients need a cardiology work-up? A review of pre-operative cardiac clearance guidelines in vascular surgery. Eur J Vasc Endovacs Surg 25:110–117 2. Boersm E, Poldermans D, Bax JJ, Steyerberg EW, Thomson IR (2001) Predictors of cardiac events after major vascular surgery: role of clinical characteristics, dobutamine echocardiography, and beta blocker therapy. J Am Med Assoc 285:1965–1873 3. Reul GJ Jr, Cooley DA, Duncan JM et al (1986) The effect of coronary artery bypass on the outcome of peripheral vascular operations in 1093 patients. J Vasc Surg 3:788–798 4. Turnbull JM, Buck C (1987) The value of preoperative screening investigations in otherwise healthy individuals. Arch Intern Med 147:1101–1105 5. UK Small Aneurysm Trial (1998) Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet 352:1649–1655 6. UK Small Aneurysm Trial (1998) Health service costs and quality of life for early elective surgery or ultrasonic surveillance for small abdominal aortic aneurysms. Lancet 352:1656–1660 7. Wallace A, Llayug B, Tateo L et al (1998) Prophylactic atenolol reduces post-operative myocardial ischaemia. Anesthesiology 88:7–17
93
95
1.9 Peri-operative Care of the Vascular Patient Anne Karin Lindahl
1.9.1 Introduction The vascular patient is at high risk of complications in the peri-operative period, due to the generalized nature of the atherosclerotic disease and other concomitant diseases. The aim of peri-operative care for the vascular patient is to minimize the risk of complications by: • careful pretreatment • peri- and postoperative monitoring • optimized anaesthesia • postoperative pain treatment. In this chapter, these aspects will be reviewed in the light of available scientific evidence.
1.9.2 Preoperative Planning The patient’s medical status must be evaluated preoperatively, and all documented preoperative measures to prevent peri-operative ischaemia need to be taken. Initiation of β-blockers and platelet inhibitors is particularly important, as are smoking cessation and the implementation of preoperative optimal regulation of blood pressure and blood glucose. Also, the use of statins seems to be associated with reduced peri-operative mortality in major noncardiac surgery, probably due to their anti-inflammatory, plaque-stabilizing effects [57, 65]. These preoperative considerations should be made in good time before admission for planned surgery, in order to optimize the high-risk vascular patient. In many centres, preoperative cardiac screening and overall evaluation are performed by a specialized anaesthetist, with or without a cardiologist, in addition to the vascular surgeon, to ensure the best preoperative medical treatment. This treatment will not only improve the peri-operative mortality and morbidity, but also the patients’ long-term
outcomes. This must be emphasized, in order to motivate the patient to be compliant and make the necessary lifestyle changes. Detailed written and oral information should be given in advance to the patient regarding the procedure and possible complications, and what to expect during the recovery period. The information should be clear and understandable, in order for the patient to give his or her informed consent to the procedure. In addition to the patient’s right to information, good preoperative information reduces preoperative anxiety, thereby decreasing stimulation of the sympathetic nerve system. Preoperative anxiety, cigarette smoking and other stimulation of the sympathetic nervous system, in addition to the surgical trauma, lead to an increase in peri-operative coronary thrombosis and vasospasms. The importance of good communications skills to convey this kind of information needs to be emphasized, as does the need to include communication skills in the education of surgeons and anaesthetists [30].
1.9.3 Effects of Anaesthesia The use of epidural anaesthesia may favourably influence early graft patency in patients undergoing infra-inguinal revascularization [12], but the evidence is not unequivocal [64]. An improved early graft patency may be explained by an increase of fibrinolysis, which has been reported with regional anaesthesia (RA), possibly mediated by a reduction in plasminogen activator inhibitor (PAI) [24, 61]. There is no evidence of beneficial effects on cardiac mortality of using RA alone for peripheral vascular surgery. For peripheral surgery, RA may be used alone, or in combination with general anaesthesia, in an attempt to dilate peripherally for best possible tissue perfusion in the
96
1.9 Peri-operative Care of the Vascular Patient
symptomatic leg [12, 24]. However, the improved blood flow with RA was more pronounced in patients who did not suffer from peripheral arterial disease, and the improvement of blood flow was the least prominent in patients with both atherosclerosis and diabetes mellitus [28]. For aneurysm surgery, general anaesthesia with opiates and a potent inhalational agent is most often used, combined with thoracic epidural anaesthesia for the perioperative effects and also for postoperative pain relief. Some procedures, most often carotid thromboendarterectomy (TEA) and acute peripheral embolectomy, may be performed under local anaesthesia. Due to the known cardiac risk of the vascular patient, it is important to treat the anxiety of a patient who is awake during surgery. However, some surgeons prefer to have the patient awake to be able to assess their level of consciousness, especially during carotid surgery, and to avoid unnecessary use of a shunt during the procedure. The choice of method of anaesthesia is often traditionbound to the hospital or even to the country. In some countries, the use of local anaesthesia for carotid TEA is very rare, while local anaesthesia is used routinely for this procedure in other countries.
1.9.4 Peri-operative Monitoring A minimum for peri-operative cardiac monitoring of the vascular patient is continuous electrocardiogram (ECG), preferably with computerized analysis of ST changes, measurements of arterial O2, end-tidal CO2, blood pressure, diuresis and body core temperature. In many hospitals, the monitoring of the hypnotic depth is also routine. For abdominal surgery or in high-risk patients, continuous central venous pressure and intra-arterial pressure should be monitored and kept as stable as possible. Continuous monitoring of O2 in mixed venous blood can be considered in patients with highly symptomatic cardiac disease, and is performed through a pulmonary artery catheter (Schwan-Ganz catheter). Some centres use transoesophageal echocardiography in order to detect myocardial ischaemia early.
1.9.4.1 Monitoring for Cardiac Ischaemia There are three major ways to monitor for cardiac ischaemia:
1. Surface ECG 2. Transoesophageal echocardiography 3. Pulmonary artery catheterization.
Due to the complexity and the possible side-effects of the two latter methods, the most practical and most used form is surface ECG. It is considered important to monitor ischaemia during and after the operation and to take measures to resolve the ischaemia if possible, to prevent myocardial infarction, although it is not shown to reduce peri-operative morbidity in controlled trials [51]. Subendocardial ischaemia is the most common type of ischaemia, and is detected by ST depression [37], while transmural ischaemia causing ST segment elevation in the leads facing the lesion is less common. In noncardiac surgery patients, 96% of ischaemic episodes were detected with a three-lead system (leads II, V4 and V5) [38]. ECG changes consistent with ischaemia are difficult to detect in patients with right bundle branch block, left ventricular hypertrophy with a strain pattern or with atrial fibrillation, and impossible in patients with left bundle branch block or on a pacemaker – this affects about 15% of vascular surgery patients [58]. The most reliable way to monitor for ischaemia is to follow the trend for ST segment elevation or depression over time by computerized ST segment analysis [51], which is now automated in most monitoring equipment. Pulmonary artery catheterization has not been proven to reduce complications or mortality in a meta-analysis [1]. Elevation of troponin postoperatively has been shown to be prognostic of both short-term mortality and long-term mortality. However, a recent report contradicted these findings, and did not identify troponin elevation to be prognostic of 2-year all-cause mortality or of major cardiac events in noncardiac surgery [18].
1.9.4.2 Peri-operative Temperature Control Although hypothermia may be of benefit in some aspects of the peri-operative period, and may provide some protection against cerebral and myocardial hypoxia, the results of hypothermia (below 36°C) may also harm the patient. Hypothermia affects blood coagulation by reducing the effect of extrinsic pathway activation (measured by the prothrombin time), slightly reducing the platelet count, and increasing peri-operative bleeding and the need for transfusion [34, 63]. Upon wakening from anaesthesia, a hypothermic patient will also use energy and increase their myocardial and total O2 consumption due
1.9.5 Prevention of Cardiac Ischaemia
to shivering to increase their body temperature. This may increase the risk of cardiac complications postoperatively [19, 20].The anaesthetic drugs profoundly impair thermoregulatory responses, but the protective mechanisms are reactivated as the anaesthetics are withheld [53]. It is therefore important to reduce temperature loss during the operation to a minimum, and to use devices such as the “bear hugger” upper body warm air blanket, in addition to warming the intravenous fluids and inspired air, to effectively warm the patient during surgery. It has also been documented that the use of warming devices and avoiding hypothermia during surgery improve survival, and reduce the stay in the intensive care unit and the hospital [8, 35].
1.9.4.3 Level of Hypnotic Depth Hypnotic depth may be measured by electroencephalogram (EEG) and quantified by Bispectral Index®, for instance, and such measurements may be used to dose the anaesthetic drugs more exactly, thus reducing cardiovascular side-effects caused by overdosage [7]. This not only affects the immediate peri-operative period – in a multivariate model of demographic, preoperative clinical and intraoperative variables, cumulative deep hypnotic time, patient co-morbidity and intraoperative systolic hypotension were found to be predictors of 1-year mortality [47].
1.9.5 Prevention of Cardiac Ischaemia 1.9.5.1 Preoperative Revascularization The preoperative cardiac evaluation will reveal the need for preoperative revascularization. The benefits of coronary artery by-pass graft (CABG) and percutaneous coronary intervention (PCI) accrue gradually; subsequent surgery should ideally be delayed for at least 6 weeks and longer, after such reconstructive procedures, if possible [72].
1.9.5.2 Good Peri-operative Haemodynamic Control Myocardial ischaemia results from an imbalance between myocardial oxygen supply and demand. Such imbalance may have many causes in the peri-operative period. The
most detrimental changes are tachycardia, hypovolaemia and anaemia – and if they occur at the same time, the oxygen demand increases as the oxygen supply decreases. Tachycardia increases oxygen demand by increasing the myocardial workload. At the same time, myocardial oxygen supply decreases due to a shorter diastole, the period during which most coronary blood flow occurs.
1.9.5.3 Anaemia This will result in both reduced oxygen supply and demand. Reduced oxygen content reduces the supply, and tachycardia and increased cardiac output as a result of anaemia will increase oxygen demand. However, a liberal transfusion policy may be more harmful than beneficial, and even for patients at risk of cardiac ischaemia haemoglobin levels of 7–9 g/l are considered adequate, except in patients with acute myocardial infarcts and unstable angina [31].
1.9.5.4 Adrenergic Tone Myocardial ischaemia and infarction occur more frequently postoperatively than pre- or peri-operatively (Table 1.9.1). Although the vascular patients have more ischaemia peri-operatively than other patient groups, the problem is even more frequent postoperatively. This intriguing discrepancy is probably due to the careful haemodynamic monitoring and balancing of the patient’s oxygen demand and supply preoperatively [51]. During the operation, the anaesthetist suppresses the adrenergic tone by β-blockade or a thoracic epidural with bupivacaine or another local anaesthetic [5]. Some advocate liberal use of β-blockers during the operation to keep the heart rate under 80 beats/min [51], while the American College of Cardiology (ACC) guidelines suggest a target heart rate of 50–60 beats/min in those with inducible ischaemia [16]. Boersma et al. [3] showed that the relative risk reduction from peri-operative β-blockade depends on the number of clinical risk factors (age >70 years, a history of current or previous angina, myocardial infarct, stroke or heart failure) and the presence or absence of inducible ischaemia. In patients with one or two clinical risk factors, the incidence of death or myocardial infarct was lower in β-blocked patients (0.9%) than in those who were not βblocked (3%). However, in patients with three or more risk factors and inducible ischaemia, the incidence of adverse cardiac events was 10% despite β-blockade [3].
97
98
1.9 Peri-operative Care of the Vascular Patient
Table 1.9.1 Incidence (percentage) of myocardial ischaemia detected by continuous Holter monitoring and ST segment analysis during preoperative, peri-operative and postoperative periods in vascular patients. Modified after Norris [51] Study
Preoperative
Peri-operative
Postoperative
Overall
Aortic/lower extremity
40
38
48
61
Carotid
38
41
54
68
Oyang et al. [54]
13
21
63
–
McCann and Clements [46]
14
–
38
–
Mangano et al. [41, 42, 43]
Pasternack et al. [56]
20
25
41
–
Raby et al. [59]
–
18
30
–
Christopherson et al. [12]
8
11
40
40
Boylan et al. [4]
–
–
35
–
Norris et al. [52]
3
4
15
16
19
23
40
46
Average
The scientific evidence for the benefit of β-blockade and α2-agonists during vascular operations to reduce ischaemia, myocardial infarction and cardiac death are unequivocal, while the evidence for the benefits of using calcium channel blockers is less clear [68]. Survival is also higher 1–2 years postoperatively when continuing such treatment. Despite the convincing evidence for the benefits of β-blockade, both peri-operatively and in the long-term, only 57% of Canadian anaesthesiologists reported in a study that they always or usually administered β-blockers to patients with known coronary disease. Only 34% of these regular users continued β-blockade beyond the early postoperative period, while 95% of the respondents were aware of the peri-operative β-blocker literature [74]. This emphasizes the importance of a specially trained and aware anaesthetist, who is also involved in preoperative patient evaluation, in order to understand the high-risk vascular patient’s need for intensive peri-operative titration of vasoactive therapies [30]. Also, the vascular surgeon should be aware and ensure that his or her patient receives optimal and evidence-based peri-operative pharmacological treatment.
1.9.5.5 Postoperative Ischaemia Prevention In the immediate postoperative period, an increased oxygen demand may be due to pain, tachycardia, hyperten-
sion, sympathetic discharge and hypercoagulability [5]. Transfer from the operating room to the intensive care unit may be made under less surveillance than peri-operatively, despite transportable monitors, and in a less controllable state. Most postoperative ischaemia and infarctions are silent, due to masking by postoperative pain and opioids, and are usually associated with an increased heart rate [36, 42]. Peri-operative blood pressure control is also important in relation to cardiac ischaemia, and a maximum 20% variation from baseline is recommended [51]. If the ratio between mean arterial pressure and the heart rate, the pressure/rate quotient, is less than 1.0, there is an increased risk of ischaemia [6].
1.9.6 Aneurysm Surgery 1.9.6.1 Effects of Clamping and Declamping Even clamping below the renal arteries reduces renal perfusion by 38%, with resulting renal failure in 2–3% of patients [21]. Therefore, most surgeons want mannitol to be given before cross clamping, although the effect of this is not documented, and the mechanism of this presumed beneficial effect is not known. Also, effects of administering calcium blockers and dopamine in low dose on renal perfusion have been tested extensively, but no conclusive beneficial effects have been found. During clamping, va-
1.9.7 Heparin
sodilatation therapy is important to avoid an abrupt increase in blood pressure. Such an abrupt increase may lead to a steep increase in left ventricular filling pressure, which may induce subendocardial hypoxia due to the pressure-induced hypoperfusion. Agents most often used for vasodilatation are nitroglycerin or nitroprusside. The latter may also improve the intestinal circulation [24]. Perfusion of the kidneys and intestines may suffer during clamping above the renal arteries. Different peri-operative measures are used to avoid ischaemic injury, including perfusion of cold Ringer’s acetate solution to the kidneys, shunting through a side branch of the graft or a temporary by-pass to circulate the distal aorta and the lower limbs during the operation [17]. On cessation of cross clamping, close cooperation between the surgeon and the anaesthetist is needed, in order to keep the blood pressure from dropping too quickly and too low. The anaesthetist can manipulate the vasoactive drugs and reduce the vasodilatation drugs before unclamping, in addition to keeping the patient filled up with fluid. It is beneficial to avoid vasopressor drugs, which add to the stress and oxygen demand of the heart. In vulnerable patients, the surgeon may want to unclamp gradually by manual external pressure on the aorta. The aim is always to keep the patient’s arterial pressure as stable as possible, in order to prevent cardiac events.
1.9.6.2 Prevention of Spinal Cord Ischaemia in Thoracic Aortic Surgery Spinal cord ischaemia resulting in postoperative paraplegia is a devastating complication of thoracoabdominal aortic aneurysm repair. To prevent spinal cord compartment syndrome, cerebrospinal fluid drainage, as well as various other methods, including hypothermia, distal aortic perfusion, reattachment of intercostals arteries and more, have been used as adjuncts to thoracoabdominal aortic aneurysm repair [70].
1.9.6.3 Autotransfusion During Surgery Autotransfusion during aortic surgery is widely used and is considered to reduce the need for allogeneic blood transfusion [25, 69]. Especially in complicated cases, where blood loss may be great, cost-effectiveness has been shown [13, 26]. Spark et al. has shown that autotransfusion reduced hospital stay and infective complications [67]. The method of autotransfusion may also be
important [60], and autotransfusion of washed red blood cells is now routinely used in most centres. These washing systems may also have the benefit and possibility of producing homologous thrombocyte/fibrin glue from the normally discarded plasma, which can be used peri-operatively.
1.9.7 Heparin 1.9.7.1 Peri-operative Heparin During most vascular surgical procedures, heparin is given intravenously or intra-arterially to prevent clotting of the temporarily clamped arteries. For intra-arterial instillation of heparin in peripheral surgery, 10–20 ml of a solution of 10 U/ml unfractionated heparin is instilled in the efferent and afferent arteries immediately after clamping. There is no documentation of the beneficial or detrimental effects of this heparin treatment, although the heparin concentration theoretically should be well above therapeutic anticoagulation treatment levels in the clamped arteries. The dose of heparin given intravenously before cross clamping varies from a standardized fixed dose to weightadjusted doses. Some surgeons neutralize part of or the whole heparin effect with protamine after declamping the arteries. Most often this is done after larger doses of heparin (e.g. 7500 or 10,000 IU in a single dose). For lower doses, 2500–5000 IU, most surgeons think the patient benefits from the heparin after the surgery and refrain from neutralizing it. Administration of intravenous heparin before cross clamping in elective aortic surgery is widely used, and is considered to reduce peripheral thrombotic complications. This has however not been proven in a randomized trial of heparin versus placebo, where there was no difference in blood loss, blood transfusion or distal thrombosis. However, this study did show a benefit of heparin administration on peri-operative myocardial infarction – 5.7% in the placebo group versus 1.4% in the heparinized group [71]. The anticoagulant effect of a single dose of 5000 IU during aortic surgery was monitored, and found to be surprisingly high even 1 h after surgery [60]. This prolonged heparin effect is probably beneficial for the clotting tendency of the arteries operated on, but may increase the frequency of bleeding episodes. Especially in aortic aneurysm surgery, where bleeding may be a major
99
100
1.9 Peri-operative Care of the Vascular Patient
obstacle, the prolonged heparin effect may be a problem of some significance. Intravenous heparin is most often not used for emergency aortic surgery. The rationale for this is the bleeding tendency resulting from consumption of coagulation factors and fibrin upon rupture. Pushing the haemostatic system further towards bleeding in this situation is considered more risky than beneficial. This is despite the well-known risk of patients with acute aneurysm rupture to experience embolic episodes peripherally.
1.9.7.2 Prophylaxis of Deep Leg Vein Thrombosis Standard regimens of deep leg vein thrombosis prophylaxis should be followed after vascular surgery. The vascular patients are not considered at particular risk of vein thrombosis, but risk factors such as thrombophilia, previous vein thrombosis, obesity, abdominal surgery, long operating time, etc. should be considered when deciding upon whether to give a low or high dose of low-molecular-weight heparin for prophylaxis of deep leg vein thrombosis. Due to the frequent use of unfractionated heparin during the operation, most surgeons prefer to wait until after the procedure to start this treatment.
1.9.8 Peri-operative Monitoring after Arterial Reconstructions During vascular surgery, quality control of the performed reconstruction is required. The options for such quality control are: • intravascular ultrasound (to visualize intima flaps and stenoses) • intraoperative angiography • Doppler flow measurements • intraoperative duplex scanning. Most surgeons use one or more such measurements of quality control, but the choice of method depends on: • the type of reconstruction • the resources available • the independent preference of the surgeon. Injections of a potent vasodilatation agent, e.g. papaverine, may be applied during such quality control, to measure the maximal flow of the reconstruction.
1.9.9 Prophylactic Antibiotic Administration The use of prosthetic grafts for vascular surgery prompts the use pf prophylactic antibiotic treatment to avoid graft and skin infections. The skin bacteria, e.g. Staphylococcus aureus or Staphylococcus albicans, cause most such infections. Most centres use prophylaxis with a cephalosporin 24 h peri-operatively. Prolonged treatment is saved for cases with known infectious focus or when infections are diagnosed. In addition to skin infections and graft infections, the vascular patient is at risk of pulmonary infection (see below) and urinary infection after urethra catheterization. For open abdominal aortic surgery, postoperative septicaemia may be one of several possible complications [23]. There is no evidence that prophylactic treatment with antibiotics peri-operatively prevents postoperative septicaemia.
1.9.10 Postoperative Pain Treatment The control of postoperative pain is vital for reducing catecholamine release [5], and the more the pain, the more stressful it is for the patient. Knowing the catecholamine effect on an already strained heart, the benefits regarding prevention of cardiac events postoperatively and of good postoperative pain control are obvious. In the immediate postoperative period, epidural analgesia with bupivacaine and morphine are associated with lower postoperative morbidity than “on demand” general opiate analgesia, especially after surgery involving the abdominal or thoracic aorta [73]. It is considered obligatory postoperative pain treatment to apply a base of paracetamol, and in patients without manifest or imminent renal insufficiency, a nonsteroidal anti-inflammatory drug. Since vascular patients are at particular risk of cardiac ischaemia, cyclooxygenase-2 (COX-2) antagonists should be avoided.
1.9.11 Pulmonary Complications, Prophylaxis and Treatment All surgical patients may suffer from pulmonary complications. The rate of complications depends on the patient’s
1.9.14 Pre- and Postoperative Gut Function and Nutrition
respiratory status preoperatively, as well as on the nature of the surgery and the speed of the recovery. To reduce pulmonary complications it is important to implement the following: • preoperative smoking cessation • general exercise • optimization of bronchodilatational therapy and preoperative information • specific breathing exercises. Postoperatively, mobilization of the patient and pulmonary physiotherapy are imperative, as are a focus on general fluid mobilization and avoidance of the development of heart failure and pulmonary oedema after larger surgery.
1.9.12 Peri-operative Care and Endovascular Surgery Patients treated with endovascular procedures need the same preoperative optimization of medical treatment, smoking cessation, etc. as those undergoing conventional open surgery, for lowest peri- and postoperative morbidity and mortality, but more so for the long-term results. Patients treated with endovascular therapy peripherally, e.g. percutaneous transluminal angioplasty or iliac or carotid stent implantation, as well as peripheral fibrinolysis are most often cared for in a postoperative unit with close monitoring, but there is usually no need for admission to the intensive care unit. Patients treated for aneurysmal disease with stent graft usually have a much easier recovery and fewer postoperative complications than those treated with open repair. Thus the need for peri- and postoperative monitoring is less extensive in these patients. There are fewer cardiac complications both peri- and postoperatively when comparing patients with the same degree of preoperative heart disease. This is probably due to the much smaller total surgical trauma, but in particular the fact that aortic cross clamping is not needed during the procedure. However, patients not fit for conventional surgical aortic aneurysm repair due to a combination of co-morbid conditions are now receiving aortic stent graft treatment, and these patients are at increased risk of postoperative complications [15]. The level of postoperative monitoring will naturally reflect the patient’s preoperative condition and possible adverse events during stent grafting.
In these patients in particular, postoperative monitoring of renal function is warranted, due to the use of relatively large quantities of nephrotoxic contrast media, to the problems that may occur upon placing the upper part of the stent above the renal arteries or due to the dislocation of the aneurysm neck thrombosis into the renal arteries [45]. The need for postoperative dialysis must be considered when the patient is suffering from prolonged renal failure. Renal failure is in these patients, as in patients with open repair, associated with a higher postoperative mortality rate [45].
1.9.13 Intensive Care Ward is Needed Only for Selected Patients There is an ongoing discussion about the need for intensive care treatment postoperatively in patients undergoing vascular surgery. While some centres practise the routine use of the intensive care unit (ICU) for one or more days after major vascular surgery, there is now a trend for selecting patients for ICU treatment, rather than admitting all vascular patients, even after larger operations such as open aortic aneurysm surgery. Several studies document the need for ICU care for some patients. In one of these, 109 out of 502 patients surviving the first 48 h needed a prolonged ICU stay [23]. Preoperative risk factors predicting the need for a prolonged ICU stay were elevated creatinine indicating renal failure, and operation for ruptured aneurysm.
1.9.14 Pre- and Postoperative Gut Function and Nutrition Some centres favour peri-oral fluids until 2–4 h preoperatively, and some advocate carbohydrate supplement to increase the gut recovery after intra-abdominal surgery [2]. The evidence for the beneficial effects of such regimens in open aortic surgery remains to be documented [66]. Immediate, transient postoperative nausea and vomiting is very common, but may be avoided using prophylactic anti-nausea treatment, particularly in vulnerable patients. The use of guidelines for the treatment of postoperative nausea has been shown beneficial [22]. In some patients undergoing abdominal surgery, postoperative gastrointestinal tract dysfunction may persist
101
102
1.9 Peri-operative Care of the Vascular Patient
beyond the first 72 h postsurgery, and may reflect injury due to manipulation of the intestines leading to postoperative paralytic ileus, or reflect more serious conditions such as multiorgan failure or ischaemic bowel [33, 49]. The postoperative dysfunction may be caused by an inflammatory response due to reperfusion injury of the intestines, e.g. in aortic surgery, but other trauma, hypoxia or infection may also induce this inflammatory response [11]. Analgesics, mainly opioids, used during and after anaesthesia may contribute to a relative gut paralysis [40]. Newer drugs with selective peripheral opioid antagonist effects have demonstrated earlier resolutions of ileus after intra-abdominal surgery, with effects on the quality of postoperative analgesia [62]. Pain itself may also contribute to postoperative gastrointestinal tract dysfunction, either directly through noxious stimuli affecting gut perfusion, or indirectly by gut pain contributing to delayed mobilization, delayed eating and breathing difficulty [27, 39]. Postoperative gastrointestinal tract dysfunction may be induced more easily upon a reduction in circulating blood volume, as in acute aortic surgery with bleeding [29], whereas replacement with larger volumes of fluid improves gut perfusion and outcome [50]. Collis et al. [14] advocate the use of hydroxyethyl starch for such plasma expansion due to its possible anti-inflammatory effects, shown by reduced rolling and sticking of white cells to vascular endothelium. Routine placement of a nasogastric tube as a preventative measure postoperatively is associated with an increase in morbidity, and thus not recommended. The nasogastric tube should be placed selectively upon post-
operative bloating and vomiting [9]. Pharmacological treatment to speed up the recovery of the bowel after the surgical trauma has not been very effective [32]. Multiple drugs have been tried, and although some have shown effects in some studies, others have not been able to reproduce these effects (Table 1.9.2). Studies on early nutrition suggest that it is associated with a more rapid return of gastrointestinal tract function regardless of the site of surgery [55]. Early nutrition is also associated with improved outcome, measured as reduced morbidity and length of hospital stay [44].
1.9.15 Discharge Planning As the length of hospital stay is shorter, most of the recovery period is at home. While patients routinely receive much information before and after cardiac surgery, the information given after vascular procedures varies [10]. • The patients need to know what to expect regarding wound healing, leg swelling, progressive ambulation and medication. • Most patients need to stop smoking and use the perioperative period as a starting point, often requiring nicotine replacement therapy and support. • The use of nicotine replacement therapy should be discouraged in patients treated for critical ischaemia, as it may induce vasospasm in the smaller vessels and aggravate the peripheral ischaemia.
Table 1.9.2 Pharmacological therapeutic possibilities for treating postoperative ileus. Table adapted from Holte and Kehlet [32] Agent
Mechanism of action
Effect on duration of postoperative ileus
Propranolol
ß-receptor antagonist
Decreased or none
Dihydroergotamine
α-receptor antagonist
Decreased or none
Neostigmine
Acetylcholinesterase inhibitor
Decreased or none
Erythromycin
Motilin agonist
None
Cisapride
Acetylcholine agonist Serotonin receptor agonist
Decreased or none
Metoclopramide
Cholinergic stimulant Peripheral dopamine antagonist
None
Cholecystokinin
Prokinetic peptide
None
Ceruletide
Cholecystokinin
Decreased
Vasopressin
Stimulation of defecation
None
References
• Information on diet, need for physical exercise and general change of lifestyle should ideally be given before, but needs to be stressed at discharge, as the patients may be especially receptive to these changes after surgery to maintain a good operative result. For cardiac surgery patients, a shorter length of stay and fewer postoperative complications have been shown to result from the preoperative teaching and predischarge preparations [48]. There is reason to believe that similar results will be valid for vascular patients as well. The most frequent postdischarge concerns for CABG patients were leg incision healing, pain, medication, leg swelling, gastrointestinal disturbance, activities, cold symptoms and sleep. Most of these occurred within the first 14 days.
1.9.16 Summary Vascular patients are at high risk of complications during surgery. Good planning, preoperative preparation and pretreatment, the right level of monitoring related to the patient’s preoperative condition and the extent of the procedure performed may all influence the outcome of the vascular surgical treatment favourably. The cooperation of several medical professions is needed round the vascular patient for the best possible outcome. Early recognition and treatment of complications are imperative. The best peri-operative treatment gives fewer complications, better survival and reduces the need for intensive care treatment and hospital stay. References 1. Barone JE (2001) Routine perioperative pulmonary artery catheterization has no effect on rate of complications in vascular surgery: a meta analysis. Am Surgeon 67:674–679 2. Basse L et al (2000) A clinical pathway to accelerate recovery after colonic resection. Ann Surg 232:51–57 3. Boersma E et al (2001) Predictors of cardiac events after major vascular surgery – role of clinical characteristics, dobutamine echocardiography and beta-blocker therapy. J Am Med Assoc 285:1865–1873 4. Boylan JF et al (1998) Epidural bupivacaine-morphine analgesia versus patient-controlled analgesia following abdominal aortic surgery: analgesic, respiratory and myocardial effects. Anesthesiology 89:585–593 5. Breslow MJ et al (1993) Determinants of catecholamine and cortisol responses to lower extremity revascularization. The PIRAT study group. Anesthesiology 79:1202–1209
6. Buffington CW (1985) Hemodynamic determinants of ischaemic myocardial dysfunction in the presence of coronary artery stenosis in dogs. Anesthesiology 63:651–662 7. Buhre W, Rossaint R (2003) Perioperative management and monitoring in anesthesia Lancet 362:1839–1846 8. Bush H Jr et al (1995) Hypothermia during elective abdominal aortic aneurysm repair: the high price of avoidable morbidity. J Vasc Surg 21:392–402 9. Cheatham ML et al (1995) A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy. Ann Surg 221:469–476 10. Chien-Yun W (1995) Assessment of post discharge concerns of coronary artery bypass graft patients. J Cardiovasc Nurs 10:1–7 11. Chieveley-Williams S, Hamilton-Davies C (1999) The role of the gut in major postoperative morbidity. Int Anesthesiol Clin 37:81–110 12. Christopherson R et al (1993) Perioperative morbidity in patients randomized to epidural or general anesthesia for lower extremity vascular surgery. Anesthesiology 79:422–434 13. Clagett GP et al (1999) A randomized trial of intraoperative autotransfusion during aortic surgery. J Vasc Surg 29:22–30 14. Collis RE et al (1994) The effect of hydroxyethyl starch and other plasma volume substitutes on endothelial cell activation: an in vitro study. Intensive Care Med 20:37–41 15. Cuypers P et al (1999) On behalf of the EUROSTAR collaborators. Realistic expectations for patients with stentgraft treatment of abdominal aortic aneurysms. Results of a European Multicentre Registry. Eur J Vasc Endovasc Surg 17:507–516 16. Eagle KA et al (2002) ACCAHA guideline update for perioperative cardiovascular evaluation for noncardiac surgery – executive summary. A report of the American College of Cardiology/American Heart Association Task force on practice guidelines Circulation 105:1257–1267 17. Eide TO et al (2003) Shunting of the coeliac and superior mesenteric arteries during thoracoabdominal aneurysm repair. Eur J Vasc Endovasc Surg 26:602–606 18. Filipovic M et al (2005) Predictors of long-term mortality and cardiac events in patients with known or suspected coronary artery disease who survive major non-cardiac surgery. Anesthesia 60:5–11 19. Frank SM (1997) Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. A randomized clinical trial. J Am Med Assoc 277:1127–1134 20. Frank SM, Christopherson R (1993) Unintentional hypothermia is associated with postoperative myocardial ischaemia. Anesthesiology 78:468–476
103
104
1.9 Peri-operative Care of the Vascular Patient
21. Gamulin Z et al (1984) Effects of infrarenal aortic crossclamping on renal hemodynamics in humans. Anesthesiology 61:394–399 22. Gan TJ et al (1993) Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003 97:62–71 23. Gefke K et al (1994) Abdominal aortic aneurysm surgery: survival and quality of life in patients requiring prolonged postoperative intensive therapy. Ann Vasc Surg 8:137–143 24. Gelman S (1993) General versus regional anaesthesia for peripheral vascular surgery. Is the problem solved? Anesthesiology 79:415–418 25. Glazier DB et al (1998) Elective aortic surgery with minimal banked blood. Am Surg 64:171–174 26. Goodnough LT et al (1996) Intraoperative salvage in patients undergoing elective abdominal aortic aneurysm repair: an analysis of cost and benefit. J Vasc Surg 24:213–218 27. Grundy D (2002) Neuroanatomy of visceral nociception: vagal and splanchnic afferent. Gut 51 8 (Suppl 1):i2–i5 28. Haljamae H, Holm FJ, Akerstrom G (1988) Epidural vs. general anesthesia and leg blood flow in patients with occlusive atherosclerotic disease. Eur J Vasc Surg 2:395–268 29. Hamilton-Davies C et al (1997) Comparison of commonly used indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med 23:276–281 30. Hepner DL, Bader AM (2001) The perioperative physician and professionalism: the two must go together! Anesth Analg 93:1088–1090 31. Herbert PC et al (2001) Is a low transfusion threshold safe in critically ill patients with cardiovascular diseases? Crit Care Med 29:227–234 32. Holte K, Kehlet H (2002) Postoperative ileus: progress towards effective management. Drugs 62:2602–2615 33. Kalff JC et al (1998) Surgical manipulation of the gut elicits an intestinal muscularis inflammatory response resulting in postsurgical ileus. Ann Surg 228:652–663 34. Kettner SC et al (2003) The effect of graded hypothermia (36°C – 32°C) on hemostasis an anesthetized patients without surgical trauma. Anesth Analg 96:1772–1776 35. Kurz A et al (1996) Perioperative normothermia to reduce the incidence of surgical wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med 334:1209–1215 36. Landesberg et al (2001) Myocardial infarction after vascular surgery. The role of prolonged stress-induced ST-depression type ischaemia. J Am Coll Cardiol 37:1839–1845 37. London MJ (1991) Monitoring for myocardial ischaemia. In Kaplan JA (ed) Vascular anesthesia. Churchill Livingstone, New York, pp 249–287
38. London MJ et al (1988) Intraoperative myocardial ischaemia: localization by 12-lead electrocardiography. Anesthesiology 69:232–241 39. Mackaway-Jones K et al (1999) Modification of the cardiovascular response to hemorrhage by somatic afferent nerve stimulation with special reference to gut and skeletal muscle blood flow. J Trauma 47:481–485 40. Manara L, Bianchetti A (1986) The central and peripheral influences of opioids on gastrointestinal propulsion. Annu Rev Pharmacol Toxicol 25:249–273 41. Mangano DT et al (1990) Association of perioperative myocardial ischaemia with cardiac morbidity and mortality in men undergoing noncardiac surgery N Engl J Med 323:1781–1788 42. Mangano DT et al (1991) Perioperative myocardial infarction in patients undergoing noncardiac surgery – I: incidence and severity during the 4 day perioperative period. The Study of Perioperative Ischaemia (SPI) Research Group. J Am Coll Cardiol 17:843–850 43. Mangano DT et al (1991) Perioperative myocardial infarction in patients undergoing noncardiac surgery – II: Incidence and severity during the 1st week after surgery. The Study of Perioperative Ischaemia (SPI) Research Group. J Am Coll Cardiol 17:851–857 44. Mangesi L, Hofmeyer GJ (2002) Early compared with delayed oral fluids and food after caesarean section. Cochrane Database Syst Rev CD 003516 45. May J et al (1999) Adverse effects after endoluminal repair of abdominal aortic aneurysms: a comparison of two successive periods of time. J Vasc Surg 29:32–39 46. McCann RL, Clements FM (1989) Silent myocardial ischaemia in patients undergoing peripheral vascular surgery: incidence and association with perioperative cardiac morbidity and mortality. J Vasc Surg 9:583–587 47. Monke TG et al (2005) Anesthetic management and oneyear mortality after noncardiac surgery. Anesth Analg 100:4–10 48. Mullen P et al (1992) A metaanalysis of controlled trials of cardiac patient education. Patient Educ Counsel 19:143–162 49. Mythen MG (2005) Postoperative gastrointestinal tract dysfunction. Anesth Analg 100:196–204 50. Mythen MG, Webb AR (1995) Perioperative plasma volume expansion reduces incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 130:423–429 51. Norris EJ (2003) Anesthesia for vascular surgery. In: Miller RD (ed) Miller’s anesthesia, Vol 2. Elsevier, Amsterdam, pp 2051–2125
References
52. Norris EJ et al (2001)Double-masked randomized trial comparing alternate combinations of intraoperative anesthesia and postoperative analgesia in abdominal aortic surgery. Anesthesiology 95:1054–1067 53. Okuyama K et al (2003) Doxapram produced a dose-dependent reduction in the shivering threshold in rabbits. Anesth analg 97:759–762 54. Oyang P et al (1989) Frequency and significance of early postoperative silent myocardial ischaemia in patients having peripheral vascular surgery. Am J Cardiol 64:1113–1136 55. Page CP (1989) The surgeon and gut maintenance. Am J Surg 159:485–490 56. Pasternack PF et al (1989) The value of silent myocardial ischaemia monitoring in the prediction of perioperative myocardial infarction in patients undergoing peripheral vascular surgery. J Vasc Surg 10:617–625 57. Poldermans D et al (2003) Statins are associated with a reduced incidence of peri-operative mortality in patients undergoing major noncardiac vascular surgery. Circulation 107:1848–1851 58. Raby KE et al (1989) Correlation between preoperative ischaemia and major cardiac events after peripheral vascular surgery. N Engl J Med 321:1296–1300 59. Raby KE et al (1992) Detection and significance of intraoperative and postoperative myocardial ischaemia in peripheral vascular surgery. J Am Med Assoc 268:222–227 60. Roald et al (1996) Reduced rate of complications with autotransfusion of washed blood as compared to unwashed blood during surgery for abdominal aortic aneurysms. Circulation 94:235 61. Rosenfeld BA et al (1993) The effects of different anaesthetic regimens on fibrinolysis and the development of postoperative arterial thrombosis. Anesthesiology 79:435–443 62. Schmidt WK (2001) (ADL8-2698) is a novel peripheral opioid antagonist. Am J Surg 182:27–38 63. Schmied H et al (1996) Mild intraoperative hypothermia increases blood loss and allogenic transfusion requirements during total hip arthroplasty. Lancet 347:289–292
64. Schunn CD et al (1998) Epidural versus general anesthesia: does anesthetic management influence early infrainguinal graft thrombosis? Ann Vasc Surg 12:65–69 65. Shouten O, Poldermans D (2005) Statins in the prevention of perioperative cardiovascular complications. Curr Opin Anaesthesiol 18:51–55 66. Smedley F et al (2004) Randomized clinical trial of the effects of preoperative and postoperative oral nutritional supplements on clinical course cost of care. Br J Surg 91:983–990 67. Spark JL et al (1997) Allogenic versus autologous blood during abdominal aortic aneurysm surgery. Eur J Vasc Endovasc Surg 14:482–486 68. Stevens RD, Burri H, Tramer MR (2003) Pharmacologic myocardial protection in patients undergoing noncardic surgery: a quantitative systematic review. Anesth Analg 97:623–633 69. Szalay D, Wong D, Lindsay T (1999) Impact of red cell salvage on transfusion requirements during elective abdominal aortic aneurysm repair. Ann Vasc Surg 13:576–581 70. Tabayashi K (2005) Spinal cord protection during thoracoabdominal aneurysm repair. Surg Today 35:1–6 71. Thompson JF et al (1996) Intraoperative heparinisation. Blood loss and myocardial infarction during aortic aneurysm surgery: a joint vascular research group study. Eur J Vasc Surg 12:86–90 72. Thompson JP (2004) Ideal perioperative management of patients with cardiovascular disease: the quest continues. Anaesthesia 59:417–421 73. Tuman KJ et al (1991) Effects of epidural anesthesia and analgesia on coagulation and outcome after major vascular surgery. Anesth Analg 73:696–704 74. VanDen Kerkhof EG, Milne B, Parlow JL (2003) Knowledge and practice regarding prophylactic perioperative β blockade in patients undergoing noncardiac surgery: a survey of Canadian anesthesiologists. Anesth Analg 96:1558–1565
105
107
1.10 Training of the Vascular Surgeon for Endovascular Procedures Giorgio M. Biasi, Claudia Piazzoni, Gaetano Deleo, Alberto Froio, Valter Camesasca, Angela Liloia, Grazia Pozzi
In the last two decades the most crucial event in the evolution of vascular surgery has been the advent of endovascular techniques. The introduction of endovascular therapies has had an extraordinary impact on vascular surgery, widening and transforming the horizons of vascular surgeons in many important ways. The number of endovascular procedures has increased in the last few years and the need to gain endovascular skills has become necessary, as changing trends strongly indicate that endovascular procedures will replace traditional open operations in many vascular territories. On the other hand, even though surgeons were the first to introduce catheter-derived procedures to the vascular field, other specialists with a historically greater experience of catheter manoeuvring and the ability to treat vascular diseases stepped into the scene of the treatment of peripheral vascular diseases. The question inevitably arose as to which specialist was most qualified to treat these cases through endoluminal access. The question remains unresolved and in some cases turf battles are conducted to assert the supremacy of one specialist over the others and to identify who is responsible for the procedure. In any case, the trend seems to be that endoluminal procedures will increasingly represent the treatment of choice for many vascular diseases and that these must be performed by appropriately trained vascular surgeons who have endoluminal devices as part of their armamentarium. It also seems that the numbers of vascular surgeons who are not inclined, or do not intend, to enter the endoluminal field will eventually diminish. A primary mission of vascular surgery is to give the best possible care to the population, offering all types of treatment. To be successful with these radical modifications, vascular surgeons need to transform their traditional methods to face and treat vascular pathologies, adopting the knowledge and skill typical of other specialists (interventional radiologists, cardiologists, etc.) [2].
This dramatic change is only partly related to new techniques and procedural manoeuvres; it mostly concerns new indications [3]. This represents an inevitable evolution for vascular surgeons, consequently it has enormous implications for vascular fellowship organization. There is currently a pressing need for full reform of traditional methods of training and certification. A dedicated training is therefore mandatory to prepare the specialist with competence to treat patients with a full range of vascular diseases: a new specialist with competence in vascular open surgery, catheter-manoeuvring ability and experience in imaging [6]. Some fellowship programmes in the USA are changing by replacing the year normally dedicated to research training with endovascular training. Other programmes have partnered with an interventional radiology fellowship to make their trainees more familiar with vascular imaging, catheters and guidewires. Others have been changed to incorporate an entire year of interventional radiology into vascular surgery training [7]. Newer methods are being explored, including computer simulation [8, 9]. The advantage of training by computer simulation is the ability to place a trainee in a graphic scenario and provide real-time feedback and discussion of actions and consequences without risk of harm. It represents an emergent approach that has yet to be validated, but it could be considered an important and realistic tool for residency training. These can be partial solutions to the problem of the educational training of the “new” vascular surgeon but many other steps have yet to be taken to create this new type of hybrid specialist [4, 10]. The association of vascular surgeons and interventional radiologists, working as partners in groups or institutes, is a sensible but less than perfect manner in which to address the question of retraining vascular surgeons. Probably the most important benefit derived from these partnerships will be to
108
1.10 Training of the Vascular Surgeon for Endovascular Procedures
facilitate the education of a new generation of vascular surgeons for whom these techniques will be as familiar as the conventional open ones. In Europe the organization and practice of vascular surgical services vary, and depend on local, regional and national traditions and needs, thus presenting a highly complex and often confusing, disorganized pattern. The training to become a vascular surgeon varies all over Europe, both in duration and content. The length of vascular training varies between 5 and 11 years, and the number of procedures undertaken by the trainees varies hugely among trainees and countries [1, 5, 11]. In several countries the training programmes are currently under revision, with formal incorporation of training in endovascular procedures as a hallmark. However, this poses some difficulties that must be solved to train the specialist for the future: • When should endovascular skill be acquired? • Will other competences have to be sacrificed to give way to endovascular training or should endovascular training just be added to the present vascular training programme? • Will endovascular training be performed only by vascular surgeon trainers or is it necessary for other specialists to be involved in the training process with the consequent need for some reciprocity? • On the other hand, are radiologists and cardiologists presently being adequately trained to perform endovascular procedures and face their potential complications? During the academic year 2001–2002 at the University of Milano-Bicocca, in Milan, Italy, Giorgio Biasi’s team started a University-certified Master in Endovascular Techniques (MET), open to vascular surgeons, interventional cardiologists and radiologists who have received the specialization or relative certification of completion of the training programme (Fig. 1.10.1). The year-long MET course, now in its fourth year, starts on 1 November of each year and ends on 31 October of the following year, divided into two semesters. The training programmes are highly professional and different according to the background of the trainee: a vascular surgeon will spend 6 months in an interventional radiology department and 6 months in an interventional cardiology department. Reciprocal programmes have been devised for radiologists and cardiologists. The programme seems to have great success, with many applications from all over the world.
Fig. 1.10.1 Master in Endovascular Techniques
The intention is to provide the formation of a new figure: the “Endovascular Specialist”. This is an extremely ambitious project considering that there is still no clear definition of an endovascular specialist, his/her limits and duties. Ideally, the training programme for the creation of such a specialist should start immediately after obtaining the medical degree. The programme should be divided into three different stages [3]: Stage 1: Two years of this new vascular fellowship could be dedicated to vascular anatomy and physiology, angiology, diagnostic vascular lab and minor general, venous and arterial surgery procedures. The young vascular surgeons should also be trained in preventive medicine in order to treat lifestyles and risk factors. At this stage basic science training should also be considered that permits intelligent interpretation of emerging knowledge and technologies, such as genetic risk factors, gene therapy, drug-eluting stents, etc.
109
Fig. 1.10.2 “Endovascular specialist” training programme, Certificate of Completion of Speciality Training (CCST)
1.12.3 Lower Extremity By-pass
Table 1.12.3 Factors contributing to graft occlusion with time Cause
Time from implant 0–30 days
1–18 18 months months to 5 years
Operative technique
++++
–
–
Graft surface thrombogenicity
++
+
–
Poor outflow
++
+
–
Obstructive venous disease ++
+
–
Neointimal fibroplasias
–
+++
–
Graft structural abnormalities (vein)
–
+++
++
Graft structural abnormalities (prosthetic graft)
–
–
++
Progressive atherosclerosis
–
+
++++
Modified from [35]
As shown in Table 1.12.3, these factors act at different times; in the early postoperative period technical errors undoubtedly play the major role in jeopardizing the patency [1]. Moreover, even if patency can be restored in occluded grafts, long-term results are rarely achieved if the occlusion occurred in the early postoperative period [27]. Therefore, any measure providing improvement of immediate results needs to be considered. Different methods have been used to obtain intraoperative quality control to ensure the adequacy of the arterial reconstructions. These are: • flowmetry • IVUS • duplex • angiography • angioscopy.
1.12.3.1 Angiography The introduction of the angiographic intraoperative control in the intraoperative field was justified by an early experience from Renwick et al. [26]: when routinely used on any type of lower extremity surgical operation, it showed technical defects in 27% of the patients. This dramatically
Fig. 1.12.1 A below-knee femoropopliteal by-pass done a few months before it thrombosed acutely. At reintervention patency was restored by using Fogarty catheters. Completion angiography showed a patent tibioperoneal trunk. Run-off was provided through the tibialis posterior and peroneal
decreased the early thrombosis rate from 18% to 0%. A landmark paper from Courbier et al. [7] reported on more than 1800 arterial procedures where a completion angi-
121
110
1.10 Training of the Vascular Surgeon for Endovascular Procedures
Stage 2: Progress to three years of training in major open vascular procedures obtaining the Certificate of Completion of Specialist Training (CCST) in Vascular Surgery. Although the appearance of endovascular techniques demands the addition of new elements of training, it has not diminished the need for advanced skills in open surgical repair; conversely, it emphasizes the need for such skills – the skill required for conversion of a failed endovascular procedure into an open repair is greater than that required for primary surgical repair. Stage 3: The next step should be a 1-year training programme for acquiring skill and experience of catheterderived endovascular procedures, as well as imaging. Possession of such knowledge will not be in conflict with open traditional surgery but will be an adjunctive and complementary part of the training (Fig. 1.10.2). Stage 3 could represent a sort of common trunk, a part of the training programme that can apply to other specialists (radiologists and cardiologists). This new specialist should have the competence to treat all vascular territories including coronary angioplasty. References 1. Barnes RW, Ernst CB (1996) Vascular surgical training of general and vascular surgery residents. J Vasc Surg 24:1057–1063 2. Berguer R (2004) Problems facing vascular surgery in 2004. Vascular 12:39–41 3. Biasi GM, Piazzoni C (2004) Postgraduated training in endovascular surgery for vascular surgeons. Int Congr Ser 1272:109–115
4. Brevetti LS, Nackman GB, Shindelman LE, Ciocca RG, Gerard Crowley J, Graham AM (2003) Influence of endovascular training on fellowship and general surgery training. J Surg Res 115:100–105 5. Calligaro KD, Dougherty MJ, Sidawy AN, Cronenwett JL (2004) Choice of vascular surgery as a specialty: survey of vascular surgery residents, general surgery chief residents, and medical students at hospitals with vascular surgery training programs. J Vasc Surg 40:978–984 6. Choi ET, Wyble CW, Rubin BG, Sanchez LA, Thompson RW, Flye MW, Sicard GA (2001) Evolution of vascular fellowship training in the new era of endovascular techniques. J Vasc Surg 33:S106–S110 7. Cronenwett JL (2004) Vascular surgery training in the United States, 1994 to 2003. J Vasc Surg 40:660–669 8. Dayal R, Faries PL, Lin SC, Bernheim J, Hollenbeck S, DeRubertis B, Trocciola S, Rhee J, McKinsey J, Morrissey NJ, Kent KC (2004) Computer simulation as a component of catheter-based training. J Vasc Surg 40:1112–1117 9. Hsu JH, Younan D, Pandalai S, Gillespie BT, Jain RA, Schippert DW, Narins CR, Khanna A, Surowiec SM, Davies MG, Shortell CK, Rhodes JM, Waldman DL, Green RM, Illig KA (2004) Use of computer simulation for determining endovascular skill levels in a carotid stenting model. J Vasc Surg 40:1118–1125 10. Lin PH, Bush RL, Milas M, Terramani TT, Dodson TF, Chen C, Chaikof EL, Lumsden AB (2003) Impact of an endovascular program on the operative experience of abdominal aortic aneurysm in vascular fellowship and general surgery residency. Am J Surg 186:189–193 11. Maurer PC (1995) Vascular surgery in European Union: current state, developments and prospects for the future. Int Angiol 14:335–338
111
1.11 Peripheral Arterial Disease and Emerging Biochemical Vascular Risk Factors Stella S. Daskalopoulou, Marios E. Daskalopoulos, Christos D. Liapis, Dimitri P. Mikhailidis
1.11.1 Introduction Peripheral arterial disease (PAD) affects more than 10 million people in the United States. The risk factors associated with PAD are similar to those for coronary heart disease (CHD) and cerebrovascular disease (CVD) [4, 7]. Medical therapy of PAD must include modification of vascular risk factors with application of strict secondary prevention guidelines [7]. Established risk factors such as smoking, diabetes, hypertension and dyslipidaemia are commonly found in patients with PAD [7]. Furthermore, several emerging risk factors such as homocysteine (Hcy), lipoprotein (a) [Lp(a)], C-reactive protein (CRP) and fibrinogen have also been documented in patients with PAD [1–3, 5–12, 15, 17, 19, 21–28]. This review briefly considers the role of these emerging risk factors in the pathogenesis and treatment of PAD.
1.11.2 Homocysteine (Hcy) Elevated Hcy levels have been reported in patients with PAD [2, 5, 15, 22–24, 27] Moreover, Hcy concentrations were found to be significantly lower in patients with isolated PAD than in patients who also had additional systemic atherosclerosis in PAD (10.1±4.4 versus 16.7±7.0 μmol/l, p<0.0001) [23]. Similarly, Hcy in type 2 diabetes was found to be associated with the angiographic severity of PAD. Even in young women, hyperhomocysteinaemia is a risk factor for PAD [27]. Furthermore, there is a strong synergistic effect between Hcy and traditional vascular risk factors, but this synergism may not be seen in CHD and CVD [27]. Thus, in a study of 6880 unselected primary care patients (aged ≥65 years) the association between atherothrombotic manifestations and Hcy diminished substantially after adjusting for age, gender, smok-
ing status, diabetes, hypertension, lipid disorders and estimated glomerular filtration rate [5]. The odds ratio (OR) for PAD decreased to 1.4; for CHD, to 1.0; and for CVD, to 1.1. Therefore, after adjusting for established risk factors, the association between Hcy and PAD is small but no longer present for CHD and CVD. There is also evidence of a relationship between Hcy and nonfatal atherothrombotic stroke in patients with symptomatic PAD [24]. This could be clinically relevant because of the high incidence of cerebrovascular complications in PAD patients. However, we need to consider that not all studies support a strong association between PAD and Hcy. The adverse effect of Hcy on the vasculature may include the accumulation of the endogenous nitric oxide (NO) synthase inhibitor, asymmetric dimethylarginine (ADMA) [24]. This may result in platelet activation. There are as yet no convincing intervention trials indicating whether lowering Hcy levels (e.g. by administering folic acid or vitamin B12) results in a decreased risk of vascular events. Nevertheless, it is unlikely that the administration of vitamin supplements is harmful in cases where there is no haematological abnormality.
1.11.3 C-reactive Protein (CRP) Circulating CRP levels are elevated in the presence of PAD [1, 2, 11, 15, 17, 21]. Moreover, symptomatic PAD patients were found to have higher CRP levels than asymptomatic PAD patients. CRP also correlated negatively with the ankle/brachial pressure index (ABPI) [1]. Higher CRP levels were associated with poorer walking performance. Among several atherothrombotic markers assessed at baseline, CRP and the total cholesterol:highdensity lipoprotein cholesterol (HDL-C) ratio were the strongest independent predictors for the development of PAD [15]. As with CHD, CRP provided additive prog-
112
1.11 Peripheral Arterial Disease and Emerging Biochemical Vascular Risk Factors
nostic information over standard lipid measures. The relationship between PAD and CRP appears to be stronger than that between PAD and Hcy. PAD is commoner in type 2 diabetic patients [1]. Therefore, it is interesting that higher CRP levels are reported in those with diabetes and PAD as compared with diabetes alone. In fact, only the serum CRP level, the duration of diabetes and use of angiotensin converting enzyme inhibitors (ACEI) were independently associated with PAD in type 2 diabetes mellitus. Physical activity may lower serum CRP levels in patients with PAD [1]. Statins reduce the event rate in PAD.[7, 18]. However, there is evidence that this benefit is limited to, or at least more obvious in, the presence of high inflammatory activity. In this context, it is interesting that statins lower the circulating levels of CRP [1]. It is not clearly established if there is a dose–response relationship between the extent of LDL-C lowering (and possibly the statin dose used) and the fall in CRP levels. In this context, it is interesting that ezetimibe (a selective cholesterol transport inhibitor) lowers CRP levels further when added to a statin [7]. Some fibrates (e.g. ciprofibrate and fenofibrate) can also lower the circulating levels of CRP [7]. Preprocedural CRP levels predict a high incidence of myocardial infarction (MI) in patients with PAD, independently of previous CHD and established vascular risk factors [17]. CRP levels at baseline and 48 h after intervention may also be independent predictors of postangioplasty outcome (e.g. restenosis at 6 months [20]). Although serum CRP levels have been used as “markers” of vascular disease, it is important to consider that there is evidence that CRP may also participate in atherogenesis (e.g. by acting as a chemoattractant).
1.11.4 Lipoprotein (a) [Lp(a)] Lp(a) is an independent risk factor for PAD [15, 25]. This is even true for type 1 and 2 diabetic patients. The relationship between PAD and Lp(a) may be stronger than that between Lp(a) and CHD and stroke. A threshold of ≥30 mg/dl has been proposed as an independent risk factor for premature peripheral atherosclerosis in men. Lp(a) levels correlated with LDL-C, total cholesterol, fibrinogen and apolipoprotein B levels as well as disease severity. An elevated Lp(a) level may be associated with more severe forms of PAD [15].
Serum Lp(a) levels are elevated in patients with early impairment of renal function and are associated with a greater prevalence of vascular disease. An inverse correlation between serum Lp(a) level and creatinine clearance may account for this elevation. This relationship may be relevant since patients with PAD may have impaired renal function (e.g. due to co-existing atherosclerotic renal artery stenosis). In a multivariate regression analysis, Lp(a) and Hcy were the best predictors for acute MI, whereas Lp(a), Hcy and the total cholesterol:HDL-C ratio were the best predictors for PAD [15]. The circulating levels of Lp(a) are largely genetically determined; therefore, it is difficult to influence this variable. Nicotinic acid can lower Lp(a) levels but compliance may be a problem because of side-effects (e.g. flushing). Correcting hypothyroidism or administering hormone replacement therapy may also lower Lp(a) levels. Since the risk attributed to Lp(a) is influenced by the LDL-C level, it may be that the overall risk of a vascular event can be decreased by aggressively lowering the LDL-C levels (e.g. with a statin [7]). The structural homology between Lp(a) and plasminogen means that Lp(a) is considered as a “bridge” between dyslipidaemia and haemostasis.
1.11.5 Fibrinogen Patients with PAD have elevated plasma fibrinogen levels that also indicate an increased risk for poor outcome, particularly for fatal cardiovascular complications [9]. There is not only a correlation between plasma fibrinogen concentration and the severity of CHD but also a correlation with the incidence of additional PAD or CVD. In CHD, the fibrinogen level is associated with the number of stenosed coronary arteries. Fibrinogen probably exerts its adverse effects by several mechanisms. These include increasing blood viscosity, activating platelets, modulating endothelial function and promoting smooth muscle cell proliferation and migration as well as participating in the coagulation process [9]. Several factors influence plasma fibrinogen levels. Among these are smoking, diabetes/insulin resistance, obesity and the acute phase response [9]. There is an inverse association between physical activity and plasma fibrinogen levels. Patients receiving statin
1.11.7 PAD and Other Potentially Relevant Emerging Risk Factors
therapy had significantly less inflammation (hs-CRP p<0.001, fibrinogen p=0.007, albumin p<0.001 and neutrophils p=0.049) and better survival [adjusted hazard ratio (HR) 0.52, p=0.022] and event-free survival rates (adjusted HR 0.48, p=0.004) than patients not treated with statins [18]. However, the short-term effect of statins on plasma fibrinogen levels remains controversial. In contrast, fibrates (with the possible exception of gemfibrozil) consistently lower plasma fibrinogen levels [7]. High fibrinogen concentrations appear to be detrimental to early angioplasty success.
1.11.6 Endothelium The endothelium is not a passive lining of the arterial tree [3]. It is an active organ that plays a key role in regulating vascular reactivity and preventing thrombosis. Inflammation is implicated in the pathophysiology of endothelial dysfunction in PAD. For example, a multivariate analysis showed an association of CRP, fibrinogen and ABPI with brachial artery flow-mediated dilation (FMD) [3]. The adhesive protein von Willebrand factor (vWF), a marker of endothelial damage, contributes to platelet function by mediating the initiation and progression of thrombus formation at sites of vascular injury. vWF is significantly associated with the risk of developing PAD [3]. Increased levels of vWF are independently associated with cardiovascular and all-cause mortality in both diabetic patients and nondiabetic subjects. The ABPI correlates positively with FMD and negatively with CRP, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) [3]. Thus, in PAD, endothelial function and inflammatory status are related to the severity of the circulatory impairment. The associated thrombotic tendency may contribute to the increased risk of MI and stroke.
1.11.7 PAD and Other Potentially Relevant Emerging Risk Factors 1.11.7.1 Creatinine Renal impairment is associated with an increased risk of mortality in advanced PAD, irrespective of the presence of hypertension and diabetes mellitus [5, 12]. This sug-
gests that impaired renal function exerts an unfavourable effect on outcome, independently of these risk factors. After multivariable proportional-hazard adjustment for potential confounders and other known risk factors for PAD, women with a decreased creatinine clearance (<60 ml·min– 1 ·1.73 m– 2 ) had a significantly increased risk of PAD (and/or other vascular problems) compared with those with a creatinine clearance ≥60 ml·min– 1 ·1.73 m– 2 [14]. Clinicians should be aware of the high prevalence of PAD among patients with renal insufficiency [7]. Type 2 diabetic patients with PAD had longer diabetic duration, higher serum creatinine levels, a higher total cholesterol: HDL-C ratio, more hypertension and a history of cerebrovascular events and higher CRP and inteleukin-6 (IL6) levels [21, 28]. The renal haemodynamic profile in atherosclerotic patients might constitute functional evidence of the silent phase of ischaemic renal disease. The findings suggest that renal function should be carefully assessed in patients with extrarenal atherosclerosis, particularly in those with classic vascular risk factors. In other words, recent evidence strongly suggests that renal and vascular disease progress in parallel. In turn, the same treatment that improves vascular disease may also preserve/restore renal function [7]. It is important to consider that impaired renal function will adversely affect other variables; for example, by raising the circulating levels of Hcy, urate and Lp(a) [5]. Future studies should determine whether correcting or preventing impaired renal function will result in a decreased risk of vascular events. In this context, there is evidence that treatment with statins and antihypertensive drugs results in improved renal function or a delay in renal disease progression [6, 7].
1.11.7.2 Urate Elevated uric acid levels were found to be a significant and independent risk factor for PAD as well as a predictor of CHD [10]. However, the link between plasma urate levels and the risk of vascular events remains controversial [6]. Hyperuricaemia is more pronounced in hypertension complicated by PAD and is associated with worse functional status of the peripheral circulation [10]. Circulating urate levels are influenced by renal function and there is evidence that hyperuricaemia is associated with an increased risk of vascular events [7].
113
114
1.11 Peripheral Arterial Disease and Emerging Biochemical Vascular Risk Factors
Statins may lower plasma urate levels by improving renal function [6]. Fenofibrate exerts a uricosuric effect [6].
1.11.7.3 Microalbuminuria Microalbuminuria is associated with increased vascular and all-cause mortality, probably because it reflects generalized atherosclerosis [7, 26]. Albuminuria is associated with diabetes mellitus, PAD, hypertension, CHD, hyperlipidaemia and in some cases with elevated plasma fibrinogen levels. Microalbuminuria and PAD are mutually independent risk indicators. Aggressive blood pressure lowering (especially with ACEI or angiotensin II receptor blockers) or statins exert a favourable effect on microalbuminuria and renal function [7, 26].
1.11.7.4 Insulin Resistance and Metabolic Syndrome The incidence of PAD is greater in patients with diabetes or impaired glucose tolerance and insulin resistance [8]. The metabolic syndrome is also associated with a higher risk of vascular events [8]. The prevalence of the metabolic syndrome in a secondary prevention population has been reported as: 58% in PAD patients, 41% in CHD patients, 43% in CVD patients and 47% in abdominal aortic aneurysm patients. With the increasing prevalence of the metabolic syndrome we expect to see more PAD associated with insulin resistance. Patients with the metabolic syndrome may have raised levels of urate and fibrinogen as well as impaired fibrinolysis [8].
1.11.7.5 Platelets, Fibrinolysis and D-Dimers Patients with PAD have impaired fibrinolytic activity, manifested primarily as raised levels of the inhibitor of fibrinolysis, plasminogen activator inhibitor-1 (PAI-1). Six months of exercise training improved fibrinolysis. Physical activity lowers D-dimer levels, which may be a sensitive marker of the extent of atherosclerosis in lower extremity arteries [11]. High D-dimer levels are associated with poorer physical activity among individuals with and without PAD. Additional work is needed to determine whether D-dimers (and CRP) are involved in the
pathophysiology of functional impairment or whether they are simply markers of the extent of systemic atherosclerosis [11]. PAD is associated with platelet activation; this may be why antiplatelet drugs exert a beneficial effect in these patients [13, 16]. Unfortunately, it is difficult to evaluate platelet function because of the need for fresh samples. It is possible that in the future this limitation will be overcome by the measurement of the plasma levels of soluble P-selectin.
1.11.7.6 Other Markers of Inflammation Low serum albumin levels are associated with a greater incidence of major adverse cardiac events (MACE: MI, percutaneous coronary interventions, coronary artery by-pass graft and death) in patients with advanced atherosclerosis [19]. Serum amyloid A, another marker of inflammation, can mirror the results seen with CRP (see above) [11, 18]. Patients with PAD also have higher levels of IL-6. Platelet activation may play a significant role through the expression of CD40 ligand as a source of activation signals to endothelial cells. This, in turn, may modulate the inflammatory response. In this context, it is relevant that both statins and the antiplatelet agent clopidogrel may influence the CD40 activation process [13, 16].
1.11.8 Conclusions Several emerging biochemical markers have shown promise in terms of predicting the probability of developing PAD, the risk of vascular events or further progression of lower limb arterial disease. Among these are Hcy, Lp(a), CRP and fibrinogen. There is a need to confirm their role as predictors of vascular risk and as targets for pharmacologic or lifestyle intervention. These factors may also prove useful for patient surveillance. The currently available medical treatment for PAD (antiplatelet, lipid-lowering, hypoglycaemic and antihypertensive drugs) may influence these emerging risk factors. It is also relevant to mention that noninvasive diagnostic imaging techniques are being developed. These techniques, when used in conjunction with biochemical markers, will help detect early vascular disease as well as evaluate the effectiveness of any treatment.
References
References 1. Bassuk SS, Rifai N, Ridker PM (2004) High-sensitivity Creactive protein: clinical importance. Curr Probl Cardiol 29:439–493 2. Bloemenkamp DG, van den Bosch MA, Mali WP, Tanis BC, Rosendaal FR, Kemmeren JM, Algra A, Visseren FL, van der Graaf Y (2002) Novel risk factors for peripheral arterial disease in young women. Am J Med 113:462–467 3. Brevetti G, Silvestro A, Di Giacomo S, Bucur R, Di Donato A, Schiano V, Scopacasa F (2003) Endothelial dysfunction in peripheral arterial disease is related to increase in plasma markers of inflammation and severity of peripheral circulatory impairment but not to classic risk factors and atherosclerotic burden. J Vasc Surg 38:374–379 4. Criqui MH, Denenberg JO, Langer RD, Fronek A (1997) The epidemiology of peripheral arterial disease: importance of identifying the population at risk. Vasc Med 2:221–226 5. Darius H, Pittrow D, Haberl R, Trampisch HJ, Schuster A, Lange S, Tepohl HG, Allenberg JR, Diehm C (2003) Are elevated homocysteine plasma levels related to peripheral arterial disease? Results from a cross-sectional study of 6880 primary care patients. Eur J Clin Invest 33:751–757 6. Daskalopoulou SS, Athyros VG, Elisaf M, Mikhailidis DP (2004) Uric acid levels and vascular disease. Curr Med Res Opin 20:951–954 7. Daskalopoulou SS, Daskalopoulos ME, Liapis CD, Mikhailidis DP (2005) Peripheral arterial disease: a missed opportunity to administer statins so as to reduce cardiac morbidity and mortality. Curr Medicinal Chem 12:763–771 8. Daskalopoulou SS, Mikhailidis DP, Elisaf M (2004) Prevention and treatment of the metabolic syndrome. Angiology 55:589–612 9. Koenig W (2003) Fibrinogen in cardiovascular disease: an update. Thromb Haemost 89:601–609 10. Langlois M, De Bacquer D, Duprez D, De Buyzere M, Delanghe J, Blaton V (2003) Serum uric acid in hypertensive patients with and without peripheral arterial disease. Atherosclerosis 168:163–168 11. McDermott MM, Greenland P, Green D, Guralnik JM, Criqui MH, Liu K, Chan C, Pearce WH, Taylor L, Ridker PM, Schneider JR, Martin G, Rifai N, Quann M, Fornage M (2003) D-dimer, inflammatory markers, and lower extremity functioning in patients with and without peripheral arterial disease. Circulation 107:3191–3198 12. Mlekusch W, Exner M, Sabeti S, Amighi J, Schlager O, Wagner O, Minar E, Schillinger M (2004) Serum creatinine predicts mortality in patients with peripheral artery disease: influence of diabetes and hypertension. Atherosclerosis 175:361–367
13. Peripheral Arterial Diseases Antiplatelet Consensus Group (2003) Antiplatelet therapy in peripheral arterial disease. Consensus statement. Eur J Vasc Endovasc Surg 26:1–16 14. Reddan DN, O’Shea JC, Sarembock IJ, Williams KA, Pieper KS, Santoian E, Owen WF, Kitt MM, Tcheng JE (2003) Treatment effects of eptifibatide in planned coronary stent implantation in patients with chronic kidney disease (ESPRIT Trial). Am J Cardiol 91:17–21 15. Ridker PM, Stampfer MJ, Rifai N (2001) Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. J Am Med Assoc 285:2481–2485 16. Robless P, Mikhailidis DP, Stansby G (2001) Systematic review of antiplatelet therapy for the prevention of myocardial infarction, stroke or vascular death in patients with peripheral vascular disease. Br J Surg 88:787–800 17. Rossi E, Biasucci LM, Citterio F, Pelliccioni S, Monaco C, Ginnetti F, Angiolillo DJ, Grieco G, Liuzzo G, Maseri A (2002) Risk of myocardial infarction and angina in patients with severe peripheral vascular disease: predictive role of Creactive protein. Circulation 105:800–803 18. Schillinger M, Exner M, Mlekusch W, Amighi J, Sabeti S, Muellner M, Rumpold H, Wagner O, Minar E (2004) Statin therapy improves cardiovascular outcome of patients with peripheral artery disease. Eur Heart J 25:742–748 19. Schillinger M, Exner M, Mlekusch W, Amighi J, Sabeti S, Schlager O, Wagner O, Minar E (2004) Serum albumin predicts cardiac adverse events in patients with advanced atherosclerosis – interrelation with traditional cardiovascular risk factors. Thromb Haemost 91:610–618 20. Schillinger M, Exner M, Mlekusch W, Rumpold H, Ahmadi R, Sabeti S, Haumer M, Wagner O, Minar E (2002) Vascular inflammation and percutaneous transluminal angioplasty of the femoropopliteal artery: association with restenosis. Radiology 225:21–26 21. Silvestro A, Scopacasa F, Ruocco A, Oliva G, Schiano V, Zincarelli C, Brevetti G (2003) Inflammatory status and endothelial function in asymptomatic and symptomatic peripheral arterial disease. Vasc Med 8:225–232 22. Spark JI, Laws P, Fitridge R (2003) The incidence of hyperhomocysteinaemia in vascular patients. Eur J Vasc Endovasc Surg 26:558–561 23. Taute BM, Taute R, Heins S, Behrmann C, Podhaisky H (2004) Hyperhomocysteinemia: marker of systemic atherosclerosis in peripheral arterial disease. Int Angiol 23:35–40 24. Taylor LM Jr (2003) Elevated plasma homocysteine as risk factor for peripheral arterial disease – what is the evidence? Semin Vasc Surg 16:215–222
115
116
1.11 Peripheral Arterial Disease and Emerging Biochemical Vascular Risk Factors
25. Tseng CH (2004) Lipoprotein(a) is an independent risk factor for peripheral arterial disease in Chinese type 2 diabetic patients in Taiwan. Diabetes Care 27:517–521 26. Tseng CH, Tseng CP, Tai TY, Chong CK (2005) Effect of angiotensin blockade on the association between albuminuria and peripheral arterial disease in elderly Taiwanese patients with type 2 diabetes mellitus. Circ J 69:965–970
27. van den Bosch MA, Bloemenkamp DG, Mali WP, Kemmeren JM, Tanis BC, Algra A, Rosendaal FR, van der Graaf Y (2003) Hyperhomocysteinemia and risk for peripheral arterial occlusive disease in young women. J Vasc Surg 38:772–778 28. Yu HI, Sheu WH, Song YM, Liu HC, Lee WJ, Chen YT (2004) C-reactive protein and risk factors for peripheral vascular disease in subjects with Type 2 diabetes mellitus. Diabet Med 21:336–341
117
1.12 Quality Control in Vascular Surgery P. G. Settembrini, M. Carmo, R. Dallatana, G. Mercandalli, G. A. T. De Angelis
1.12.1 Introduction Intraoperative assessment of technical adequacy is a necessary part of all arterial reconstructions. Detection of any technical imperfection in the operating room allows the surgeon to provide immediate correction of the abnormalities that may lead to early thrombosis. Technical imperfection accounts for about 2.4–26% of all failures according to different studies [6]. In the past most surgeons used to check the reconstruction through the palpation of a pulse in the vessel distal to the anastomosis; only later was continuous wave (CW) Doppler adopted, providing data on the physiology of the reconstruction (flow velocity). Intraoperative angiography was introduced in the 1970s, thus providing information on the morphology of the by-pass. In recent years duplex scan and colour duplex scan have been widely used, thus permitting us to check the reconstruction for its physiological and morphological parameters (vessel wall and lumen).
1.12.1.2 Angiography Angiography is still considered the gold standard for the assessment of vessel patency. Introduced in the intraoperative setting, this technique was able to accurately depict the anatomy of reconstruction and the outflow. However, it remains an invasive procedure, which requires direct injection of contrast dye into the vessel. Angiography requires two projections to obtain an appropriate vision of the vessel. Complications related to needle insertion (dissection and thrombosis) or the contrast dye (nephrotoxicity or allergic reaction) have been described. Their incidence is probably less frequent than commonly thought [7], and the introduction of digital subtraction (available also on portable machinery) has further lowered this rate. Its disadvantages are the same as those encountered for preoperative diagnosis: besides the cost of the machinery and the necessity for specifically trained personnel, its accuracy has been questioned. The presence of air inside the lumen, and an excessive or poor concentration of the contrast dye can easily cause over- or underestimation of the defects.
1.12.1.1 Physical Examination This is frequently forgotten in an era of advanced technology. Pulsatility of distal arteries, pink colour of the skin and warm temperature of the limbs often indicate that a normal blood supply has been restored. These findings alone cannot ensure the technical adequacy of the reconstructions, however their absence is not always indicative of the presence of a defect: spasm and calcification of the peripheral arteries can prevent a pulsation from being palpable. A thrill on the anastomosis can indicate the presence of a stenosis, but at the same time the turbulence associated with a high flow can produce the same “sound”.
1.12.1.3 Continuous Wave (CW) Doppler In the earliest era of vascular surgery, CW Doppler was the first method used to test construction. It remains valid due to its simplicity and cost-effectiveness: the probes are cheap, easy to use and always available, and can be directly sterilized or covered by a sterile sheath. They detect the velocity inside the vessel by direct contact with the external wall, providing indirect measurement of the relative decrease in the diameter of the lumen. The older CW Doppler machines were only able to transform the velocity into sound. Interpretation relied only on the experience of the operator. More recent machines have a screen showing the flow wave, allowing precise measurement of the peak systolic velocity (PSV) and the end-
118
1.12 Quality Control in Vascular Surgery
diastolic velocity (EDV), expressed in cm/s. The absolute maximum PSV and the ratio between the maximum PSV and the value measured in the vessel before the increase are the two parameters commonly used to characterize the stenosis. The simplicity of the method represents its major limit. In fact it does not enable one to see inside the vessel in order to choose the point where to detect the velocity. This would allow one to precisely correlate the morphologic defect with the increased velocity. Its measurement is prone to large variation due to the angle of the probe with the vessel: 45° is the required angle. Experienced operators are therefore required to correctly perform and interpret the examination. Moreover any minor defect not producing a significant change in flow velocity is difficult to detect with this method.
1.12.1.4 Duplex and Colour Duplex Scan The colour duplex scan machine associates a B-mode ultrasound with a pulsed wave (PW) Doppler. The colour is the visual translation of the PW Doppler to help the operator test the exact point where the defect is visible (area of stenosis, turbulence, etc.). Initially used in the preoperative setting, it has recently been introduced for intraoperative use. The implementation of the technology has produced smaller probes (now measuring about 2 cm), with longer wavelength, thus providing better two-dimensional resolution. The major advantage of this technique is the possibility of obtaining both anatomic and functional information about the vessel. Direct vision of the lumen and wall allows one to visualize the presence of stenosis, thrombus, dissection or intimal flap. Measurement of flow velocity can confirm findings from a B-mode examination and provide more reliable parameters in order to grade the lesion (as discussed in Section 1.12.1.3). This technique is applicable to any vessel and does not require the use of nephrotoxic contrast dye. The major limitation in this case is its dependence on the operator. Polytetrafluoroethylene (PTFE) grafts and patches cannot be appropriately scanned due to the presence of air inside the wall of the graft, which masks the lumen. Moreover the outflow vessel can be scanned only within the limit of the surgical wound, where the probe can be appropriately placed directly on the artery.
1.12.1.5 Intravascular Ultrasonography (IVUS) This application was introduced in the 1980s but has become more popular recently, and has been widely used during endovascular procedures. Moreover, over the years catheters have reduced in diameter from 2.5–3 mm to less than 1 mm. The wavelength of the ultrasound reaches 40 MHz, allowing a high resolution for the view of the surrounding tissues. The probe is placed on the tip of a flexible catheter introduced inside the artery. The image is a 360° transverse scan of the vessel, obtained through either a single rotating transducer or a phased array. The major advantage is the accuracy of its measurements. For this reason it is being used in some centres during endovascular aneurysm repair (EVAR), enabling the operator to take measurements of neck diameter and length, to check the exact position of the graft and to verify the patency of the renal arteries at the end of the procedure. It accuracy is applicable to all different kinds of arterial and venous lesions, such as restenosis and flaps.
1.12.1.6 Angioscopy This technique allows direct vision of the inner wall of any artery, vein or by-pass by using optic fibres. The blood represents the major obstacle. For this reason blood flow needs to be interrupted and the vessel to be filled with saline. Catheter diameters range from 0.5 to 3.5 mm depending on the presence of a coaxial channel used for irrigation with water. Blood flow is usually interrupted through an inflatable balloon. The optic fibres have a high resolution and are very flexible. When the fibre is connected to a camera, the images obtained are visible on a monitor and the inner wall can thus be directly visualized, distinguishing between different plaque characteristics (ulcers or heavy calcifications). The presence of the light at the end of the fibre helps one to correlate the lesion found to the skin surface, thus allowing one to make small incisions in exactly the right area when open surgery is required. For in situ or non-reversed vein by-pass surgery, this method is helpful when checking for the presence of residual valves inside the vein graft. Gloviczki has described another particular application [12] for valvuloplasty of the femoral vein without venotomy: the stitches are placed under direct vision of the inner surface by introducing the angioscopic fibre through the great saphenous vein.
1.12.2 Arteries of the Abdomen
The limitations are mainly the cost and the fact that the procedure remains invasive: lesion on the wall, with flaps or dissection, and trauma due to water pressure or fluid overload secondary to excessive irrigation are the most common complications.
1.12.1.7 Flowmetry This method has been used particularly in the USA. The method uses an electromagnetic or ultrasonographic flow meter: a small cuff (an appropriate diameter needs to be chosen) is placed around the vessel (graft or native artery) and the transducer measures the flow inside the conduit. Usually papaverine is injected in the distal outflow vessel to maximize the sensitivity of the test. The technique is very simple and precise. The cost is related to the machinery, as the probes can be re-sterilized. This method has a high specificity but a low sensitivity, as minor defects or even major ones are not detectable if they do not decrease the flow. Moreover, PTFE isolates the flow from the transducer both for the ultrasound flow meter (because of the air inside the wall of the graft) and the electromagnetic one (PTFE is a good electric isolator). For these reasons this method is usually associated with another technique as quality control.
1.12.2 Arteries of the Abdomen 1.12.2.1 Abdominal Aorta Due to the large calibre of the abdominal aorta and iliac arteries, the issue of possible technical defects during the reconstruction is less important. In any case (and in particular for the iliac arteries), any time an unsatisfactory pulse is present at the end of the procedure some kind of quality control is required. Flow meters, CW Doppler and duplex are all used in this setting. Endovascular techniques are obviously different: in this case the angiography is part of the procedure itself. However, even in the presence of increased creatinine, long procedures or other relative contraindications, a completion angiography should always be performed at the end of the procedure to test for patency of the renal and iliac arteries and the presence of endoleaks [24]. The use of angioscopy in this setting has already been discussed.
1.12.2.2 Visceral Arteries Papers on visceral artery revascularization rarely report on intraoperative controls used after surgery. A recent article from the Mayo Clinic reviewed their experience with intraoperative duplex scan. Oderich et al. [21] described 68 patients who received arterial revascularization on 120 visceral arteries [coeliac artery in 52 cases, superior mesenteric artery (SMA) in 60, inferior mesenteric artery (IMA) in 8] between 1992 and 2001 [21]. Intraoperative duplex ultrasound was performed at the end of the procedure in all of them. Table 1.12..1 describes the parameters used to classify the defects for the coeliac artery and SMA. One hundred and two had normal findings (85%); 13 of them had nonfocal increased velocity due to vessel–graft mismatch. Eight arteries (6.6%) had minor defects, while ten (8.4%) presented major alterations: four had a residual stenosis, two had a thrombus, another two a kink, and bidirectional flow and dissection were present in one artery each. All arteries with a major defect were immediately revised. In all cases the abnormality was confirmed during re-intervention. Only one case had a persistent major defect (bidirectional flow) after revision, while another two had a reduction of the residual stenosis to a minor defect. Perioperative mortality was 4.4% (3 cases): in two of them it was correlated to graft occlusion and in one there was a minor unrepaired defect in the vessel. Patients with abnormal intraoperative findings had a higher incidence of early thrombosis (14.2% versus 1%; p=0.04), late restenosis (18.2% versus 3.2%; p=0.08) and visceral re-intervention (21.4% versus 3.2%; p=0.03). Univariate analysis identified a positive association between graft-related complication/death and both abnormal intraoperative findings (55.5% versus 7.8%, Table 1.12.1 Classification of intraoperative duplex findings for visceral artery revascularization. Presence of abnormal velocities in the absence of any kind of visible defect was classified as calibre mismatch between graft and native vessel PSV (cm/s)
Ratio
B-mode
Coeliac artery
Superior mesenteric artery
-
Normal
< 2.0
< 2.75
<2
Normal
Minor defect
< 2.0
< 2.75
<2
Abnormal
Major defect
> 2.0
> 2.75
>2
Abnormal
119
120
1.12 Quality Control in Vascular Surgery
p=0.04) and single vessel revascularization (35.7% versus 10.8%, p=0.4). Multiple regression analysis confirmed the presence of abnormal intraoperative findings as the only independent risk factor for graft-related complication/ death (OR 7.08; 95% CI 1.65–30.4; p=0.08).
1.12.2.3 Renal Arteries For renal revascularization ultrasound has always been the first choice. In fact angiography has its major limitation in the poor renal function of the patients undergoing this type of surgery. Moreover, due to its anterior location, the proximal anastomosis of an aorto-renal by-pass is not easily shown with the distal one in a single projection. For this reason a second shot is usually required, thus increasing the use of contrast dye. Four different studies aimed to report on intraoperative ultrasound for renal revascularization. In the first experience, Okuhn et al. [22] reported on 96 arterial reconstructions: out of these only 83 were renal. B-mode scans (narrowing, flap or thrombus), spectral broadening and flow velocities determined the classification of the examination as normal or abnormal. Sixtyfive arteries had normal findings (68%) and 31 abnormal (32%). A postoperative confirmatory examination was available for 73 of 96 arteries (76%). Assuming these examinations to be truthful, this means that intraoperative duplex findings among renal arteries have 85% sensitivity and 75% specificity. The Winston–Salem group published in 1991 their experience with intraoperative ultrasound [13]. In a 25month period they performed 41 renal reconstructions followed by intraoperative ultrasound. Only 35 patients with 57 arteries had follow-up, but in one case the examination was not satisfactory, leaving 56 arteries for analysis. Table 1.12.2 shows the classification of the defects used for this study. There were 13 defects. Seven minor
defects were not revised. Six major were revised: at revision the abnormality was confirmed to be present in all cases. Follow-up was obtained on all living patients (two deaths). Normal intraoperative findings resulted in a 98% patency at follow-up. Minor defects had a 100% patency (one case at autopsy). Among six major defects four arteries were patent, one had an early restenosis and one occluded. These results lead to 86% sensitivity and 100% specificity for intraoperative ultrasound. The Mayo Clinic experience was reported by Dougherty et al. [10]. In all, 35 patients had 64 arteries reconstructed. Intraoperative classification was similar to that used by Winston–Salem; only severely dampened systolic/diastolic flow was added as a major defect. Seven arteries were revised because of major defects (11%); in all cases ultrasound findings were confirmed at revision and in all but one the defect was correctable. Postoperative studies were obtained in 43 of 64 arteries. If we consider only a major defect as the primary end-point, intraoperative ultrasound had 100% sensitivity and 98% specificity. A more recent paper from van Weel et al. [34] reports on 73 renal revascularization procedures where both intraoperative duplex was performed and follow-up studies were available. Sixty-seven arteries (91.8%) were found to be normal at intraoperative duplex, while only six (8.2%) required revision. In only two cases was the presence of the defect confirmed at re-intervention. However, despite the absence of surgical correction, the subsequent duplex showed improvement of the parameters in all cases. The authors conclude that, assuming those four cases as true positive, duplex had 66.7% sensitivity and 100% specificity. In conclusion the available literature indicates that intraoperative duplex is an accurate mean of obtaining quality control during renal artery revascularization. This seems to be mandatory, especially if we consider that early occlusion has a prohibitive rate of kidney loss [14].
1.12.3 Lower Extremity By-pass Table 1.12.2 Classification of intraoperative duplex findings for renal artery revascularization. Presence of abnormal velocities in the absence of any kind of visible defect was classified as calibre mismatch between graft and native vessel PSV
B-mode
Normal
< 2.0 m/s
Normal
Minor defect
< 2.0 m/s
Abnormal
Major defect
> 2.0 m/s and turbulence
Abnormal
Five factors contribute substantially to maintaining the patency of lower extremity by-passes. They are: • appropriate inflow • appropriate outflow • low thrombogenicity of the conduit • absence of technical defects • individual factors such as the patient’s coagulation function.
122
1.12 Quality Control in Vascular Surgery
ography was performed. Among by-passes in the lower extremities, angiography showed technical problems in 2.2% of the grafts. Papers published later confirmed the role of completion angiography in the improvement of the patency of the reconstructions and its superiority to physical examination and CW Doppler. Mills et al. [20] performed a completion angiography at the end of the procedure on all but one of the 214 reversed vein by-passes. In 18 cases a technical error was shown (8%); femoropopliteal grafts had fewer defects (6%) than femorodistal ones (12%). In only three cases was the presence of a defect suspected on the basis of the physical examination or CW Doppler measurement. Early occlusion occurred in seven cases, but only in two of them was a technical defect found, leading to 90% sensitivity and 98% specificity for angiography. Marin et al. [19] evaluated 78 infrapopliteal by-passes to grade the lesions found at angiography into four classes. Six class I lesions did not require revision. Eighteen by-passes in classes I and II received minimal treatment, such as urokinase or papaverine infusion. Surgical revision was performed on 15 grade III lesions (total cut-off of the graft or outflow artery, opacification or irregular intraluminal filling defects of distal by-pass or outflow artery). When compared to 39 by-passes with no visible defect (class 0) classes I and II together showed no difference in their patency rates at 30 days and 1 year (87% and 82% versus 87% and 79%). Grade III lesions had poorer results (33% and 27%) despite surgical revision. The authors concluded that angiography might not always be able to define appropriately the extent of the problem associated with the defect. Later, angiography was further improved with the introduction of digital subtraction. However, this technique requires expensive equipment, trained personnel and a longer time to be performed. The advantage of angiography is the ability to provide information on both the reconstruction and distal run-off. This fact is particularly important in the emergent procedures: in these cases the surgeon often faces an unknown vascular tree, where the poor status due to the underlying disease can compromise any successful attempt to solve the acute problem (Fig. 1.12.1).
1.12.3.2 Ultrasound (CW Doppler, PW Doppler, Duplex, Colour Duplex) In the 1980s some authors explored the possibility of testing the reconstruction with CW Doppler and pulsed Doppler, in an effort to avoid using angiography. The re-
sults were encouraging, but the technology was still poor, not allowing different defects to be distinguished, such as valve cusps or the presence of a fistula [32]. With the introduction of duplex scanners and colour duplex scanners, the accuracy of this method increased. MacKenzie, of the McGill University in Montreal, reported on 78 infra-inguinal by-passes where duplex was used as an intraoperative control [18]. The cut-off used to determine the need for re-intervention was: PSV > 200 cm/s and < 45 cm/s and a velocity ratio >2. Thirty bypasses met the criteria for revision, but only 12 were reopened. In the latter group, surgeons felt the defects were reversible or not correctable. When they analysed the 6-months primary and secondary patency for the three groups, they found a significant difference between the first two groups (93% and 97% for the normal and 91% and 100% for the revised) when compared to the group that was not revised (53% and 71%); this result was confirmed by the log-rank test on the Kaplan–Meier curves (p<0.001). Doppler and later duplex have been extensively studied by the group of Bandyk. The landmark paper reported in 2000 on 626 infra-inguinal procedures receiving intraoperative duplex at the end of the procedure [16]. The protocol required a 30-mg papaverine injection inside the by-pass to be performed before scanning to obtain maximum vasodilatation of the run-off, thus enhancing the sensitivity of the test. Table 1.12.4 shows the classifica-
Fig. 1.12.2 Intraoperative duplex showed an end-diastolic velocity (EDV) of 0 cm/s and an increase in the peripheral vascular resistance (PVR) on the tibioperoneal trunk. The by-pass occluded a few days later despite aggressive antithrombotic and anticoagulant therapy
1.12.3 Lower Extremity By-pass
Table 1.12.4 Classification of intraoperative duplex findings for infra-inguinal by-passes. (Vr Velocity ratio) Stenosis category
PSV (cm/s)
Normal
Vr
Interpretation
<125
1–2
Moderate
125–180
2–2.5
Severe
180–300
2.5–5
>300
>5
High-grade
Normal Residual abnormality: rescan after a second papaverine dose. Consider angiography Significant abnormality. Revise or perform angiography Critical lesion: revise
Modified from [16]
Table 1.12.5 Algorithm for management of low-flow infra-inguinal by-passes. (LMWH Low molecular weight heparin, PVR peripheral vascular resistance) Category
Graft flow velocity
PVR
Interpretation and management
Normal
> 45 cm/s
Low
Normal graft flow: dextran and aspirin
Low flow, low PVR
< 45 cm/s
Low
Heparin or LMWH, dextran, aspirin
Low flow, high PVR
< 45 cm/s
High
Consider adjunctive procedure to increase flow; if not possible, treat as low flow graft
Low
Repair stenosis; heparin or LMWH, dextran, aspirin
Low flow, graft stenosis
> 200 cm/s at anastomosis
Modified from [16]
tion of the stenosis according to the parameters recorded. Ninety-six by-passes (15%) had major defects at duplex scan and 53 (8%) had minor defects, which were left unrepaired. All major defects were revised and only one was not confirmed at redo surgery. If 67 of them normalized after revision, 29 had a residual moderate stenosis, leaving a total of 82 arteries with moderate stenosis and 531 normal arteries for follow-up. Among the abnormal group the 90-days thrombosis/stenosis rate was 40%, which was significantly higher than the 2.5% rate for normal arteries. The aforementioned classification was used to grade only normal flow conduits. For this reason Bandyk considered another two factors for judging low-flow conduits: a PSV less than 45 cm/s and peripheral vascular resistance (PVR). Table 1.12.5 shows the algorithm used according to different patterns. It is remarkable to note that among 13 low-flow conduits, 38% developed a thrombosis within 3 months. Clearly the classification adopted from Bandyk applies only to normal-flow conduits. For this reason the group of Walsh and Cronenwett of New Hampshire [28] studied 45 infrapopliteal by-passes at high risk of failure: 20% had poor outflow (defined as small, <1 mm, arteries, need for endarterectomy at the anastomotic site or
no direct line to the foot); and 31% had “disadvantaged” conduits (composite grafts, sclerotic segments in the vein and spliced veins). At 12 months 25 were patent and 20 occluded. Two of them were found to have retained valve leaflets, while in 18 cases the reason was attributed to the poor outflow or disadvantaged conduit. Among failed by-passes PSV <45 cm/s failed to predict occlusion (35% sensitivity and 36% specificity). With regression analysis only EDV <8 cm/s was able to predict thrombosis at 12 months (p<0.05), with 76% sensitivity and 75% specificity (Fig. 1.12.2). It is important to note that all by-passes with EDV = 0 cm/s failed within 6 months. A recent paper compared, in a small series, duplex with angiography in a community hospital, resulting in a 100% correlation between the two methods [29]. However, angiography was more expensive (650 $) when compared to duplex (350 $) and took longer.
1.12.3.3 Angioscopy Angioscopy was introduced in the late 1960s, when Vollmar first used a rigid angioscope to evaluate an endar-
123
124
1.12 Quality Control in Vascular Surgery
terectomy performed with rings. Since then the improvement of technology and the introduction of optic fibres has led to smaller, flexible instruments. Its use is mainly limited to in situ vein grafts, where it allows direct visualization of the whole vein, allowing complete lyses of the valves and ligation of collateral branches. Gilbertson et al. [11] published the first series that compared angioscopy to angiography and duplex on this particular type of graft. Twenty patients underwent the three tests. Angioscopy had the best sensitivity for side branches (66% versus angiography 44% and duplex 11%; p<0.01) and cusps (100% versus 22% and 11%; p<0.01). Since none of the stenoses found were confirmed at revision, comparison needs to be performed using the false-positive rate: again angioscopy had the best results, with 0% compared to 20% for angiography and 10% for duplex. One of the advantages of this method is the possibility of immediately correcting the defects, by introducing operating instruments through the angioscope inside the vessel or allowing small skin incisions through the exact location of a side branch. The limit is mainly the cost and the difficulty of examining the distal anastomosis. The latter is particularly important, as this is the site where most of the defects are usually located.
1.12.3.4 Flowmetry Lepäntalo and coworkers in Finland have extensively studied this technique. Two recent papers from this group showed the benefits of flowmetry in predicting poor patency and stenosis development. In the first one [2], they recorded rest flow and maximum flow capacity, the latter by injecting 40 mg of papaverine before measurement. There was a significant difference (p<0.001) in the primary assisted patency for infrapopliteal by-passes with a maximum flow >90 ml/min and those with a flow <90 ml/min. In a logistic regression model aimed at finding predictors of 1-year failure, maximum flow capacity had a 0.53 relative risk for every 30 ml/min increase in blood flow (protective effect); this was highly significant (p<0.001). A later study divided the by-passes according to flow quartiles [15]. Using Kaplan–Meier survival analysis, the authors were able to correlate poor flow to the development of stenosis (10% at 2 years for the highflow group, compared to 39%, 38% and 36% for the other three groups; p=0.027). This was confirmed also at multiple regression analysis, where low flow and female sex were the only independent predictors.
1.12.3.5 Conclusions All the methods described above were able, when appropriately used, to provide accurate evaluation of the technical adequacy of lower extremity arterial reconstructions. It is our opinion that, due to its accuracy and lack of potential harm, duplex scan should be the first choice. Angiography is certainly preferred whenever outflow status knowledge is missing, such as during emergency procedures, and if a combined endovascular procedure is planned or potentially required. Angioscopy is undoubtedly best used for in situ vein grafts, but needs to be associated with another method able to provide information on the distal anastomosis. Flowmetry has the advantage of being the fastest and cheapest method, but its sensitivity is still poor and it seems to be a better predictor of mid-term results rather than technical adequacy.
1.12.4 Carotid Arteries The role for carotid endarterectomy in the prevention of stroke is well established. Randomized trials have confirmed its effectiveness when compared to best medical treatment. However, surgery needs to maintain high-level standards; in fact morbidity and mortality should be under 7% for symptomatic, and under 3% for asymptomatic, disease. To be able to obtain these results technical perfection is mandatory. Angiography was the first method tested as quality control. In 1978 Anderson et al. [3] reported on 131 angiographies. Seven patients (5.3%) had major defects, which were revised. Only three with complications related to angiography were observed: all of them required surgical correction (for carotid occlusion), and one of them resulted in a stroke. None of the patients revised for the presence of defects had complications. Coubier et al. [8] published a comparison between two consecutive series before and after the introduction of intraoperative angiography. Out of 100 patients in the second series, only 5 were revised due to major defect, while another 37 had minor defects (3 were spasms) and 58 had normal results. Among patients with normal angiography only 3.5% were found to have a restenosis at a mean follow-up of 19 months. When comparing clinical outcome in the two series, patients undergoing intraoperative angiography had 2% stroke rate; patients without angiography, 8.2%. However, there is a substantial differ-
1.12.4 Carotid Arteries
ence in the preoperative characteristics: only 38% were asymptomatic in the old series compared to 58% in the new one. When ultrasounds were first introduced, they did not obtain the expected results: Seifert and Blackshear [31] used CW Doppler on 229 carotid endarterectomies and found 30 abnormal cases: in 10 of them the internal carotid artery was involved. Two underwent immediate revision, while in 8 an angiography was performed. Five defects were confirmed, thus leading to 70% sensitivity only when compared to angiography. Dilley used B-mode echotomography to detect anomalies after endarterectomy and compared it to angiography [9]. Twelve defects were found in 158 patients (8.3%); four were found by both techniques, three by B-mode only and five by angiography only. These results confirmed angiography as the gold standard. In 1988 Bandyk compared angiography and duplex in 235 patients undergoing 250 CEA [5]. Duplex found 20 severe defects, but only 10 were confirmed by angiography. These patients were promptly revised and surgery confirmed the diagnosis. In another 10 carotids duplex indicated the presence of a severe flow disturbance, while no defect was visible at angiography. For this reason none was revised. Two of them experienced major neurological deficit in the recovery room and were revised. Both had a complete thrombosis and experienced a stroke; one patient died. Eight patients were asymptomatic, but developed restenosis of >50% in three cases and of <50% in the remaining five. This study showed that the more the ultrasound technology improved, the more this was able to overcome angiography. The problem encountered with duplex was that a lot of minor defects were visible and physicians were not sure about the behaviour of these lesions. Sawchuck studied the fate of 21 unrepaired minor defects found at duplex [30]. Only one flap of the external carotid artery occluded. Among nine defects on the internal, seven resolved and two developed a stenosis of <30%. An elegant paper from University of California, San Francisco (UCSF) reported in 1990 on 131 carotids where a completion duplex was performed at the end of the procedure [25]. They divided the carotid bifurcation into operated and nonoperated segments. They recorded if any segment was not visible or poorly visualized. They also classified the defects detected according to their size. Any defect in a nonoperated segment was defined as residual disease, while defects in the operated ones were flaps. Excluding the external carotid artery, only 10% of the com-
mon-internal segments were not visualized. This rate further reduced down to 5% if the proximal common carotid was not taken into consideration. The percentage of narrowing and length of the flap relative to segment diameter classified the defects. Fifteen arteries were found to have at least one defect at intraoperative control and were therefore revised. In seven cases the internal carotid was involved; the common carotid artery in three. Follow-up studies were performed at 1, 3 and 6 months. Restenosis was classified according to the percentage of narrowing from 0 (no restenosis) to 6 (100%). The authors built an ordinal logistic regression model using several local and systemic factors to predict the severity of restenosis. Among technical factors only intraoperative size defect predicted severity of restenosis (p=0.0175). Among systemic factors hypertension, smoking and cholesterol were positively associated with restenosis. Similar results were found by Kinney a few years later [17]. Among 461 carotids operated in 430 patients, 410 (89%) received an intraoperative duplex scan. An angiography was added in 268 of them, while the remaining 51 patients received physical examination and clinical inspection only. Twenty-six carotids were revised based on the classification in Table 1.12.6 (Figs. 1.12.3, 1.12.4). Three of them had moderate flow disturbance at redo duplex scan. After all revisions 337 arteries had normal flow, 73 moderate disturbance and 51 were unknown, not having had any test. At 1 month no strokes were recorded in the group not receiving any test. Seven strokes occurred in the 337 patients in the normal-flow group, compared to 3/73 (4.1%) among the moderate abnormal flow one (p=NS). This difference increased at 5 years (3.9% versus 9.3%) but still it was not statistically significant. Estimated survival analysis for freedom from restenosis showed a significant difference between normal duplex arteries when compared to either the untested group or the abnormal one. Multiple regressions indicated that female gender had 2.8 relative risk of developing carotid restenosis (95% CI 1.21–6.723; p=0.024), while normal completion duplex had a protective effect (RR 0.276; 95% CI 0.126–0.604; p=0.0015). Only normal duplex was significantly inversely related to long-term ipsilateral stroke (RR 0.173; 95% CI 0.031–0.965; p=0.037). Baker et al. [4] reviewed 316 carotids operated in 283 patients. They patched 153 vessels (48.4%), the remaining being primary closure. A 3-mm cut-off was used to distinguish between major and minor defects at intraoperative duplex (Fig. 1.12.5). This was positive in 254 arteries (80.4%) and abnormal in 62 (19.6%). Nine of
125
126
1.12 Quality Control in Vascular Surgery
Fig 1.12.3 Normal intraoperative duplex scan of a carotid artery. PSV reaches 60 cm/s
Fig. 1.12.5 Small flaps inside an operated internal carotid artery
Table 1.12.6 Classification of intraoperative duplex findings for carotid endarterectomy. (SB Spectral broadening) Grade Normal
Diameter reduction (%) 0–15
PSV (cm/s)
Spectral analysis
< 100 No or minimal SB
Mild
16–49
100–125 SB only in diastole
Moderate
50–75
126–150 SB in systole and diastole
> 75
> 150 SB in systole and diastole
Severe
Modified from [17]
Fig. 1.12.4 Abnormal velocities recorded during intraoperative duplex following carotid endarterectomy. A platelet aggregate is clearly visible. The PSV right after the defect is about 300 cm/s
them were major defects (14.5%); all of them were revised and the abnormality was confirmed at surgery in all but one (only turbulent flow). None of the 53 minor defects (85.5%) was reopened. Early stroke rate was 1.6%; duplex follow-up was done at 1 day, 6 months and then every 12 months. Among normal carotids four patients experienced a stroke (1.3%); this was not significantly different from the percentage for the group with unrepaired defects (1 stroke – 1.9%). Recurrent stenosis occurred in eight patients with normal intraoperative findings (3.1%),
four of them on the first postoperative day and four at late controls. Nine restenoses occurred among those 52 patients who had unrepaired defects (17.5%). The difference was highly significant (p=0.002). No neurological complications were recorded among patients revised and only one restenosis was seen at 6 months. A significant difference in restenosis rate was noted when patched arteries were compared to primary closure technique (2.6% versus 9.2%, p=0.025). Another recent study confirmed the correlation between unrepaired minor defects and restenosis. Padayachee studied 244 arteries [23]; in 76 cases a shunt was used and only 37 cases were patched. Intraoperative duplex found 52 stenoses: according to flow velocity 18 were severe stenosis of the internal carotid, but they re-
References
vised only 9 of them where a flap was associated with the increased PSV. This left 41 arteries with an untreated defect for follow-up and 172 with normal findings. In the latter group restenosis rate was 23%, significantly lower (p<0.0001) than the 51% observed in the normal one. It is interesting to note that all the nine arteries with severely increased flow velocity that were left untreated showed some kind of stenosis regression at follow-up. No correlation was shown between the presence of defects at intraoperative control and postoperative stroke or occlusion. A comparison between intraoperative duplex and angiography was the aim of a study by Valenti et al. [33]. They reported on 141 CEA on 138 patients. All arteries received an intraoperative duplex and angiography at the end of the procedure. The operating surgeon read the results. Thirty-six defects were detected, but only four were major defects, which required revision. Among 32 minor defects, duplex was able to pick up 28 of them, while only 19 were visible at angiography. These results led to 100% sensitivity and specificity for both techniques, but 87% specificity for duplex compared to 59% of angiography for minor defects. To conclude, the reported studies underline the importance of coupling morphology and physiological parameters. Flaps alone are often benign lesions, which improve with time and usually disappear during the remodelling that occurs after endarterectomy. At the same time increased flow velocity without visible defects might be caused by spasm or calibre change and rarely threaten the operated artery. Duplex scan can provide both kinds of information. It is relatively cheap, safe and accurate. The major flaw is that the operator needs adequate training and experience to be able to discriminate between small benign lesions and the others that can really jeopardize the short- and long-term results of the operation. References 1. Albäck A, Lepäntalo M (1998) Immediate occlusion of in situ saphenous vein bypass grafts: a survey of 329 reconstructions. Eur J Surg 164:745–750 2. Albäck A, Roth WD, Ihlberg L, Biancari F, Lepäntalo M (2000) Preoperative angiographic score and intraoperative flow as predictors of the mid-term patency of infrapopliteal bypass grafts. Eur J Vasc Endovasc Surg 20:447–453 3. Andersen CA, Collins GJ, Rich NM (1978) Routine operative arteriography during carotid endarterectomy: a reassessment. Surgery 83:67–71 4. Baker WH, Koustas G, Burke K, Littoy FN, Greisler HP (1994) Intraoperative duplex scanning and late carotid artery stenosis. J Vasc Surg 19:829–833
5. Bandyk DF, Kacbnick HK, Adams MB, Towne JB (1988) Turbulence after carotid bifurcation endarterectomy: a harbinger of residual and recurrent carotid stenosis. J Vasc Surg 7:261–274 6. Carmo M, De Angelis GAT, Tassinari L, Roveri S, Mercandalli G, Merlini D, Settembrini PG (2002) Controllo di qualità intraoperatorio con ecocolor doppler in chirurgia carotidea. In: Pratesi C, Pulli R (eds) Chirurgia della carotide extracranica. Minerva Medica, Turin, pp 292–298 7. Courbier R, Jausseran JM, Reggi M (1977) Detecting complications of direct arterial surgery. The role of intraoperative arteriography. Arch Surg 112:1115–1118 8. Courbier R, Jausseran JM, Reggi M, Bergeron P, Formichi M, Ferdani M (1986) Routine intraoperative carotid angiography: its impact on operative morbidity and carotid restenosis. J Vasc Surg 3:343–350 9. Dilley RB, Bernestein EF (1986) A comparison of B-mode real-time imaging and arteriography in the intraoperative assessment of carotid endarterectomy. J Vasc Surg 4:256–262 10. Dougherty MJ, Hallett JW, Naessens JM, Bower TC, Cherry KJ, Gloviczki P, James EM (1997) Optimizing technical success of renal revascularization: the impact of intraoperative color-flow duplex ultrasonography. J Vasc Surg 17:849–857 11. Gilbertson JJ, Walsh DB, Zwolak RM, Waters MA, Musson A, Magnant JG, Schneider JR, Cronenwett JL (1992) A blinded comparison of angiography, angioscopy and duplex scanning in the intraoperative evaluation of in situ saphenous vein bypass grafts. J Vasc Surg 15:121–129 12. Gloviczki P, Merrell SW, Bower TC (1991) Femoral vein valve repair under direct vision without venotomy: a modified technique with use of angioscopy. J Vasc Surg 14:276–279 13. Hansen KJ, O’Neil EA, Reavis SW, Craven TE, Plonk GW, Dean RH (1991) Intraoperative duplex sonography during renal artery reconstruction. J Vasc Surg 14:364–374 14. Hansen KJ, Deitch JS, Oskin TC, Ligush J, Craven TE, Dean RH (1998) Renal artery repair: consequence of operative failures. Ann Surg 227:678–689 15. Ihlberg LHM, Albäck NA, Lassila R, Lepäntalo M (2001) Intraoperative flow predicts the development of stenosis in infrainguinal vein grafts. J Vasc Surg 34:269–276 16. Johnson BL, Bandyk DF, Back MR, Avino AJ, Roth SM (2000) Intraoperative duplex monitoring of infrainguinal vein bypass procedures. J Vasc Surg 31:678–690 17. Kinney EV, Seabrook GR, Kinney LY, Bandyk DF, Towne JB (1993) The importance of intraoperative detection of residual flow abnormalities after carotid artery endarterectomy J Vasc Surg 17:912–923
127
128
1.12 Quality Control in Vascular Surgery
18. MacKenzie KS, Hill AB, Steimetz OK (1999) The predictive value of intraoperative duplex for early vein graft patency in lower extremity revascularization. Ann Vasc Surg 13:275–283 19. Marin ML, Veith FJ, Panetta TF, Suggs WD, Wengerter KR, Bakal C, Cynamon J (1993) A new look at intraoperative completion arteriography: classification and management strategies for intraluminal defects. Am J Surg 166:136–139 20. Mills JL, Fujitani RM, Taylor SM (1992) Contribution of routine intraoperative completion arteriography to early infrainguinal bypass patency. Am J Surg 164:506–511 21. Oderich GS, Panneton JM, Macedo TA, Noel AA, Bower TC, Lee RA, Cha SS, Gloviczcki P, Cherry KJ (2003) Intraoperative duplex ultrasound of visceral revascularizations: optimizing technical success and outcome. J Vasc Surg 38:684–691 22. Okuhn SP, Reilly LM, Bennett JB, Hughes L, Goldstone J, Ehrenfeld WK, Stoney RJ (1987) Intraoperative assessment of renal and visceral artery reconstruction: the role of duplex scanning and spectral analysis. J Vasc Surg 5:137–147 23. Padayachee TS, Arnold JA, Thomas N, Aukett M, Colchester ACF, Taylor PR (2002) Correlation of intra-operative duplex findings during carotid endarterectomy with neurological events and recurrent stenosis at one year. Eur J Vasc Endovasc Surg 24:435–439 24. Reed A, Mozes G, Carmo M, Andrews JC, Macedo TA, Gloviczki P (2004) Renal artery coverage during endovascular aortic aneurysm repair: proximal migration or misplacement of the graft. Persp Vasc Endovasc Surg 16:135–140 25. Reilly LM, Okhun SP, Rapp JH, Bennett JB, Ehrenfeld WK, Goldstone J, Stoney RJ (1990) Recurrent carotid stenosis: a consequence of local or systemic factors ? The influence of unrepaired technical defects J Vasc Surg 11:448–460 26. Renwick S, Royle JP, Martin P (1968) Operative angiography after femoropopliteal arterial reconstruction: its influence on early graft failure rate. Br J Surg 55:134–136
27. Robinson KD, Sato DT, Gregory RT, Gayle RG, DeMasi RJ, Parent FN, Wheeler JR (1997) Long term outcome after early infrainguinal graft failure. J Vasc Surg 26:425–437 28. Rzucidlo EM, Walsh DB, Powell RJ, Zwolak RM, Fillinger MF, Schermerhorn ML, Cronenwett JL (2002) Prediction of early graft failure with intraoperative completion duplex ultrasound scan. J Vasc Surg 36:975–981 29. Sawaqed RS, Podbielski FJ, Rodriguez HE, Wiesman IM, Connolly MM, Clark ET (2001) Prospective comparison of intraoperative angiography with duplex scanning in evaluating lower extremity bypass grafts in a community hospital. Am Surg 67:601–604 30. Sawchuck AP, Flanigan DP, Machi J, Schuler JJ, Sifel B (1989) The fate of unrepaired minor technical defects detected by intraoperative ultrasonography during carotid endarterectomy. J Vasc Surg 9:671–676 31. Seifert KB, Blackshear WM (1985) Continuous-wave doppler in the intraoperative assessment of carotid endarterectomy. J Vasc Surg 2:817–820 32. Spencer TD, Goldman MH, Hyslop JW, Lee HM, Barnes RW (1984) Intraoperative assessment of in situ saphenous vein bypass grafts with continuous-wave Doppler probe. Surgery 96:874–877 33. Valenti D, Gaggiano A, Berardi G, Ferri M, Mazzei R, Roda G, Palombo D (2003) Intra-operative assessment of technical defects after carotid endarterectomy: a comparison between angiography and colour duplex scan Cardiovasc Surg 11:26–29 34. van Weel V, van Bockel JH, van Wissen R, van Baalen JM (2000) Intraoperative renal duplex sonography: a valuable method for evaluating renal artery reconstructions. Eur J Vasc Endovasc 20(3):268–272 35. Walsh DB (2000) Technical adequacy and graft thrombosis. In: Rutherford RB (ed) Vascular surgery. Saunders, Philadelphia, p 720
Cerebrovascular Arteries
131
2.1 Haemodynamic Changes and Other Risk Factors for Complications During Carotid Procedures Hakan N. Parsson
2.1.1 Cerebral Blood Flow
Table 2.1.1 Cerebral blood flow pathology Loss of autoregulation
The brain’s ability to keep cerebral blood flow (CBF) relatively constant despite changes in systemic blood pressure (BP) is due to cerebrovascular autoregulation. The actual cerebral perfusion pressure (CPP) depends on the BP and the intracranial pressure (ICP). The aim with cerebral autoregulation is to keep CBF independent of systemic changes in BP. In clinical practice, transcranial Doppler (TCD) is commonly used for both dynamic and static measurements of intra-cerebral flow velocity as an indicator of cerebral perfusion [10]. Other methods less frequently used to measure cerebral perfusion include: • Arterio-jugular oxygen content difference, • Transit time flowmetry, • Cerebral oximetry, • Positron emission tomography (PET) [14]. Loss of autoregulation in areas of previous cerebral infarction and those compromised by recent embolization is well recognized [23] (Table 2.1.1). This makes the brain more vulnerable to changes in BP. The association of severe carotid artery stenosis with cerebral haemodynamic dysfunction has also been documented. Insufficient cerebral collateral flow during occlusion of the internal carotid artery (ICA), such as by cross-clamping or balloon occlusion, may also result in inadequate perfusion. It is also important to recognize the possibility of adequate ipsilateral flow (>100 ml/min) even in the presence of a severely stenosed ICA (>90%) [14].
2.1.2 General Complications During carotid endarterectomy (CEA) as well as carotid angioplasty and stent placement (CAS), a significant in-
Insufficient collateral flow Hypoperfusion Hyperperfusion (HPS) Intracerebral haemorrhage (ICH)
stability of BP is frequently noted and can result in both hypertension and hypotension [18, 21]. The mechanism behind systemic hypertension during and after carotid artery manipulation seems to be transient dysfunction of adventitial baroreceptors in the endarterectomized area [6]. Infiltration of local anaesthetic into the periadventitial tissue around the carotid sinus might abolish this response [3]. Release of metabolic factors such as renin, vasopressin and cranial norepinephrine has also been described [2]. Sudden increases in CBF due to removal of a significant stenosis may also contribute to the hypertension. Postprocedural hypertension is a critical finding associated with hyperperfusion syndrome (HPS) or intracranial haemorrhage (ICH). This has been well described following CEA and is associated with significant morbidity and mortality. The incidence of HPS after CEA is <3%, with symptoms such as irritability, seizure and confusion, and rarely progresses to ICH if treated in time. The incidence of HPS and ICH after CAS seems to be about equal to that after CEA [1, 7]. The mechanisms involved include a chronic low-flow CBF due to significant carotid artery disease in combination with impaired autoregulation. Following reperfusion, loss of ability to change resistance in response to BP changes results in increased CBF. Patients with severe (>90%) carotid stenoses may be predisposed to ICH, particularly with concurrent hypertension and contralateral carotid occlusion. A more intense haemodynamic monitoring and aggressive treatment of hypertension such as β-blockers, nitroprusside
132
2.1 Haemodynamic Changes and Other Risk Factors for Complications During Carotid Procedures
Table 2.1.2 General haemodynamic complications and treatment options Systemic hypertension
Nitroprusside, calcium antagonists, β-blockers
Systemic hypotension
Vasopressors, dopamine, phenylephrine
Bradycardia
Atropine
Table 2.1.3 Cerebral monitoring and protection General versus local anaesthesia Transcranial Doppler (TCD) Transit time flowmetry Arterio-jugular oxygen content difference Cerebral oximetry Positron emission tomography (PET)
and calcium antagonists are recommended (Table 2.1.2). A CT scan in patients with symptoms is recommended to exclude secondary haemorrhage and visualize cerebral oedema. Bradycardia sometimes in combination with hypotension is also frequently seen intraoperatively as well as in the immediate postoperative period. This has been attributed to increased activity from the carotid baroreceptors related to increased stretch and compliance in the arterial wall after removal of the atherosclerotic plaque. History of myocardial infarction (MI) also predisposes to postprocedural hypotension probably due to increased sensitivity of baroreceptors in patients with coronary artery disease. This is important during CAS too, which also involves manipulation of baroreceptors and the carotid sinus and contributes to haemodynamic instability. Bradycardia during CAS can be severe and result in asystole unless treated. Hypotension in the post dilatation period is common and adequate postprocedural monitoring of BP and electrocardiographic changes is important. Sameday discharge for patients after CAS may not be adequate with such a risk of instability [26]. Treatments include early administration of atropine and vasopressors. The need for significant pressor therapy may, however, contribute to postoperative myocardial ischaemia and infarction. In selected patients, prophylactic placement of a transvenous pacemaker can be used to treat periprocedural haemodynamic changes [6, 13].
2.1.3 Cerebral Monitoring and Protection During CEA Indications as well as methodology for cerebral monitoring and protection during surgical interventions are controversial issues. Several methods have been used to estimate adequate cerebral perfusion during ICA clamping (Table 2.1.3). Most patients have sufficient collateral flow
to allow for clamping without using a shunt, as demonstrated in CEA performed under local anaesthesia (LA). Shunting for ischaemia was necessary in 4.5% of all cases and in 19% of patients with contralateral occlusion using LA as the sole method for monitoring [15]. Four different approaches can be used to perform CEA with regard to cerebral monitoring and/or protection [12]: 1 Regional anaesthesia and shunting for patients who have changes in neurological status. 2 Deep general anaesthesia with no shunt. 3 General anaesthesia and use of cerebral monitoring such as TCD, EEG, stump pressure or oximetry. Patients with threshold values or changes are selectively shunted. 4 General anaesthesia with routine shunting. Regional anaesthesia is advocated by some clinicians because of the possibility of continuous neurological assessment and less haemodynamic instability. Disadvantages may include restlessness, anxiety and discomfort. It is well recognized that general anaesthetics have the ability to protect the brain during ischaemic conditions, mainly by decreasing oxygen demand (cerebral metabolic rate). Hypotension and tachycardia are frequent during general anaesthesia and often the administration of α1-adrenergic agonists such as phenylephrine is required, which in turn can lead to myocardial ischaemia. Controversy still exists over the optimal means for cerebral monitoring and anaesthesia, and no consensus has been agreed upon. An ongoing randomized clinical trial such as the GALA trial (General Anaesthesia vs Local Anaesthesia) might clarify these matters.
2.1.5 Adjuvant Medical Therapy
2.1.4 Cerebral Embolization during CEA and CAS Perioperative cerebral embolization during CEA or CAS is a potentially devastating complication and is probably correlated with the embolic potential of the plaque (Table 2.1.4). Echolucent plaques as measured by grey-scale median (GSM), obtained from standardized preoperative ultrasonography Duplex, seem to have increased plaque cellularity and a larger embolic potential [4, 11]. Some plaques also show thrombus associated with plaque rupture, indicating a possible vulnerable state [25]. This has been associated with an increased risk of stroke in both the preoperative and intraoperative period. Using ex vivo flow models, the highest embolic potential seems to be in the most severe stenoses. The use of preoperative statin treatment may reduce the amount of embolization, possibly by a stabilizing and anti-inflammatory effect [5]. Embolization during dissection and in particular during CA seems to be associated with the presence of an ulcerated plaque and associated thrombus. Intraoperative TCD monitoring can detect potentially harmful embolization during this stage, enabling the surgical technique to be modified appropriately [16]. The use of cerebral emboli protection devices during CAS, such as filters, can reduce the amount of embolization as measured by TCD [24] but currently no consensus has been agreed upon. Diffusion-weighted MRI (DWI) offers the possibility of visualizing even small and asymptomatic cerebral lesions shortly after their emergence. Recent studies have demonstrated more frequent ischaemic lesions after CAS as compared with CEA but the detected lesions did not cause neurological deficits [9, 20]. Following CEA or CAS the optimal flow surface should not be flow-limiting, and all embolic sources should be removed and minimally thrombogenic. Residual disease and technical defects are associated with perioperative strokes and restenosis. The aetiology includes:
Table 2.1.4 Cerebral embolization during carotid endarterectomy (CEA) and carotid angioplasty and stent placement (CAS) Embolic potential of the plaque During surgical dissection During CAS Postoperative embolization; technical problems
• • • •
Kinking of the vessel, Dissection, Flaps, Residual atheroma with embolic potential.
2.1.5 Adjuvant Medical Therapy Adjuvant medical therapy helps in decreasing the initial complication rate and includes pre- and postoperative antiplatelet agents [8] and perioperative anticoagulation (Table 2.1.5). Antiplatelet therapy should not be discontinued during the operative period. Agents include aspirin and clopidogrel. In a recent study preoperative clopidogrel in combination with aspirin significantly reduced the number of cerebral emboli as compared with heparin alone, however with some concerns of increased bleeding and an increased amount of ICH [19]. Intraoperative anticoagulation includes heparin, which promotes inactivation of thrombin and inhibits the activation of prothrombin. Ideally a target activated clotting time (ACT) should be used for heparin monitoring. However, heparin may, in combination with antiplatelet agents, predispose to postoperative bleeding. A recent study demonstrated increased platelet aggregation in response to arachidonic acid after heparin administration, despite adequate inhibition by aspirin administered preoperatively. This apparent reversal in antiplatelet activity persisted into the immediate early postoperative period, and could explain why a small proportion of patients are at increased risk for acute cerebrovascular and cardiovascular events despite aspirin therapy [27]. Heparin reversal by means of protamine carries an increased risk of postoperative complications. Several studies have demonstrated sustained micro-embolization in the immediate perioperative period following CEA as measured by TCD [17]. Intravenous administration of dextran seems to be beneficial in these situations. Abciximab, a nonselective glycoprotein IIb/IIIa inhibitor, has also been used during CAS with a
Aspirin Clopidogrel Heparin Dextran Abciximab Statins
Table 2.1.5 Adjuvant medical therapy
133
134
2.1 Haemodynamic Changes and Other Risk Factors for Complications During Carotid Procedures
reduced frequency of ischaemic stroke in high-risk patients. However, the benefit was lost because of an increased rate of ICH [22].
2.1.6 Conclusion The overall benefit of prophylactic CEA or CAS is dependent on the perioperative results regarding the combined risks of stroke and death. Major risk factors involve perioperative embolization and haemodynamic instability. Restoration of cerebral perfusion without neurological damage is the final endpoint. Meticulous techniques in respect to both the actual carotid lesion and cardiovascular care are extremely important in order to achieve a good outcome. References 1. Abou-Chebl A, Yadav JS, Reginelli JP, Bajzer C, Bhatt D, Krieger DW (2004) Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: risk factors, prevention, and treatment. J Am Coll Cardiol 43:1596–1601 2. Ahn SS, Marcus DR, Moore WS (1989) Post-carotid endarterectomy hypertension: association with elevated cranial norepinephrine. J Vasc Surg 9:351–360 3. Al-Rawi PG, Sigaudo-Roussel D, Gaunt ME (2004) Effect of lignocaine injection in carotid sinus on baroreceptor sensitivity during carotid endarterectomy. J Vasc Surg 39:1288–1294 4. Biasi GM, Froio A, Diethrich EB, Deleo G, Galimberti S, Mingazzini P, Nicolaides AN, Griffin M, Raithel D, Reid DB, Valsecchi MG (2004) Carotid plaque echolucency increases the risk of stroke in carotid stenting: the Imaging in Carotid Angioplasty and Risk of Stroke (ICAROS) study. Circulation 110:756–762 5. Bicknell CD, Cowling MG, Clark MW, Delis KT, Jenkins MP, Hughes AD, Thom SA, Wolfe JH, Cheshire NJ (2003) Carotid angioplasty in a pulsatile flow model: factors affecting embolic potential. Eur J Vasc Endovasc Surg 26:22–31 6. Bush RL, Lin PH, Bianco CC, Hurt JE, Lawhorn TI, Lumsden AB (2004) Reevaluation of temporary transvenous cardiac pacemaker usage during carotid angioplasty and stenting: a safe and valuable adjunct. Vasc Endovascular Surg 38:229–235 7. Coutts SB, Hill MD, Hu WY (2003) Hyperperfusion syndrome: toward a stricter definition. Neurosurgery 53:1053–1058
8. Engelter S, Lyrer P (2003) Antiplatelet therapy for preventing stroke and other vascular events after carotid endarterectomy. Cochrane Database Syst Rev CD001458 9. Flach HZ, Ouhlous M, Hendriks JM, Van Sambeek MR, Veenland JF, Koudstaal PJ, Van Dijk LC, Van Der Lugt A (2004) Cerebral ischemia after carotid intervention. J Endovasc Ther 11(3):251–257 10. Gaunt ME, Brown L, Hartshorne T, Bell PR, Naylor AR (1996) Unstable carotid plaques: preoperative identification and association with intraoperative embolisation detected by transcranial Doppler. Eur J Vasc Endovasc Surg 11:78–82 11. Goncalves I, Moses J, Pedro LM, Dias N, Fernandes e Fernandes J, Nilsson J, Ares MP (2003) Echolucency of carotid plaques correlates with plaque cellularity. Eur J Vasc Endovasc Surg 26:32–38 12. Hamdan AD, LoGerfo FW (2000) Should all patients be shunted? If not, how can I predict which patients will require a shunt? In: Naylor RA, Mackay WC (eds) Carotid artery surgery. Harcourt, London, pp 249–254 13. Harrop JS, Sharan AD, Benitez RP, Armonda R, Thomas J, Rosenwasser RH (2001) Prevention of carotid angioplastyinduced bradycardia and hypotension with temporary venous pacemakers. Neurosurgery 49:814–820 14. Kragsterman B, Parsson H, Bergqvist D (2004) Local haemodynamic changes during carotid endarterectomy – the influence on cerebral oxygenation. Eur J Vasc Endovasc Surg 27:398–402 15. Lawrence PF, Alves JC, Jicha D, Bhirangi K, Dobrin PB (1998) Incidence, timing, and causes of cerebral ischemia during carotid endarterectomy with regional anesthesia. J Vasc Surg 27:329–334 16. Lennard N, Smith J, Dumville J, Abbott R, Evans DH, London NJ, Bell PR, Naylor AR (1997) Prevention of postoperative thrombotic stroke after carotid endarterectomy: the role of transcranial Doppler ultrasound. J Vasc Surg 26:579–584 17. Mauney MC, Buchanan SA, Lawrence WA, Bishop A, Sinclair K, Daniel TM, Tribble CG, Kron IL (1995) Stroke rate is markedly reduced after carotid endarterectomy by avoidance of protamine. J Vasc Surg 22:264–269 18. Mendelsohn FO, Weissman NJ, Lederman RJ, Crowley JJ, Gray JL, Phillips HR, Alberts MJ, McCann RL, Smith TP, Stack RS (1998) Acute hemodynamic changes during carotid artery stenting. Am J Cardiol 82:1077–1081 19. Payne DA, Jones CI, Hayes PD, Thompson MM, London NJ, Bell PR, Goodall AH, Naylor AR (2004) Beneficial effects of clopidogrel combined with aspirin in reducing cerebral emboli in patients undergoing carotid endarterectomy. Circulation 109:1476–1481
References
20. Poppert H, Wolf O, Resch M, Theiss W, Schmidt-Thieme T, Graefin von Einsiedel H, Heider P, Martinoff S, Sander D (2004) Differences in number, size and location of intracranial microembolic lesions after surgical versus endovascular treatment without protection device of carotid artery stenosis. J Neurol 251:1198–1203 21. Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, Guterman LR, Hopkins LN (1999) Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke 30:2086–2093 22. Qureshi AI, Suri MF, Ali Z, Kim SH, Lanzino G, Fessler RD, Ringer AJ, Guterman LR, Hopkins LN (2002) Carotid angioplasty and stent placement: a prospective analysis of perioperative complications and impact of intravenously administered abciximab. Neurosurgery 50:466–473 23. Reinhard M, Muller T, Roth M, Guschlbauer B, Timmer J, Hetzel A (2003) Bilateral severe carotid artery stenosis or occlusion - cerebral autoregulation dynamics and collateral flow patterns. Acta Neurochir 145:1053–1059
24. Schmidt A, Diederich KW, Scheinert S, Braunlich S, Olenburger T, Biamino G, Schuler G, Scheinert D (2004) Effect of two different neuroprotection systems on microembolization during carotid artery stenting. J Am Coll Cardiol 44:1966–1969 25. Spagnoli LG, Mauriello A, Sangiorgi G, Fratoni S, Bonanno E, Schwartz RS, Piepgras DG, Pistolese R, Ippoliti A, Holmes DR (2004) Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke. J Am Med Assoc 292:1845–1852 26. Tan KT, Cleveland TJ, Berczi V, McKevitt FM, Venables GS, Gaines PA (2003) Timing and frequency of complications after carotid artery stenting: what is the optimal period of observation? J Vasc Surg 38:236–243 27. Webster SE, Payne DA, Jones CI, Hayes PD, Bell PR, Goodall AH, Naylor AR (2004) Anti-platelet effect of aspirin is substantially reduced after administration of heparin during carotid endarterectomy. J Vasc Surg 40:463–468
135
137
2.2 Extracranial Carotid Artery Disease José Fernandes e Fernandes, Luís Mendes Pedro
2.2.1 Introduction Ischaemic stroke represents a major health problem and an important cause of morbidity and mortality in several western countries [12]. Mortality from stroke ranges between 10% and 30% [61] and its survivors remain at a high annual risk of recurrent ischaemic events and mortality both from myocardial infarct and repeated stroke [76]. Atherosclerosis from supra-aortic vessels, especially from the common carotid bifurcation, is the major single aetiology of ischaemic stroke in developed countries as opposed to intracranial occlusive disease and cardioembolization. The association between internal carotid artery occlusion and severe ischaemic stroke was first credited to Savory [82], obtained from the autopsy of a woman
Fig. 2.2.1 First cerebral arteriogram performed by Egas Moniz
with a history of monocular blindness and contralateral hemiplegia and occlusion of the left carotid artery associated with bilateral subclavian occlusions. Subsequent descriptions were reported [33, 87] and in 1914 Ramsey Hunt published an important paper, which correlated the presence of diminished cervical carotid pulsations with intermittent neurological symptoms and drew attention to the need for “careful examination of the neck vessels” in such patients [49]. With the introduction of angiography, Egas Moniz [62] provided the first demonstration in vivo of occlusion of the internal carotid and stroke (Fig. 2.2.1) and also described the correlation between transient strokes and carotid bifurcation stenosis [63]. His observations were confirmed in subsequent studies using angiography [18, 51], although the established arteriographic technique routinely practised often failed to visualize the extracranial vessels [13, 42]. Embolization from carotid bifurcation lesions was suggested by Miller Fisher [35, 36] to be the pathogenic mechanism of ischaemic brain symptoms associated with extracranial carotid disease and led to the possibility of preventing stroke by eventual surgical correction of the diseased arteries. The most frequent lesion is stenosis at the common carotid bifurcation and origin of the internal carotid artery; however, atheroma of the aortic arch protruding into the ostia of the innominate and left common carotid arteries may cause severe flow-reducing stenosis and act as a source of cerebral embolization. Reconstructive surgery for chronic arterial occlusive disease started in Lisbon in 1947, with the introduction of endarterectomy by João Cid dos Santos [19], a technique conceived to be used for the obliteration of limb occlusive disease ideally in short segmental obstructions. The first carotid intervention was performed in Buenos Aires in 1951 by Carrea, Mollins and Murphy [17], consisting of resection of the proximal internal carotid segment and re-establishment of flow by anastomosing the external carotid to the distal internal carotid.
138
2.2 Extracranial Carotid Artery Disease
DeBakey [24] described the first carotid disobliteration in 1953, in a patient with a complete occlusion, which succeeded in restoring flow. Eastcott, in 1954 [27], performed the first successful elective carotid operation on a patient with internal carotid stenosis and multiple transient ischaemic attacks (TIAs) in order to prevent stroke, resulting in the patient remaining asymptomatic for more than 30 years. Successful endarterectomy of the innominate artery with a 2-year follow-up was described in 1956 [21], followed by several reports of correction of proximal and/or ostial lesions at the aortic arch through by-pass procedures. The development of arterial catheterization for arteriography [83] and its widespread use provided easier diagnosis of extracranial disease as a major cause of brain ischaemia and set the stage for the generalized use of carotid surgery, aiming to restore arterial perfusion to the brain and avoid distal atheroembolization to prevent severe ischaemic syndromes. The 80 multicentre cooperative studies, in both Europe and the USA [29, 70], provided level 1 evidence for the benefit of carotid endarterectomy (CEA) in patients with transient neurological symptoms (TIAs) and reversible stroke; for carotid stenosis it was greater than 70%, contributing to a more appropriate and rational use of CEA. Reduction of surgical risk and the need for specific accreditation of surgeons and institutions for the treatment of extracranial carotid disease were recognized [64] in order to ensure greater benefit from CEA. The selection of patients for surgical treatment, and the need to reduce overall morbidity and mortality in patient management, both for symptomatic and asymptomatic patients, must be considered; the impact of the new endovascular surgical procedures requires careful re-evaluation of established concepts, to offer the best available treatment for each patient, and to provide guidelines for institutions and individual practitioners dealing with extracranial carotid disease.
2.2.2 Pathogenesis of Brain Ischaemia The mechanisms of neurological dysfunction in extracranial carotid disease are: • Atheroembolization – from local thrombosis associated with unstable plaques [53, 88]
• Haemodynamic – with reduction of cerebral blood flow, associated with sudden occlusion of a carotid artery, severe bilateral disease and ostial stenosis in the aortic arch Local thrombosis in ulcerated plaques results from disruption of its endothelial surface and fibrous cap causing: • Ulceration or subintimal haemorrhage • Platelet and erythrocyte aggregation to the subendothelial layer • Distal embolization of the thrombus and debris from the plaque contents These events are associated with clinical symptoms and progression of the atheromatous plaque [5, 7, 37, 54]. High-definition ultrasonography [9, 72, 79] and magnetic resonance imaging [90, 91] allow in vivo visualization of carotid bifurcation lesions in patients with symptoms of brain ischaemia. It is possible to identify markers of plaque activity, such as: • Echolucency • Presence of heterogeneity in its echostructure • Presence of echolucent areas near the arterial lumen • Surface disruption and/or ulceration (Fig. 2.2.2), which correlates with the presence of ipsilateral appropriate neurological symptoms [72] • Increased levels of elastin degradation products, cellularity and DNA contents of the plaque [39–41] Stroke occurs when there is brain infarct due to local reduction of cerebral blood flow (CBF), which is maintained around 45–50 ml/100 g of tissue per min by the mechanisms of autoregulation, for systolic blood pressures between 60 and 130 mmHg [4, 23, 31, 38, 56, 60]. With flow reduction (CBF <16 ml/100 g tissue per min) there is cessation of electrical brain activity, flattening of the EEG and failure to synthesize biochemical neurotransmitters, but the neuron may still be viable. When CBF is <10 ml/100 g tissue per min, disruption of aerobic metabolism, reduction of depolarization of the cell membrane and cell necrosis occur, leading to infarct [38]. There is a central area of necrosis, surrounded by an area of impaired function but viable tissue known as the ischaemic penumbra, its extent depending upon the functional capability of the collateral circulation. The severity of the stroke is correlated with the location and extent of the brain infarct, and also with the dysfunction of the penumbra area, which may be recovered by re-establishment
2.2.2 Pathogenesis of Brain Ischaemia
Fig. 2.2.2 High-definition ultrasonographic markers of risk in carotid plaques
of arterial flow. Haemorrhagic transformation may occur in 20% to 40% of brain infarcts during the first week after onset of symptoms [32], which limits the scope of arterial intervention in acute stroke with established infarct [89]. The onset, severity and duration of the neurological symptoms associated with carotid disease depend upon several factors: • Progression of the atheromatous plaque and presence of structural alterations predisposing to local thrombotic events. • Location of the atheroembolic material and the extent of the brain tissue area with flow impairment. • Compensation by the collateral circulation, with functional integrity of the circle of Willis and patency of the remaining extracranial arteries. The presence of transient or reversible neurological symptoms carries a higher risk of stroke at 1 year, repre-
senting a 16-fold increase when compared to the age- and sex-matched normal population. The European Carotid Surgery Trial (ECST) and North American Symptomatic Carotid Endarterectomy Trial (NASCET) confirmed a significant risk of stroke in patients with stenosis ≥70%, despite adequate antiplatelet treatment with aspirin [29, 70]. The stroke risk with severe incapacitating deficit increases to 60% and 70% in patients with progressing stroke. Asymptomatic carotid stenosis has an annual risk of ipsilateral stroke of between 1% and 2% [45, 59], but recent observations from multicentre randomized studies suggest that a significant risk reduction of stroke may be achieved by CEA in the presence of stenosis greater than 70% [30, 66]. Also, this benefit may be enhanced by the identification of high-risk lesions [68], that is those with higher potential for instability and embolization where a 5.3% annual risk of ipsilateral stroke was demonstrated.
139
140
2.2 Extracranial Carotid Artery Disease
2.2.3 Clinical Manifestations 2.2.3.1 Amaurosis fugax • Monocular sudden loss of vision lasting for seconds or minutes, followed by full recovery of the normal vision. • Often related to atheroembolization from the carotid plaque, consisting mainly of cholesterol crystals, into the retinal vessels (Fig. 2.2.3). • Recent studies seem to suggest reduced risk of ipsilateral stroke in patients with amaurosis fugax when compared with hemispheric transient ischaemic attacks (TIAs) [86].
2.2.3.2 Transient/Reversible Cerebral Ischaemia Its clinical manifestations result from neurological dysfunction in the territory of the internal carotid artery and its main branches, the anterior and middle cerebral arteries. They can be: • Transient (TIAs), when lasting less than 24 h with full recovery. • Reversible, when the symptoms disappear after 24 h without neurological deficit. Symptoms depend upon the involved area, giving rise to contralateral motor and/or sensory deficit. Dysphasia/aphasia may also arise following dominant hemisphere lesions. • Crescendo TIAs, characterized by a succession of TIAs in a short period of time which could correspond to multiple embolization from active carotid plaques carrying an increased risk of permanent neurological deficit.
2.2.3.3 Established Stroke • A major neurological deficit lasting for more than 24 h with/without partial recovery, which may determine physical incapacity.
Fig. 2.2.3 Histologic examination of a carotid plaque removed by endarterectomy with cholesterol crystals surrounded by inflammatory infiltrate
2.2.3.5 Global Cerebral Ischaemia 2.2.3.4 Stroke in Evolution (“Waving and Waning”) • Persistent neurological dysfunction, with repeated exacerbations, corresponding to dysfunction of the ischaemic penumbra area.
• Progressive deterioration of the intellectual capacities. • Related to reduced cerebral perfusion associated with multiple occlusive lesions in the supra-aortic vessels.
2.2.4 Diagnosis
2.2.3.6 Asymptomatic Carotid Disease • Often associated with cervical bruits. • More prevalent in patients with atherosclerotic occlusive lesions in other territories (coronary and lower limbs). • May represent an increased risk of stroke without warning. • The specificity of cervical bruit as an indicator of carotid disease is only 50%, its absence being recognized in complete carotid occlusions or pre-occlusive stenosis with a residual luminal diameter <2 mm, where turbulence may be insufficient to produce an audible bruit.
2.2.4 Diagnosis 2.2.4.1 Arteriography • Arteriography has been the gold standard technique to demonstrate extracranial carotid occlusive disease. • It outlines the inner surface of the arterial wall by providing direct visualization of blood flow inside the artery acting as a mould of the lesions from the arterial wall. • It was first obtained by direct puncture of the common carotid. • Following the development of arterial catheterization, it became standard practice to do it through selective retrograde catheterization, from the femoral or brachial/axillary arteries, providing full visualization of the extracranial vessels (Fig. 2.2.4) and also of the intracranial circulation. • It provides no direct visualization of the arterial wall and its morphologic alterations, thus limiting its ability to reveal the underlying changes leading to stenosis or occlusion. • Its use as a diagnostic tool in extracranial carotid disease was limited by local complications from arterial access (haematomas, false aneurysms) requiring treatment, allergic reactions to the contrast and deterioration of renal function. • Digital subtraction techniques and the introduction of safer nonionic contrast media reduced its complications and improved the outcome of carotid arteriography, although recent published results [30] documented a stroke risk of 1.2%.
Fig. 2.2.4 Angiography of the carotid bifurcation showing a complex stenotic lesion involving the first portion of the internal carotid artery
2.2.4.2 Colour Flow Duplex Scan • Colour flow Duplex scan was introduced by Strandness et al. [85]. • It was a major turning point in vascular diagnosis, by providing safe, noninvasive and reliable technology to evaluate both the morphological changes within the arterial wall and their repercussions on blood flow. • It combines real-time B-mode ultrasound imaging technology with a pulsed Doppler flow detector and spectral analyser. • The effect of arterial stenosis on flow is recognized by acceleration with a significant increase in peak systolic and diastolic velocities in association with increased disorganization of the velocity spectra (Fig. 2.2.5c).
141
142
2.2 Extracranial Carotid Artery Disease
Fig. 2.2.5a–c Quantification of the degree of stenosis by colour flow Duplex scan. a Diameter measurement of longitudinal section. b Area measurement on cross-section. c Haemodynamic assessment with peak systolic and end diastolic velocities calculation
Fig. 2.2.6 Computer-assisted carotid plaque analysis and determination of echogenicity using the GSM and P40 parameters
Several limitations of colour flow Duplex scan are recognized: • Difficult insonation at the base of the neck with failure to identify proximal stenotic lesions (innominate artery, left common carotid) that may require treatment, suspected by abnormal velocity tracings in the proximal common carotid artery. • Impossibility to visualize the distal segments of the internal carotid artery, which may be diseased (distal and/or siphon stenosis).
• Distinction between high-grade stenosis and complete occlusion, which could be overcome by new technological advances for recording low velocities and the use of acoustic contrast [57]. • Absence of information on the intracranial circulation and detection of stenosis and arterial aneurysms. • The clinical relevance of concomitant intracranial occlusive disease for the management of extracranial carotid disease has been controversial; siphon stenosis is rare – <6% – and its significance as a risk factor af-
2.2.4 Diagnosis
fecting the outcome of carotid endarterectomy or as a cause of recurrence of symptoms has not been confirmed [77]. • Cerebral aneurysms are also a rare event (<2%) [2] and can be suspected on the basis of clinical symptomatology, or by modern brain imaging techniques.
2.2.4.3 High-resolution Ultrasonography • High-resolution ultrasonography (HDU) with computerized analysis of the plaque structure provides a more precise and detailed study of the arterial wall and also objective measurement of plaque echogenicity, expressed as gray scale median (GSM) and P40 (percentage of pixels of echolucency) (Fig. 2.2.6) [73]. • Markers of plaque instability, such as disruption of its cap, ulceration, juxta-luminal location of echolucent areas and plaque heterogeneity, as described previously [73], can be identified. • These markers are powerful new tools for diagnosing vulnerable carotid plaques, monitoring their progression and assessing the potential effect of new pharmacological agents. • These wall changes identified by HDU may have clinical relevance, particularly in asymptomatic patients; in fact, plaque ulcerations identified by angiography represent an independent risk factor for cerebral events, with a cumulative effect, in association with the degree of stenosis [78].
2.2.4.4 Measuring the Degree of Stenosis • Appropriate measurement of degree of stenosis is essential for treatment selection [29, 30, 66, 70]. • Different methods have been suggested based on arteriography (Fig. 2.2.7) and discrepancies between these methods have been reported [69]. • Discrepancies can be overcome by B-mode ultrasonography and colour flow Doppler assessment, which provides accurate measurements of diameter and area reduction in complex and eccentric lesions (Fig. 2.2.5b). • Transcervical measurements have an excellent correlation with intraoperative evaluation of cross-sectional area reduction, obtained previously to endarterectomy.
Fig. 2.2.7 Most common methods for quantification of carotid stenosis by angiography
• Transcervical measurements combined with flow velocity changes provide higher specificity for the identification of severe carotid stenosis [71].
143
144
2.2 Extracranial Carotid Artery Disease
2.2.4.5 Transcranial Doppler Examination • Transcranial Doppler examination (TCD) was first described by R. Aaslid [1] for the diagnosis of intracranial severe stenosis, and to assess the patency and function of the circle of Willis. • It can be obtained with colour flow Duplex imaging, allowing more precise evaluation of the intracranial arteries and it should be included in the overall evaluation of the patient suspected of having carotid artery disease. • Colour flow Duplex scan and TCD provide information equivalent to the classic four-vessel arteriography, without its risks, and are used routinely in our practice.
2.2.4.6 Other Flow-imaging Techniques • Other flow-imaging techniques such as MR angiography and rapid sequence CT scans of the neck may provide useful information; their accuracy and reproducibility are not superior to those of the colour flow Duplex scan when performed by an experienced operator, and their evaluation tends to overestimate the degree of stenosis [74].
2.2.4.7 Indications for Arteriography The present indications for arteriography in our practice today are limited to: • Failure to meet the requirements for adequate colour flow Duplex scan. • Patients with nonhemispheric symptoms and evidence of multi-vessel occlusive disease on the Duplex scan examination. • Suspicion of proximal/ostial stenosis amenable to treatment by endovascular procedures. • Patients with stroke-in-evolution considered for carotid surgery, where it may be useful to exclude significant occlusions of the intracranial vessels. • Suspicion of severe siphon stenosis which could be treated by endovascular interventions.
2.2.4.8 Computerized Tomography and Magnetic Resonance Imaging • It is mandatory that all patients for whom carotid intervention is proposed undergo a preoperative brain imaging study, with either computerized tomography (CT) or magnetic resonance imaging (MRI). • CT and MRI provide direct visualization of the brain and are important for the investigation of patients with cerebrovascular disease. • Using these techniques enables distinction between ischaemic infarct and haemorrhage [8, 81], essential information for the proper management of acute strokes. • The precise location and type of ischaemic infarct may bear clinical relevance: cortical and subcortical lesions may correspond to atheroembolic phenomena, watershed infarcts are more common in the presence of haemodynamic impairment of cerebral blood flow and deep lacunae small infarcts are usually associated with small-vessel disease [25]. • Routine use of CT scan investigations in patients with TIAs confirmed the presence of unsuspected, silent infarcts [22, 48], which may increase the risk of carotid surgery. • Cerebral atrophy – leuko-ariosis – may be associated with carotid disease and reduced survival following carotid surgery (NASCET). • There is a clear advantage on the use of MRI over CT scan, despite its higher costs, particularly in acutely symptomatic patients. • The new weighted-diffusion techniques may detect early unsuspected infarcts, provide assessment of the status of the blood–brain barrier and are essential for identifying a subgroup of patients with acute stroke that could benefit from early carotid intervention without a significant increase in haemorrhagic transformation of an ischaemic infarct [3, 67].
2.2.4.9 Examination of the Retina • Overlooked in more recent practice. • The classical description of the Hollenhorst plaque [45] with bright cholesterol crystals impacted in the retinal vessels with associated localized infarct has been confirmed by several observations in patients with amaurosis fugax.
2.2.5 Selection, Treatment and Results
• There are some specific retinal alterations in giant-cell arteritis [47] and it is important to recognize occlusion of the central retinal artery, a condition rarely associated with atheroembolization, from a carotid lesion and a potential cause of severe and persistent unilateral blindness.
2.2.5 Selection, Treatment and Results 2.2.5.1 Medical Treatment • Medical treatment is based on the use of antiplatelet medication with aspirin [26], ticlopidine and clopidogrel [15].
Aspirin • Several trials have shown the advantage of aspirin over placebo in the prevention of stroke [14, 34]. • Data from both ECST and NASCET confirmed the advantage of aspirin over surgical treatment in patients with minimal carotid disease and stenosis <30%. • The exact dose of aspirin remains controversial; in both multicentre trials it was 300 mg daily, but there is a trend to reduce its dosage to 150 mg daily.
• Floating thrombus in the carotid bifurcation • Patients with pre-occlusive stenosis before surgery Long-term anticoagulation is not recommended except for patients with atrial fibrillation because of the risk of haemorrhagic complications.
Correction of Metabolic Risk Factors for Atherosclerosis Correction of metabolic risk factors for atherosclerosis should be carried out thoroughly and are integral parts of adequate management of atherosclerosis: • Cessation of smoking • Correction of dyslipidaemias • Diabetes mellitus • Control of hypertension • Appropriate correction of hyperhomocysteinemia with folic acid Statins have been shown to reduce the incidence of stroke [44] and to have a stabilizing effect on the atheromatous plaque [20] beyond its effect on lowering cholesterol. Its routine use in diabetic patients with arterial disease has been recommended recently [84] to reduce cardiovascular events, but as yet there is no definitive evidence that it should be used in all patients despite a normal cholesterol level.
Antiplatelet Treatment 2.2.5.2 Surgical Treatment • Antiplatelet treatment is also indicated because of concomitant coronary artery disease and during the peri-operative period following endarterectomy, to reduce platelet aggregation and thrombus formation in the operated segment [55]. • Long-term antiplatelet therapy should be maintained to reduce the incidence of cardiovascular events, particularly in those patients with evidence of systemic atherosclerosis.
Surgical treatment is dominated by carotid bifurcation endarterectomy, proven to be effective in the prevention of stroke for symptomatic patients with transient or reversible ocular and hemispheric dysfunction associated with stenosis >70% and also in asymptomatic patients [29, 30, 70] with severe stenosis.
Moderate Stenosis Anticoagulation Anticoagulation with unfractionated heparin, warfarin or low-molecular weight heparins may be indicated in: • “Crescendo” TIAs • Waning and waving neurological deficits
For moderate stenosis (50–70%) the benefit of endarterectomy in patients with (1) TIAs (single or multiple) or crescendo with or without plaque ulceration, or (2) mild or moderate stroke irrespective of antiplatelet therapy was evident, if neurological morbidity and mortality of the procedure was kept under 5% [6].
145
146
2.2 Extracranial Carotid Artery Disease
Asymptomatic Patients In asymptomatic patients several factors, other than the severity of stenosis, should be considered: • Presence of contralateral carotid occlusion • Ipsilateral brain infarcts and leuko-ariosis detected in pre-operative CT/MR scans [50] • The structure of the atheromatous plaque In fact, there is some criticism of the data from both the Asymptomatic Carotid Atherosclerosis Study (ACAS) and ACST, prompted by the following observations: • The need to perform a substantial number of operations to prevent a single stroke. • Operation with a risk <3%, probably not achievable outside centres of excellence. • Heterogeneity of asymptomatic carotid disease, with different stroke risks, and the need to identify a subgroup of patients with a higher risk of stroke [68]. Surgical decision requires careful evaluation of the overall risk for the individual patient, the presence of concomitant cardiac and respiratory disease and also the individual surgeon’s experience and institutional capabilities.
Patients with Severe Coronary Disease • Patients with severe coronary disease require careful evaluation and should be appropriately treated, either by surgery or pharmacotherapy. • Routine use of β-blockers has been recommended to reduce peri-operative myocardial infarct in patients with arterial disease [75]. • Prophylactic carotid endarterectomy, particularly in the presence of severe bilateral stenosis or associated contralateral occlusion, may be required before coronary revascularization to reduce the incidence of postoperative stroke [80].
Stroke • Established stroke with partial recovery carries a higher risk of repeated neurological events and mortality [65]; there is indication for endarterectomy, despite its higher risk than for TIAs or reversible stroke. • For acute stroke there is evidence that prompt intervention in adequately selected noncomatose patients,
and in whom there is evidence of a viable area of ischaemic penumbra confirmed by functional imaging techniques (diffusion-weighted NMR and/or positron-emission tomography), may benefit the patient by reducing the severity of the stroke. However, this should only be carried out within strict experimental protocols [11] because of the high risk of intracerebral haemorrhage. Appropriate selection of patients and reduced surgical risk are essential factors to support the efficacy of carotid artery surgery in the prevention of stroke; reduction of its associated morbidity and mortality is a major requirement to be pursued in all centres dealing with these patients.
2.2.5.3 Technique of Carotid Endarterectomy Carotid endarterectomy (CEA) can be performed under general or regional anaesthesia and requires full cardiac and blood pressure monitoring. Transcranial Doppler is a major adjuvant for: • Identifying embolic events (microembolic signals, MES) that may occur during surgical dissection. • Deciding whether to use shunt when the operation is performed under general anaesthesia. • Assessing function and cerebral flow post-operatively. Persistent MES after carotid declamping and/or in the recovery room may represent an increased risk of thrombus formation at the operated carotid and subsequent stroke. Longitudinal or oblique (skin crease) cervical incision is performed and exposure of the carotid bifurcation obtained by division of the facial vein. Careful dissection is mandatory to avoid iatrogenic lesions of the hypoglossal, vagus and recurrent laryngeal nerve, causing dysphonia and hoarseness; unnecessary manipulation of the arteries should be avoided to prevent cerebral embolization. Heparin (2500–5000 U) is routinely administered before clamping and a longitudinal arteriotomy is performed from the distal common carotid to the internal carotid as far as the end of the plaque. Subsequent steps of the operation are shown in Fig. 2.2.8. Insertion of a shunt to preserve flow depends upon the appearance of appropriate neurological symptoms when the operation is performed with the patient awake, or based upon indirect evidence of insufficient collateral flow assessed by:
2.2.5 Selection, Treatment and Results
Fig. 2.2.8 Carotid endarterectomy: plaque removal and final aspect before artery closing
147
148
2.2 Extracranial Carotid Artery Disease
• A carotid stump pressure <50 mmHg • A 50% reduction in flow velocity detected in the middle cerebral artery by TCD if the operation is performed under general anaesthesia. To remove the plaque, dissection is initiated in a sub-adventitial plane using the Watson–Cheyne dissector and it is carried out meticulously, separating the lesion from the arterial wall. Complete removal of the lesion should always be attempted; when the dissection is in the correct plane the plaque “feathers out” distally, so tacking sutures of the distal intima are very seldom required. Clearing of the external carotid artery ostium and of its initial segment is performed routinely, and proximally, in the common carotid, the lesion is cut with scissors to avoid fragmentation and irregularities. Extreme care is taken to remove all remaining fragments of plaque and intimal flaps, which may be a source of secondary embolization or lead to secondary thrombosis. The arteriotomy is routinely closed with a Dacron patch, aiming to enlarge the artery and to prevent early recurrent restenosis secondary to proliferative fibrosis [71], to correct kinking of the artery immediately distal to the endarterectomized segment and to reduce post-operative neurological morbidity [28]. Clamps are released sequentially in order to allow an initial flush through the external carotid and to prevent cerebral embolization. Vein can also be used, but there is no convincing evidence of its additional advantage over the Dacron patch. Peri-operative completion assessment is routinely performed with colour flow Duplex scan to identify technical defects such as thrombus, floating flaps >2 mm or residual stenosis, which, if present, require prompt correction. Monitoring with transcranial Doppler is continued in the recovery room to detect brain embolization; if there is evidence of repeated high-intensity transient signals (HITS), this could correspond to thrombus formation at the endarterectomized segment. Administration of 250 ml Dextran 40 is performed intravenously, and usually this is sufficient to ensure its disappearance. However, if there is persistence of HITS despite Dextran administration, immediate cervical re-exploration is carried out, the arteriotomy opened and thrombectomy of the carotid artery performed to prevent a major stroke [43]. Drainage is always applied and routine closure of subcutaneous tissues and skin performed after careful inspection and perfect haemostasis. Other techniques have been described, such as eversion endarterectomy. Details of this technique can be
Table 2.2.1. Early results of carotid endarterectomy. (TIA Transient ischaemic attack) Morbidity and mortality < 30 days Asymptomatic disease
0.7 % (1/129)
TIAs/reversible stroke
1.5 % (6/376)
Stroke with partial deficit
4.8 % (2/41)
Acute stroke
10 % (1/10)
found in this volume in Chapter 2.3, Reversed Carotid Endarterectomy, by D. Kiskinis. Our preference is for conventional endarterectomy and our personal experience is based upon 556 patients and 610 procedures, two-thirds symptomatic patients, either TIAs or reversible strokes, and the overall morbidity and mortality was 1.7%. Its stratification according to clinical presentation is as in Table 2.2.1. Complications of CEA in our patients were acute thrombosis in three patients, leading to major stroke and death in two; two patients had haemorrhagic stroke, with full recovery after several weeks and two patients died during the first 30 days postoperatively, one from pulmonary embolus and the second from acute myocardial infarct. Peripheral nerve injuries have been described in association with CEA; in our patients its incidence was 2.5%, mainly dysphonia due to vocal cord paralysis and reversible in all patients except one, who required transient tracheotomy followed by laser segmental cord resection, because of contralateral cord paralysis following previous stroke. Neck and submandibular paraesthesia are common and transient. The impact of completion assessment in our practice was analysed in a consecutive group of 114 patients; 4 required immediate re-operation to correct minor defects such as free-floating flaps, thrombi at the endarterectomy area and/or significant residual stenosis. There was no mortality or neurological morbidity in this group of patients. Long-term results were analysed during a follow-up period, mean 48 months, ranging from 6 to 120 months; restenosis was identified by colour flow Duplex scan and its overall incidence was 7.5%, but for >70% it was only 3.3%, and the majority were asymptomatic. The annual stroke incidence in the operated patients was 0.9% and the major cause of death in this group was myocardial infarct.
2.2.6 Endovascular Treatment
2.2.6 Endovascular Treatment Kerber et al. [52] reported the first dilatation of the proximal common carotid during conventional endarterectomy of a bifurcation lesion, and it was followed by several anecdotal reports of cases where the procedure was attempted with several degrees of success. Mathias [58] performed the first successful transluminal angioplasty (PTA) of a carotid bifurcation stenosis and a surge of enthusiasm followed several reports confirming the feasibility, safety and patency of the carotid arteries following PTA. The advantages of endovascular treatment are obvious: • Absence of surgical incision • Ability to perform the procedure under local anaesthesia • Monitoring of the neurological status of the patient during the procedure • Avoidance of peripheral nerve injuries. Disadvantages have also been recognized: • Embolism during manipulation (crossing the lesion with guidewires and balloons, balloon inflation and deflation during PTA) • Acute thrombosis • Spasm and failure to treat some calcified lesions. Carotid tortuosity and the specific anatomy at the aortic arch and origin of the supra-aortic vessels may cause additional difficulties for selective carotid catheterization, and increase the risk of peri-procedural cerebral embolization.
Fig. 2.2.9 PTA/stenting of the innominate artery
Details on endovascular treatment can be found in Chapter 2.6, Endovascular Treatment of Carotid Stenosis, by T. Gerasimidis. The durability of endovascular treatment needs to be determined with accuracy; results vary from 10% to 25%; early restenoses have been reported, although recent series suggest a restenosis rate of between 5% and 10%. Refinement of endovascular procedures, with the development of new and more suitable stents, increased experience and adequate selection of the lesions [10] will yield better results in the future. Prospective randomized studies comparing carotid angioplasty and stent placement (CAS) and CAE will be required to provide definitive evidence of the relative merits and indications of CAS compared to the established procedure of CAE. For ostial lesions of the innominate and of the left common carotid arteries PTA/STENT has been reported as a durable and safe procedure as shown in Fig. 2.2.9, reducing the indication for conventional open surgery with median sternotomy or extra-anatomic by-pass reconstructions.
2.2.6.1 What are the Established Indications for Endovascular Procedures in Extracranial Carotid Disease? Published evidence [16] suggests that PTA/STENT may yield comparable or better results than conventional surgery for: • Early restenosis following carotid bifurcation endarterectomy, a fibrous lesion which seems to be associat-
149
150
2.2 Extracranial Carotid Artery Disease
ed with a smaller embolic risk than the atheromatous lesion, and wherever conventional surgery may cause higher incidence of peripheral nerve injury. • Radiation arteritis and “hostile neck” situations. • Distal lesions of the internal carotid artery inaccessible to conventional surgery. • Ostial disease of the innominate and common carotid arteries. References 1. Aaslid R, Markwalder TM, Nornes H (1982) Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg 57:769–774 2. Akers DL, Bell WH 3rd, Kerstein MD (1988) Does intracranial dye study contribute to evaluation of carotid artery disease? Am J Surg 156:87–90 3. Albers G, Lansberg M, Norbash A et al (2000) Yield of diffusion-weighted MRI for detection of potentially relevant findings in stroke patients. Neurology 54:1562–1567 4. Astrup J, Siesjo BK, Symon L (1981) Thresholds in cerebral ischaemia. The ischaemic penumbra [editorial]. Stroke 12:723–725 5. Badimon JJ, Gallo R, Badimon L et al (1998) The role of atherosclerotic plaque disruption and thrombosis in acute coronary heart disease. In: Mercuri M, McPherson DD, Bassiouny H, Glagov S (eds) Non-invasive diagnosis of atherosclerosis. Kluwer, Boston 6. Barnett HJ, Taylor DW, Eliasziw M, Fox AJ, Ferguson GG, Haynes RB, Rankin RN, Clagett GP, Hachinski VC, Sackett DL, Thorpe KE, Meldrum HE (1998) Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 339:1415–1425 7. Bassiouny HS, Sakaguchi Y, Mikucki SA, McKinsey JF, Piano G, Gewertz BL, Glagov S (1997) Juxtalumenal location of plaque necrosis and neoformation in symptomatic carotid stenosis. J Vasc Surg 26:585–594 8. Bentsson JR (1996) Computed tomography in stroke. In: Moore WS (ed) Surgery for cerebrovascular disease. Churchill Livingstone, New York, pp 201–216 9. Biasi GM, Sampaolo A, Mingazzini P, De Amicis P, El Barghouty N, Nicolaides NA (1999) Computer analysis of ultrasonic plaque echolucency in identifying high risk carotid bifurcation lesions. Eur J Vasc Endovasc Surg 17:476–479 10. Biasi GM, Frio A, Diethrich EB et al (2004) Carotid plaque echolucency increases the risk of stroke in carotid stenting. Circulation 110:756–762
11. Biller J, Feinberg WM, Castaldo JE, Whittemore AD, Harbaugh RE, Dempsey RJ, Caplan LR, Kresowik TF, Matchar DB, Toole J, Easton JD, Adams HP Jr, Brass LM, Hobson RW 2nd, Brott TG, Sternau L (1998) Guidelines for carotid endarterectomy: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 29:554–562 12. Bonita R, Stewart A, Beaglehole R (1990) International trends in stroke mortality: 1970–1985. Stroke 21:989–992 13. Cadwater WB (1912) Unilateral optic atrophy and contralateral hemiplegia consequent on occlusion of the cerebral vessels. J Am Med Assoc 59:2248 14. Canadian Cooperative Study Group (1978) A randomized trial of aspirin and sulfinpyrazone in threatened stroke. N Engl J Med 299:53–59 15. CAPRIE Steering Committee (1996) Lancet 348:1329–1339 16. Caps MT (2004) Summary of results of carotid bifurcation angioplasty and stenting. In: Schneider PA, Bohannon W, Sila MB (eds) Carotid interventions. Dekker, New York, Chapter 16 17. Carrea R, Mollins M, Murphy G (1955) Surgical treatment of spontaneous thrombosis of the internal carotid artery in the neck: carotid carotideal anastomosis. Acta Neurol Latinoamer 1:71–78 18. Chao WH, Kwan ST, Lyman RS et al (1938) Thrombosis of the left internal carotid artery. Arch Surg 37:100–111 19. Cid dos Santos J (1947) Sur la desobliteration des thromboses arterièlles anciènnes. Mem Acad Chir (Paris) 73:409 20. Crisby M, Nordin-Fredriksson G, Shah PK, Yano J, Zhu J, Nilsson J (2001) Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization. Circulation 103:926–933 21. Davies JB, Grove WJ, Julian OC (1956) Thrombotic occlusion of the branches of the aortic arch, Martorell’s syndrome: report of a case treated surgically. Ann Surg 144:124–126 22. Davies PH, Clarke WR, Bendixen BH et al (1996) Silent cerebral infarction in patients enrolled in the TOAST study. Neurology 46:942–948 23. Dearden NM (1985) Ischaemic brain. Lancet 2:255–259 24. DeBakey ME (1975) Successful carotid endarterectomy for cerebrovascular insufficiency: nineteen year follow-up. J Am Med Assoc 233:1083–1085 25. DeWitt LD, Buonanno FS, Kistler JP et al (1984) Nuclear magnetic resonance imaging in evaluation of clinical stroke syndromes. Ann Neurol 16:535–545 26. Dyken ML (1979) Assessment of the role of antiplatelet aggregating agents in transient ischemic attacks, stroke and death. Stroke 10:602
References
27. Eastcott HHG, Pickering GW, Robb CG (1954) Reconstruction of the internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 2:994–999 28. Eikelboom BC, Ackerstaff RG, Hoeneveld H, Ludwig JW, Teeuwen C, Vermeulen FE, Welten RJ (1988) Benefits of carotid patching: a randomized study. J Vasc Surg 7:240–247 29. European Carotid Surgery Trialists‘ Collaborative Group (1991) MRC European Carotid Surgery Trial. Interim results for symptomatic patients with severe (70-99%) and with mild (0-29%) stenosis. Lancet 337:1235–1243 30. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study (1995) Endarterectomy for asymptomatic carotid artery stenosis. J Am Med Assoc 273:1421–1428 31. Fernandes e Fernandes J (2003) Extracranial carotid disease. University of Lisbon, Lisbon, 1985 32. Ferro JM (2003) Cardioembolic stroke: an update. Lancet Neurol 2:177–188 33. Fields WS, Lemak NA (1989) A history of stroke. Oxford University Press, Oxford 34. Fields WS, Lemak NA, Frankowski RH, Hardy RJ (1977) Controlled trial of aspirin in cerebral ischemia. Stroke 8:301–314 35. Fisher CM (1951) Occlusion of the internal carotid artery. Arch Neurol Psychiatry 65:346–377 36. Fisher CM (1952) Transient monocular blindness associated with hemiplegia. Arch Ophthalmol 47:167–203 37. Fuster V, Badimon JJ, Chesebro JH (1998) Atherothrombosis: mechanisms and clinical therapeutic approaches. Vasc Med 3:231–239 38. Garcia J, Ye Z, Liu K (1999) Mechanisms of neuronal cell death after ischemic injury to the brain. In: Fisher M, Bogousslavsky J (eds) Cerebrovascular disease, 3rd edn. Current Medicine, Philadelphia, Chapter 2 39. Gonçalves I, Moses J, Dias N, Pedro L, Fernandes e Fernandes J, Nilsson J, Ares M (2003) Changes related to age and cerebrovascular symptoms in the extracellular matrix of human carotid plaques. Stroke 34:616–622 40. Gonçalves I, Moses J, Pedro L, Dias N, Fernandes e Fernandes J, Nilsson J, Ares M (2003) Echolucency of carotid plaques correlates with plaque cellularity. Eur J Vasc Endovasc Surg 26:32–38 41. Gonçalves I, Lindholm M, Pedro L, Dias N, Fernandes e Fernandes J, Fredrikson G, Nilsson J, Moses J, Ares M (2004) Elastin and calcium rather than collagen or lipid content determine the echogenicity of human carotid plaques. Stroke 35:2795–2800 42. Guthrie LH, Mayou S (1908) Right hemiplegia and atrophy of left optic nerve. Proc R Soc Med 1:180
43. Hayes PD, Lloyd AJ, Lennard N et al (2000) Transcranial Doppler-directed Dextran-40 therapy is a cost-effective method of preventing carotid thrombosis after carotid endarterectomy. Eur J Vasc Endovasc Surg 19:56–61 44. Heart Protection Study Collaborative Group (2002) MRC/ BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 360:7–22 45. Hobson R, Weiss D, Fields W et al (for Veterans Affairs Cooperative Study Group) (1993) Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. N Engl J Med 328:221–227 46. Hollenhorst RW (1961) The significance of bright plaques in the retinal arteries. J Am Med Assoc 178:123–129 47. Hollenhorst RW, Brown JR, Wagener HP (1967) Neurologic aspects of temporal arteritis. Neurology 10:490–498 48. Hougaku H, Matsumoto M, Hashikawa K, Hori M (2000) The role of brain imaging in the preoperative evaluation of carotid surgical patients. In: Loftus CM, Kresowik TF (eds) Carotid artery surgery. Thieme, New York, pp 81–96 49. Hunt JR (1914) The role of the carotid arteries in the causation of vascular lesions of the brain, with remarks on certain special features of the symptomatology. Am J Med Soc 147:704–713 50. Inzitari D, Eliasziw M, Gates P (2000) The causes and risk of stroke in patients with asymptomatic internal-carotid-artery stenosis. N Engl J Med 342:1693–1701 51. Johnson HC, Walker AE (1951) The angiographic diagnosis of spontaneous thrombosis of the internal and common carotid arteries. J Neurosurg 8:631–659 52. Kerber CW, Cromwell LD, Loehden OL (1980) Catheter dilatation of proximal carotid stenosis during distal bifurcation endarterectomy. AJNR Am J Neuroradiol 1:348–349 53. Lammie GA, Path MR, Sandercock PA, Dennis MS (1999) Recently occluded intracranial and extracranial carotid arteries. Relevance of the unstable atherosclerotic plaque. Stroke 30:1319–1325 54. Libby P (1998) The interface of atherosclerosis and thrombosis: basic mechanisms. Vasc Med 3:225–229 55. Lindblad B, Persson N, Takolander R, Bergqvist D (1993) Does low-dose acetylsalicylic acid prevent stroke after carotid surgery? A double-blind, placebo-controlled randomized trial. Stroke 24:1125–1128 56. Lobo Antunes J, Fernandes e Fernandes J (1992) Cerebral ischemia. Surgical aspects. In: Ribeiro C, Carvalho LS, Braz Nogueira J (eds) Ischemia. University of Lisbon, Lisbon, pp 189–209 57. Martin RP, Lerakis S (2004) Contrast for vascular imaging. Cardiol Clin 22:313–320
151
152
2.2 Extracranial Carotid Artery Disease
58. Mathias K (1977) Ein neuartiges Kathetersystem zur percutanen transluminalen Angioplastie von Karotisstenosen. Fortschr 95:1007–1011 59. Mayo Asymptomatic Carotid Endarterectomy Study Group (1992) Results of a randomized controlled trial of carotid endarterectomy for asymptomatic carotid stenosis. Mayo Clin Proc 67:513–518 60. Millikan CH (1965) The pathogenesis of transient focal cerebral ischaemia. Circulation 32:438 61. Mohr JP, Caplan LR, Melski JW, Goldstein RJ, Duncan GW, Kistler JP, Pessin MS, Bleich HL (1978) The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 28:754–762 62. Moniz E (1927) L’éncephalographie artérielle: son importance dans la localization des tumeurs cérébrales. Rev Neurol 2:172 63. Moniz E, Lima A, Lacerda R (1937) Hemiplegies par thrombose de la carotide interne. Presse Med 45:977 64. Moore WS, Barnett HJ, Beebe HG et al (1995) Guidelines for carotid endarterectomy. A multidisciplinary consensus statement from the ad hoc committee. AHA Stroke 26:188–201 65. Moore WS, Barnett HJ, Beebe HG et al (1995) Guidelines for carotid endarterectomy. A multidisciplinary consensus statement from the ad hoc committee. AHA Circulation 91:566–579 66. MRC Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group (2004) Prevention of disabling and fatal strokes by successful endarterectomy in patients without recent neurological symptoms: randomized controlled trial. Lancet 363:1491–1502 67. Neumann-Haefelin T, Moseley ME, Albers G et al (2000) New magnetic resonance imaging methods for cerebrovascular disease: emerging clinical applications. Ann Neurol 31:559–570 68. Nicolaides AN (2004) Carotid endarterectomy: coming of age and the future. Presentation at the Coronaries, Carotids, Peripherals, Renals Endovascular Therapy Meeting (CCPR 2004), Greece 69. Nicolaides AN, Shifrin EG, Bradbury A, Dhanjil S, Griffin M, Belcaro G, Williams M (1996) Angiographic and duplex grading of internal carotid stenosis: can we overcome the confusion? J Endovasc Surg 3:158–165 70. North American Symptomatic Carotid Endarterectomy Trial Collaborators (1991) Beneficial effect of carotid endarterectomy in symptomatic patients with high grade carotid stenosis. N Engl J Med 325:445–463
71. Pedro LM (2003) A window to atherosclerosis: high definition ultrasonography in the study of the arterial wall. University of Lisbon, Lisbon 72. Pedro LM, Pedro MM, Goncalves I, Carneiro TF, Balsinha C, Fernandes e Fernandes R, Fernandes e Fernandes J (2000) Computer-assisted carotid plaque analysis: characteristics of plaques associated with cerebrovascular symptoms and cerebral infarction. Eur J Vasc Endovasc Surg 19:118–123 73. Pedro LM, Fernandes e Fernandes J, Pedro MM, Gonçalves I, Dias NV, Fernandes e Fernandes R, Carneiro TF, Balsinha C (2002) Ultrasonographic risk score of carotid plaques. Eur J Vasc Endovasc Surg 24:492–498 74. Phan T, Huston J III, Bernstein MA, Riederer SJ, Brown RD Jr (2001) Contrast-enhanced magnetic resonance angiography of the cervical vessels: experience with 422 patients. Stroke 32:2282–2286 75. Poldermans D, Boersma E, Jeroen D et al (1999) The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. N Engl J Med 341:1789–1794 76. Robinson RE et al (1968) Natural history of cerebral thrombosis: 9–19 years follow-up. J Chronic Dis 21:221 77. Roederer GO, Langlois YE, Chan ARW et al (1983) Is siphon disease important in predicting outcome of carotid endarterectomy? Arch Surg 118:1177–1181 78. Rothwell PM, Gibson R, Warlow CP (2000) Interrelation between plaque surface morphology and degree of stenosis on carotid angiograms and the risk of ischemic stroke in patients with symptomatic carotid stenosis. On behalf of the European Carotid Surgery Trialists’ Collaborative Group. Stroke 31:615–621 79. Sabetai MM, Tegos TJ, Nicolaides AN, Dhanjil S, Pare GJ, Stevens JM (2000) Reproducibility of computer-quantified carotid plaque echogenicity: can we overcome the subjectivity? Stroke 31:2189–2196 80. Salasidis GC, Latter DA, Steinmetz OK et al (1995) Carotid artery duplex scanning in preoperative assessment for coronary artery revascularization: the association between peripheral vascular disease, carotid artery stenosis, and stroke. J Vasc Surg 21:154–160 81. Sandercock P, Molyneux A, Warlow C (1985) Value of computed tomography in patients with stroke: the Oxfordshire Community Stroke Project. Br Med J 290:193–196 82. Savory WS (1856) Case of a young women in whom the main arteries of both upper extremities and of the left side of the neck were throughout completed obliterated. MedChir Tr London 39:205–219 83. Seldinger SI (1953) Catheter replacement of the needle in percutaneous arteriograhy. Acta Radiol 39:368–376
References
84. Sever P, Dahlof B, Poulter N et al (2003) Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial – Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 361:1149–1158 85. Strandness Jr DE (1993) Duplex scan in vascular disorders. Raven, New York 86. Streifler JY, Eliasziw M, Fox A et al (1995) The risk of stroke in patients with first-ever retinal versus hemispheric transient ischemic attacks and high-grade carotid stenosis. Arch Neurol 52:246–249 87. Thompson JE (1996) The evolution of surgery for the treatment and prevention of stroke. Stroke 27:1427–1434
88. Torvik A, Svindland A, Lindboe CF (1989) Pathogenesis of carotid thrombosis. Stroke 20:1477–1483 89. Wylie E, Ehrenfeld W (1970) Extracranial occlusive cerebrovascular disease. Saunders, Philadelphia 90. Yuan C, Mitsumori LM, Ferguson MS, Polissar NL, Echelard D, Ortiz G, Small R, Davies JW, Kerwin WS, Hatsukami TS (2001) In vivo accuracy of multispectral magnetic resonance imaging for identifying lipid-rich necrotic cores and intraplaque hemorrhage in advanced human carotid plaques. Circulation 104:2051–2056 91. Yuan C, Zhang SX, Polissar NL, Echelard D, Ortiz G, Davis JW, Ellington E, Ferguson MS, Hatsukami TS (2002) Identification of fibrous cap rupture with magnetic resonance imaging is highly associated with recent transient ischemic attack or stroke. Circulation 105:181–185
153
155
2.3 Eversion Carotid Endarterectomy Technique D.A. Kiskinis, N.A. Saratzis, A. Saratzis
2.3.1 Introduction Carotid endarterectomy (CEA) is well established as a stroke-preventing treatment. Since the 1960s, two different techniques have evolved, namely conventional and eversion carotid endarterectomy, which is a modified version of the original method. 1. Conventional endarterectomy is the most common option for carotid bifurcation endarterectomy. It involves a longitudinal arteriotomy extending to the internal carotid distal to the lesion, and arteriotomy closure, which is made either using a patch or with primary closure. 2. The second technique is eversion endarterectomy, which was initially reported by De Bakey and later described by Etheredge, while a modification of the technique was presented by Kasprzak and Raithel in 1989 [4]. Eversion endarterectomy involves the oblique transection of the internal carotid artery (ICA) at its origin at the carotid bifurcation, endarterectomy by eversion of the ICA, endarterectomy of the carotid bifurcation and of the external carotid artery, and reimplantation of the ICA on the common carotid artery. The advantages of eversion endarterectomy, like those of earlier eversion techniques, are that: • It avoids longitudinal arteriotomy of the ICA • It avoids the need for patch angioplasty • It offers good visualization of the distal endpoint’s smooth luminal surface throughout the length of the vessel that is being operated on • It provides very effective management for the correction of carotid elongations with kinking and carotid tortuosities. Also, in subsequent studies this technique has been found to be associated with lower stroke and restenosis rates [2,
4, 5]. However, no long-term double-blind studies supporting the superiority of this method compared to the conventional procedure have yet been published. As a result, despite numerous innovations and reports, no unique CEA technique has yet become generally accepted for all patients and clinical situations. Furthermore, the superiority of one CEA method over another remains highly controversial and, thus, the optimal CEA technique to reduce postoperative complications and prevent late restenosis remains unclear. Under those circumstances, the EVEREST trial was designed to assess the major perioperative and late complication rates and durability of eversion CEA [1]. • EVEREST is a randomized multicentre trial. • A total of 1353 patients with carotid stenosis requiring surgical treatment were randomly assigned to receive standard (n = 675) or eversion (n = 678) CEA. • The primary endpoints included carotid occlusion, major stroke, death and restenosis rate. • The results of the EVEREST Trial suggest that eversion CEA is a safe and rapid procedure. • Also, the major complication rates appear to be low. • No significant differences in restenosis rates were observed between eversion and standard CEA at followup. • Longer-term results are necessary to assess whether the eversion technique influences the durability of CEA. • Still, it appears that eversion CEA has many advantages in selective cases.
2.3.2 Technique • Under general anaesthesia the patient is placed on the operating table in the supine position with the head hyperextended and turned away from the operative side.
156
2.3 Eversion Carotid Endarterectomy Technique
Fig. 2.3.1 Carotid bifurcation. A right bulldog clamp is used to control the internal carotid artery
• The skin incision is made parallel to the anterior border of the sternocleidomastoid muscle. • Exposure and clamping of the common carotid artery (CCA), external carotid artery (ECA) and ICA are made in the usual way. • Systemic heparinization is used. • A right-angled bulldog clamp should control the ICA well beyond the distal end of the atheromatous plaque (Fig. 2.3.1). • The CCA is entered with a scalpel while with angulated Pott’s scissors the arteriotomy is extended in the distal direction toward the fork of the carotid bifurcation (Fig. 2.3.2). • The incision should be made precisely parallel to the axis of the ECA. • A common pair of scissors is then used for complete transection of the ICA (Fig. 2.3.3). • Transection permits complete mobilization of the artery and additional traction downward offers additional length of exposure. • Endarterectomy is started at the stump of the ICA and the plane is developed between the outermost layers of the media and the adventitia (Fig. 2.3.4a). • The atheroma is circumferentially separated and detached while the outer layer of the vessel is everted (Fig. 2.3.4b). • Fine atraumatic vascular forceps are required for these manipulations.
Fig. 2.3.2 The arteriotomy is extended by Pott’s scissors towards the fork of the bifurcation
Fig. 2.3.3 Complete transection of the internal carotid artery permits further mobilization
• The eversion is progressively continued distally and the atheroma is detached like a cast (Fig. 2.3.5). • Gentle traction results in complete removal of the atheromatous core providing a thin fading and tapering endpoint.
2.3.2 Technique
Fig. 2.3.4a,b Eversion endarterectomy of the internal carotid artery. a The plane of cleavage is developed by a closed fine mosquito. b As the atheroma is circumferentially detached the outer layer of the vessel is everted
Fig. 2.3.5a,b Eversion endarterectomy of the internal carotid artery. a Further eversion of the outer layer of the vessel. b Removal of the atheromatous plaque by gentle traction; a smooth distal endpoint is left
157
158
2.3 Eversion Carotid Endarterectomy Technique
Fig. 2.3.6 Endarterectomy of the external carotid artery. Complete detachment of the plaque is achieved by the jaws of a closed dissector
Fig. 2.3.7 Reimplantation of the internal carotid artery. The anastomosis is started at the fork of the bifurcation and the posterior wall is reconstructed first
Fig. 2.3.8 Reconstruction of the anterior wall of the anastomosis. Dilators may be used to dilate the extracranial segment of the internal carotid artery
Fig. 2.3.9 In cases with distal plaque detachment and intimal flaps intraoperative stent deployment may secure the distal endpoint
References
• As the atheroma is removed, the luminal surface and the transition between the endarterectomized and nonendarterectomized segment of the ICA are assessed carefully. • Copious quantities of heparinized saline are used to flood the field in order to remove intimal or medial debris. • Flaps or loose “residuals’’ are gently removed only by circumferential traction since cephalic traction can cause inadvertent intimal dissection of the ICA endpoint. • The next step is attempted endarterectomy of the ECA and CCA. • Circumferential mobilization of the plaque is achieved by utilizing the closed jaws of a dissector (Fig. 2.3.6). • After proximal division of the plaque the endarterectomy is carried out into the ECA orifice as distal as possible. • The arterial wall of the ICA is drawn proximal and the reimplantation of the artery to its normal position is started (Fig. 2.3.7). • The anastomosis begins at the bifurcation fork using a simple running 6-0 synthetic monofilament suture. • The posterior wall is reconstructed first with tiny bites (Fig. 2.3.8). • Prior to completion of the anterior wall of the anastomosis, all clamps are removed sequentially to allow back bleeding and to wash out any thrombogenic debris. • At this stage of the procedure dilators of appropriate size, up to 4.5 mm in diameter, may be used to dilate the extracranial segment of the ICA. • Angioscopy may be also used to verify the anatomic result. Angioscopy yields an excellent visualization of the whole endarterectomized luminal surface and the endpoint of the ICA. • After completion of the anastomosis the blood flow is restored first to the ECA and then to the ICA. • In cases with distal flaps or plaque detachment, intraoperative stent deployment may secure the distal endpoint (Fig. 2.3.9).
2.3.3 Advantages • The advantage of this modified CEA technique over the open endarterectomy is that longitudinal arteriotomy of the ICA is avoided and subsequently the suture line does not interfere with the lumen of the vessel.
• Furthermore, the use of a patch in patients with small arteries, such as women and children, is not necessary. • This method is appropriate for the correction of coiling, kinking or tortuosity of the ICA in the presence of arteriosclerotic lesions. • After completion of the endarterectomy an ICA segment of appropriate length is resected and the vessels reimplanted.
2.3.4 Disadvantages • Among the disadvantages of the method is the limitation of an internal shunt placement when it is required. • During the procedure of eversion endarterectomy of the ICA, only a CCA to ECA shunt can be easily used for cerebral protection. • In some complex cases, when the transition endpoint of the ICA is not smooth and/or the plaque is extended distally, replacement of the ICA by a graft may be necessary [3]. • In such cases, interposition of synthetic or saphenous vein grafts may be used.
2.3.5 Conclusion In conclusion, eversion endarterectomy is a feasible and safe alternative technique for the management of extracranial carotid arteriosclerosis. The major advantages of this technique are optimum correction of an elongated ICA, a lower restenosis rate and the avoidance of patch material for arteriotomy closure. References 1. Cao P, Giordano G, Rango P, Zannetti S, Chiesa R, Coppi G, Palombo D, Spartera C, Stancanelli V, Vecchiati E (1998) A randomized study on eversion versus standard carotid endarterectomy: Study design and preliminary results: The Everest Trial. J Vasc Surg 27:595–605 2. Cao P, Giordano G, De Rango P, Zannetti S, Chiesa R, Coppi G, Palombo D, Peinetti F, Spartera C, Stancanelli V, Vecchiati E (2000) Eversion versus conventional carotid endarterectomy: late results of a prospective multicenter randomized clinical trial. J Vasc Surg 31:19–30
159
160
2.3 Eversion Carotid Endarterectomy Technique
3. Cormier JM, Cormier F, Laurian C, Gigou F, Fichelle JM, Bokobza B (1987) PTFE bypass for revascularization of the atherosclerotic internal carotid artery. Ann Vasc Surg 1:564–571
4. Kasprzak PM, Raithel D (1989) Eversion carotid endarterectomy. J Cardiovasc Surg 30:495 5. Raithel D, Kasprzak P (1993) The eversion endarterectomy: a new technique. In: Greenhalgh RM, Hollier LH (eds) Surgery for stroke. Saunders, London, pp 183–191
161
2.4 Fibromuscular Dysplasia M.N. Sechas
2.4.1 Basics
2.4.1.2 Physiology, Pathophysiology Renal Arteries
Arterial fibromuscular disease encompasses a heterogeneous group of nonatherosclerotic vascular occlusive and aneurysmal diseases. A principal forum of fibrodysplastic stenoses includes: • Intimal fibroplasia • Medial hyperplasia • Medial fibroplasia • Perimedial dysplasia [2, 11, 17]. The first two are distinctly different pathological entities, whereas the latter two appear to represent a common disease in evolution. Compounding this classification are hypoplastic dysplastic vessels occurring as true developmental lesions. Various combinations of dysplastic lesions exist, as do other less easily categorized vessel wall derangements. It is also important to distinguish primary arterial fibrodysplasia from secondary disease found in vessels subjected to earlier inflammatory attacks, physical insults and other distinct disease entities.
Renal artery fibromuscular disease was first described in 1938 and is second only to atherosclerosis as the most common cause of surgically correctable hypertension [15].
Intimal Fibroplasia
• Intimal fibroplasia of the renal artery affects male and female patients with equal frequency. • It accounts for approximately 5% of all dysplastic renal artery stenoses and is observed in infants, adolescents and young adults. • Most often it affects the main renal artery, usually occurring as a smooth focal stenosis. • Segmental vessel involvement is a more uncommon manifestation of intimal disease [13].
Intimal Hyperplasia
2.4.1.1 Anatomy Fibromuscular disease affects the following: • Renal arteries • Extracranial and intracranial cerebral arteries • Axillary, subclavian and brachial arteries • Coeliac, superior mesenteric and inferior mesenteric arteries • Iliac, femoral, popliteal, tibial and peroneal arteries • Aorta. Venous involvement is extremely rare. There have been reports of the disease in superficial veins of the lower extremities as well as in the renal veins. However, the existence of primary venous fibrodysplasia is controversial.
• Once a haemodynamically important arterial stenosis develops, progression of intimal hyperplasia appears a likely consequence of abnormal blood flow, even if the initiating aetiological factors have resolved. • The specific cellular messengers responsible for this tissue proliferation have not been identified. • Intimal lesions appear to progress at a much slower rate than do medial fibroplastic stenoses.
Medial Hyperplasia
• Medial hyperplasia without associated fibrosis is an unusual cause of renal artery stenosis. • In fact, the existence of this particular dysplastic disease is subject to discussion.
162
2.4 Fibromuscular Dysplasia
• It has been most often described in women during their fourth and fifth decades of life. • If indeed this type of lesion actually exists, it accounts for fewer than 1% of dysplastic renovascular lesions. • Focal stenoses caused by medial hyperplasia usually involve the mid-portion of the renal artery, not its branching or segmental vessels.
Medial Fibrodysplasia
• Medial fibrodysplasia accounts for nearly 85% of dysplastic renovascular disease. • More than 90% of patients with medial fibrodysplasia are female. • The morphological appearance of renal artery medial fibrodysplasia ranges from a solitary focal stenosis to its more common presentation as a series of stenoses with intervening aneurysmal outpouchings. • The latter, which cause a string-of-beads appearance, has not been observed in female patients before menarche, with the exception of a single case report. • Medial fibrodysplasia most commonly affects the distal main renal artery, with extensions into first-order segmental branches occurring in approximately 25% of cases. • Progression of medial fibrodysplasia appears to occur in 12–66% of patients with main renal artery lesions. • Progression is thought to be more likely to affect premenopausal women, but some authors have noted no differences related to age. • Hypertension develops in approximately 26% of cases. • In 18% of cases the disease progressed to complete occlusion, although acute changes are uncommon. • Two histological forms of renal artery medial fibrodysplasia are well recognized: the first is evident by disease of the outer media (peripheral form) and the second by disease throughout the entire media (diffuse form). • The second form is noted twice as often as the former. • The peripheral form is usually encountered in younger patients. • This observation lends support to the tenet that both forms represent the same disease process.
Perimedial Dysplasia
• Perimedial dysplasia is the dominant abnormality affecting approximately 10% of dysplastic renal arteries. • It may coexist with medial fibrodysplasia. • Most patients with this type of disease are female in their fourth or fifth decade of life, and these lesions present as either focal stenoses or multiple constrictions involving the midportion of the main renal artery without mural aneurysms. • Excessive elastic tissue at the junction of the media and the adventitia is the distinguishing feature of perimedial dysplasia.
Extracranial and Intracranial Cerebral Arteries: Carotid and Vertebral Arteries Arterial fibrodysplasia in these arteries is a clinical entity of potential importance, although controversy exists beyond the simple assertion that certain lesions cause symptoms of cerebral ischaemia.
Epidemiology
• The precise incidence of this disease is poorly defined, although lesions of the extracranial internal carotid artery (ECICA) were noted in 0.42% of 3600 patients undergoing cerebral arteriograms [3]. • This finding was identical to the 0.4% reported from the Mayo Clinic [16]. • Many of these examinations were for suspected cerebrovascular disease and thus the true frequency of ECICA fibrodysplasia in the general population would be expected to be lower. • Unfortunately the much lower 0.02% incidence of the disease among necropsy examination is likely to be too low, because of the uncommon removal of distal segments of the ECICA during routine autopsies. • Vertebral artery disease is even less common, having been noted in approximately 20% of patients manifesting ECICA fibrodysplasia.
Aetiology/Pathology of Carotid Artery Disease
• Various pathologic processes have been categorized as ECICA fibrodysplasia. • The two major subgroups include: (1) intimal fibrodysplasia and (2) medial fibrodysplasia.
2.4.1 Basics
• The intimal form is often associated with elongation, kinking and coiling of the carotid artery and appears for the most part to be a secondary rather than a primary dysplastic process. • This seems to be particularly true of intracranial intimal fibroplasias. • Occasional atypical lesions appear as isolated webs of the ECICA. • Medial fibrodysplasia of the ECICA was first documented arteriographically and histologically more than three decades ago. • These lesions invariably occur in female patients. • Medial fibrodysplasia of the ECICA typically involves a segment of 2–6 cm of the mid-carotid artery adjacent to the second and third cervical vertebrae. • The serial stenoses are often evident on examination of the external surface. • Bilateral disease has been reported to occur in 35–85% of patients with these lesions, with an average incidence of approximately 65%. • Involvement of the ECICA at its origin with the classic form of this dysplastic lesion has not been described. • Carotid arteries affected by medial fibrodysplasia are often elongated, and kinking occurs in approximately 5% of cases. • Typical medial fibrodysplastic lesions of the anterior intracranial arteries are uncommon. • Similar lesions of the external carotid artery or its branches have been reported, but they are exceedingly rare.
Aetiology/Pathology of Vertebral Artery Disease
• Vertebral artery disease, in the form of either multiple stenoses or nonocclusive mural aneurysms, has often been overlooked. • These lesions develop in the lower vertebral artery at the level of the fifth cervical vertebra, or higher at the level of the second vertebra. • They exhibit marked irregularities and are often accompanied by eccentric mural aneurysms, but they do not manifest the typical string-of-beads appearance noted in other muscular vessels affected with medial fibrodysplasia. • Dysplastic lesions of the basilar artery are an uncommon form of intracranial medial fibrodysplasia.
Involvement of Other Vessels
• Noncerebrovascular medial fibrodysplasia occurs in many patients with ECICA lesions. • Renal artery involvement affects as many as 25% of these individuals. • The frequency of simultaneous ECICA and renal artery dysplasia may be even higher, and it has been reported to be 50% in patients who underwent arteriographic assessments of both vessels. • Similar lesions have also been observed in the external iliac and superior mesenteric arteries.
Aneurysms
• Coexistent intracranial aneurysms have been documented in 12–25% of patients with ECICA medial fibrodysplasia. • Solitary intracranial aneurysms are present in 80% of these patients, with multiple aneurysms occurring in the remaining 20% of cases. • A meta-analysis of 18 series, excluding those with subarachnoid haemorrhage, revealed a 7.3% prevalence of cerebral aneurysms in patients with carotid or vertebral fibrodysplasia. • Although intracranial arteries are occasionally the site of dysplastic disease, aneurysms do not develop in the involved vessel. Instead they appear to evolve as a generalized dysplastic arteriopathy, manifested by weakening in arterial branches, which increases the likelihood of berry aneurysm formation. These aneurysms tend to occur on the same side as the ECICA disease. • The anatomical distribution of aneurysms in patients with medial fibrodysplasia is the same as that in patients not affected with dysplastic ECICA. • Hypertension may contribute to the evolution of these aneurysms, but it has not been identified as a dominant factor in their pathogenesis.
Complications
• Complications occurring with medial fibrodysplasia of the ECICA appear to be related to: • Encroachment on the lumen that causes flow reduction. • Occasional collection of thrombi within the cul-desacs. • Potential distal embolization. • Dissections and rupture with arteriovenous fistula formation.
163
164
2.4 Fibromuscular Dysplasia
• The precise incidence of these complications has not been determined, but they appear to occur in fewer than 10% of cases. • Frequently, dissection obliterates clear evidence of the underlying fibrodysplastic process, and many individuals experiencing this complication are thought to have suffered from spontaneous dissections. • Progression of ECICA medial fibrodysplasia may approach 30%, but the exact rate has yet to be defined. • Complications occurring with medial fibrodysplasia of the vertebral arteries are rare and are usually related to thromboembolism or dissections.
• There is a slight predominance of women among patients with these dysplastic lesions [7]. • Dysplastic disease compatible with medial fibrodysplasia, with characteristic dilatations and constrictions or histological confirmation of this form of dysplasia, may affect the subclavian, brachial, radial and ulnar arteries. • However, these particular lesions of the upper extremity arteries are too uncommon to be rigorously classified as to type and clinical importance.
Splanchnic Arteries: Coeliac and Mesenteric Iliac, Femoral, Popliteal and Tibial Arteries • The third vessel most commonly affected with medial fibrodysplasia is the external iliac artery. • Serial stenoses with intervening mural aneurysms typically affect the proximal third of this vessel. • These lesions are similar to those of the renal and ECICA vessels and may in fact occur in patients with other lesions. • Fibroproliferative processes primarily involve the medial tissue adjacent to areas of relative thinning. • Occasional fibrodysplastic lesions of the iliac vessels appear as solitary dilatations. • Complications of external iliac artery fibrodysplasia usually reflect encroachment on the lumen, with restriction of blood flow or the development of microthrombi that embolize peripherally. • Acute dissection may occur with these lesions, but it is not common. • Although exceedingly rare, similar lesions reflecting the systemic nature of medial fibrodysplasia have been reported to affect the femoral, popliteal and tibial vessels of the lower extremity. • In some instances, these extremity lesions have thrombosed; in others they have been associated with aneurysmal changes [19].
Axillary, Subclavian and Brachial Arteries • The most common dysplastic lesion affecting upper extremity vessels appear to be intimal hyperplasia, which is usually manifested by smooth focal or long tubular stenoses.
Intimal Fibroplasia
• Intimal fibroplasia may affect the origins of the three principal splanchnic vessels: coeliac, superior and inferior mesenteric. • The basis of these lesions is unknown, but this fibrodysplasia may reflect a secondary phenomenon occurring in developmentally narrowed vessels. • Ostial fibrodysplastic lesions are quite common in patients with intestinal angina and often exhibit associated atherosclerotic changes. • Intimal fibroplasias tend to occur more often in women than in men, with nearly equal involvement of the coeliac and superior mesenteric artery (SMA) [20].
Medial Fibrodysplasia
• Medial fibrodysplasia is rare within the splanchnic circulation, although histological evidence of it has been reported. • When present, this form of splanchnic vascular disease is often associated with similar renal or carotid lesions. • Histological evidence of medial dysplasia is also common among patients with splenic artery aneurysms. In fact the development of these aneurysms may be a reflection of compromised vascular integrity due to the disruptive dysplastic process. • Similar aneurysms have been noted in other splanchnic vessels, including the SMA. • The proximal SMA may exhibit medial fibrodysplastic occlusive disease a few centimetres beyond its origin as it exits beneath the pancreas over the top of the highest point of the duodenum.
2.4.1 Basics
Other Vessels
Carotid Disease
• Most other vessels affected with dysplastic disease involve intimal fibroplasia. Exceptions are: medial fibrodysplasia also affecting coronary arteries and exhibiting dissections as well as thromboses. • Other dysplastic lesions have been noted, among patients ranging from neonates to the elderly, in large arteries the size of the aorta to very small vessels such as the coronary sinus node artery. • It is unlikely that the changes in these vessels represent a systemic arteritis in its active stage, although they may represent an end stage of an earlier arteritis. • Again, experience with these rare forms of arterial dysplasia is so meagre as to preclude rendering of any firm conclusions about their aetiology or clinical relevance.
• Neurological examination for neurological deficits from a previous event (stroke), Horner’s syndrome and cranial nerve palsies. • Intracranial or extracranial cerebrovascular fibromuscular dysplasia may be discovered incidentally as the cause of a cervical bruit.
Lower Extremity Disease • Palpation of peripheral arterial pulses. • Examination of capillary circulation and critical limb ischaemia.
2.4.1.5 Technical Diagnostic Procedures 2.4.1.3 Organ-related Questions
Renal Fibromuscular Disease
For renal fibroplasia, organ-related questions regarding the special case history include the search for: • arterial hypertension (headaches, dizziness, tinnitus) • arterial infarction (sudden severe pain) or • renal insufficiency.
• Duplex imaging of the renal arteries can accurately detect elevated blood-flow velocities, especially in the distant portion of the arteries, which are most often due to fibromuscular dysplasia. • Computed tomography may play an important part in the diagnosis and follow-up of renal artery fibromuscular dysplasia, but is inferior to catheter-based angiography at present [8, 9].
For cerebrovascular fibroplasia, organ-related questions regarding the special case history include the search for symptoms of: • transient ischemic attacks • carotid dissection (stroke). For fibroplasia of the arteries of the lower extremities, organ-related questions regarding the special case history include the search for: • intermittent claudication • blue toe syndrome resultant from acute thromboembolism.
Cerebrovascular Fibromuscular Dysplasia • Duplex ultrasonography of the carotid arteries may demonstrate irregular patterns of stenosis and aneurysm. • Since fibromuscular dysplasia affects the middle and distal portions of the carotid and vertebral arteries, it may be difficult to visualize these lesions by means of Duplex ultrasound, which has a lower sensitivity than angiography.
2.4.1.4 Principles of Clinical Examination Clinical examination includes a search for signs of arterial hypertension: • measurement of arterial blood pressure • fundoscopy for lesions of the retinal vessels.
Lower Extremity Fibromuscular Arterial Disease • Duplex ultrasonography may demonstrate high velocities due to arterial stenosis or give a low ankle/brachial blood pressure index.
165
166
2.4 Fibromuscular Dysplasia
2.4.1.6 Organ-specific Radiology
2.4.2.2 Definition
Renal Artery Disease
• Nonatheromatous noninflammatory vascular disease most commonly affecting the renal and internal carotid arteries, but described in almost every arterial bed in the body.
• Catheter-based angiography remains the most accurate method for diagnosing fibromuscular dysplasia. • Although captopril renography was once the noninvasive diagnostic method of choice for patients with renal artery disease, it has now been relegated to use in secondary screening, since the quality of noninvasive methods is so high. • The role of magnetic resonance angiography in the evaluation of the disease remains uncertain, since its resolution remains inferior to that of catheter angiography.
Cerebrovascular Disease • Angiography has a higher resolution than Duplex ultrasonography for the detection of cerebrovascular fibromuscular disease. • There has been little experience with computed tomography or magnetic resonance angiography, but the latter should be performed to rule out the presence of intracranial aneurysms in patients with dysplasia.
Lower Extremity Disease • Digital angiogram is the method of choice depicting fibromuscular lesions in the lower extremities.
2.4.2 Organ-related Diseases • • • •
Arterial hypertension Cerebrovascular insufficiency Lower extremity insufficiency Splanchnic ischaemia.
2.4.2.1 Synonyms • Arterial dysplasia • Arterial fibrodysplasia • Arterial fibromuscular dysplasia (FMD).
2.4.2.3 Epidemiology/Aetiology • The precise incidence of renal artery disease in the general population is unknown, but it is less than 0.5%. • The frequency among black hypertensive patients appears to be even lower. • Renal artery dysplasia is second only to atherosclerosis as the most common cause of surgically correctable hypertension. • The pathogenesis of medial fibrodysplasia and perimedial dysplasia has been the subject of much speculation. • Hormonal effects on smooth muscle, mechanical stresses on the vessel wall and a peculiar distribution of vasa vasorum in arteries exhibiting these lesions are all considered to be contributing factors. The exact relation of these factors to each other, or their association with other unrecognized pathogenetic mechanisms, remains unknown. • Because of the familial nature of the disease, a geneticrelated autosomal dominant aetiology has been suggested, but not established. Genetic factors may play a part in the development of FMD, since the disease is more common among the first-degree relatives of patients with FMD of the renal arteries and among persons with type-I angiotensin-converting enzyme (ACE-I) [4, 10]. • Hormonal influences seem likely in view of the unusual female predilection pertaining to arterial dysplasia. More than 95% of patients exhibiting medial and perimedial disease are women. • Pregnancy is not an obvious aetiological factor in arterial fibrodysplasia. • Also no association between antiovulants or oral contraceptives and the disease was demonstrated. • It is speculated that physiological preconditioning of vascular smooth muscle cells to a secretory state by normal circulating oestrogens associated with the reproductive cycle may account for the more frequent occurrence of medial dysplastic disease in females.
2.4.2 Organ-related Diseases
• Unusual physical stresses due to ptosis of the kidneys may be associated with fibrodysplastic changes in the renal arteries. • A final aetiological factor may be related to mural ischaemia in dysplastic arteries. The renal, extracranial internal carotid and external iliac arteries are the three vessels most likely to develop medial fibrodysplasia. The latter two arteries, in particular, have relatively few branches compared with similar-sized vessels. Compromise of vasa vasorum in these vessels, in which scarcity of these nutrient vessels already exists, may lead to significant mural ischaemia. • Cigarette smoking has been implicated as an important aetiological factor in this disease, although the mechanism has not been defined. • Medial fibrodysplasia of the ECICA was first documented arteriographically and histologically more than three decades ago. These lesions invariably occur in female patients, with a mean patient age at the time of recognition being approximately 55 years. Similarly, these lesions, like those of the renal artery, have been infrequently recognized among Afro-American patients. • The pathogenesis of ECICA medial fibrodysplasia is poorly understood, but it appears to be similar to that occurring in the renal vessels. The role of mural ischaemia may be greater because very few muscular branches have origins from the extracranial portion of the internal carotid artery, thus reducing the number of intrinsic vasa vasorum in this vessel. Certainly, unusual traction or stretch stresses that occur with hyperextension and rotation of the neck appear to be another dominant factor in the development of these lesions. • Trauma has been cited as an aetiological factor in instances of vertebral artery fibrodysplasia. In fact, unrecognized adventitial bleeding due to vertebral artery injury during birth may be important in the later development of these lesions. • Most individuals with medial fibrodysplasia of the iliac vessels have been women in their fifth or sixth decade of life, about 10 years older than those presenting with similar renovascular disease. The aetiology of dysplastic lesions of the iliac and femoral arteries may be related more to a paucity of vasa vasorum than to any physical stretch or traction stresses.
• The incidence of external iliac artery fibrodysplasia in the general population is unknown, but this condition has been reported to occur in 1–6% of patients with renal artery fibrodysplasia. • Intimal fibroplasia of the external iliac artery, as well as that of the femoral, popliteal and tibial vessels is usually considered to be a secondary pathological phenomenon rather than a primary aetiological process. Although most instances of intimal disease affecting these vessels may be the consequence of prior trauma, the result of thromboembolism with recanalization of intraluminal thrombus, or the sequela of prior arthritis, certain cases appear to represent primary intimal hyperplasia. • The most common dysplastic lesion affecting upper extremity vessels appears to be intimal hyperplasia. There is a slight predominance of women. Speculation exists as to the aetiology, although the most likely underlying cause is related to an arteritis. Other intimal fibroplastic lesions affecting the subclavian and axillary vessels may be a consequence of injury (that associated with repetitive subclavian trauma at the thoracic outlet) or of abnormal flow associated with anatomical bands causing vascular narrowing. • Dysplastic disease compatible with medial fibroplasias with characteristic dilatations and constrictions may affect the subclavian, brachial and radial and ulnar arteries. However, these lesions are common. • Characteristic medial fibrodysplasia is rare within the splanchnic circulation. The basis of these lesions has not been established, although unusual stretch forces at the root of the mesentery may contribute to dysplastic changes.
2.4.2.4 Symptoms • Hypertension may be present in renal disease. • Renal failure is rare. • Cerebrovascular fibromuscular dysplasia may be asymptomatic or associated with a variety of nonspecific symptoms, including headache, tinnitus, vertigo, light-headedness and syncope. • The more specific neurological syndromes of transient ischaemic attack, amaurosis fugax, stroke, Horner’s syndrome and cranial nerve palsies may be the first presentation of FMD involving the carotid or vertebral arteries.
167
168
2.4 Fibromuscular Dysplasia
• In lower extremity disease intermittent claudication is the common symptom, but critical limb ischaemia or peripheral microembolism may also present. • Intestinal angina may occur when at least two of the major mesenteric arteries are obstructed. In unusual cases, the stenosis progresses to total occlusion, leading to acute intestinal ischaemia. • In upper extremity disease, patients experience weakness, paraesthesias, or claudication in their arms.
Imaging and Laboratory Tests
2.4.2.5 Complications
2.4.2.7 Treatment
Renal Disease
Conservative Treatment
• Hypertension (cerebral haemorrhage or cardiac insufficiency).
• Pharmacological therapy for hypertension in patients with renal artery FMD should follow the Recommended European standard therapeutic steps. • Clopidogrel (75 mg daily) or acetylsalicylic acid (ASA) alone or in combination could be given for cerebrovascular FMD to prevent stroke. These drugs may also help in peripheral arterial disease.
Cerebrovascular Disease • Rupture of an intracranial aneurysm. • Cerebral embolism originating from intravascular thrombi in stenotic regions.
Additional useful diagnostic procedures include: • Duplex ultrasonography • Computed tomography • Catheter-based digital angiography • Magnetic resonance angiography • Plasma renin activity and angiotensin II determination for evaluation of renal sufficiency.
Recommended European Standard Surgical Procedures Lower Extremity Disease • Peripheral atheroembolism or critical limb ischaemia.
Splanchnic Disease • Intestinal ischaemia or necrosis.
2.4.2.6 Diagnosis Examination • Inspection for the presence of neurological deficits in cerebrovascular disease or the presence of ischaemia of the lower extremities. • Palpation of peripheral arterial pulses. • Auscultation for bruits in the neck or in the abdomen or femoral areas. • Arterial pressure measurements.
• Revascularization should be considered for certain types of hypertensive patients: • Those with a recent onset of hypertension in whom the goal is to cure the hypertension. • Those in whom blood pressure control has proved difficult despite the use of a comprehensive antihypertensive regimen. • Those with an intolerance of antihypertensive medications. • Those whose blood pressure has been difficult to control because of noncompliance. • Those who have lost renal volume because of ischaemic nephropathy. • Before the advent of percutaneous transluminal angioplasty (PTA), surgical revascularization was the primary therapeutic alternative for patients with refractory hypertension. • Overall, the technical success rates ranged from 89% to 97%. • Hypertension was cured in 33–63% of patients, improved in 24–57% and failed to improve in 3–33%.
2.4.2 Organ-related Diseases
• A longer duration of hypertension, concomitant atherosclerotic disease and complex branch-vessel repair all adversely affect the results of surgical revascularization. • Although there are no available prospective data demonstrating the superiority of PTA over surgical revascularization, the percutaneous approach has emerged as the mainstay of treatment for patients with FMD who meet the criteria for intervention. • Although stents have been used extensively for the treatment of atherosclerotic renal artery stenosis, the use of stents for FMD has been reserved as a “bailout” procedure in cases in which there are suboptimal results with balloon angioplasty or in which renal artery dissection occurs. • There is no role for stent implantation as a primary treatment for FMD, since angioplasty alone is quite efficient [1, 14, 18]. • For patients with aneurysms or complex occlusive lesions of the renal artery, renal autotransplantation (RAT) is a well-established alternative to PTA in cases where catheter-based techniques are contraindicated [6]. • Similarly, before the use of PTA became widespread, surgery was the mainstay of therapy for patients with symptomatic cerebrovascular FMD. The surgical techniques used depended on the type of lesion and its location, but the most widely used procedure was graduated intraluminal dilatation. • Other procedures that have been used include intraoperative PTA, placement of a polytetrafluoroethylenecovered endograft, resection of the diseased segment and primary anastomosis, grafting of autogenous saphenous vein, resection of the aneurysm and carotid endarterectomy. • During the last 10 years, PTA has become the preferred treatment for symptomatic cerebrovascular FMD. There have been no randomized, controlled trials comparing surgery with balloon angioplasty in this condition. • The use of cerebral protection devices may reduce the frequency of ischaemic neurological events during stenting of the carotid artery [12]. • For symptomatic FMD in the arms or legs, treatment consists of PTA. • Treatment options for FMD of the visceral arteries include PTA and surgical by-pass.
2.4.2.8 Differential Diagnosis • Atherosclerosis generally occurs at the origin or proximal portion of the artery in older patients with typical cardiovascular risk factors. • Ehlers–Danlos syndrome (type IV) has been associated with medial fibroplasias in patients with multiple aneurysms in addition to the typical angiographic findings of FMD. There have been isolated reports of FMD associated with Alport’s syndrome, phaeochromocytoma, Marfan’s syndrome and Takayasu’s arteritis. • Vasculitis is an inflammatory process, associated with anaemia, thrombocytopaenia or abnormalities of acute-phase reactants. Large-vessel vasculitis may occur in the absence of changes in acute-phase reactants in up to 40% of cases. When histological proof or markers of inflammation are not available, it may be difficult to distinguish between these entities, because their angiographic appearance may be similar. • Although MR angiography may show wall thickening in patients with giant-cell arteritis or Takayasu’s arteritis, it is not useful in patients with renal or intestinal FMD, because the resolution of MR angiography is inadequate for the visualization of branch-vessel involvement. • In some cases intravascular ultrasound may help to distinguish FMD from vasculitis.
2.4.2.9 Prognosis • Although the loss of renal mass occurs in up to 63% of patients with renal artery FMD, renal failure is rare in these patients. • Multiple-organ involvement in FMD is particularly troublesome, since ischaemia may be associated with increased risk of complications and death.
2.4.2.10 Exemplary Surgical Procedures Procedure 1 Aortorenal By-pass
• An extended flank or subcostal incision is reserved for unilateral fibrodysplastic lesions. • The supracoeliac aorta may be selected as an in-flow source for the unilateral aortorenal by-pass.
169
170
2.4 Fibromuscular Dysplasia
• With the ipsilateral flank elevated, the incision is extended from the opposite semi-lunar line into the flank, between the costal margin and iliac crest. • A left or right visceral mobilization allows access to the renal vasculature and the aortic crus. • If necessary, the crus can be divided, and an extrapleural dissection of the descending thoracic aorta can provide access to the lower thoracic aorta for proximal control and anastomosis. • Exposure of the distal portion of the right renal artery is achieved by colonic and duodenal mobilization. • Mobilization of the left renal vein by ligation and division of the adrenal, gonadal and lumbar veins allows exposure of the entire left renal artery to the hilum. • The autologous saphenous vein is used as a graft. • When an end-to-side renal artery by-pass is performed, the anastomosis between the renal artery and the graft is performed first with a 6-0 or 7-0 monofilament polypropylene continuous suture (Fig. 2.4.1). • Following this, the aortic anastomosis is performed, removing an ellipse of the anterolateral aortic wall. Sometimes an end-to-end anastomosis between the graft and the renal artery provides a better reconstruction. • If the vein is small or sclerotic, a synthetic prosthesis preferable. A 6-mm thin-walled PTFE graft is quite satisfactory when the distal renal artery is of large calibre (≥ 4 mm).
Possible Complications of the Surgical Procedure
• Haemorrhage and/or thrombosis of the graft are the main complications of aortorenal by-pass, as is transient or permanent worsening of renal function [5].
Procedure 2 Dilatation of the Internal Carotid Artery
• The carotid bifurcation is dissected through a longitudinal incision in the neck along the anterior border of the sternocleidomastoid muscle. • A graduated dilatation of the internal carotid artery is performed through a small arteriotomy, using arterial dilators.
Possible Complications of the Procedure
• Haemorrhage through perforation of the carotid artery is possible, and also thrombosis of the artery and cerebrovascular episode (stroke).
2.4.2.11 Special Remarks As is the case with most rare diseases, it is difficult to conduct a prospective study of various treatment options for fibromuscular dysplasia. Therefore, most treatment decisions are based on data derived from retrospective case and anecdotal reports. Thanks to advances in imaging methods and enhancement of the interventional armamentarium, treatment has become less invasive and is now at least as effective as previous surgical approaches, while being associated with lower morbidity. Further study of the pathogenesis of fibromuscular dysplasia is needed in order to gain a better understanding of this disease. References 1. Anderson CA, Hansen KJ, Benjamin ME, Keith DR, Craven TE, Dean RH (1995) Renal artery fibromuscular dysplasia: results of current surgical therapy. J Vasc Surg 22:207–216 2. Begelman SM, Olin JW (2000) Fibromuscular dysplasia. Curr Opin Rheumatol 12:41–47 3. Begelman SM, Olin JW (2000) Nonatherosclerotic arterial disease of the extracranial cerebrovasculature. Semin Vasc Surg 13:153–164
Fig. 2.4.1 Aorto-renal by-pass with autogenous vein
References
4. Bofinger A, Hawley C, Fisher P, Daunt N, Stowasser M, Gordon R (2001) Polymorphisms of the renin-angiotensin system in patients with multifocal renal arterial fibromuscular dysplasia. J Hum Hypertens 15:185–190 5. Bonelli FS, McKusick MA, Textor SC et al (1995) Renal artery angioplasty: technical results and clinical outcome in 320 patients. Mayo Clin Proc 70:1041–1052 6. Chiche L, Kieffer E, Sabatier J et al (2003) Renal autotransplantation for vascular disease: late outcome according to etiology. J Vasc Surg 37:353–361 7. Cutts S, Grewal RS, Downing R (2000) Bilateral brachial artery fibromuscular dysplasia. Eur J Vasc Endovasc Surg 19:667–668 8. Funabashi N, Komiyama N, Komuro I (2003) Fibromuscular dysplasia in renovascular hypertension demonstrated by multislice CT: comparison with conventional angiogram and intravascular ultrasound. Heart 89:639 9. Gowda M, Loeb AL, Crouse LJ, Kramer PH (2003) Complementary roles of color-flow duplex imaging and intravascular ultrasound in the diagnosis of renal arterial fibromuscular dysplasia: should renal arteriography serve as the “gold standard”? J Am Coll Cardiol 41:1305–1311 10. Grimbert P, Fiquet-Kempf B, Coudol P et al (1998) Etude genetique de la dysplasie fibromusculaire des arteres renales. Arch Mal Coeur Vaiss 91:1069–1071 11. Harrison EG Jr, McCormack LJ (1971) Pathologic classification of renal arterial disease in renovascular hypertension. Mayo Clin Proc 46:161–167
12. Henry M, Henry I, Klonaris C et al (2002) Benefits of cerebral protection during carotid stenting with the PercuSurge GuardWire system: midterm results. J Endovasc Ther 9:1–13 13. Mounier-Vehier C, Lions C, Jaboureck O et al (2002) Parenchymal consequences of fibromuscular dysplasia renal artery stenosis. Am J Kidney Dis 40:1138–1145 14. Reiher L, Pfeiffer T, Sandmann W (2000) Longterm results after surgical reconstruction for renal artery dysplasia. Eur J Vasc Endovasc Surg 20:556–559 15. Safian RD, Textor SC (2001) Renal-artery stenosis. N Engl J Med 344:431–442 16. Schievink W, Bjornson J (1996) Fibromuscular dysplasia of the internal carotid artery. A clinicopathological study. Clin Neuropathol 15:2–6 17. Slovut DP, Olin JW (2004) Fibromuscular dysplasia. New Engl J Med 350:1862–1871 18. Tegtmeyer CJ, Selby JB, Hartwell GD, Ayers C, Tegtmeyer V (1991) Results and complications of angioplasty in fibromuscular disease. Circulation 83 (Suppl I):I155–I161 19. Van den Dungen JJ, Boontje AH, Oosterhuis JW (1990) Femoropopliteal arterial fibrodysplasia. Br J Surg 77:396–399 20. Yamaguchi A, Isogai M, Hori A, Kin Y (1996) Fibromuscular dysplasia of the visceral arteries. Am J Gastroenterol 91(8):1635–1638
171
173
2.5 Aneurysms of the Extracranial Carotid Arteries J. Daniel Menezes, Maria José Barbas, J. Goulão
2.5.1 Definition and Historical Background • Carotid artery aneurysm can be defined as a more than 50% localized increase of carotid calibre diameter when compared to reference values: • Internal carotid: 0.55±0.06 in men and 0.49±0.07 in women • Carotid bulb: 0.99±0.10 in men and 0.92±0.10 in women. • Unlike occlusive or ulcerated atherosclerotic lesions carotid aneurysms are quite uncommon, with very few cases reported in the literature, which influences the correct knowledge of the natural history of this entity. • In 1808 Sir Ashley Cooper made history when he performed, at Guy’s Hospital in London, the first successful treatment of a carotid aneurysm. The operation consisted of ligation of the common carotid artery, and the patient, a 50-year-old man, left the hospital after a 3-month period of recovery (because of a “smouldering wound infection”) [4, 5]. • The patient died 14 years later from a cerebral haemorrhage. • Through autopsy, Sir Ashley Cooper noticed that the haemorrhage was on the same side as the previous carotid ligation, and there was a large posterior communicating artery supplying collateral circulation to the ipsilateral middle cerebral artery. • In 1936 Nathan Winslow and colleagues reported an exhaustive review of 124 cases published in the literature. Surgical ligation of the carotid was the main therapeutical option (82 patients) with cure or improvement in 71%, and a mortality rate of 28%, while the conservative approach (42 patients) carried a mortality of 71% with 12% cure or improvement [16]. • Ligation remained the main therapeutical option until the late 1960s, when direct arterial reconstruction and/ or autogenous vein grafting had definitely become the best surgical option irrespective of the aetiology.
• Since then several series have been published, such as those of McCollum and deBakey with 37 cases operated in 20 years, representing 0.5% of all aneurysms performed in the same period [3]. • More recently El Sabrout and Cooley [2] published, in 2000, the largest single centre series of 67 carotid aneurysms operated between 1960 and 1995. • Nowadays endovascular techniques are being used particularly for lesions that are inaccessible to surgery.
2.5.2 Epidemiology/Aetiology • Extracranial carotid aneurysms are a rare situation representing 1–4% of all peripheral aneurysms and 0.5–2% of the total number of carotid operations [2, 8, 11, 16]. • They are distributed almost equally in the internal and common carotid arteries and only 2% are located in the external carotid artery. • In the past, the main causes of the development of this disease were syphilis and infections in surrounding structures, such as the throat and ears, as well as trauma. • In recent times atherosclerosis, previous carotid surgery especially with patch closure, and trauma represent most of the cases reported [2].
2.5.2.1 Atherosclerosis Aneurysms • Representing 70% of all these aneurysms, they affect predominantly older and hypertensive patients, and are sometimes associated with manifestations of occlusive or aneurysmatic disease at other locations. • They are localized at bifurcations and have a fusiform shape.
174
2.5 Aneurysms of the Extracranial Carotid Arteries
2.5.2.2 Previous Surgery/POS Endarterectomy • False aneurysm has occurred after carotid surgery mostly with synthetic patch closure but sometimes even with vein patch angioplasty. • The endarterectomized artery, infection, and the use of silk sutures (now abandoned) are the main factors implicated.
a break in the intimae followed by haemorrhage into the media, enlarging the vessel wall and reducing the true lumen. • If haemorrhage dissects into a plane between the media and the adventitia, an aneurysm forms. • This situation usually causes neurological symptoms owing to cranial nerve compression.
2.5.2.6 Other Possible Causes 2.5.2.3 Trauma • Represents the second most important cause of these aneurysms. • They are usually sacular and are really false aneurysms which as a group represent more than 50% of all cases in published series. • Closed trauma may be associated with extension, with sudden head rotation promoting intimae disruption and parietal damage, or with direct compression of the atlas transverse process or styloid process, or with mandibular fracture. • The extracranial high internal carotid is mainly affected, because it has no collaterals, thus promoting the mobility of this arterial segment compared to its intracerebral section. • Open trauma may affect different parts of the carotids, but mostly in exposed areas such as the common carotid. • Open trauma causes total or partial parietal disruption complicated by torrential haemorrhage, as well as false aneurysm and/or arterio-venous fistulae, as reported in World War II surgical registries [10].
Other possible causes are (Table 2.5.1): • Fibromuscular dysplasia • Congenital disorders • More rarely associated with intracerebral or visceral aneurysms (systemic inflammatory vasculopathy) • Marfan’s syndrome • Behçet’s disease • Periarteritis nodosum • Post-radiation. There is an association between saccular aneurysms and kinking and coils of the internal carotid artery (ICA), as personally observed by the authors. In these cases, the increased turbulence and shear stress on these vulnerable artery segments probably causes a locus of minor resistance, with intimae or transmural disruption and the formation of false or true aneurysms [7]. Table 2.5.1 Causes of extracranial carotid aneurysms • Atherosclerosis • Trauma (open/closed) • Post-endarterectomy
2.5.2.4 Infection • Syphilis was the main cause at the beginning of twentieth century and predominantly affects adults. • Tonsillitis and otitis are main causes in children. • Staphylococcus aureus infection is present in drug addicts and is carried by direct punctures with contaminated needles.
• Post-dissection • Mycotic (syphilis, tuberculosis, otitis, tonsillitis) • Congenital • Rare causes • Association with intracerebral aneurysms • Association with visceral aneurysms • Marfan‘s syndrome and Behçet‘s disease • PAN
2.5.2.5 Dissections • As these are spontaneous or traumatic they cause acute occlusion or chronic aneurysm, by developing
• Post-radiation
2.5.5 Diagnosis
2.5.3 Symptoms The symptoms of extracranial carotid aneurysms vary according to their location, size and aetiology. They can be fusiform or saccular in shape. The most frequent are fusiform aneurysms. Most often these affect the bifurcation of the common carotid artery and have a bilateral predilection, whereas the saccular type is mainly unilateral and located in the retrostyloid region [1]. • They are mainly asymptomatic, and present as a pulsating mass in the neck, with bruit and thrill [1]. They may cause symptoms, due to either compression of adjacent structures or cerebral embolization. • At present, neurological manifestations, such as transient ischaemic attack (TIA) or cerebral vascular accident, are the most frequent revealing sign of the fusiform type [1, 17]. • The symptoms of compression, of which pain is the most common local symptom, caused by the pulsated and expansible cervical mass (Fig. 2.5.1) characteristic of the saccular type can cause laryngeal and oesophageal compression or glossopharyngeal nerve or sympathetic nerve (Horner’s syndrome) compres-
sion [1] and cranial nerve dysfunction (II, III, IV, V and VI). • Raeder’s paratrigeminal syndrome, characterized by oculosympathetic paresis and intermittent facial pain, in some cases has been caused by a carotid aneurysm at the base of the skull [3]. • There are references in the literature to the propensity of the extracranial carotid aneurysms to imitate peritonsillar abscess, which were drained with consequent mortal haemorrhage [4]. The classic paper by Shipley’s group emphasized that aneurysms of the ICA present inwardly into the throat, whereas those of the common carotid present outwardly in the neck [3].
2.5.4 Complications • Cerebral embolization, causing TIA or stroke, is the most frequent complication. • Haemorrhage from spontaneous rupture is rare [13]. If rupture occurs into the oropharynx, the bleeding can be massive and can lead to suffocation and death.
2.5.5 Diagnosis 2.5.5.1 Recommended European Standard Diagnostic Steps of Investigation
Fig. 2.5.1 Cervical mass
• Colour Doppler (Fig. 2.5.2) is the most simple diagnostic tool, but has limitations, especially if the patient has a short neck or if the lesion is localized too distal in the carotid artery [11]. B-mode gray-scale imaging allows excellent definition of the size and extent of the arterial dilatation, and the use of colour flow imaging can determine the presence of thrombus and the flow characteristics [12]. • Enhanced CT scanning with three-dimensional reconstruction gives the most information. It allows complete analysis of the aneurysm, estimating the upstream and downstream ICA, and assesses the possible existence of a false lumen channel, representing the existence of a previous dysplastic or traumatic dissection. It also estimates the distance between the upper limit of the aneurysm and the temporal bone [11]. • The two-dimensional magnetic resonance inflow angiography technique with reconstruction (Fig. 2.5.3)
175
176
2.5 Aneurysms of the Extracranial Carotid Arteries
Fig. 2.5.2 Colour Doppler
Fig. 2.5.4 Angiography
balloon catheter [14], which is relevant to defining the surgical strategy. One clear disadvantage of arteriography is that it sometimes fails to visualize the aneurysm due to intramural thrombus formation [13]. • Two angiographic features help to differentiate saccular from fusiform aneurysms: saccular aneurysms show an outpouching off the arterial lumen, usually with a neck, whereas the fusiform type shows frank dilatation of the arterial lumen with no additional contrast outside the lumen. This latter type of aneurysm is usually accompanied by distortion of the arterial lumen and dilatation or stenosis in other segments of the vessel [9].
2.5.6 Treatment Fig. 2.5.3 Two-dimensional magnetic resonance
2.5.6.1 Conservative Treatment yields good opacification of the ICA, but the lesion may be underestimated in the case of a partially or completely thrombosed aneurysm [11]. • Arteriography (Fig. 2.5.4) precisely defines the location, and detects any associated lesion, such as stenosis, or wall irregularities [11]. It also has the advantage of preoperative assessment of the patient’s ability to tolerate carotid artery occlusion using an angiographic
Conservative treatment based on anticoagulation is recommended for some small aneurysms especially postdissection and requires regular ultrasonography control [15]. In 1984 Zwolak [18] described an overall stroke/major complications rate of 21% managing one-fifth of these aneurysms nonoperatively, but the group only included 6 cases. However, conservative treatment can be indicated for a subgroup of young patients with traumatic and
2.5.6 Treatment
spontaneously dissecting small aneurysms. Surgical repair is mandatory whenever neurological complications appear or progressive expansion occurs.
2.5.6.2 Surgery • Nowadays, surgery is generally accepted as the main treatment of extracranial carotid artery aneurysms, thus preventing cerebral embolization and rupture. • There is however some degree of uncertainty regarding the few cases treated in each institution (mean of one per year), and the different aetiologies, types and technical options chosen. • Aetiology and the type of presentation are the main factors that influence the surgical approach, which, until we have a better understanding of the natural history and results of the different therapeutical options, represents the gold standard for treatment. Fig. 2.5.5 Resection and interposition
Resection and Reconstruction using Saphenous Vein or PTFE Resection of the aneurysm and reconstruction using saphenous vein is the preferred technique (Fig. 2.5.5). The external carotid may be ligated or anastomosed to the graft. Shunt is used if there is evidence of impaired intracranial collateral perfusion or in cases of a previous stroke [15]. A high aneurysm location requires some technical details for achieving distal carotid control, such as: • division of the sternocleidomastoid muscle from its mastoid attachment with elevation of the parotid, • division of the digastrics, • removal of the styloid process and its attached muscles, • control of back bleeding by balloon catheter. The Marseille group [11] obtained reasonably good results in 25 ICA reconstructions, using an aggressive approach to get access to the last segment of the ICA via an anterior infratemporal route. This approach was used in ten cases, and included: • cutting the external auditory canal, • isolating the branches of the facial nerves, • retracting the styloid process and • luxation of the mandibular condyle. The mastoid process was reduced and the intrapetrous segment of the ICA exposed [11].
Resection and Primary Anastomosis or Reimplantation • In the case of a long and tortuous ICA, aneurysms can be treated simply by resection and primary anastomosis or reimplantation (Fig. 2.5.6). • The most frequent complications associated with this type of surgery are strokes related to embolization during manipulation and injury of the cranial nerves, particularly the X and the XII. • Occasionally neurogenic hypertension can result from transection of the carotid sinus and loss of baroreceptor function [15]. To avoid cranial nerve injury, El-Sabrout and Cooley [2], in their article describing the Texas Institute experience, express their preference for partial aneurysmectomy and patch closure of large fusiform aneurysms evolving carotid bifurcation. This option avoids extensive dissection of the posterior wall of the aneurysm, reducing the rate of cranial nerve dysfunction to 6%. Results of reconstructive surgery for atherosclerotic carotid aneurysms are reasonably acceptable with: • <2% mortality, • 6% stroke rate [15].
177
178
2.5 Aneurysms of the Extracranial Carotid Arteries
Ligation • Ligation nowadays is rarely used, being reserved for cases when reconstruction is not technically possible (about 10% of cases), where there is extensive local infection or for high-risk patients [18]. • McCann, in a literature survey with this technique, showed a stroke risk of 25% and a mortality rate of 20% [11] and others a death/stroke rate of 12%, in correlation with the back pressure of the clamped carotid artery [18]. • To obviate these effects some propose extracranial–intracranial by-pass graft, which is rarely used (4% of cases) but its effectiveness and long-term patency have not been demonstrated.
Endovascular Techniques
Fig. 2.5.6 Resection and reimplantation
The meta-analysis of the results of reconstructive surgery for all causes shows: • a mortality risk of 1.2%, • a stroke risk of 6%, • a cumulative morbidity-mortality risk of 7.2% [11]. Worse results can be expected when surgery is performed on an emergency basis for rupture or neurological manifestations, for re-operation and for high located aneurysms, which also promotes a higher incidence of cranial nerve injury [2]. The timing of surgery depends on aetiology and can influence the results. In post-traumatic or post-dissection cases, a delay of at least 3 months for revascularization is preferable, allowing the performance of a distal anastomosis on sclerotic and recovered scar tissue [11]. After a neurological event the delay depends on the presence of a stable neurological status and the absence of recent cerebral lesions defined by CT scan [11].
Endoaneurysmorraphy • When reconstruction is not feasible, endoaneurysmorraphy reducing the aneurysm diameter is an option in fusiform aneurysms, but long-term success has not been established [15].
• Endovascular techniques using stenting and embolization are now being used especially in inaccessible surgical cases, such as far distal lesions or re-operation. • The immediate and late results of a consistent number of cases are awaited but there are already some reports of good experiences using bare or covered stents, the latter being preferred in large defects in pseudoaneuryms complicating trauma or endarteriectomy [6, 11]. • McCready reports two cases, out of his experience of four, of embolization of branches of the middle cerebral arteries during the procedure and one stent occlusion at 12 months [6]. • So embolization constitutes a major hazard of this kind of therapy and the use of filters for cerebral protection is recommended.
Conservative Treatment • Doubts about the natural history of carotid artery aneurysms still persist, and, as Hertzer [4] said, one can ask if they are sufficiently dangerous to justify operations of the magnitude described by Rosset et al. [11] or if patients can be managed just as safely, or perhaps even more so, by modern antiplatelet therapy or oral anticoagulation. • However, the combined stroke and mortality rate of surgical reconstruction from the series of the Texas Heart Institute and in 12 previously published studies cited by this group was 9%.
References
• In comparison the rate was 12% for patients submitted to carotid ligation and 21% for patients receiving conservative treatment [2, 4]. • We can conclude that surgical treatment appears to be appropriate for most aneurysms located near the carotid bifurcation, although the stroke risk is higher than that associated with carotid endarterectomy, probably because of the higher potential for embolization from the thrombus and the tendency for the vein graft to kink and occlude. References 1. Bemelman M, Donker DN, Ackerstaff RG, Moll FL (2001) Bilateral extracranial aneurysm of the internal carotid artery. Vasc Surg 35:225–228 2. El-Sabrout R, Cooley D (2000) Extracranial carotid artery aneurysms: Texas Heart Institute experience. J Vasc Surg 31:702–712 3. Goldstone J (2000) Aneurysms of the extracranial carotid artery. In Rutherford R (ed) Vascular surgery, 5th edn. Saunders, Philadelphia, pp 1850–1852 4. Hertzer N (2000) Extracranial carotid aneurysms: a new look at an old problem. J Vasc Surg 31:823–825 5. Irwin RJ, Jacocks MA (2000) Internal carotid artery pseudoaneurysm related to pregnancy. Ann Vasc Surg 14:405–409 6. McCready RA, Divelbiss JL, Bryant MA, Denardo AJ, Scott JA (2004) Endoluminal repair of carotid artery pseudoaneurysms: a word of caution. J Vasc Surg 40:1020–1023 7. Menezes JD et al (2004) Aneurismas saculares da carotida interna. Revista da Sociedade Portuguesa de Angiologia e Cirurgia Vascular, Vol 1, N° 5, pp 33–38 8. Moore W (1996) Surgery of cerebrovascular disease, 2nd edn. Saunders, Philadelphia, pp 424–431
9. Munoz A, Campollo J, Vergas J (2001) Bilateral internal carotid aneurysms presenting as a nonpulsatile parapharyngeal mass: complementary diagnosis by CT, MR imaging and digital subtraction angiography. AJNR Am J Neuroradiol 22:864–866 10. Rich N et al (2004) Penetrating cervical vascular injuries. In: Rich N (ed) Vascular trauma, 2nd edn. Saunders, Philadelphia, pp 224 11. Rosset E, Albertini JN, Magnan PE, Ede B, Thomassin JM, Branchereau A (2000) Surgical treatment of extracranial internal carotid artery aneurysms. J Vasc Surg 31:713–723 12. Seabrook GR (2004) Nonatherosclerotic cerebrovascular disease. Haimovici’s vascular surgery, 5th edn. Blackwell, Oxford, pp 847–848 13. Skau T, Hillman J, Harder H, Magnuson B (2000) Surgical treatment of distal, extracranial, internal carotid artery aneurysms involving the base of the skull – a multidisciplinary approach. Eur J Vasc Endovasc Surg 20:308–311 14. Sood S, Timothy J, Anthony R, Strachan DR, Fenwick JD, Marks P (2000) Extracranial internal carotid artery pseudoaneurysm. Am J Otolaryngol 21:259–262 15. Stanley J (2000) Extracranial carotid artery aneurysms. In: Stanley J, Ernst CB (eds) Current therapy in vascular surgery, 4th edn. Mosby, new York, pp 102–104 16. Winslow H et al (1926) Extracranial aneurysm of internal carotid artery: history and analyses of cases registered into August 1925. Arch Surg 13:689–729 17. Zhang Q, Duan ZQ, Xin SJ, Wang XW, Dong YT (1999) Management of extracranial artery aneurysms: 17 years experience. Eur J Vasc Endovasc Surg 18:162–165 18. Zowlak RM, Whitehouse WM, Knake JE et al (1984) Atherosclerotic extracranial carotid artery aneurysms. J Vasc Surg 1:415–422
179
181
2.6 Endovascular Treatment of Carotid Stenosis THOMAS GERASIMIDIS, DIMITRIOS KARAMANOS, KONsTANTINOS KONSTANTINIDIS, ALEXANDROS MALLIOS
2.6.1 Introduction Endovascular treatment of carotid stenosis using carotid angioplasty and stenting (CAS) was first implemented experimentally on dogs in 1977 [33]. Since the early 1980s there have been reports of its implementation, mainly on patients suffering from fibromuscular dysplasia [18] and, later on, on patients with atherosclerosis and post-endarterectomy restenosis [34, 41, 57]. Stenting was performed electively in order to treat possible dissection or residual stenosis after the angioplasty procedure. Later this technique was abandoned to a routine stenting procedure. In 1986 Theron introduced a cerebral protection device using an occlusion balloon in the internal carotid artery (ICA) with simultaneous aspiration of possible microemboli [54–56]. The aim of the angioplasty and stenting procedure is – as in the case of carotid endarterectomy (CEA) – the prevention of stroke. Although initially it was considered to be an alternative solution only for high-risk patients, it is gradually gaining ground over endarterectomy and the number of patients treated by endovascular procedures is growing rapidly. Reports from the first trials comparing CAS to CEA came up with equally satisfactory results, raising the question of which of the two methods could be considered as the treatment of choice.
ferring to its composition and eventually to its stability) are to be considered essential for determining the indication for intervention. Asymptomatic patients are to be presented if they have a stenosis grade >70% with coexistence of contralateral occlusion, with a stenosis grade >80%, or if they are scheduled to undergo another major surgical operation. Clear indication for intervention is for symptomatic patients with a stenosis grade >70%, or a stenosis grade 50– 70% with the coexistence of contralateral occlusion, or a history of transient ischaemic attacks under antiplatelet treatment. Stenosis rate should be estimated using digital subtractive angiography (DSA) [35]. Two different ways for estimating stenosis grade are reported according to criteria of the NASCET and ECST trials respectively [17, 40]. According to the NASCET trial, the percentage of stenosis was determined by calculating the ratio of the luminal diameter (on two views) at the point of greatest stenosis to that at the normal part of the artery beyond the ste-
2.6.2 Indications for Surgery – Indications for Angioplasty Essential criteria for determining indications for operative treatment of carotid occlusive disease are the grade of stenosis as well as whether the patient is symptomatic. Furthermore, reports indicate that plaque characteristics as given by Duplex ultrasound controls (mainly those re-
Fig. 2.6.1 Digital subtraction angiography (DSA) evaluation of stenosis grade based on NASCET and ECST criteria
182
2.6 Endovascular Treatment of Carotid Stenosis
nosis site. According to ECST, the percentage diameter stenosis is calculated by using as a denominator an estimate of the original width of the artery at the point of the carotid bulb (as if there were no stenosis lesion). This difference in method results in great differences in patient classification, as a calculation of stenosis according to ECST tends to overestimate the percentage diameter stenosis compared to the NASCET method (Fig. 2.6.1). The same results are produced when calculation of stenosis is based on Duplex ultrasound as well as when, instead of an accurate calculation method, stenosis is estimated approximately by comparing DSA images [35]. Plaque characteristics as given by Duplex ultrasound play a vital role in determining indications for intervention treatment of carotid stenosis. Hypoechoic and heterogeneous plaques are very likely to produce microemboli because of their high lipid content as well as possible intraplaque haemorrhagic lesions (Fig. 2.6.2). Hyperechoic and homogeneous plaques, however, are indicative of plaque stability due to their high fibrous element content. The ICAROS study [8] was planned with the aim of correlating the risk of microemboli migration during carotid stenting to plaque echographic characteristics in order to achieve better patient selection for interventional treatment. Using a computer-programmed Duplex ultrasound device, lesion grey colour imaging was graded according to a grey scale median (GSM). It was proved that hypoechoic lesions with GSM <25 were related to a higher percentage of neurological complications after carotid angioplasty, to such a degree that these lesions are to be
considered contraindicative for interventional treatment. According to the study, stenotic lesions of GSM ranging 25–50 are considered safe to be treated with CAS, however in all these cases the use of a cerebral protection device is mandatory. Finally lesions of GSM >50 are considered so stable and safe that cerebral protection devices are not necessary during the CAS procedure. Apart from high-risk patients, special indications for CAS exist for patients with a haemorrhagic tendency, postendarterectomy restenosis, occlusion of the contralateral ICA and lesions located high in the neck area where a surgical approach is difficult; and also in hostile neck patients (due to previous neck operations, tracheotomy, local radiation therapy, or cervical vertebrae pathology for example ankylosing spondylitis) [7], or even in nonatherosclerotic lesions such as fibromuscular dysplasia or Takayasu’s arteritis, which are specific indications for angioplasty [26, 51].
Fig. 2.6.2 Internal carotid artery (ICA) Duplex image: heterogeneous plaque possible due to intraplaque haemorrhage (red arrow)
Fig. 2.6.3 Atherosclerotic plaque in ICA with ulcer lesion (red arrows)
2.6.3 Types of Stents
In contrast, unstable plaques with a floating surface clot or aortic arch lesions seem to be related to a high risk of microemboli migration, especially when guidewire and catheters are advanced through the lesions, and for this reason may be considered contraindications for angioplasty [7]. This is also the case for severely coiled carotid arteries as well as for plaques with intense calcification, which increase the risk of technical failure depending of course on the surgeon’s experience. Ulcerative plaques are not considered contraindications for angioplasty (Fig. 2.6.3). Renal failure is also not considered to be an absolute contraindication for angioplasty, provided that certain precautions and care have been taken to prevent the toxic effects of radiography contrast agents.
Fig. 2.6.4 Types of stents commercially available
2.6.3 Types of Stents During the first few years of this method’s implementation, the stenting procedure after angioplasty was done electively. Today, stenting is mandatory, as the use of stents produces better results both in preventing microemboli migration due to plaque destruction during angioplasty and also in avoiding recoiling. During the early days of stenting, stainless-steel balloon-expandable stents were the most commonly used. Palmaz® stents (Cordis-J&J, Miami Lakes, Fla.) were among the types initially used. Balloon-expandable stents have the advantage of exerting a constant radial force, which prevents stent collapse and allows embedding of
183
184
2.6 Endovascular Treatment of Carotid Stenosis
the stent in the vessel wall as well as accurate delivery. They are a reliable choice for lesions located at the origin of the common carotid artery (CCA), or extremely distal stenosis and occasionally in cases of highly calcified recoiling stenosis. However, they are not flexible and there are reports of compression when they are subjected to extreme mechanical force [36]. Also, it is rather difficult to use them in the carotid bifurcation area because of the difficulty of expanding vessels of varying diameter. Consequently, they are considered suitable for short localized lesions. Self-expandable stents are now considered the best choice for angioplasty and stenting procedures. Wallstents® (Boston Scientific, Natick, Mass.) were among the first stents of this kind to be used on a large scale. Eventually new types of self-expandable stents employing new materials, such as nitinol, were made. There are certain differences among various kinds of stents, such as in strut design and size. Some types have two different shapes, straight and tapered, with the latter being suitable for cases where stents should be placed partly in the internal and partly in the CCA. Currently available stents include: Carotid Wallstent® (Boston Scientific, Natick, Mass.), Exponent® (Medtronic, Minneapolis, Mn.), Xact Carotid Stent® (Abbot, South Pasadena, Calif.), RX Acculink® (Guidant, Santa Clara, Calif.), Sinus-Carotid® (OptiMed, Ettlingen), Nexstent® (EndoTex, Cupertino, Calif.), Conformexx® (Bard, Tempe, Ariz.), Precise® (Cordis-J&J, Miami Lakes, Fla.), Zilver Stent® (Cook, Winston-Salem, N.C.) and Protégé GPS® (ev3, Plymouth, Minn.) (Fig. 2.6.4).
2.6.4 Brain Protection Devices Neurological events due to microemboli migration towards the intracranial circulation are the most important among the possible complications of the method. Microemboli can be produced in practically all of the angioplasty phases, including guidewire and catheter manoeuvres inside the aortic arch, the advancement of wires through the lesions into the ICA, balloon advancement and delivery at the lesion area as well as balloon or stent dilatation at the site of stenosis. In order to decrease the risk of embolic events, brain protection devices have been used since the late 1980s, based on different concepts [54–56]. • Distal occlusion balloons, derived from Theron’s technique
Fig. 2.6.5 Schematic image of distal occlusion balloon protection device (PercuSurge GuardWire® )
• Filters • Proximal occlusion systems which produce flow reversal, derived from Kachel’s technique
2.6.4.1 Distal Occlusion Balloon (Theron’s System, PercuSurge GuardWire® Medtronic) (Fig. 2.6.5) This technique is based on the temporary occlusion of the ICA, distally to the stenosis area, by inflating a balloon and consequently reversing blood flow towards external carotid artery (ECA) and at the same time aspirating possible microemboli. The most important disadvantage of the method is that it blocks blood circulation. It is now used very rarely.
2.6.4.2 Filters This technique is based on the advancement and deployment of an umbrella-shaped system inside the ICA and distally to the stenosis area, which blocks possible microemboli. It constitutes of a mesh allowing blood flow through very small pores (100–150 μm), which is essential in cases of poor collateral circulation due to severe
2.6.4 Brain Protection Devices
Fig. 2.6.6 Types of filters commercially available
contralateral ICA lesion or a poor circle of Willis. However, several types of filters have a large cross-sectional profile leading to difficulties in passing tight, tortuous or high-grade stenoses. Also, filters can cause severe vasospasm or even dissection of the vessel wall and there is the possibility of thrombosis. There are reports of difficulties during closure and retrieval of the filters, sometimes leading to their contents being dislodged. The filter should be of such a size that it matches the lumen diameter in both systole and diastole and also after predilatation or stent deployment, which increase blood flow and lumen diameter.
Like distal occlusion balloons, filters do not offer protection throughout the whole CAS procedure. A large variety of filters is now commercially available, varying in terms of mesh pore size, delivery systems, ways of embedding in the arterial wall and in other features, details of which are beyond the aims of this chapter. The surgeon’s choice is based on personal preference and experience with each device. Filter protection devices currently available or under evaluation in clinical trials include: AngioGuard XP® (Cordis-J&J, Miami Lakes, Fla.), E.P.I Filter wire® (Boston Scientific, Natick, Mass.), Spider® (ev3, Plymouth, Minn.),
185
186
2.6 Endovascular Treatment of Carotid Stenosis
Fig. 2.6.7a–c a, b Proximal occlusion system. Parodi Anti-Emboli System®. a, b Extracorporeal flow. c The device inside the carotid artery
Emboshield® (Abbott, South Pasadena, Calif.), Accunet® (Guidant, Santa Clara, Calif.), Interceptor® (Medtronic, Minneapolis, Minn.) and Rubicon® (Rubicon, Salt Lake City, Utah) (Fig. 2.6.6).
Kachel’s System
2.6.4.3 Proximal Occlusion System
The use of this system was first reported in 1996 [28]. It consists of a double coaxial system with a balloon occluding the upper part of the CCA, producing flow towards the ECA, as well as an angioplasty balloon for the treatment of stenosis.
The concept of this system is to create a reversed flow within the ICA which prevents antegrade blood flow by sending the debris to the cerebral circulation.
Parodi Anti-Emboli System® (ArteriA Medical Science, San Francisco) (Fig. 2.6.7a–c) Parodi created a system that produced flow reversal in the ICA by occluding the CCA and the ECA. The reversed
2.6.5 Preoperative Evaluation
flow is then returned through an arteriovenous shunt with a filter to the femoral vein. It consists of a 10-Fr catheter with an occlusion balloon attached at the distal end. After the guidewire is inserted into the ECA, the catheter is advanced in the ECA and the balloon is inflated in the CCA. A second balloon is then placed in the ECA through the lumen of the catheter and inflated. The proximal end of the catheter is then connected to a femoral vein sheath via a connector with a filter inside to trap the emboli. Due to the difference of pressure, reversed blood flow from the ICA to the femoral vein is then established. The operator is now able to cross the lesion and place the stent under protection. The major advantage of this technique is that the protection starts before crossing the lesion. Disadvantages include the potential danger of spasm or dissection of the CCA or ECA and the intolerance of blood flow occlusion by some patients with reduced collateral supply and large introducer size.
Proximal occlusion systems offer protection before crossing the lesion, and in that sense can be considered as safer than other brain protection systems. However, it is understood that they cannot offer protection during guidewire manoeuvres into the aortic arch or during their advance through the carotid arteries. Also as with distal occlusion balloons, some patients cannot tolerate blood flow occlusion of the ICA. In order to deal with this problem, Parodi implemented a combination of two techniques calling it the “seatbelt and airbag technique”. According to this technique the Parodi AntiEmboli System® is initially used, creating reversed blood flow into the ICA, and then a second type of protection device using a filter is advanced distally into ICA. After filter deployment blood flow reversal is stopped and the procedure is continued under filter protection.
2.6.5 Preoperative Evaluation MO.MA® (Invatec, Roncadelle) (Fig. 2.6.8) Protection action occurs by interrupting the antegrade flow from the CCA and the retrograde flow from the ECA by inflating two occlusive balloons. Debris is stopped at the bifurcation and, after completion of the angioplasty procedure, removed by syringe aspiration. The balloons are then deflated and blood flow restored. Advantages and disadvantages are the same as in the Parodi AntiEmboli System®.
Fig. 2.6.8 Proximal occlusion system. MO.MA®
Patient history is vital in choosing and posing indication for treatment. Patients also undergo routine preoperative control, including physical examination, chest X-ray, electrocardiography (ECG), blood tests (haematological and biochemical profile as well as screening tests of the coagulation system). Special attention is given to renal function as any disorder may negatively affect the patient’s postoperative recovery.
187
188
2.6 Endovascular Treatment of Carotid Stenosis
2.6.5.1 Neurological Examination Clinical evaluation by an independent neurologist is necessary both to determine indications for intervention and to estimate accurately the patient’s preoperative condition and possible residual neurological signs due to previous brain ischaemic attacks. It is also necessary to have a postoperative clinical evaluation by the same neurologist in order to make sure there are no neurological complications due to the angioplasty procedure.
2.6.5.2 Special Imaging Examination Patients undergo a thorough imaging control, consisting of Duplex ultrasound, digital subtraction angiography (DSA) of the aortic arch and its branches [or magnetic resonance angiography (MRA) if necessary] and brain computed tomography (CT) scan.
it is very dependent on the examiner, it is subject to overestimation, and it cannot provide information regarding the aortic arch and most of the proximal part of the carotid arteries where the cause of the patient’s symptoms may lie.
2.6.5.4 Digital Subtraction Angiography (DSA) While the decision for endarterectomy can be based only on results of Duplex ultrasound, this cannot be the case for angioplasty. Preoperatively, precise evaluation of the grade of stenosis and of the anatomical features of the aortic arch and its branches are necessary. There are cases where excessive coiling, extreme angulations or other anatomical variations (for example, bovine arch) (Fig. 2.6.9) may be considered as either contraindicative for the an-
2.6.5.3 Duplex Ultrasound Duplex ultrasound usually acts as the screening test for diagnosis of carotid occlusive disease. In most cases it is part of a diagnostic procedure following a brain ischaemic incident, the onset of neurological signs or just the detection of a bruit in neck vessels during clinical examination. Duplex ultrasound provides information regarding carotid artery morphology, detection of stenosis site, as well as a rough estimation of the grade of stenosis and special plaque features regarding its stability and composition [6]. Using computerized programs for analysing grey scale images, Duplex enables the discrimination between homogeneous and heterogeneous plaques, with hyperechoic sites representing fibrous elements and hypoechoic sites representing lipids or places of intraplaque haemorrhage. It has been proved that heterogeneous and hypoechoic plaques, especially on the surface, are prone to be unstable and have a poor prognosis [38]. Using Doppler and coloured Duplex ultrasound an indirect functional evaluation of stenosis grade can be done by calculating maximum blood flow velocity. When values are >120 cm/s stenosis grade is estimated to be over 50%, thus being of clinical relevance and in need of thorough evaluation and treatment. Duplex ultrasound has the advantage of being atraumatic, repeatable (both for preoperative control and also for follow-up), reliable and costeffective. It has, however, some significant disadvantages:
Fig. 2.6.9 Abnormal origin of the left common carotid artery from the innominate artery (bovine arch) (red arrow). Significance of sufficient preoperative mapping of the aortic arch
2.6.5 Preoperative Evaluation
gioplasty procedure, or requiring a different approach (brachial access or direct catheterization of the CCA). DSA may also detect proximal lesions of the aortic arch, which may be thought responsible for the patient’s symptoms and must be treated at the same time as the carotid stenosis, as they have a high risk of causing perioperative embolic events.
2.6.5.5 Magnetic Resonance Angiography (MRA) (Fig. 2.6.10) MRA is based on different features of moving blood protons when detected under a strong magnetic field. MRA actually produces images of blood flow inside the lumen and not the exact anatomical morphology of the lumen. It is safer than DSA and has a high sensitivity but low specificity. A normal MRA is quite preclusive of possible significant stenosis, while pathological results cannot give the stenosis grade with high accuracy thus it is not absolutely positive for angioplasty indication [32]. In patients with impaired renal function the combination of Duplex ultrasound and MRA can provide a reliable preoperative evaluation while MRA has the advantage of providing brain scan images during the same examination. MRA is an evolving method whose results are improving.
2.6.5.6 Brain Computed Tomography (CT) Computed tomography (CT) of the brain is considered necessary for preoperative evaluation according to many reports [32]. Old or recent brain ischaemic incidents, history of neurosurgical operations or of accidents involving brain damage are absolute indications for preoperative brain imaging. This author’s view is that recent brain imaging, whether it involves CT or MRI, is easy, quick, inexpensive, safe and is necessary for all patients as a basic preoperative procedure in case of postoperative neurological complications.
Fig. 2.6.10 Magnetic resonance angiography (MRA): image of bilateral lesions (red arrow)
189
190
2.6 Endovascular Treatment of Carotid Stenosis
2.6.6 Technique 2.6.6.1 Step 1: Approach to the Common Carotid Artery Access Site The most common and widely used access site is via percutaneous catheterization of the femoral artery. Brachial or radial access or direct catheterization of the CCA following neck incision can be chosen in cases of severe aorta–iliac stenosis or occlusion, or in cases of a difficult approach to the aortic arch with an angulated carotid artery origin. Direct percutaneous catheterization of the
carotid artery, which was used previously, has now been abandoned because of serious disadvantages (difficulties with haemostasis, collapsed stents during manual compression for haemostasis or even puncture at the site of the plaque).
Femoral Access • Local anaesthesia of the inguinal area. • Percutaneous transfemoral catheterization followed by advancement of a stiff hydrophilic guidewire (0.035 inch, 0.1 cm) and then a sheath over the wire.
Fig. 2.6.11 Common carotid artery’s puncture after neck incision and preparation
2.6.6 Technique
Fig. 2.6.12 Various types of catheters and catheterization techniques regarding aortic arch anatomy
• Over the wire and through the sheath – a guide catheter is advanced along with the wire into the aortic arch.
Brachial Access This technique is used in cases of severe aorta–iliac stenosis or occlusions. Technical aspects are the same. For catheterization of the left ICA, right brachial or radial artery access is preferred; for the right ICA, the left brachial or radial arteries.
Cervical Access Via Preparation (Fig. 2.6.11) • • •
Local neck anaesthesia Preparation of the CCA following small incision CCA puncture (antegrade or retrograde depending on the stenosis site) • Advancement of guidewire and sheath
• Pre-interventional angiography to determine ICA’s morphology and stenosis site.
2.6.6.2 Step 2: Cannulation of the Common Carotid Artery (Fig. 2.6.12) Cannulation of the left or the right CCA is achieved using the proper guide catheter, by first advancing the guidewire just proximally to the bifurcation site and then proceeding with guide catheter advancement. Alternatively, CCA cannulation can be achieved by placing a soft guidewire and diagnostic catheter in the external carotid, exchanging that with a stiff wire and then withdrawing the catheter and inserting a guide catheter into the CCA. Finally, an alternative option is to use a long guide sheath instead of a guide catheter. When cannulation of the CCA and angiographic control are completed, the decision can be made as to whether a cerebral protection device can be used.
191
192
2.6 Endovascular Treatment of Carotid Stenosis
Fig. 2.6.13a,b Left ICA angioplasty: perioperative DSA before angioplasty (a) and after balloon-expandable stenting (b) without the use of a brain protection system (red arrow)
2.6.6.3 Step 3: Angioplasty and Stenting Without Cerebral Protection (Fig. 2.6.13a,b) A 0.035-cm (0.014-in) or 0.046-cm (0.018-in) guidewire is advanced distally to the stenosis site in the ICA. Then, after verifying the proper position of the guidewire, the stent is inserted at the site of stenosis. The stent can be inserted using either the over-the-wire-technique or the rapid exchange monorail technique (Fig. 2.6.14). The second technique is easier and quicker, and therefore more popular. The stent can be self-expandable or balloon-expandable. In cases of high-grade stenosis insertion of the stent can prove impossible, and there is also the danger of the premounted stent of the balloon slipping. In these cases, predilatation of the stenosis using a coronary balloon of 2–4 mm diameter and 20–40 mm length can help when inserting the stent at the stenosis site. Fig. 2.6.14 Monorail system
With Cerebral Protection (Fig. 2.6.15a,b) The stenting technique, in which a distal occlusion balloon or filter is used for cerebral protection, is quite similar. Crossing of the lesion with the protection device and inflation of the protection balloon or filter deployment
follow cannulation of the CCA using a guide catheter or a guide sheath. Then procedure is continued – if necessary and always under protection – with predilatation of the lesion, stent implantation and (also if necessary) postdilatation of the stent. When insertion of a brain protection
2.6.8 Complications
device is impossible, predilatation of the lesion using a coronary balloon can be done in order to help pass the protection device distally to the lesion. When the procedure is finished, the protection device is withdrawn. Using a proximal occlusion device as a protection system is quite a different procedure. After inserting the guide catheter into the CCA, an occlusion balloon is inflated in the upper part of the CCA and, according to the type of system, a second occlusion balloon is inflated in the ECA and so reversed blood flow is created. The procedure is then continued with stenting and, if necessary, pre- or post-dilatation is done and the protection system is withdrawn.
rate of technical failure was up to 10%, but continuous improvement in materials and experience has reduced this rate to less than 2% [59, 60].
2.6.6.4 Step 4: Control Angiography
2.6.8.3 Access Site Complications
Intervention is completed with angiographic control of the extra- and intracranial circulation.
The most common complication of this kind is haematoma at the puncture site or in the retroperitoneal area. Rarely, a false aneurysm may develop. There are also reports of common femoral artery dissection, most likely secondary to closure-device misplacement leading to occlusion and needing surgical exploration [53].
2.6.7 Peri-operative Monitoring Carotid angioplasty and stenting is performed using local anaesthesia under the anaesthetist’s care, checking the patient’s consciousness, motility and sensitivity levels during the whole procedure. Preoperatively, the patient is given salicylic acid and clopidogrel. During the procedure a bolus administration of 70–100 IU/kg unfractionated heparin is given in order to raise their activated partial prothrombin time to 200–300 s. An intravenous bolus of atropine (0.6–1 mg) is administered before dilatation in order to decrease the risk of major bradycardia due to carotid sinus stimulation when the carotid bulb is dilated. In very rare situations a temporary pacemaker may be needed. During the intervention, monitoring of blood pressure, cardiac pulse, arterial blood oxygen saturation as well as roughly the neurological condition of the patient is essential. When possible a transcranial Doppler ultrasound is performed.
2.6.8 Complications 2.6.8.1 Technical Failure In most cases the procedure is successfully completed with a residual stenosis of <30%. In the early days, the
2.6.8.2 Contrast Encephalopathy This is a rather rare complication involving patient confusion and neurological deficit. It is attributed to blood– brain barrier disturbance and extravasation of contrast agent. A CT scan can reveal signs of oedema and cortical enhancement which, however, soon vanish without leaving permanent neurological deficit [15].
2.6.8.4 Hyperperfusion Syndrome (Fig. 2.6.16) Brain cells have the ability to autoregulate blood circulation in response to a large range of systematic arterial blood pressure values. The presence of high-grade stenosis in the ICA leads to maximal arterial vasodilatation in order to preserve cerebral perfusion. When stenosis is treated by CAS, blood flow is increased in dilated cerebral vessels. If autoregulation does not respond accordingly, there is the possibility of increased perfusion, oedema or even brain haemorrhage [22]. The patient may suffer from headaches, seizures or even focal neurological symptoms and changes in their level of consciousness. The hyperperfusion occurrence rate ranges from 1.1% to 6.8% and is related to a high death rate (up to 40%) [1, 11]. It is associated with patients who have high-grade stenosis, a significant contralateral lesion and periprocedural hypertension. Patients should therefore be closely monitored for their ability to maintain systemic arterial blood pressure at the level of 140 mmHg. Transcranial Doppler findings of increased velocities are indicative of the patient’s high risk of developing the syndrome and may help in early diagnosis and treatment [45].
193
194
2.6 Endovascular Treatment of Carotid Stenosis
Fig. 2.6.15a Schematic image of carotid angioplasty and stenting (CAS) using a brain protection system
2.6.8.5 Hypotension and Bradycardia
2.6.8.6 Embolic Complication
Angioplasty and stenting of plaques located in the carotid bulb may result in haemodynamic alterations due to stimulation of the carotid sinus reflex. Stimulation of baroreceptors leads to increased parasympathetic discharge and a reduction in the sympathetic discharge, which results in hypotension and bradycardia. Rates vary between 7% and 68% [14, 47]. This complication may develop late after angioplasty (after the first 24 h) and may last for up to 10 days, without however increasing the risk of neurological complications [31]. Treatment initially involves fluid and atropine administration. Persistent hypotension may require the administration of vasoconstriction drugs and rarely a temporary pacemaker [21, 37].
Neurological events due to emboli are one of the most severe and life-threatening complications. Emboli production is possible in nearly all phases of angioplasty. Neurological event rates are decreasing as materials improve and experience grows. The combined 30-day stroke and death rate in various reports range between 4% and 10%. Brain protection systems have improved angioplasty results in such a way that recent reports estimate 30-day combined stroke and death rate at 1.8–3.3% [2, 13, 16, 19, 24, 25, 27, 29, 42, 48].
2.6.9 Follow-up
Fig. 2.6.15b Accunet® type of filter immediately after retrieval in one of the author’s cases
2.6.8.7 Complications Involving Brain Protection Devices The use of brain protection devices is now considered almost mandatory in carotid artery angioplasty procedures. However, their use is also linked with certain complications. These complications refer to the introduction and deployment of the devices as well as to tolerance, effectiveness and, most commonly, to device retrieval. Balloon occlusion devices are not always tolerated and filters can be the cause of spasm and dissection of the artery [12]. Debris may well end up in the brain, being transferred by the collateral circulation of the ECA [3]. Also they may not be captured by the filter device or slip out as the withdrawal catheter is being retrieved [43, 44, 58]. Finally brain protection systems increase the duration, technical difficulty and the cost of the procedure.
2.6.9 Follow-up Patients who do not suffer from any kind of complication after angioplasty may safely leave hospital on the first or second postoperative day, while in some cases patients can leave hospital in the evening of the day of operation [53]. It is necessary that patients undergo an examination of their neurological condition at regular periods as well as Duplex ultrasound control for possible asymptomatic restenosis, which in several trials is reported to be 5–20% after 5 years [30, 50, 53]. Complete physical and neurological examination along with Duplex control of the carotid arteries in 6 and 12 months and then yearly is considered a sufficient postoperative follow-up. In cases where Duplex control reveals gradient restenosis, pa-
195
196
2.6 Endovascular Treatment of Carotid Stenosis
Fig. 2.6.16 CT scan after left ICA angioplasty. Signs of left hemisphere oedema during hyperperfusion syndrome
tients should be examined more frequently. If restenosis becomes haemodynamically important and over 70%, a new DSA of the carotid arteries will be necessary in order to verify Duplex findings and determine the need for a possible new angioplasty.
2.6.10 Carotid Angioplasty and Stenting (CAS): Present and Future Carotid endarterectomy (CEA), having good results for symptomatic and asymptomatic patients [4, 40], was considered the gold standard for carotid occlusive disease. It is therefore for CAS plus brain protection systems to prove that it is at least as effective as endarterectomy. There are two main questions to be answered:
• Endarterectomy or angioplasty? • Use brain protection systems or not? The question of whether to use stents or not with carotid angioplasty does not exist. The CAVATAS trial [10] showed equal results regarding major complications (stroke and death) for CAS and CEA, while there was a statistically significant difference in favour of angioplasty regarding lesser complications such as cranial nerve injury or haematomas. The 1-year follow-up showed an increased rate of restenosis for the endovascular treatment but the 3-year follow-up, however, did not reveal any difference in stroke events between the two methods. The SAPHIRE trial [49], focusing on mortality as well as stroke and myocardial infarction rates in the 1-year follow-up, showed results such as 12.2% and 20.1% for
References
CAS and CEA respectively (p=0.004). Reoperation rates in the 1-year follow-up were 0.6% and 4.3% for CAS and CEA, respectively (p=0.04). The CARESS trial [9] revealed the same 30-days stroke- and myocardial ischaemia-related mortality rate (2%) for both methods. Based on these results carotid angioplasty and stenting with the use of brain protection systems seem to have equally good results as endarterectomy, and have the additional advantage of being minimally interventional. Furthermore, materials are being improved and have become less traumatic, more flexible and have a smaller cross-sectional profile. Drug-eluting stents have already given good results in coronary interventions by reducing the restenosis rate, while implementation of biodegradable stents is thought to produce natural remodelling of the vessels [5, 39, 52]. There is also significant progress in the study of plaques, which will enable better patient selection, while progress in drugs research has produced agents capable of reducing stroke rates [23, 46]. Bearing in mind that CAS is a new method, with continuous evolution of materials and technique it seems that the treatment of carotid occlusive disease is entering a new era. Results from new and larger clinical trials will answer our questions. Reports showed that CAS represented 8% of all interventions for carotid stenosis in Europe for the year 2000 [20]. It is estimated that this percentage will grow to 60% by the year 2006. References 1. Abou-Chebl A, Yaclar JS, Reginelli JP, Bajzer C, Bhatt D, Krieger DW (2004) Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: risk factors, prevention and treatment. J Am Coll Cardiol 43:1596–1601 2. Ahmadi R, Willfort A, Lang W, Schillinger M, Alt E, Gschwandtner ME, Haumer M, Maca T, Ehringer H, Minar E (2001) Carotid artery stenting: effect of learning curve and intermediate-term morphological outcome. J Endovasc Ther 8:539–546 3. Al-Mubarak N, Vitek JJ, Lyer S, New G, Leon MB, Roubin GS (2001) Embolization via collateral circulation during carotid stenting with the distal balloon protection system. J Endovasc Ther 8:354–357 4. Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group (MRC) (2004) Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet 363:1491–1502
5. Babapulle MN, Joseph L, Belisle P, Brophy JM, Eisenberg MJ (2004) A hierarchical Bayesian meta-analysis of randomized clinical trials of drug-eluting stents. Lancet 364:583–591 6. el-Barghouty N, Geroulakos G, Nicolaides A, Androulakis A, Bahal V (1995) Computer assisted carotid plaque characterization. Eur J Vasc Endovasc Surg 9:389–393 7. Becquemin JP (2004) Carotid artery disease: endovascular treatment of carotid disease. In: Hallet JW, Milla JL, Earnshaw JJ, Reekers JA (eds) Comprehensive vascular and endovascular surgery. Mosby, New York 8. Biasi GM, Ferrari SA, Nicolaides AN, Mingazzini PM, Reid D (2001) The ICAROS Registry of Carotid Artery Stenting. J Endovasc Ther 8:46–52 9. CARESS Steering Committee (2003) Carotid revascularization using endarterectomy or stenting systems (CARESS): phase I clinical trial. J Endovasc Ther 10:1021–1230 10. CAVATAS Investigators (2001) Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): a randomized trial. Lancet 357:1729–1737 11. Couts SB, Hill MO, Hu WY (2003) Hyperperfusion syndrome: toward a stricter definition. Neurosurgery 53:1053–1058 12. Cremonesi A, Manetti R, Setacci F, Setacci C, Castriota F (2003) Protected carotid stenting clinical advantages and complications of embolic protection devices in 442 consecutive patients. Stroke 34:1936–1943 13. Criado Frank, Lingel Bach JM, Ledesma DF, Lucas PR (2002) Carotid artery stenting in a vascular surgery practice. J Vasc Surg 35:430–434 14. Dangas G, Laird JR Jr, Satler LF, Mehran R, Mintz GS, Larrain G, Lansky AJ, Gruberg L, Parsons EM, Laureno R, Monsein LH, Leon MB (2000) Postprocedural hypotension after carotid artery stent placement: predictors and short and long term clinical outcomes. Radiology 215:677–683 15. Dangas G, Monsein LH, Laureno R, Peterson MA, Laird JR Jr, Satler LF, Mehran R, Leon MB (2001) Transient contrast encephalopathy after carotid artery stenting. J Endovasc Ther 8:111–113 16. Diethrich EB, Ndiye M, Reid DB (1996) Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 3:42–62 17. European Carotid Surgery Trialists Collaborative Group (1998) Randomized trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet 351:1379–1387 18. Garrido E, Montoya J (1981) Transluminal dilatation of internal carotid artery in fibromuscular dysplasia: a preliminary report. Surg Neurol 16:469–471
197
198
2.6 Endovascular Treatment of Carotid Stenosis
19. Golledge J, Mitchell A, Greenhalg RM, Davies AH (2000) Systematic comparison of the early outcome of angioplasty and endarterectomy for symptomatic carotid artery disease. Stroke 31:1439–1443 20. Greenhalgh RM et al (2002) Carotid stenting will become the gold standard: against the motion. In: Greenhalgh RM et al (eds) The evidence for vascular or endovascular reconstruction. Saunders, Philadelphia 21. Harrop JS, Sharan AD, Benitez RP, Armonda R, Thomas J, Rosenwasser RH (2001) Prevention of carotid angioplasty induced bradycardia and hypotension with temporary venous pacemakers. Neurosurgery 49:814–822 22. Hartman M, Weber R, Zouba S, Schranz C, Knauth M (2004) Fatal subarachnoid hemorrhage after carotid stenting. J Neuroradiol 31:63–66 23. Heart Protection Study Collaborative Group (2002) MRS / BHF Heart Protection study of cholesterol lowering with simvastatin in 20536 high-risk individuals: a randomised placebo-controlled trial. Lancet 360:7–22 24. Henry M, Amor M, Henry I, Klonaris C, Chati Z, Masson I, Kownator S, Luizy F, Hugel M (1999) Carotid stenting with cerebral protection: first clinical experience using the Percu Surg Guard Wire System. J Endovasc Surg 6:321–331 25. Henry M, Polydorou A, Henry I, Polydorou A, Hugel M (2004) Carotid angioplasty under cerebral protection with the PercuSurge Guardwire system. Catheter Cardiovasc Interv 61:293–305 26. Hui C, Baker D, Platts A (2003) The role of percutaneous transluminal angioplasty in the treatment of carotid fibromuscular dysplasia. Eur J Vasc Endovasc Surg Extra 5:102–105 27. Jaeger HJ, Mathias KD, Hauth E, Drescher R, Gissler HM, Hennigs S, Christmann A (2002) Cerebral ischemia detected with diffusion-weighted MR imaging after stent implantation in the carotid artery. Am J Neuroradiol 23:200–207 28. Kachel R (1996) Results of balloon angioplasty in the carotid artery. J Endovasc Surg 3:22–30 29. Kastrup A, Groschel K, Krapf H, Brehm BR, Dichgans J, Schulz JB (2003) Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke 34:813–819 30. Lal B, Hobson R, Goldstein J, Geohagan M, Chakhtoura E, Pappas P, Jamil Z, Haser P, Varma S, Padberg F, Cerveira J (2003) In stent recurrent stenosis after carotid artery stenting: life table analysis and clinical relevance J Vasc Surg 38:1162–1167
31. Leisch F, Kerschner K, Hofmann R, Steinwender C, Grund M, Bibl D, Leisch FA Jr, Bergmann H (2003) Carotid sinus reactions during carotid artery stenting: predictors, incidence and influence or clinical outcome. Catheter Cardiovasc Intervent 58:516–523 32. Mackey W, Naylor R (2004) Carotid artery disease: natural history and diagnosis. In: Hallet JW, Milla JL, Earnshaw JJ, Reekers JA (eds) Comprehensive vascular and endovascular surgery. Mosby, New York 33. Mathias K (1977) Ein neuartiges Katheter-System zur percutanen transluminalen Angioplastie von Karotis stenosen. Fortschr Med 95:1007–1011 34. Mathias K, Bockenheimer S, von Reutern G, Heiss HW, Osthein-Dzerowycz W (1983) Katheter dilatation hirnversorgender Arterien. Der Radiologe 23:208–214 35. Mathias K, Jager H, Hennigs S, Gissler HM (2001) Endoluminal treatment of internal artery carotid artery stenosis. World J Surg 25:328–326 36. Mathur A, Dorros G, Iyer SS, Vitek JJ, Yadav SS, Roubin GS (1997) Palmaz stent compression in patients following carotid artery stenting. Cathet Cardiovasc Diagn 41:137–140 37. Mlekush W, Schillinger M, Sabeti S, Nachtmann T, Lang W, Achmadi R, Minar E (2003) Hypotension and bradycardia after elective carotid stenting: frequency and risk factors. J Endovasc Ther 10:851–859 38. Montauban van Awijndregt A, Elbers HRJ, Moll FL, de Letter J, Ackerstaff RGA (1998) Ultrasonographic characterization of carotid plaques. Ultrasound Med Biol 24:489–493 39. Moses JW, Leon MB, Popma JJ, Fitzgerald PJ, Holmes DR, O’Shaughnessy C, Caputo RP, Kereiakes DJ, Williams DO, Teirstein PS, Jaeger JL, Kuntz RE; SIRIUS Investigators (2003) Sirolimus eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med 349:1315–1323 40. North American Symptomatic Carotid Endarterectomy Trial Collaborators (1998) Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 339:1415–1425 41. Numaguchi Y, Puxau FA, Provenza LJ, Richardson PE (1984) Percutaneous transluminal angioplasty of the carotid artery. Its application to post surgical stenosis. Neuroradiology 26:527–530 42. Ohki T, Marin ML, Lyon RT, Berdejo GL, Soundararajan K, Ohki M, Yuan JG, Faries PL, Wain RA, Sanchez LA, Suggs WD, Veith FJ (1998) Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg 27:463–471
References
43. Ohki T, Roubin GS, Veith FJ, Iyer SS, Brady E (1999) The efficacy of a filter device in preventing embolic events during carotid artery stenting: an ex-vivo analysis. J Vasc Surg 30:1034–1044 44. Ohki T, Veith FJ, Grenell S, Lipsitz EC, Gargiulo N, McKay J, Valladares J, Suggs WD, Kazmi M (2002) Initial experience with cerebral protection devices to prevent embolization during carotid stenting. J Vasc Surg 36:1175–1185 45. Pfefferkorn T, Mayer T, Von Stuckrad-Barre S, Covi M, Hamann GF (2001) Hyperperfusion-induced intracerebral hemorrhage after carotid artery stenting documented by TCD. Neurology 57:1933–1935 46. PROGRESS Collaborative Group (2001) Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack. Lancet 358:1033–1041 47. Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, Guterman LR, Hopkins LN (1999) Frequency and determinants of post procedural hemodynamic instability after carotid angioplasty and stenting. Stroke 30:2086–1093 48. Reimers B, Schluter M, Castriota F, Tubler T, Corvaja N, Cernetti C, Manetti R, Picciolo A, Liistro F, Di Mario C, Cremonesi A, Schofer J, Colombo A (2004) Routine use of cerebral protection during carotid artery stenting: results of a multicenter registry of 753 patients. Am J Med 116:217–222 49. SAPPHIRE Investigators (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy) (2004) Protected carotid-artery stenting versus endarterectomy in high-risk patients. 351:1493–1501 50. Setacci C, Pula G, Baldi I, de Donato G, Setacci F, Cappelli A, Pieraccini M, Cremonesi A, Castriota F, Neri E (2003) Determinants of in stent restenosis after carotid angioplasty: a case control study. J Endovasc Ther 10:1031–1038 51. Sharma BK, Jain S, Bali HK, Jain A, Kumari S (2000) A follow up study of balloon angioplasty and de novo stenting in Takayasu arteritis. Int J Cardiol 75:147–152
52. Stone GW, Ellis SG, Cox DA, Hermiller J, O’Shaughnessy C, Mann JT, Turco M, Caputo R, Bergin P, Greenberg J, Popma JJ, Russell ME; TAXUS-IV Investigators (2004) A polymer based, paclitaxel eluting stent in patients with coronary artery disease. N Engl J Med 350:221–231 53. Tan K, Cleveland T, Berczi V, McKevitt F, Venables G, Gaines P (2003) Timing and frequency of complications after carotid artery stenting: what is the optimal period of observation? J Vasc Surg 38:236–242 54. Theron J, Cosgrove R, Melanson D, Ethier R (1986) Embolization with temporary balloon occlusion of the internal carotid of vertebral arteries. Neuroradiology 28:246–253 55. Theron J, Raymond J, Casasco A, Courtheoux F (1987) Percutaneous angioplasty of atherosclerotic and postsurgical stenosis of carotid arteries. AJNR Am J Neuroradiol 8:495–500 56. Theron J, Payelle G, Coskum O, Huet H, Guimaraens C (1996) Carotid artery stenosis: treatment with protected balloon angioplasty and stent placement. Radiology 201:627–636 57. Tievsky AL, Droy EM, Mardiat JG (1983) Transluminal angioplasty in postsurgical stenosis of the extracranial carotid artery. Am J Neuroradiol 4:800–802 58. Tubler T, Schluter M, Dirsch O, Sievert H, Bosenberg I, Grube E, Waigand J, Schofer J (2001) Balloon protected carotid artery stenting. Relationship of periprocedural neurological complications with the size of particulate debris. Circulation 104:2791–2796 59. Wholey MH, Wholey M, Mathias K, Roubin GS, Diethrich EB, Henry M, Bailey S, Bergeron P, Dorros G, Eles G, Gaines P, Gomez CR, Gray B, Guimaraens J, Higashida R, Ho DS, Katzen B, Kambara A, Kumar V, Laborde JC, Leon M, Lim M, Londero H, Mesa J, Musacchio A, Myla S, Ramee S, Rodriquez A, Rosenfield K, Sakai N, Shawl F, Sievert H, Teitelbaum G, Theron JG, Vaclav P, Vozzi C, Yadav JS, Yoshimura SI (2000) Global experience in cervical carotid artery stent placement. Catheter Cardiovasc Interv 50:160–167 60. Wholey MH, Al-Mubarek N, Wholey M (2003) Updated review of the global carotid artery stent registry. Catheter Cardiovasc Interv 60:259–266
199
201
2.7 Carotid body tumour Fabrizio Benedetti Valentini, Rita Massa, Antonella Laurito
2.7.1 Synonyms • Carotid body tumour (CBT) • Chemodectoma • Paragangliomas.
2.7.2 Definition of the Disease • Carotid body tumour (CBT) is a non-chromaffin paraganglioma of the carotid body • It originates from the mesodermal cells of the third branchial arch and from the neural part of the ectoderm crest [14].
2.7.3 Epidemiology/Aetiology CBT location is predominantly at the carotid bifurcation, but similar paragangliomas can be found: • at the base of the skull • in the nasopharynx • at the aortic arch • along the mediastinum • or at the retroperitoneum. They can also originate from the glossopharyngeal or the vagus nerve. In a few cases there is multicentricity of the disease such as multiple associated tumours in various sites, which should not be confused with distant metastases [19]. In other cases the CBT is a component of a multiple endocrine neoplasia (MEN) in association with a medullary thyroid tumour or a phaeochromocytoma [3]. Two forms of CBT can be distinguished biologically:
• The familial form is transmitted by an autosomal dominant pattern [7]; it is usually fairly aggressive and bilateral in over 30% of cases [7, 8]. • The sporadic form is less aggressive and bilateral in no more than 5% [9–15]. Only a minority, perhaps 5%, is endocrinologically active, secreting catecholamines in various amounts [4–10]. Men and women are reported to be affected equally, but in the experience of this author, many more females are affected. It is also reported that the CBT becomes apparent between 40 and 50 years of age [19], however the extremes can extend from the paediatric to the geriatric age. The main source of vascularization of a CBT is the external carotid artery, however in larger tumours afferent vessels can grow from the internal carotid artery, the distal vertebral artery and the thyreocervical trunk. The CBT is basically a benign form, but it does not show any true capsule. It adheres tenaciously to the carotids and other adjacent structures, so that dissection can be difficult, leftovers though minimal are rather frequent and recurrence a real possibility. Malignant forms are suggested to be only around 5% [19] and cannot be detected on the basis of histology since mitotic figures or nuclear abnormalities are not evident. Only lymph node invasion and metastases in distant locations and in sites other than known ones for paragangliomas can identify the rare malignancy. The CBT grows slowly but progressively, adhering to and encasing the vessels and the nerves, compressing and dislocating the pharynx, even eroding the base of the skull. They should never be left untreated since the outcome is poor. In general the larger the tumour, the worse the symptoms, thus resulting in a more severe prognosis [1]. Macroscopically, the CBT appears as a dark reddish mass located at the carotid bifurcation and mainly on its
202
2.7 Carotid body tumour
postero-medial aspect; on its surface multiple enlarged and engorged vessels are evident. The tumour is elastic and tense, and bleeds easily and at high pressure. Both external and internal carotid arteries are dislocated and the bifurcation is enlarged; in large tumours the mass encases one or both carotids or even the hypoglossal, the superior laryngeal or the vagus nerve. In most cases the internal jugular vein is spared. Lymph nodes can be enlarged, even greatly, but histology is needed to judge about possible invasion. Histological features of the tumour are no different from those of the normal carotid body. A large number of capillaries surround clusters of cells where some are the supporting cells and others are epithelioid cells with granular eosinophilic cytoplasm (Fig. 2.7.1). Even in malignant forms no nuclear abnormalities or karyokinesis is seen. Fibrous septa containing blood vessels are evident.
When therapeutic preoperative embolization is done, rather large pale areas of ischaemia appear on the surface of the CBT and histology shows vessels either thrombosed or filled with occluding material and cell necrobiosis. Under the surgical perspective, the CBT, as suggested by Shamblin et al. [15], can be divided into three groups: • Group I is formed by small tumours, not yet strongly adhering to the carotids, that are fairly easily removed with no neurological complications. • Group II includes larger tumours, partially encasing the vessels and with tight adhesions to some nerves, particularly the superior laryngeal, the hypoglossal and vagus nerve: they can be resected, but their dissection is difficult and there is risk of damage to the nerves. • Group III is the highest degree of surgical difficulty and danger for the nerves; the tumour is very large, it encases completely one or both carotids; it extends towards the pharynx and the base of the skull; external carotid resection and/or internal carotid resection and reconstruction are needed, and in extreme cases nerve resection is not avoidable if radicality is to be reached.
2.7.4 Symptoms • A CBT remains asymptomatic until it involves the adjacent nerves and pharynx. • Painless swelling at the angle of the mandible is the first and main clinical sign. • At palpation it is elastic and mildly sore, fixed vertically but mobile laterally; a continuous bruit can be heard over the mass.
2.7.5 Complications Progressively with nerve involvement, the following can appear: • hoarseness • dysphasia • dysphagia • tinnitus • other cranial nerve dysfunctions. Fig. 2.7.1 Large clusters of cells are separated by fibrous septa. Numerous and enlarged capillaries are seen. The tumoural cells show granular eosinophilic cytoplasm
In some cases the tumour can be seen and palpated from inside the pharynx. Movements of the tongue can become impaired.
2.7.6 Diagnosis
2.7.6 Diagnosis 2.7.6.1 Recommended European Standard Diagnostic Steps of Investigation
• • •
At present there are highly reliable and noninvasive or minimally invasive techniques to reach a firm diagnosis and to determine the details for posing indications and planning treatment.
•
at the carotid bifurcation, which appears widened as much as the carotids are dislodged (Fig. 2.7.2). Dimensions of the tumour can be measured. In larger tumours, some afferent vessels suitable for preoperative embolization can also be identified. Differentiating a CBT from a carotid aneurysm is possible, as is detecting contemporary carotid intrinsic disease [16], such as atherosclerotic stenosis, which is rare but possible in older patients. Duplex scanning is definitely the most convenient screening examination.
Colour-coded Duplex Scanning • Colour-coded Duplex scanning is a very simple means to identify an oval shaped, highly vascularized mass
Magnetic Resonance Imaging (MRI) Scans Plus MR Angiography • MRI scans plus MR angiography (Fig. 2.7.3) can further visualize the carotids and the vessels afferent to the mass and help in differential diagnosis from other cervical masses as well as in estimating the tumour’s relationship with adjacent structures. • Precise measurement of the tumour’s size can be done, and its superior level in the neck estimated, thus contributing to the plan for the best surgical approach.
Fig. 2.7.2 Colour-coded Duplex scanning shows the tumoural mass (above) dislocating the internal carotid artery and rich vascularization through enlarged vessels (below)
Fig. 2.7.3 MR angiography clearly depicts the highly vascularized mass and deviation of the carotid arteries
203
204
2.7 Carotid body tumour
Computed Tomography and Angiograms (Angio CT) • Angio CT is more or less equivalent to MRI. • By this technique the position of the CBT as compared to the bony structures of the neck is usually best assessed. • Afferent vessels are also depicted rather sharply (Fig. 2.7.4). • By both MRI and CT bilateral investigation of the carotid bifurcation is carried out automatically and this is very useful while investigating a disease that is so often bilateral. • Both techniques are also employed when suspicion arises of multicentricity or of an associated tumour such as a phaeochromocytoma.
Nuclear Medicine Investigations
Fig. 2.7.4 Spiral CT of the same case as in Fig. 2.7.3 showing the tumour and some enlarged feeding vessels, which could be used for preoperative embolization
• Rather recently, nuclear medicine investigations have been applied both preoperatively and intraoperatively as radio-guided surgery.
Fig. 2.7.5a,b a SPECT 4 h postinjection of 111In-labelled pentetreotide, transaxial; large mass at the right carotid bifurcation with obvious uptake and accumulation of radiotracer. b Static planar scintigraphy 24 h postinjection, antero-posterior projection, same mass at the right carotid bifurcation
2.7.6 Diagnosis
• Patients with suspected CBT, or any functioning paraganglioma, are studied by somatostatin receptor scintigraphy (SRS) and single photon emission computed tomography (SPECT). • The radiotracer is 111In-labelled pentetreotide, better known as OctreoScan®, which is administered intravenously. • Radioactivity measurements and computed imaging are carried out between 4 and 24 h postinjection.
• The uptake by the tumour tissue is very high and identifies the mass, or masses, determining its nature (Figs. 2.7.5, 2.7.6). • This method is excellent in the follow-up of operated patients in order to detect any recurrence or to check residuals. • Further radioactivity measurements are carried out during surgery by a hand-held gamma-detecting probe connected to a special counting unit. • This method is particularly helpful in detecting even small leftovers of tumour tissue, which would surely entail a recurrence.
2.7.6.2 Additional Useful Diagnostic Procedures Selective Carotid Angiography • Selective carotid angiography was considered the gold standard exam until recently, since it accurately depicts the CBT (Fig. 2.7.7) and its highly vascularized mass with a “blush” effect. • It also shows the widening of the carotid bifurcation, identifies the afferent vessels and possible intrinsic carotid disease.
Fig. 2.7.6 Above: static planar scintigraphy 24 h postinjection of 111In-labelled pentetreotide, antero-posterior projection, preoperative; large mass with huge uptake of radiotracer at the left carotid bifurcation. Below: same examination, repeated after resection of the carotid body tumour; no radioactivity is detected at the previous tumoural site, all uptake is with the thyroid gland and maxillofacial centre
Fig. 2.7.7 Conventional angiography showing the tumour, the dislodgement of the carotid arteries and some enlarged vessels (left). An occlusion test of the internal carotid can be carried out (right) to assess tolerance to carotid blockade. In some cases the same technique can be used for cerebral protection during preoperative embolization
205
206
2.7 Carotid body tumour
• All the methods previously described allow the same information to be obtained by far less invasive means; therefore, some surgeons believe that angiography is only warranted when a preoperative embolization is judged to be useful. • There is no consensus whatsoever on the use of preoperative embolization: many surgeons think that it does not reduce the vascularization of the CBT and the bleeding during surgery and therefore it should not be done since it can cause cerebral embolization or internal carotid thrombosis [2, 11, 13]. • However in large tumours, when good calibre afferent vessels are clearly seen, selective embolization of those vessels can be helpful. • In such cases rather large spots of ischaemia have been seen during surgery with less intensive bleeding, though still abundant. • The safety of such a procedure can also be increased by contemporary internal carotid blockade; thus allowing an occlusion test to determine the patient’s tolerance to carotid clamping (Fig. 2.7.7). • This test can also be sensitized by the use of transcranial Doppler monitoring.
2.7.7 Therapy 2.7.7.1 Conservative therapy • There is no room for conservative treatment in CBT, since it grows slowly but progressively and causes severe damage of cranial nerves and can proceed to become intracranial or to compress the pharynx. • Chemotherapy is ineffective. • Radiotherapy carries definite danger such as necrosis of the mandible, laryngeal fibrosis and carotid lesions [5, 10, 12, 17]. Therefore, it should be restricted to old and high-risk patients or to recurrence at the base of the skull.
2.7.7.2 Surgery Recommended European Standard Surgical Procedures Surgery is carried out under general anaesthesia with complete haemodynamic monitoring and autotransfusion equipment. When manoeuvres on the mandible are
planned, nasotracheal intubation should be done. Bipolar coagulation is advisable in order to avoid heat damage to the nerves. A pre-sternomastoid muscle incision is carried out, extended upwards anterior to the external auditory meatus when needed. In such cases the parotid gland is mobilized and the facial nerve is identified and preserved. When the CBT grows high above the angle of the mandible a better approach to the distal segment of the internal carotid artery is needed for a more radical resection of the tumour, safer dissection of the nerves and vascular reconstruction. There are two ways to obtain this: anterior subluxation of the tempo-mandibular joint or vertical osteotomy of the mandibular ramus. The second approach has been shown to provide a wider space almost up to the base of the skull [18]. The bone is later reconstructed by internal rigid fixation. Posterior resection of the digastric muscle can improve access to the distal internal carotid also when mandibular osteotomy is not carried out. Proximal control of the common carotid artery is easy; conversely, it may be difficult to reach distal control of the internal and external carotid. All the manoeuvres should be started from the external carotid and go upwards. This is described as a periadventitial plane, named “white line” [6], where the dissection is supposedly easier. This is only a theoretical assumption since in most cases, and particularly in the most advanced ones, the surgeon must adapt to whatever plane is found. Sometimes dividing and resecting a segment of the external carotid may help to decrease the blood supply to the tumour and can act as a lever of traction on the tumorous mass. The lowest part of the CBT is tightly attached to the posterior aspect of the carotid bifurcation and may be very hard to detach. Occasionally it is best removed last. Cranial nerves should be identified, dissected and spared very carefully. In extreme situations, with large aggressive tumours encasing carotids and nerves, resection of some of them becomes mandatory, although the result can be a very disabling one. The involved nerves are the vagus, the hypoglossal and the superior laryngeal nerve. The latter lies immediately behind the carotid bifurcation and proximal segment of the external carotid and is particularly vulnerable since it is regularly involved in the dissection. In CBT moderately extended upwards the glossopharyngeal nerve may be involved and should also be identified and spared if severe disturbances to swallowing are to be avoided. When external carotid resection is carried out there is no indication to reconstruct it, but no stump should be left on the carotid bifurcation since it could become
2.7.7 Therapy
the site of thrombosis and consequent embolization to the brain. When the internal carotid artery cannot be dissected free from the tumour or is injured during the manoeuvres its reconstruction becomes mandatory. Simple angioplasty may suffice in few cases; in most of them graft reconstruction is needed. It is generally agreed that the graft of choice is a segment of autogenous saphenous vein (Fig. 2.7.8) and actually good results were obtained that way. However, the interposition of a segment of thin-walled PTFE tube performed just fine and was easier to manage when an internal shunt was needed. Such a need can be predicted preoperatively by an internal carotid occlusion test, during angiography, or more simply by a common carotid compression test during transcranial Doppler examination (TCD). TCD is also used intraoperatively to monitor flow velocity changes in the intracranial vessels and particularly in the middle cerebral artery or to detect embolizations; it is also the simplest way to know when a shunt should be used and to monitor its function.
Radioactivity measurements were very reliable and useful. They were undertaken on the tumour in vivo and on the background for comparison, on the lymph nodes to detect invasion and in the tumorous bed to detect remnants: even small ones were readily identified and removed.
Possible Complications of the Surgical Procedure Two are the main concerns of surgery for CBT: recurrence and neurological complications. • Recurrence was more frequent some time ago, when technical means, from investigations to surgery, were much less refined. The possibility of safely reconstructing the internal carotid artery attains two goals: it allows for radical resection of large tumours and avoids strokes. However, since even tiny remnants may lead to recurrence, radionuclide investigations and radio-guided surgery can ameliorate the outcome even more.
Fig. 2.7.8 Intraoperative view after resection of a tumour of the carotid body together with external and internal carotid arteries. A segment of autogenous saphenous vein was inserted to repair the internal carotid artery
207
208
2.7 Carotid body tumour
• Neurological complications, that is cranial nerves injuries, are largely proportional to tumour size, pace of growth and clinical symptoms. The superior laryngeal nerve is often hurt since it is almost invariably involved also in rather small tumours. The hypoglossal and the vagus nerve can be dissected safely in most cases; some deviation of the tongue is seen rather frequently after surgery but disappears in a few days. The glossopharyngeal nerve is usually the last involved and gets easily hurt because it is not easily identified. Cranial nerve complications are reported as high as up to 40%. There are however big differences in the degree and clinical significance from mild dysphonia to severe dysphagia and/or total tongue deviation. The latest estimates of permanent disabling complications are around 5%. CBT should be operated upon as early as possible.
2.7.8 Differential Diagnosis In the early phase of the disease a high level of suspicion is needed to reach the diagnosis of CBT, while in the most advanced stage it becomes rather obvious and only a differential diagnosis pathway has to be followed. Lymph node enlargement, thyroid diseases, submandibular or parotid gland disease and carotid aneurysms are taken into consideration. References 1. Benedetti-Valentini F, Stumpo R, Massa R, Romeo S (2001) I Chemodectomi. In: Benedetti-Valentini F (ed) Chirurgia Vascolare. Minerva Medica, Turin, pp 519–523 2. Berguer R, Kieffer E (1992) Carotid body tumours and other paragangliomas. In: Surgery of the arteries to the head. Springer, Berlin Heidelberg New York, pp 201–204 3. Bolande RP (1976) The neurocristopathies: a unifying concept of disease arising in the neural crest development. Hum Pathol 5:409–413 4. Crowell WT, Grizzle WE, Siegel AL (1982) Functional carotid paragangliomas: biomedical, ultrastructural, and histochemical correlation with clinical symptoms. Arch Pathol Lab Med 106:599–603 5. Evenson LJ, Mendenhall WM, Parsons JT, Cassisi NJ (1998) Radiotherapy in the management of chemodectomas of the carotid body and glomus vagale. Head Neck 20:609–613
6. Gordon-Taylor G (1940) On carotid body tumours. Br J Surg 28:163–167 7. Grufferman S, Gillman MW, Pasternak LR, Peterson CL, Jung WG Jr (1980) Familial carotid body tumours: case report and epidemiologic review. Cancer 46:2116–2122 8. Hallett JW, Nora JD, Hollier LH, Cherry KJ, Pairolero PC (1988) Trends in neurovascular complications of surgical management for carotid body and cervical paragangliomas: a 50-year experience with 153 tumours. J Vasc Surg 7:284–291 9. Javid H, Chawla SK, Dye WS, Hunter JA, Najafi H, Goldin MD, Serrj C (1976) Carotid body tumours: resection or reflection. Arch Surg 111:344–347 10. Lees CD, Levine HL, Beven EG, Tucker HM (1981) Tumours of the carotid body: experience with 41 operative cases. Am J Surg 142:362–365 11. Mansfield AO (2001) Excision of carotid body chemodectoma. In: Greenhalgh RM (ed) Vascular and endovascular surgical techniques. Saunders, London, pp 43–48 12. Martin CE, Rosenfeld L, McSwain B (1973) Carotid body tumours: a 16-year follow-up of seven malignant cases. South Med J 66:1236–1243 13. Pandya SK, Nagpal RD, Desai AP, Purohit AT (1978) Death following external carotid arterial embolization for a functioning glomus jugular chemodectoma. J Neurosurg 48:1030–1034 14. Pryse-Davies J, Dawson IMP, Westbury G (1964) Some morphological histochemical and chemical observations on chemodectomas and the normal carotid body, including a study of the chromaffin reaction and possible ganglion cell elements. Cancer 17:185–202 15. Shamblin WR, ReMine WH, Sheps SG, Harrison EGJ (1971) Carotid body tumour (chemodectoma): clinicopathologic analysis of ninety cases. Am J Surg 122:732–739 16. Steinke W, Hennerici M, Aulich A (1989) Doppler colour flow imaging of carotid body tumours. Stroke 20:1574–1577 17. Valdagni R, Amichetti M (1990) Radiation therapy of carotid body tumours. Am J Clin Oncol 13:45–48 18. Valentini V, Fabiani F, Nicolai GL, Torroni A, Battisti A, Iannetti G, Irace L, Faccenna F, Siani A, Pascucci Marzia, Benedetti-Valentini F (2002) Surgical approach to the third area of the internal carotid artery through vertical osteotomy of the mandibular ramus. J Craniofac Surg 13:816–820 19. Whitehill TA, Krupski WC (2000) Uncommon disorders affecting the carotid arteries. In: Rutherford RB (ed) Vascular surgery. Saunders, Philadelphia, pp 1856–1862
209
2.8 Combined Treatment of Coronary Plus Other Arterial Pathologies: the Magnitude of the Polyatherosclerotic Patient Nicos S. Angelides
2.8.1 Introduction Atherosclerosis is a generalized disease [2, 4, 9, 11, 21, 22, 41]. Therefore, it is of no surprise that simultaneous atherosclerotic lesions may exist in the carotid arteries, the coronary arteries, the aorta and the peripheral arteries in the form of unifocal, bifocal and multifocal occlusive or aneurysmal disease [1, 14, 15, 18, 26, 38, 39]. Coexistence of severe coronary artery disease with carotid artery stenosis, aortic aneurysm and critical limb ischaemia is a frequent event and the management of these patients is still unclear and in some cases controversial [12, 16, 17, 24, 27, 31, 32, 36, 37]. Therefore, multifocal atherosclerosis remains a challenge for the cardiothoracic and vascular surgeon who has, nowadays, the therapeutic alternative of open or endovascular repair.
2.8.2 The Magnitude of Multifocal Arterial Disease In order to identify the magnitude of multifocal atherosclerosis, a study on 387 consecutive patients admitted for arterial operation was carried out by the team of The Cardiovascular and Thoracic Unit of the Nicosia General Hospital, Cyprus. The aim of this study was to calculate the percentage of modification of the surgical or endovascular reconstruction initially planned and, also, to demonstrate the way in which endovascular techniques have affected the management of polyatherosclerotic patients with multifocal occlusive or aneurysmal disease.
• • • • •
Symptomatic carotid artery stenosis – 74 patients. Severe coronary artery disease – 198 patients. Thoracic aortic aneurysms – 10 patients. Abdominal aortic aneurysms – 55 patients. Severe peripheral arterial disease – 60 patients.
Preoperative evaluation included noninvasive assessment, calculation of a five-step cumulative illness scale and angiography in the form of digital subtraction, spiral CT, or MR angiography. Noninvasive assessment utilized: • Carotid Duplex scan, to show the site and extent of stenosis and type of atherosclerotic plaque • ECG, to demonstrate ischaemic changes and changes in cardiac rhythm. • Treadmill exercise test, to show changes that may occur in the coronary or the peripheral circulation during exercise. • Thallium perfusion scan, to detect myocardial ischaemia at rest or after exercise. • Muga scan, to investigate the pumping efficiency of the heart. • Segmental pressure measurements using Doppler ultrasound and cuffs. • Coloured Duplex scan, to perceive the anatomical outlook of the aorta and the peripheral arteries as well as the spectrum of blood flow at any site of stenosis. Finally, the five steps of the cumulative illness scale were: 1 for normal 2 for mild problems 3 for moderate problems 4 for severe problems 5 for life-threatening impairment.
2.8.2.1 Material and Methods
2.8.2.2 Results
Patients were classified in five groups according to their initial diagnosis:
• The overall incidence of multifocal arterial disease was 61.9% (Fig. 2.8.1).
210
2.8 Combined Treatment of Coronary Plus Other Arterial Pathologies: the Magnitude of the Polyatherosclerotic Patient
Fig. 2.8.1 Patients with multifocal and unifocal arterial disease
Fig. 2.8.2 Patients with multifocal arterial disease
Fig. 2.8.3 Severe multifocal arterial disease
Fig. 2.8.4 Five-step cumulative illness scale in patients with multifocal and unifocal atherosclerosis
The distribution location of multifocal arterial disease is shown in Fig. 2.8.2: • 44.9% of multi-atherosclerotic patients had severe combined coronary and peripheral arterial disease • 30.8% combined carotid and coronary • 13.2% combined carotid and peripheral arterial disease • 11.3% combined carotid, coronary and peripheral arterial disease. Severe forms of multifocal arterial disease represented 9.5% of the total (Fig. 2.8.3). The five-step cumulative illness scale showed that cardiovascular, respiratory and renal problems, as well as hypertension and diabetes mellitus were significantly increased in multifocal compared to unifocal disease (Fig. 2.8.4). These results agree with those published throughout the world [4, 5, 7, 11, 16, 20, 23, 24, 29, 41].
The main focus of the study was the need to modify the initially planned treatment as a result of other vascular priorities; this proved to be necessary mainly in patients with critical limb ischaemia, as a result of severe peripheral arterial disease; 9.4% of these patients‘ plans were in need of modification, in the sense that the coexistence of carotid and coronary artery disease affected the initially planned treatment, altering the priorities. The results demonstrated that endovascular treatment was the first treatment of choice for patients with critical limb ischaemia due to aorto-iliac disease. The endovascular procedures carried out showed an 85% immediate success rate. The 3-year primary patency rate was 53% for angioplasty alone and 62% for angioplasty and stenting. Surgical treatment for severe aorto-iliac disease, leading to critical limb ischaemia, was performed simultaneously with carotid endarterectomy whenever endovascular treatment was technically impossible. Endovascular treatment was
2.8.3 Multifocal Occlusive and Aneurysmal Arterial Disease
also carried out for infra-inguinal arterial disease causing critical limb ischaemia. The results showed a 75% initial success rate for superficial femoral artery occlusion and 61% for popliteal occlusion. The 1-year patency rate for both locations decreased to approximately 44%, while the 3-year patency rate was even worse, decreasing to about 28% for both locations. Endovascular reconstruction was not introduced for infra-popliteal lesions; instead, a long femorocrural by-pass graft was preferred, using either vein – when available – or a composite graft. The initial success rate was 69%; the 1-year patency rate was 58% and the 3-year patency rate 51%. In these patients other existing factors were always taken into consideration, such as sepsis, neuropathy and the presence of chronic renal and venous disease. Results demonstrated that in patients with aortic aneurysms the need to modify the initially planned treatment as a result of other vascular priorities was 1.2%; in such cases, the treatment of choice was endovascular repair of the abdominal aortic aneurysm (EVAR); general anaesthesia over local was preferred, as was the use of self-expandable grafts. The immediate and late results were free of complications, but it should be clearly noted that EVAR was used in highly selected cases. Reviews of the international literature indicate that EVAR was applied in about 4% of cases. Finally, the need for modification was similarly low (3.3%) in patients with severe symptomatic carotid and coronary artery disease, but this will be discussed further on [3, 13, 33–35, 43, 46]. The results of the study demonstrate that the coexistence of severe carotid, coronary and peripheral arterial disease is particularly high in vascular patients admitted to hospital for treatment. Similarly, a high need was also identified for modifying the initially planned treatment in polyatherosclerotic patients. In these patients, any modification of treatment was always based on the location of the multilevel occlusive or aneurysmal arterial disease, and on its severity. Angioplasty, alone or in combination with stenting, was the treatment of choice whenever possible, which is in agreement with international literature [6, 10, 19, 30, 45, 47]. The results demonstrate that, in polyatherosclerotic patients, whenever there was a need to modify the initially planned therapy, endovascular surgery monopolized the field of treatment, because it is easily applied and does not affect the patient’s status considerably. According to the results of the study, surgery provided better immediate and long-term patency and is the first line of treatment in occlusive and aneurysmal vascular disease. Finally, the use of intravascular ultrasonography (IVUS) before angioplasty may facilitate
the selection of patients for endovascular treatment, especially in the polyvascular patients.
2.8.3 Multifocal Occlusive and Aneurysmal Arterial Disease Combined occlusive coronary artery disease and aortic aneurysm may frequently exist in the same patient and represents a difficult vascular condition from the management point of view [14, 42–45]. In such patients, it is not easy to predict the necessity for coronary artery by-pass grafting (CABG) without conducting coronary angiography. Consequently, this can justify the routine enforcement of preoperative coronary catheterization in most cases of aortic aneurysm [18, 20, 21]. However, it has been demonstrated that in the presence of abdominal aortic aneurysm the incidence of patients requiring CABG first was small (about 4.5%). A similarly small percentage was reported in cases of thoracic aortic aneurysms [3, 38, 46]. According to this information, routine preoperative cardiac evaluation before aortic aneurysm repair may contribute little information with an impact on treatment, and therefore most patients with aortic aneurysm may undergo surgery safely with no cardiac workup [14]. In the case of staging of the corrective procedures, surgical repair of coronary artery disease in patients with coexisting large abdominal aortic aneurysms may increase the rate of aortic aneurysm rupture. This is why one-stage CABG and aortic aneurysm repair has been recommended by several surgeons as an alternative to staged intervention, but with a higher mortality rate [5, 20]. Data analysis of the study led to the following six options concerning escalation of the corrective procedure: • Option 1. One-stage CABG and simultaneous aortic aneurysm repair carried out either during or after cardiopulmonary by-pass. Abdominal aortic aneurysm repair during cardiopulmonary by-pass is recommended in patients with established left ventricular dysfunction. • Option 2. One-stage CABG performed with a beating heart and simultaneous abdominal aortic aneurysm repair. • Option 3. Two-stage procedure consisting of CABG followed by aortic aneurysm repair at a later stage. Recommended timing for the repair of the abdominal aortic aneurysm is 2 months after myocardial revascularization.
211
212
2.8 Combined Treatment of Coronary Plus Other Arterial Pathologies: the Magnitude of the Polyatherosclerotic Patient
• Option 4. Reversed two-stage procedure consisting of repairing the abdominal aortic aneurysm first and the CABG later. • Option 5. Angioplasty and stenting for the coronary artery disease, performed as a first procedure to correct unstable angina, followed by the repair of the abdominal aortic aneurysm. • Option 6. Endovascular repair of the abdominal aortic aneurysm performed as a first procedure, followed by CABG.
• Also, there are reported cases of simultaneous carotid endarterectomy, CABG and repair of abdominal aortic aneurysm, as well as reports of one-stage operations in combined thoracoabdominal aortic aneurysm and coronary artery disease [5, 12, 23, 27, 29].
The above options are based on the experience of the team that conducted the study. In patients with unstable angina options 5 and 6 are recommended. In patients with severe coronary artery disease combined with large aortic aneurysm options 2 and 6 are preferred. In patients with stable angina and an asymptomatic, non-tender abdominal aortic aneurysm, option 3 is recommended. Option 1 is recommended in younger patients with a combination of severe coronary artery disease and a quickly expanding large abdominal aortic aneurysm, although in such patients a one-stage operation with off-pump CABG is also an attractive option (option 2). Option 1 is also recommended for the repair of combined aneurysm of the ascending aorta and CABG. On reviewing the international literature, it may be noted that it is not possible to proceed with firm recommendations regarding the management strategy, mainly due to the lack of a large series of patients with critical coronary artery disease and aortic aneurysm. The following extra recommendations are debated on the basis of published literature: • If the abdominal aortic aneurysm is not tender and has a diameter of 5.45–8 cm a combined approach may be a better option [14, 45]. • Performing CABG with a beating heart will help to avoid the risk of abdominal aortic aneurysm rupture during the interval between the two operations. • Endoluminal repair of abdominal aortic aneurysm offers a further option, both for stage and reversed-stage approaches and may be applied in patients with large aneurysms amenable to this therapeutic modality. • The same options exist for patients with coexistent coronary, aortic and severe peripheral disease (critical limb ischaemia) [22, 24, 25, 47]. In these patients endoluminal repair becomes even more attractive because it repairs some of the existing arterial problems of the polyvascular patient, with low mortality and morbidity.
Stroke is a devastating complication of coronary bypass surgery and is associated with significant mortality (20%). There has been a debate over the last 25 years concerning the relationship between carotid endarterectomy and CABG. Which one has priority? This issue remains controversial but becomes more demanding with the passing of time. This is because there the population needing CABG is ageing, which in consequence increases the coexistence of carotid and coronary artery disease. Although there is now a significant reduction in the morbidity and mortality following myocardial revascularization, the incidence of post-operative stroke in patients undergoing coronary surgery has remained unchanged. This observation can be explained by the fact that the causes of perioperative stroke after CABG are multifactor. They include: • Ventricular mural thrombi • Emboli from atherosclerotic plaques in the ascending aorta • Showers of microemboli from air, platelet aggregation and fat during cardiopulmonary by-pass • Perioperative hypotension • Intracranial haemorrhage [5, 10, 25].
2.8.4 Multifocal Carotid and Coronary Occlusive Disease
However, the most powerful predictor of perioperative stroke during CABG is ipsilateral carotid artery stenosis [1, 2, 15, 43]. Today, coronary patients needing myocardial revascularization are frequently screened preoperatively, which allows an increased percentage of severe asymptomatic carotid disease to be detected. Many studies have shown increased postoperative stroke rates in patients with carotid artery disease. Brener et al. [11] reported a stroke rate of 9.2% in patients undergoing cardiac revascularization with a less than 50% ipsilateral carotid artery stenosis; the same authors found a stroke rate of 20% in patients with greater than 50% stenosis. Faggioli et al. [16] reported that the highest postoperative risk of stroke was
2.8.4 Multifocal Carotid and Coronary Occlusive Disease
in patients with greater than 75% symptomatic carotid artery stenosis. They also found that a very high risk of perioperative stroke exists in patients with >80% asymptomatic bilateral carotid artery stenosis, as well as >80% asymptomatic ipsilateral carotid artery stenosis and contralateral occlusion [16]. What is the prevalence of severe carotid artery disease in coronary patients needing surgery? Carotid Duplex imaging has provided information regarding the prevalence of carotid artery disease in patients requiring myocardial revascularization. The reported incidence of severe symptomatic carotid artery disease in such patients fluctuates from 3.2% to 8.7% [8, 16, 40, 42]. This percentage may increase with age [1, 2, 12, 15, 16]. Examination with Duplex ultrasound in patients scheduled for CABG also revealed a high prevalence of asymptomatic internal carotid artery stenosis. About 25% of these patients had a less than 50% stenosis while 12% had a severe stenosis of >80% [7, 9, 39, 44]. What is the incidence of stroke perioperatively in myocardial revascularization? The values in the international literature vary widely between 0.6% and 15.8% [1, 11, 28]. Remarkable variation exists also in the proportion of post-CABG strokes within a 5-year follow-up that are of carotid origin. The values vary widely between 0% and 6%! These remarkable variations may partially result from different criteria in the selection of patients, study design, type and timing of follow-up, etc., but they cannot be explained completely only on these grounds. What do we know about severe symptomatic and asymptomatic carotid artery stenosis in coronary patients needing myocardial revascularization? There can be very little doubt that carotid endarterectomy in patients with symptomatic severe carotid artery stenosis must be performed before CABG. The possible exception is for patients with unstable angina where a combined carotid and coronary procedure could have merit but with an increased perioperative risk. There are two options for avoiding this: • Unstable angina can be corrected with coronary angioplasty • Carotid artery stenosis can be treated with balloon angioplasty and stenting under cerebral protection and therefore combined carotid and coronary surgery may no longer be indicated. In contrast, there is a lack of evidence in terms of controlled trials in asymptomatic carotid disease. The Asymptomatic Carotid Atherosclerosis (ACAS) study failed
to give a clear result in terms of stroke without warning [1]. The results of the ACST study (Asymptomatic Carotid Stenosis Trial) have recently been published. These results demonstrated that, among otherwise healthy patients under 75 years of age with tight carotid stenosis and a 5-year stroke risk of about 12%, carotid endarterectomy will reduce the net 5-year risk to about 6% [2]. The ACST study also demonstrated that the 5-year probability of a carotid stroke, and hence the 5-year benefit of a successful carotid endarterectomy, was as great for those with 70% stenosis on ultrasound as for those with 80% and 90% stenosis, irrespective of plaque echolucency [2]. This surgical benefit was more significant for men than for women. Finally the ACST study demonstrated that although the main reduction of 5-year stroke was in the risk of ipsilateral carotid stroke, the results showed that contralateral carotid stroke was also significantly reduced after carotid endarterectomy, presumably via mechanisms involving the circle of Willis [2]. Which coronary patients will benefit from carotid intervention prior to CABG and when? • Patients with symptomatic carotid stenosis >70% and patients with asymptomatic carotid stenosis >70% combined with contralateral occlusion will benefit from carotid intervention prior to CABG. It is still unclear whether there is a benefit in performing prophylactic carotid endarterectomy for bilateral asymptomatic carotid artery stenosis >80% in coronary patients needing by-pass surgery. Concerning the timing of carotid endarterectomy and coronary revascularization, it seems that the scientific literature is not strong enough to recommend carotid endarterectomy prior to CABG both in symptomatic and asymptomatic patients [1, 2, 9, 39]. In order to objectively identify the prevalence of asymptomatic severe carotid artery disease in coronary patients and to determine the timing of carotid and coronary intervention we carried out the study detailed below.
2.8.4.1 Material and Methods A total of 1250 consecutive patients admitted to the Cardiovascular and Thoracic Unit of the Nicosia General Hospital for coronary by-pass surgery were routinely examined with a colour Duplex ultrasound machine for carotid artery stenosis. Two skilful technicians in the vascular laboratory carried out these investigations. Two independent vascular surgeons evaluated the ultrasound
213
214
2.8 Combined Treatment of Coronary Plus Other Arterial Pathologies: the Magnitude of the Polyatherosclerotic Patient
results. Descriptive statistics, correlation coefficients and regression analysis were used for the statistical analysis.
2.8.4.2 Results The prevalence of significant asymptomatic carotid artery disease in 1250 coronary patients was 7.36% (92 patients). Furthermore, the prevalence of severe asymptomatic disease increased significantly with age. It was 2.14% in patients under 60 years old, rising to 5.23% in patients over 60 years old. In contrast, the prevalence of severe symptomatic carotid artery disease was almost the same in patients with stable angina as in those with unstable angina: 3.95% in 930 patients with stable angina and 3.42% in 320 patients with unstable angina. Staged intervention (carotid before coronary) was performed on 74 patients (80.4%) with stable angina. They all had either bilateral severe stenosis (>70%) or ipsilateral severe stenosis and contralateral occlusion. Combined or synchronous intervention was carried out on 13 patients (14.2%). All were suffering from unstable angina, and had ipsilateral severe stenosis of >70% and contralateral occlusion. Reverse staged intervention was performed on five patients only with unstable angina. Coronary angioplasty was not recommended and CABG surgery was urgently needed. A staged procedure in stable angina was preferred because it is safer and more sensible. Its main advantage is a significant reduction in perioperative CABG stroke risk. Its main disadvantage is the necessity for two general anaes-
Fig. 2.8.5 Carotid endarterectomy performed with and without shunt and patch
thetics in a short period of time and longer hospitalization with an increased economic burden. Synchronous and reverse staged carotid endarterectomy was adopted in cases with unstable angina. Mortality in these cases was significantly higher. Carotid endarterectomy was the only intervention used in this study. It was performed without a shunt in 92.2% of cases, and using a patch graft in 94.8% of cases (Fig. 2.8.5). Perioperative complications of carotid endarterectomy were found in 6.2% of cases and were mild and short lived. Total mortality was 2.2% (0% for staged intervention, 7.1% for synchronous intervention and 20% for reverse staged intervention). Suggested options to the adopted protocol are: • Off-pump coronary revascularization particularly in the elderly. • Carotid angioplasty and stenting under cerebral protection, which may become the treatment of choice in polyvascular patients requiring myocardial revascularization. Acknowledgements The author expresses his thanks to Ms I. Tsiappa and Dr Chr. Bekos for their assistance in the statistical analysis of the results. References 1. ACAS (1994) Clinical advisory: carotid endarterectomy for patients with asymptomatic internal carotid artery stenos is. Stroke 25:2523–2524 2. ACST (2004) Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. MRC Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group. Lancet 363:1491–1502 3. Alric P, Berthet JP, Branchereau P, Veerapen R, Marty-Ane CH (2002) Endovascular repair for acute rupture of the descending thoracic aorta. J Endovasc Ther 9 [Suppl 2]: II51–II59 4. Ashton HA, Buxton MJ, Day NE, Kim LG, Marteau TM, Scott RA, Thompson SG, Walker NM; Multicentre Aneurysm Screening Study Group (2002) The Multicentre Aneurysm Screening Study (MASS) into the effect of the abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet 360:1531–1539 5. Bashar AH, Kazui T, Washiyama N, Yamashita K, Terada H (2002) Simultaneous carotid endarterectomy, coronary artery by-pass grafting and abdominal aortic aneurysm surgery. Ann Thorac Cardiovasc Surg 8:167–169
References
6. Beard J, Gaines P (2001) Vascular and endovascular surgery, 2nd edn. Saunders, London 7. Bilfinger TV, Reda H, Giron F, Seifert FC, Ricotta JJ (2000) Coronary and carotid operations under prospective standardized conditions: incidence and outcome. Ann Thorac Surg 69:1792–1798 8. Bonardelli S, Portolani N, Tiberio GA, Nodari F, De Lucia M, Quartierini G, Maffeis R, Ghilardi G, Lorusso R, Latini C, Zogno M, Giulini SM (2002) Combined surgical approach for carotid and coronary stenosis. Sixty four patients and review of Literature. J Cardiovasc Surg 43:385–390 9. Borger M, Fremes S (2001) Management of patients with concomitant coronary and carotid disease. Semin Thoracic Cardiovasc 13:192–198 10. Bradbury AW, Bell J, Lee AJ, Prescott RJ, Gillespie I, Stansby G, Fowkes FG (2002) By-pass or angioplasty for severe limb ischaemia. A Delphi Consensus Study. Eur J Vasc Endovasc Surg 24:411–416 11. Brener BJ, Brief DK, Alpert J, Goldenkranz RJ, Parsonnet V (1987) The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow up study. J Vasc Surg 5:269–279 12. CAVATAS Investigators (2001) Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Transluminal Angioplasty Study: a randomized trial. Lancet 357:1729–1737 13. Chuter TAM (2003) Opinions on endoleaks. In: Veith FJ, Baum RA (eds) Endoleaks and endotension. Marcel Dekker, New York 14. D’Angelo AJ, Puppala D, Farber A, Murphy AE, Faust GR, Cohen JR (1997) Is preoperative cardiac evaluation for abdominal aortic aneurysm repair necessary? J Vasc Surg 25:152–156 15. ECST (1998) Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery trial (ECST). Lancet 35:1379–1387 16. Faggioli GL, Curl GR, Ricotta J (1990) The role of carotid screening before coronary artery by-pass. J Vasc Surg 12:724–731 17. Greenberg RK, Srivastava SD, Ouriel K, Waldman D, Ivancev K, Illig KA, Shortell C, Green RM (2000) An endoluminal method of haemorrhage control and repair of ruptured abdominal aortic aneurysms. J Endovasc Ther 7:1–7 18. Haas GE, Parr GV, Hargrove WC, Trout RG (1989) Coronary artery by-pass surgery prior to resection of abdominal aortic aneurysm in patients with unstable coronary artery disease. J Am Osteopath Assoc 307:310–313
19. Harris PL, Vallabhaneni SR, Desgranges P, Becquemin JP, van Marrewijk C, Laheij RJ (2000) Incidence and risk factors of late rupture, conversion and death after endovascular repair of infrarenal aortic aneurysms: the EUROSTAR experience. J Vasc Surg 32:739–749 20. Haverich A, Miller DC, Scott WC (1985) Acute and chronic aortic dissections: determinants of long-term outcome for operative survivors. Circulation 72 [Suppl II]:22–31 21. Hertzer NR, Young JR, Kramer JR, Phillips DF, deWolfe VG, Ruschhaupt WF 3rd, Beven EG (1979) Routine coronary angiography prior to elective aortic reconstruction: results of selective myocardial revascularization in patients with peripheral vascular disease. Arch Surg 114:1336–1344 22. Ingle H, Nasim A, Bolia A, Fishwick G, Naylor R, Bell PR, Thompson MM (2002) Subintimal angioplasty of isolated infragenicular vessels in lower limb ischaemia: long term results. J Endovasc Ther 9:411–416 23. Jackson MJ, Wolfe JH (2001) Are infra-inguinal angioplasty and surgery comparable? Acta Chirurg Belg 101:6–11 24. Jamsen T, Manninen H, Tulla P (2002) The final outcome of primary infrainguinal percutaneous transluminal angioplasty in 100 consecutive patients with chronic critical limb ischaemia. J Vasc Interv Radiol 41:73–77 25. Korn P, Khilnani NM, Fellers JC, Lee TY, Winchester PA, Bush HL, Kent KC (2001) Thrombolysis for native arterial occlusions of the lower extremities: clinical outcome and cost. J Vasc Surg 33:1148–1157 26. Lederle FA, Johnson GR, Wilson SE, Ballard DJ, Jordan WD Jr, Blebea J, Littooy FN, Freischlag JA, Bandyk D, Rapp JH, Salam AA; Veterans Affairs Cooperative Study no. 417 Investigators (2002) Rupture rate of large abdominal aortic aneurysms in patients refusing or unfit for elective repair. J Am Med Assoc 287:2968–2972 27. Martin JB, Pache JC, Treggiari-Venzi M, Murphy KJ, Gailloud P, Puget E, Pizzolato G, Sugiu K, Guimaraens L, Theron J, Rufenacht DA (2001) Role of the distal balloon protection technique in the prevention of cerebral embolic events during carotid stent placement. Stroke 32:479–484 28. Morimoto K, Taniguchi I, Miyasaka S, Aoki T, Kato I, Yamaga T (2004) Usefulness of one-stage coronary artery by-pass grafting on the beating heart and abdominal aortic aneurysm repair. Ann Thorac Cardiovasc Surg 10:29–33 29. Muradin GS, Bosch JL, Stijnen T, Hunink MG (2001) Balloon dilatation and stent implantation for treatment of femoropopliteal arterial disease: meta-analysis. Radiology 221:137–145
215
216
2.8 Combined Treatment of Coronary Plus Other Arterial Pathologies: the Magnitude of the Polyatherosclerotic Patient
30. Nasr MK, McCarthy RJ, Hardman J, Chalmers A, Horrocks M (2002) The increasing role of percutaneous transluminal angioplasty in the primary management of critical limb ischaemia. Eur J Vasc Endovasc Surg 23:398–403 31. Naylor A, Mehta Z, Rothwell P, Bell PR (2002) Carotid artery disease and stroke during coronary artery by-pass; a critical review of the literature. Eur J Vasc Endovasc Surg 23:283–294 32. Ohki T, Marin ML, Lyon RT, Berdejo GL, Soundararajan K, Ohki M, Yuan JG, Faries PL, Wain RA, Sanchez LA, Suggs WD, Veith FJ (1998) Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg 27:463–471 33. Ohki T, Veith FJ (2001) Late abdominal aortic aneurysm rupture after endorepair. J Vasc Surg 33:599–606 34. Oz MC, Ashton RC Jr, Singh MK, Serra JS, Lemole GM (1990) Twelve year experience with intraluminal sutureless ringed graft replacement of the descending thoracic and thoracoabdominal aorta. J Vasc Surg 11:331–336 35. Paty PS, Darling RC 3rd, Chang BB, Lloyd WE, Kreienberg PB, Shah DM (2000) Repair of large aortic aneurysm should be performed early after coronary artery by-pass surgery. J Vasc Surg 31:253–159 36. Powell JT, Greenhalgh RM (2003) Small abdominal aortic aneurysms. N Engl J Med 348:1895–1901 37. Propranolol Aneurysm Trial Investigators (2002) Propranolol for small abdominal aortic aneurysms: results of a randomized trial. J Vasc Surg 35:72–79 38. Rehders T, Nienaber CA (2001) Complications of stent graft placement in the thoracic aorta. In: Branchereau A, Jacobs M (eds) Complications in vascular and endovascular surgery. Futura, New York, pp 185–191 39. Ricotta J (1995) The approach to patients with carotid bifurcation disease in need of coronary by-pass grafting. Semin Vasc Surg 8:62–69
40. Rizzo RJ, Whittemore AD, Couper GS, Donaldson MC, Aranki SF, Collins JJ Jr, Mannick JA, Cohn LH (1992) Combined carotid and coronary revascularization: the preferred approach to the severe vasculopath. Ann Thorac Surg 54:1099–1109 41. Roddy SP, Darling RC 3rd, Abrishamchian AR, Ozsvath KJ, Kreienberg PB, Paty PS, Mehta M, Chang BB, Shah DM (2002) Combined coronary artery by-pass with carotid endarterectomy: Do women have a worse outcome? J Vasc Surg 36:555–558 42. Sasaki Y, Isobe F, Kinugasa S, Iwata K, Murakami T, Saito M, Motoki M (2004) Influence of coronary artery disease on operative mortality and long-term survival after abdominal aortic aneurysm repair. Surg Today 34:313–317 43. Takahashi J, Okude J, Gohda T, Murakami T, Hatakeyama M, Sasaki S, Yasuda K (2002) Coronary artery by-pass surgery in patients with abdominal aortic aneurysm: detection and treatment of concomitant coronary artery disease. Ann Thorac Cardiovasc Surg 8:213–219 44. Terramani TT, Rowe VL, Hood DB, Eton D, Nuno IN, Yu H, Yellin AE, Starnes VA, Weaver FA (1998) Combined carotid endarterectomy and coronary artery by-pass grafting in asymptomatic carotid artery stenosis. Am Surg 64:993–997 45. Teufelsbauer H, Prusa AM, Wolff K, Polterauer P, Nanobashvili J, Prager M, Holzenbein T, Thurnher S, Lammer J, Schemper M, Kretschmer G, Huk I (2002) Endovascular stent grafting versus open surgical operation in patients with infrarenal aortic aneurysms: a propensity score-adjusted analysis. Circulation 106:782–787 46. Thompson CS, Gaxotte VD, Rodriguez JA, Ramaiah VG, Vranic M, Ravi R, DiMugno L, Shafique S, Olsen D, Diethrich EB (2002) Endoluminal stent grafting of the thoracic aorta: initial experience with the Gore Excluder. J Vasc Surg 35:1163–1170 47. Vraux H, Hammer F, Verhelst R, Goffette P, Vandeleene B (2000) Subintimal angioplasty of tibial vessel occlusions in the treatment of critical limb ischaemia. Eur J Vasc Endovasc Surg 20:441–446
Upper Extremity Arteries
219
3.1 Upper Extremity Occlusive Disease P. Berg, S. Schmitz, V. Lens, H. Farghadani
3.1.1 Introduction Unlike the lower extremity, the upper extremity is less likely to be affected with occlusive disease (10%) [17]. Diagnosis and treatment of upper limb occlusive disease is often difficult for the following reasons: • Most of the lesions are asymptomatic until the appearance of trophic lesions. • Only 2.8% of all vascular reconstructive techniques are applied to the upper extremity. • One-third of the lesions are proximal and accessible to reconstructive or endovascular techniques while twothirds are distal lesions, where treatment is considered to be a therapeutic challenge [18]. • Ischaemic problems in the upper extremity have many causes. Local, regional and systemic causes have been recognized. A precise aetiology is often difficult to establish.
3.1.2 Types of Upper Extremity Occlusive Disease 3.1.2.1 Acute and Chronic Ischaemia Epidemiology/Aetiology
Diagnosis/Investigations A detailed workup, often including arteriography, is necessary [34, 44]. A careful medical history and physical examination is primordial. Physical examination includes auscultation, palpation of pulses and the Allen test [1]. This test is useful in establishing the patency of the ulnar and radial artery, palmar arch and digital arteries. The procedure is as follows: • The radial and ulnar artery are compressed at the wrist by the examiner after blood has been forced out of the hand by clenching it into a fist. • The occlusion should be maintained for 20 s. • Compression of the ulnar artery is released. Immediate “pinking” of the hand indicates that the ulnar artery is patent; if the hand remains pale, the ulnar artery is occluded; if the hand remains pale on the radial side, the palmar arch is occluded. • The same procedure is repeated on the radial artery.
3.1.2.2 Raynaud’s Phenomenon Epidemiology/Aetiology • This is a clinical sign, and describes the characteristic and intermittent colour changes that occur in acral skin following exposure to cold or to stress [2].
• A precise aetiology is often difficult to establish. Symptoms Symptoms • Rarely, ischaemia will have severe initial manifestations.
• Clinical examination may reveal scleroderma, the most common reason for secondary Raynaud’s phenomenon in women. • Dry eye and/or mouth syndromes also suggest a collagen vascular disease such as scleroderma, Sjögren’s syndrome, or rheumatoid arthritis.
220
3.1 Upper Extremity Occlusive Disease
• In men, arteriopathies such as Buerger’s disease or digital arteritis in an atherosclerotic heavy smoker are more suspect.
Diagnosis/Investigations • If the cause of the bilateral Raynaud’s phenomenon is not apparent from the clinical examination, it is reasonable to prescribe tests such as radiographs of the chest and hands and blood tests. • Capillaroscopy of the nail bed may be useful.
shoulder girdle syndrome, carpal tunnel syndrome, occasionally, in acute attacks of pain, humeroscapular periarthritis and finally epicondylitis.
3.1.3 Embolism 3.1.3.1 Definition • Embolism is a common, acquired vascular disease of the upper extremity.
3.1.2.3 Trophic Lesions
3.1.3.2 Epidemiology/Aetiology
• Ulcerations and gangrene are seen with distal arterial disease (Buerger’s disease, vasculitis, arteritis) or in chronic ischaemia due to embolism. • The medical history and clinical examination help point to a diagnosis. • Doppler, colour-flow Doppler, magnetic resonance angiography and traditional arteriography are often necessary.
• The emboli may have several possible origins that affect the size of the embolus and consequently the level at which it stops. • Emboli are the most frequent cause of secondary ischaemia of the upper limb. • Of all arterial embolizations, 10–20% involve the upper limb. • More than two-thirds of those involving the upper extremity originate from heart disease, the aetiology most often being fibrillation (Table 3.1.1). • A small percentage follows acute myocardial infarction, be it clinically apparent or occult. Because the latter is not infrequent, silent infarction should be borne in mind. • Emboli of cardiac origin often precipitate an acute arterial occlusion of the upper extremity. Thrombi originating from the heart are usually larger and tend to lodge at the proximal site especially on the bifurcation of the brachial artery, whereas arterial emboli travel more distally [6]. But this cannot be considered as a rule, as shows Fig. 3.1.1.
3.1.2.4 Differential Diagnosis of Upper Extremity Occlusive Disease Phlegmasia cerulea dolens is an exceptionally rare cause of acute upper limb ischaemia. It arises due to progressive venous thrombosis, which leads, eventually, to complete blockage of venous drainage. As a result, arterial input is progressively dammed and the result is genuine arterial ischaemia. Aetiologically, all possibilities should be considered that may give rise to venous thrombosis. The most likely are compression syndromes in the costoclavicular space (see Chapter 3.3, Thoracic Outlet Syndrome). Distinction from purely arterial ischaemia is simple: • The limb is swollen, cyanosed instead of pale, and, on elevation, the discoloration resolves, which does not happen with arterial disorders. • Pulses are not palpable, initially because of the swelling and later because of the reduced arterial input. Acute ischaemia is clinically so impressive that other causes of pain can scarcely be considered. Most likely, and therefore worth excluding, are cervical disc problems,
3.1.3.3 Symptoms • The magnitude of the resultant ischaemia is a function of the anastomoses. • The most frequent signs of an embolus are an altered limb colour, decreased temperature as compared with the contralateral site, absence of peripheral pulses, sensory changes, pain and loss of some or all motor function.
3.1.3 Embolism
Table 3.1.1 Emboli of the upper extremity Aetiology
Incidence (%)
Cardiac
87
Atrial fibrillation Ischaemic cardiopathy Myocardial infarction Rheumatic heart disease Ventricular aneurysm Bacterial endocarditis Atherosclerotic heart disease Atrial myxoma Non obstructive cardiopathy Mitral prolapse Paradoxical emboli via a patent foramen ovale [48] Sequelae of cardiac valve replacement Noncardiac
Fig. 3.1.1 Male, 54 years old, subacute ischaemia of the left hand. Angiogram: occlusion of arcus palmaris profundus and of digital arteries, particularly of the thumb and index finger. Aetiology: benign tumour of mitral valve 13
Poststenotic aneurysm Aortic aneurysms Atheromatous plaques Proximal dialysis access shunt Post-traumatic subclavian aneurysm Atherosclerotic aneurysm Poly aneurysmal dystrophies Fibromuscular dysplasia Thoracic outlet syndrome Foreign bodies (bullets) Aneurysms induced by axillary crutches
from a propagating clot. It is imperative, under these circumstances, that surgery be performed immediately. Physical findings are helpful in distinguishing embolism from thrombosis: • An embolus lodges at a bifurcation. • The pulse proximal to an embolus is bounding and full, whereas the pulse proximal to a thrombus is weak. • Collateral circulation does not develop distal to emboli as it so often does in chronic arterial sclerotic occlusion.
• Acute ischaemia of the entire limb or of a single digit, as well as chronic and progressive ischaemia of the fingers, resulting in the long term in severe distal ischemic necrosis, may occur.
Since the surgical procedure to be performed is dictated by the type of occlusion, differentiation between embolism and thrombosis is important. When in doubt, arteriography is called for and will enable the physician to establish the diagnosis.
3.1.3.4 Diagnosis
3.1.3.5 Therapy
Medical history and clinical examination help point to a diagnosis. • Pulsed Doppler examination is sufficient to localize the embolus. • Arteriography is not necessary. • Significant sensory changes or peripheral paralysis may be signs of advanced ischaemia and may warn of impending gangrene, likely to be the result of emboli
Reestablishment of the arterial flow by embolectomy or thrombolysis may become necessary in the presence of marked sensory changes and, above all, in the presence of ischaemic paralysis. This occurs most commonly when the embolus lies in the brachial artery. • For axillary artery embolism, the incision is made in the medial bicipital groove immediately distal to the axillary fold.
221
222
3.1 Upper Extremity Occlusive Disease
• Embolism of the brachial artery is operated through an S-shaped incision at the elbow. The bifurcation is incised longitudinally. The embolus usually extrudes itself. If this does not happen, it must be extracted with the aid of a stripper or Fogarty catheter. • The proximal and distal patency must be checked by testing forward and backward flow. If this is not adequate, proximal and distal thrombus must be evacuated with a Fogarty catheter until satisfactory patency has been established. Compensation through collaterals is usually so good that late sequelae are not to be expected and treatment is conservative. This consists of immediate anticoagulation to prevent further (often cerebral) emboli from establishing, of treating this source of embolism and of preventing hand injuries [26].
3.1.4 Occlusive Arterial Disease 3.1.4.1 Definition Two types of occlusion can be distinguished based on the level of stenosis and occlusion. • Proximal arterial lesions, including the subclavian and brachial arteries. A specific feature consists of aortic arch syndrome: all branches of the aortic arch are occluded and the pulses in the upper limbs are absent (pulseless disease). Mostly, however, only isolated branches occlude or become stenosed (partial aortic arch syndrome). The same symptoms are caused by isolated stenosis or occlusion of the subclavian artery [47]. • Distal arterial lesions including the arteries of the forearm and the hand [16].
3.1.4.2 Proximal Arterial Disease Atherosclerosis Epidemiology/Aetiology
• Atheroma is the most common lesion affecting the first segment of the subclavian arteries. • Symptomatic left subclavian disease occurs three times more frequently than right-sided symptoms.
Table 3.1.2 Proximal and distal arterial disease [21] Proximal arterial disease Occlusive disease Atherosclerosis Giant cell arteritis Takayasu’s disease Thoracic outlet syndrome Congenital anomalies Thrombo-embolism Cardiac emboli Noncardiac emboli Distal arterial disease Occlusive disease Autoimmune arteritis, vasculitis Buerger’s disease Fibromuscular dysplasia Thrombo-embolism Hypothenar hammer syndrome, ulnar aneurysm Acute arterial occlusion Thrombophilic state Cancer
• Causative factors associated with the disease are hypertension, diabetes, hyperlipidemia, obesity and cigarette smoking.
Symptoms
• Atherosclerosis can affect other segments of the upper limb; usually, however, the subclavian and brachiocephalic arteries and those of the forearm are afflicted. • The clinical expression is often slight, found only with effort. • In prevertebral stenosis or occlusion of the subclavian artery, reversal of the flow in the vertebral artery known as the subclavian steal can be observed. • Neurological signs such as dizziness can be observed during effort of the respective upper limb (Figs. 3.1.2, 3.1.3). • Obliterative disease of the arteries of the forearm, hand and fingers is usually caused by distal embolism from proximal atheromatous plaques. • The symptomatology only becomes more severe with coexisting downstream lesions or if there are pre-existing anastomoses, inadequate at the level of the hand
3.1.4 Occlusive Arterial Disease
(incomplete palmar arches, radial or ulnar dominance).
Diagnosis
• Diagnosis is usually made clinically. • When a proximal disease is suspected, arteriography is helpful in establishing the exact nature and location of the disease.
Ulcerations Definition
• An ulceration is a break in the intimal covering of a plaque that exposes the media and the atheromatous core of the lesion to the bloodstream. • Ulcerations of the subclavian artery are a potential embolic source.
Fig. 3.1.2 Female, 46 years old, pain left upper extremity and vertigo after slight exertion, history of renal transplantation, occluded AV fistula in left arm with occlusion of radial artery, CT angiography (1) and DSA (2): sub-occlusion of a highly calcified left prevertebral subclavian artery, demonstration of a subclavian steal (3)
Fig. 3.1.3 Left subclavian-to-carotid transposition (1), protection of vagus and phrenic nerve. Postoperative CT angiogram (2) showing a patent end-to-side anastomosis and a patent VA
223
224
3.1 Upper Extremity Occlusive Disease
Fig. 3.1.4 Male, 69 years old, dysphagia lusoria, left retroesophageal subclavian artery with compression of the oesophagus. CT scan (1), opacification of oesophagus (2)
Fig. 3.1.6 Tip necrosis of right index finger, embolic occlusion
Fig. 3.1.5 Female, 60 years old, stenosis of a right retroesophageal subclavian artery with floating thrombus, common carotid trunk, right VA originating from right common carotid artery (CCA)
3.1.4 Occlusive Arterial Disease
Fig. 3.1.7 Carotid–subclavian by-pass, protection of phrenic nerve, postoperative MR angiogram
Symptoms
• Their presentation is more frequently subacute or chronic than acute.
Diagnosis/Investigations
• The pulsed Doppler is the preferred diagnostic test. • Arteriography confirms the lesion and demonstrates any downstream lesions.
Thoracic Outlet Syndrome • See Chapter 3.3.
Congenital Anomalies • The aortic arch gives off its three branches as it curves around the tracheoesophageal axis between the ascending and descending portions of the aorta. • Variations in the anatomy of the branches of an aortic arch include the innominate artery originating at the left side of the trachea. • In adults this disposition predisposes to arterial erosions after prolonged endotracheal intubation or cannulation through a tracheostomy. • The most common anomaly of the aortic arch branches is the retroesophageal subclavian artery (RSA), seen in 0.5% of the population [8]. • The compression of the oesophagus by the posterior RSA is known as dysphagia lusoria (Fig. 3.1.4). • These patients may have other anomalies, such as: a common carotid trunk and a right vertebral artery originating directly from the right common carotid artery (Figs. 3.1.5, 3.1.6, 3.1.7)
225
226
3.1 Upper Extremity Occlusive Disease
• At the origin of the RSA there may be a congenital dilatation of the wall called the diverticulum of Kommerel, a remnant of the posterior part of the right fourth aortic arch [12]. • A rare anomaly is isolation of the left subclavian artery (SA), where the first part of the SA is absent. The left upper limb gets its blood supply through the left vertebral artery. • Variations in the arterial anatomy of the upper extremities, although uncommon, occur in up to one in five patients. Most of these variants occur in either the radial or ulnar artery; brachial artery variations are less common [22, 43]. • These congenital anomalies may create: (1) stenoses, (2) aneurysms and (3) occlusive disease of the upper extremities.
Arteritis • Takayasu’s arteritis can involve the supra-aortic trunks, mostly the innominate artery and the left common carotid artery or subclavian artery, in continuity with aortic arch lesions. • Giant cell arteritis involves the distal SA often extending to the axillary artery. • A radiation arteritis can occur on irradiated arteries.
Malignant Tumours • Malignant vascular tumours of the upper extremity have been reported but are infrequently seen. • Hemangiosarcoma, hemangioendotheliosarcoma and hemangiopericytoma [30] as well as Kaposi’s sarcoma do occur [35], however, and should be treated with the same principles governing cancer surgery in other locations. • Tumour growth more rapid than the normally slow progression of a vascular lesion, increase in pain, signs of local ischaemia, and even infectious complications should alert one to the possibility of malignant change [46].
the upper limb, in particular in patients with associated distal lesions, may present a contraindication [14]. • The surgical technique should favour an extrathoracic approach. The transposition technique is the preferred technique. The transposition of the prevertebral SA into the common carotid artery (CCA) is particularly well suited and has the advantage of the absence of a synthetic graft (Fig. 3.1.3). This technique is contraindicated in patients who have had myocardial revascularization using the ipsilateral internal mammary artery, extensive vascular disease and concomitant lesions of the CCA. • A stenosis of the ipsilateral carotid bifurcation can be treated at the same time [8]. • Cervical by-pass provides an easy and safe solution and is best indicated in high-risk patients. Synthetic prostheses are the material of choice. Two techniques can be employed: (1) ipsilateral by-pass, carotid-subclavian by-pass, or (2) crossover by-pass, axillary–axillary or subclavian–subclavian. This is rarely advised, and then only if there are cerebral symptoms or ischaemia with threatening or established necrosis. • Surgical repair of an RSA is indicated in the presence of dysphagia lusoria, occlusive disease, aneurysmal disease, or associated aortic disease. Necrosis is more likely to occur in the peripheral occlusive type. In such cases, the circulation can be improved when there are frequent Raynaud’s attacks or necrosis by surgical or chemical thoracocervical sympathectomy or by spinal cord stimulation. Otherwise treatment consists largely of recognizing the underlying condition and improving it (change of occupation, prophylaxis against the cold and trauma, treatment of the underlying disease in cryoglobulinemia, polycythaemia, or atherosclerosis, or treatment of infection).
3.1.4.3 Distal Arterial Disease Thrombangiitis obliterans (TAO) Epidemiology/Aetiology
Therapy of Proximal Occlusive Arterial Disease • Stenosis of the first segment of the SA may be corrected by balloon angioplasty or by stent implantation. The risk of an embolization of the vertebrobasilar territory or
• TAO or Buerger’s disease is a vasculitis of unknown aetiology that can be defined as a nonspecific inflammatory and occlusive arteritis primarily affecting the midsized and small-calibre vessels of young men who are heavy smokers [28].
3.1.4 Occlusive Arterial Disease
Fig. 3.1.8 Male, 34 years old, smoker, ulcerations on right thumb and left index finger, atypical Raynaud’s syndrome on both upper extremities
• It differs from other vasculitis in that the serological makers of inflammation and autoantibody formation are either absent or normal. • Pathologically, it differs from other forms of vasculitis in that there is progressive organization of a highly inflammatory thrombus in the vessel lumen, the vessel wall architecture is relatively spared and fibrinoid necrosis is absent [23].
• Patients are often seen with ischaemia or claudication in the arch of the foot, legs, arms or hands (Figs. 3.1.8, 3.1.9) [33]. • There is almost always more than one limb affected. Ulceration, finger tip necrosis and gangrene may be present.
Diagnosis Symptoms
• The upper extremity involvement is classic, especially if it includes Raynaud’s syndrome of recent onset in a young man. • The Raynaud’s symptoms are mostly atypical, affecting only a few digits. This can be explained by the normal vasoconstriction occurring in digits with occluded arteries.
• The diagnosis is usually made on the basis of the presence of distal artery disease in individuals who smoke and in whom other disease entities (diabetes, hyperlipidemia, autoimmune disease, traumatism, haematological diseases) have been excluded. • The association between tobacco use and the development of TAO is incontestable. • Arteriographic findings typical of TAO include small- and medium-calibre arteries of the forearm and hand involvement, segmental occlusive disease, distal disease greater than proximal, collateralization
227
228
3.1 Upper Extremity Occlusive Disease
Fig. 3.1.9 Angiogram: segmental occlusions of small- and medium-calibre arteries of all extremities. Diagnosis: thromboangiitis obliterans
by-passing occlusive segments and normal proximal vessels. • Typical angiographic findings are twisted collaterals presenting the vaso vasorum of the occluded digital arteries. • Although arteriographic differentiation from atherosclerosis is relatively obvious, TAO is difficult to differentiate from scleroderma and collagen vascular disease.
Therapy
• The mainstay of therapy is the absolute avoidance of smoking and exposure to tobacco products. • When ischaemic pain predominates and patients require potent narcotic analgesics or sympathetic blockade, beneficial effects can be expected by intravenous prostaglandin analogues. These drugs appear to have
some beneficial effect in ischaemic pain and in healing ischaemic ulcerations. Spinal Cord Stimulation
• Implantable spinal cord stimulators have been used successfully in patients with atherosclerotic and vasospastic peripheral arterial disease. This method provides good pain control and healing of distal necrosis has been observed [3, 45]. • Spinal cord stimulation (SCS) is performed in most cases in two stages. A temporary (trial) SCS lead is placed percutaneously in the dorsal aspect of the epidural space opposite the segments of the spinal cord that control the target dermatomes. In treating lesions of the upper extremities, the lead has to be placed at the level C3–C5. (Figs. 3.1.10, 3.1.11, 3.1.12). • After a successful trial on the basis of evidence of improved circulation and decreased pain, evidenced
3.1.4 Occlusive Arterial Disease
Fig. 3.1.10 Male, 55 years old, thromboangiitis obliterans (TAO) of upper extremities. He had stopped smoking 6 years previously, had chronic ischaemia of the right fingers, particularly the index finger, atypical Raynaud’s syndrome and rest pain
both subjectively and by decreased narcotic requirements, permanent SCS with a pulse generator implant is performed. • The advantages of this technique are that it is relatively simple, nondestructive and reversible. However, it is an expensive method and should be reserved for patients who have severe, but stable, symptoms, failed medical management and are not candidates for reconstructive by-pass grafting surgery.
Vasculitis Epidemiology/Aetiology
• Vasculitis of varying pathogenesis can be an important cause of occlusive disease of the upper extremity [29]. • Digital ischaemia should initiate a search for the underlying pathological condition that precipitated the process of vasculitis.
• Arteritis due to systemic infections (typhus, paratyphus, diphtheria, influenza, pneumonia), allergy (also after drugs [40], penicillin), cannabis arteritis [13], or in association with neoplastic disease are quite rare.
DigitalArteritis
• The principle symptom is Raynaud’s phenomenon. • In the presence of cryoglobulinemia it should be established whether tumour (multiple myeloma, leukaemia, and bronchial or breast carcinoma), collagen disease, liver disease (cirrhosis), or systemic infection (sepsis, endocarditis, hepatitis, malaria, pneumonia, among others) is the underlying aetiology. • Treatment of digital arteritis is dietetic, hygienic and medical.
229
230
3.1 Upper Extremity Occlusive Disease
Fig. 3.1.11 Implantation of a cervical spinal cord stimulator. Immediate pain relief with excellent long-term result (8 years). To treat the dermatomes C6–C8, the lead has to be placed between C3 and C5
vasculitis affects small vessels, especially postcapillary venules, and has a good prognosis under medical treatment. • Serum sickness. • Henoch-Schönlein purpura. • Malignancies.
ConnectiveTissue Disorders
Fig. 3.1.12 Same patient as Figs. 3.1.8 and 3.1.9, 4 months after stopping smoking, 2 weeks of intravenous prostaglandin analogues and cervical spinal cord stimulation
HypersensitivityVasculitis
• Antigens causing hypersensitivity vasculitis can be drugs, bacteria (β-haemolytic streptococcus), tumour antigen or serum protein; allergic (or hypersensitivity)
Antigen–antibody complex deposition in digital vessels is a common factor in this group of heterogeneous conditions. These changes (fibrinoid degeneration, intimal thickening) produce the clinical features of digital ischaemia. • Systemic lupus erythematosus (SLE) – vasculitis accounts for the Raynaud’s phenomenon [41] of SLE, which occurs in one-fifth of SLE patients. Digital ischaemia may indeed be the presenting symptom of SLE and may predate arthritic symptoms. Arteriolar endothelial destruction, with eosinophilic infiltration of the intima of the common digital arteries, narrows the lumen.
3.1.4 Occlusive Arterial Disease
• Scleroderma – Patients with CREST syndrome (calcinosis cutis, Raynaud’s phenomenon, oesophageal dysmotility, scleroderma and telangiectasia) develop vasculitis and digital ischaemia, quite frequently predating systemic disease by many years. Arterial involvement occurs in the digital arteries. There is intimal thickening secondary to fibrin deposition in the vessel wall, resulting in narrowed arterial lumen and digital ischaemia [27]. • Polyarteritis nodosa – Polyarteritis nodosa affects small- and medium-sized vessels with segmental involvement [50]. • Rheumatoid arthritis – Seropositive rheumatoid arthritis gives rise to endoarteritis obliterans in the digital arteries. Postcapillary venules in the skin are also affected. Generally, severely affected hands and digits are subject to vasculitis. A careful search for vasculitis must be made before surgical reconstruction of these deformed hands.
• Accidental intra-arterial injection of certain drugs almost always leads to irreversible changes if treatment is not instituted early. • The mildest permanent change is weakness of the forearm or finger muscles. • Necrosis of fingertips, whole fingers, or, indeed, several fingers may develop.
Ischaemia-inducing Agents • Catecholamines and vasopressin cause injury by local ischaemia. • Epinephrine, norepinephrine, metaraminol, dopamine and dobutamine have all been reported to cause tissue slough as a result of ischaemic necrosis after their extravasation.
Ulnar Artery Thrombosis
• The pathology of fibromuscular dysplasia (see Chapter 2.4, Fibromuscular Dysplasia, by M. Sechas) involves the media of the arteries of small and medium calibre. • In the upper extremity [9, 11, 34], these lesions are extremely rare and found more commonly in women who are generally younger than those seen because of atheromatous disease. • Fibrous dysplasia and atherosclerosis may coexist in the same artery. • In its most common form the media develops annular thickenings separated by segments of normal or thinned artery. • The result is an artery that is elongated and has the appearance of a string of beads, with alternating stenoses and dilatations. • Segmental narrowings may occur and create turbulence and a critical stenosis.
This occurs in people who use the palms of their hands during such daily activities as pushing, hammering, pounding or twisting (hypothenar hammer syndrome, see “Ulnar Artery Aneurysm” below) [32]. • Repeated trauma to the hypothenar area causes periadventitial scarring, which results in damage to the media, disruption of the internal elastic lamina, intimal damage and subintimal haematomas. • Subsequently, the thrombosis may extend to the common digital arteries and even to the digital arteries. • Embolization can also take place, and showers of emboli can occlude flow downstream in the digital vessels. • In the presence of significant arterial obstruction, night pain or even rest pain may be a very troublesome symptom. • Cold intolerance manifests in 80% of this population and is often a disabling symptom. • Most patients have unilateral involvement.
Drug Injection
Treatment of Distal Arterial Disease
• Digital ischaemia secondary to intra-arterial injection of drugs, particularly heroin [19]. • Treatment is symptomatic, consisting of vasodilators and anticoagulants.
• Treatment of distal arterial lesions is quite difficult and surgical revascularization is done only exceptionally. • Treatment consists of medical treatment (prostaglandins, steroids, antibiotics, etc.), spinal cord stimulation, sympathectomy, hygienic and dietetic measures.
FibromuscularDysplasia
231
232
3.1 Upper Extremity Occlusive Disease
3.1.5 Aneurysms 3.1.5.1 Epidemiology/Aetiology
• Other causes include vascular reconstruction procedures, haemodialysis shunts, urinary tract infections, gonorrhoea, osteomyelitis and penetrating trauma. • The most commonly associated offending organisms are Staphylococcus aureus and Streptococcus. Others include enterococci, salmonellae, gonococci and clostridia.
• True or false aneurysms both occur in the upper extremity [20]. • The traumatic false aneurysm is the most common aneurysm of the hand [25]. • Proximal aneurysms are the most frequent type of true aneurysms.
The classic sign of a mycotic aneurysm is fever associated with a painful, tender, pulsatile mass adjacent to a blood vessel.
Proximal Aneurysms
3.1.5.2 Diagnosis
• Aneurysms of the supra-aortic trunks, especially of the first portion of the left SA, require a left thoracotomy.
• A pulsatile swelling is readily identified in the brachial, radial or ulnar arteries because of their superficial position, but is more difficult in the hand. • A thrill can commonly be felt in an aneurysm and a bruit heard on auscultation. • Localized tenderness is often the only symptom that prompts surgical exploration without prior diagnosis. Differential diagnosis includes ganglion, cysts and lipomas.
Ulnar Artery Aneurysm • Ulnar artery aneurysms are more common than other aneurysms in the hand. • Repeated blunt trauma to the hypothenar eminence by using this part of the hand as a hammer has resulted in the term hypothenar hammer syndrome [15] (post-traumatic digital ischaemia or pneumatic tool disease). • Ulnar artery aneurysm may manifest as a pulsatile mass with ischaemic changes in the form of cold intolerance, pain and mottling. • If digital embolization occurs, subungual haemorrhage, ulceration, or gangrene can occur.
Digital Artery Aneurysm • Digital artery aneurysms are relatively rare. • Only a few cases of false aneurysms have been reported.
Mycotic Aneurysm • Mycotic aneurysms result from intravascular infection and from direct extension of a septic focus into an adjacent blood vessel [24]. • Drug addiction has increased the incidence of mycotic aneurysms in the brachial artery.
If doubt exists, angiography is the preferred diagnostic method.
3.1.5.3 Therapy • The preferred treatment for aneurysms of the subclavian, axillary and brachial arteries is resection and insertion of a synthetic prosthetic graft. Surgery is indicated because of the risk of complications. • Aneurysms involving only the radial, ulnar or palmar arteries can be resected after ligation. Reconstruction of the artery is unnecessary as long as collateral arteries are open [42].
3.1.6 Arteriovenous Fistulae 3.1.6.1 Epidemiology/Aetiology • AV fistulae are characterized by direct communication between an artery and a vein.
3.1.8 Iatrogenic Aetiologies
• These are rarely congenital [39] and are usually traumatic in origin. • Arteriovenous fistulae occur following trauma or infection or are created surgically to provide circulatory access for patients undergoing haemodialysis.
3.1.6.2 Symptoms • An AV fistula secondary to trauma or infection may produce distal ischaemic symptoms by the creation of a “steal” phenomenon. • AV fistulae from chronic haemodialysis can be a source of distal emboli [49] when an aneurysm forms at the proximal anastomoses. • They can also be the source of effort-induced ischaemia by shunting [31], which may require reduction of the outflow (surgically or by an endovascular route). • Like the angiodysplasia, the proximal venous hypertension they can cause can be the origin of distal trophic problems, pain and Raynaud’s phenomenon.
(Fig. 3.1.13), and aneurysms. The superficial ulnar artery is the usual site of trauma of this type.
3.1.7.2 Symptoms • The existence of an intraluminal thrombus explains the possibility of migration of this material, causing occlusion of the proper or common digital arteries; these distal occlusions are usually responsible for ischaemic digital complications. • Although segmental occlusion of an artery of the hand may remain asymptomatic because of the collateral circulation, this is not always true. • The unexpected arrival of ischaemia remains linked to the conformation of the palmar arcades; if these are discontinuous, the risk increases. • Certain professions and sports are particularly prone [36].
3.1.7.3 Therapy 3.1.6.3 Investigations • Examination reveals a thrill and a bruit. • Arteriography shows the fistula and the downstream shunting.
3.1.6.4 Therapy • Embolization and surgery can provide definitive cures.
3.1.7 Vascular Trauma 3.1.7.1 Epidemiology/Aetiology • Repetitive trauma is usually responsible for isolated intimal lesions that are the sources of thrombi (hammer syndrome, Raynaud’s syndrome [37, 38]). • A severe single blow can cause rupture of the different layers of the arterial wall, resulting in an aneurysm. Thus all types of lesions can be seen [4]: thrombosis of a minimally pathological or dysplastic artery, stenosis corresponding to partial thrombosis or dissection
• If acute ischaemia develops after elbow dislocation or a supracondylar fracture of the humerus [10], traumatic thrombosis or a tear of the artery is to be assumed and surgical treatment is equally necessary.
3.1.8 Iatrogenic Aetiologies Iatrogenic ischemic accidents secondary to axillary, brachial and radial catheterizations are more and more frequent. The rate of surgical intervention after cardiac catheterization is approximately 1% [5]: • Axillary catheterization may be ischaemic, less by in situ thrombosis than by axillary-subclavian dissection. The symptomatology, which is usually severe, improves rapidly, leaving a residual effort-induced ischaemia. Diagnosis is made by echo Duplex scan more often than by arteriography. The formation of a pseudoaneurysm may be a later source of distal emboli. • Brachial catheterization has a very low morbidity, barring any pre-existing lesions downstream. Brachial catheterizations can be complicated by dissection at the point of puncture or thrombosis in situ formed after an initial spasm. The symptomatology is that of an acute regressive ischaemic attack. It may pass un-
233
234
3.1 Upper Extremity Occlusive Disease
Fig. 3.1.13 Male, 31 years old, traumatic occlusion of the digital arteries of the right index finger. Kite flying with guiding of the kite by a ring placed around the index
noticed, only being discovered at an evaluation, or it may have more serious manifestations if there are preexisting lesions downstream. The manoeuvres of catheterization may mobilize endoluminal material that will precipitate distal embolic ischaemia. Radial artery puncture in the course of anaesthetic procedures poses the problem of preliminary analysis of the palmar arterial anastomoses [7]. In effect, an occlusion of the radial artery in the absence of intact palmar anastomoses can be accompanied by a severe digital-palmar ischaemia. The Allen test is better than nothing and should be done when there is no other method of testing available.
3.1.9 Conclusion Noninvasive evaluation now plays a major role in the management of patients with vascular disease of the upper extremity, in many instances eliminating the need for invasive techniques such as arteriography, but some cases remain where a precise diagnosis may be difficult to establish. If no cause for embolism or thrombosis can be found or none can be excluded, anticoagulation should be for life, especially after embolism, because further episodes are common and one-third of these affect the cerebral circulation. References 1. Allen EV (1929) Thromboangiitis obliterans: methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases. Am J Med Sci 178:237–244
References
2. Allen EV, Brown GE (1932) Raynaud’s disease: a critical review of minimal requisites for diagnosis. Am J Med Sci 183:187–200 3. Amann W, Berg P, Gersbach P, Gamain J, Raphael JH, Ubbink DT (2003) Spinal cord stimulation in the treatment of non-reconstructable stable critical leg ischaemia: results of the European Peripheral Vascular Disease. Eur J Vasc Endovasc Surg 26:280–286 4. Axelrod TS, Buchler U (1991) Severe complex injuries to the upper extremity: revascularisation and replantation. J Hand Surg 16A:574–584 5. Babu SC, Piccorelli GO, Shah PM, Stein JH, Clauss RH (1989) Incidence and results of arterial complications among 16350 patients undergoing cardiac catheterization. J Vasc Surg 10:113–116 6. Banis JC, Rich N, Whelan TJ (1977) Ischaemia of the upper extremity due to noncardiac emboli. Am J Surg 134:131–139 7. Bedford RF, Wollman H (1973) Complications of percutaneous radial artery catheterization. Anaesthesiology 38:228–236 8. Berguer R, Kieffer E (1992) Surgery of the arteries to the head. Springer, Berlin Heidelberg New York 9. Billig DM, Hallman GL, Cooley DA (1967) Arterial embolism: surgical treatment and results. Arch Surg 95:1–6 10. Bishara RA, Pasch AR, Lim LT, Meyer JP, Schuler JJ, Hall RF, Flanigan DP (1986) Improved results in the treatment of civilian vascular injuries associated with fractures and dislocations. J Vasc Surg 3:707–711 11. Crawford ES, De Bakey ME, Morris GC, Howell JF (1969) Surgical treatment of occlusion of the innominate, common carotid and subclavian arteries. A 10 year experience. Surgery 65:17 12. Ciervo A, Kahn M, Pangilinan J, Dardik H et al (2001) Absence of the brachial artery: report of a rare human variation and review of upper extremity arterial anomalies. J Vasc Surg 33:191–194 13. Disdier P, Granel B, Serratrice J, Constans J et al (2001) Cannabis arteritis revisited – ten new case reports. Angiology 52:1–5 14. Edwards JM, Antonius JI, Porter JM (1985) Critical hand ischaemia caused by forearm fibromuscular dysplasia. J Vasc Surg 2:459–463 15. Ferris BL, Taylor LM, Oyama K, McLafferty RB, Edwards JM, Moneta GL, Porter JM (2000) Hypothenar hammer syndrome: proposed etiology. J Vasc Surg 31:104–113 16. Fuchs JCA (1993) The pathology of upper extremity arterial disease. Hand Clin 9:1–4
17. Fujitani MR, Mills JL et al (1993) Acute and chronic upper extremity ischaemia. II. Small vessel arterial occlusive disease. Ann Vasc Surg 7:195–199 18. Fujitani RM, Mills JL; Lackland Air Force Base, USA (1993) Acute and chronic upper extremity ischaemia. I. Large vessel arterial occlusive disease. Ann Vasc Surg 7:106–112 19. Goldberg I, Bahar A, Yosipovitch Z (1984) Gangrene of the upper extremity following intraarterial injection of drugs. A case report and review of the literature. Clin Orthop 188:223–229 20. Green DP (1973) True and false traumatic aneurysms in the hand. Report of two cases and review of the literature. J Bone Joint Surg 55A:120–128 21. Harris RW, Andros G, Dulawa LB, Oblath RW, Salles-Cunha SX, Apyan R (1984) Large-vessel arterial occlusive disease in symptomatic upper extremity. Arch Surg 119:1277–1282 22. Hill RA, Pho RWH, Kumar VP (1993) Resection of vascular malformations. J Hand Surg 18B:17–21 23. Hirai M, Shionoya S (1979) Arterial obstruction of the upper limb in Buerger’s disease: its incidence and primary lesion. Br J Surg 66:124–128 24. Ho PK, Yarenchuk MJ, Dellon AL (1986) Mycotic aneurysm in the upper extremity. Report of two cases. J Hand Surg 11B:271–273 25. Ho PK, Weiland AJ, McClinton MA, Wilgis EFS (1987) Aneurysms of the upper extremity. J Hand Surg 12A:39–46 26. Iwai T, Konno S, Hiejima K, Satake S, Suzuki S, Hiranuma S et al (1985) Fibromuscular dysplasia in the extremities. J Cardiovasc Surg 26:496–501 27. Jones NF, Raynor SC, Medsger TA (1987) Microsurgical revascularisation of the hand in scleroderma. Br J Plas Surg 40:264–269 28. Joyce JW (1990) Buerger’s disease. Thromboangiitis obliterans. Rheum Dis Clin North Am 16:463–470 29. Kallenberg CGM (1990) Early detection of connective tissue disease in patients with Raynaud’s phenomenon. Rheum Dis Clin North Am 16:11–30 30. Kato N, Kato S, Ueno H (1990) Hemangiopericytoma. Characteristic features observed by magnetic resonance imaging and angiography. J Dermatol 17:701–706 31. Kinnaert P, Struyven J, Mathieu J et al (1980) Intermittent claudication of the hand after creation of an arteriovenous fistula in the forearm. Am J Surg 139:838–843 32. Koman LA, Urbaniak JR (1985) Ulnar artery thrombosis. Hand Clin 1:311–326 33. Lambeth JT, Yong NK (1970) Arteriographic findings in thromboangiitis obliterans with emphasis on femoropopliteal involvement. AJR Am J Roentgenol 109:553–562
235
236
3.1 Upper Extremity Occlusive Disease
34. Lin WW, McGee GS, Patterson BK, Yao JST, Pearce WH (1992) Fibromuscular dysplasia of the brachial artery: a case report and review of the literature. J Vasc Surg 16:66–70 35. McCarthy WD, Pack GT (1950) Malignant blood vessel tumors. A report of 56 cases of angiosarcoma and Kaposi’s sarcoma. Surg Gyn Obstet 91:465–482 36. McCarthy WJ, Yao JST, Schafer MF, Nuber G, Flinn WR, Blackbun D, Suker JR (1989) Upper extremity arterial injury in athletes. J Vasc Surg 9:317–327 37. McLafferty RB, Edwards JM, Ferris BL, Moneta GL et al (1999) Raynaud’s syndrome in workers who use vibrating pneumatic air knives. J Vasc Surg 30:1–7 38. McNamara MF, Takaki HS, Yao JS, Bergan JJ (1978) A systematic approach to severe hand ischaemia. Surgery 83:1–11 39. Merland JJ, Riche MC, Chiras J, Melki JP et al (1980) Les malformations artério-veineuses congénitales. Conséquences évolutives et thérapeutiques des ligatures artérielles. Plaidoyer pour leur abandon et solutions actuelles. Ann Chir 34:389–395 40. Plaza S, Alvarez-Sala JL, Sicilia JJ, Espinos D (1986) Diffuse digital ischaemia caused by vasculitis in a heroin addict. Med Clin (Barc) 87:737 41. Priollet P, Vayssairat M, Housset E (1987) How to classify Raynaud’s phenomenon. Long term follow-up study of 73 cases. Am J Med 83:494–498
42. Rothkopf DM, Bryan DJ, Cuadros CL, May JW Jr (1990) Surgical management of ulnar artery aneurysms. J Hand Surg 15A:891–897 43. Schwartz CJ, Werthessen NT, Wolf W (1980) Structure and function of the circulation. Plenum, New York 44. Sumner DS (1989) Evaluation of acute and chronic ischaemia of the upper extremity. In : Rutherford RB (ed) Vascular surgery, 3rd edn. Saunders, Philadelphia, p 806 45. Swigris JJ, Olin JW, Mekhail NA (1999) Implantable spinal cord stimulator to treat the ischemic manifestations of thromboangiitis obliterans (Buerger’s disease). J Vasc Surg 29:928–935 46. Taylor LM, Hauty MG, Edwards JM, Porter JM (1987) Digital ischaemia as manifestations of malignancy. Ann Surg 206:62–68 47. Thompson BW, Read RC, Campbell GS (1969) Aortic arch syndrome. Arch Surg 98:607–611 48. Travis JA, Fuller SB, Ligush J, Plonk GW, Geary RL, Hansen KJ (2001) Diagnosis and treatment of paradoxical embolus. J Vasc Surg 34:860–865 49. Yeager RA, Moneta GL, Edwards JM, Landry GJ, Taylor LM Jr, McConnell DB, Porter JM (2002) Relationship of hemodialysis access to finger gangrene in patients with end-stage renal disease. J Vasc Surg 36:245–249 50. Zeek PM (1953) Periarteritis nodosa and other forms of necrotizing arteritis. New Engl J Med 248:764
237
3.2 Vasospastic Disorders of the Upper Extremities Armando Mansilha , Sérgio Sampaio
3.2.1 Raynaud’s Syndrome 3.2.1.1 Definition • Raynaud’s syndrome is named after Maurice Raynaud, who first identified it in 1862 [12]. • It is characterized by recurrent episodes of digital numbness, tingling and a skin tricolour sequence: pallor, cyanosis and rubor. • Formerly subcategorized into Raynaud’s disease and Raynaud’s phenomenon. • Raynaud’s disease is a benign form with no underlying disease. • Raynaud’s phenomenon is an aggressive form, associated with vascular collagen diseases or other concomitant processes. • Nowadays patients tend to be currently diagnosed simply with Raynaud’s syndrome, since long periods of time may elapse between the vasospastic episodes and any underlying first identifiable features of this condition.
3.2.1.3 Symptoms • Colour changes correspond to the vasospastic phases: • extreme vasospasm – white (Fig. 3.2.1) • early resolution with fast blood deoxygenation in the capillaries – blue • arteriolar dilation – red. • Severe pain seems to be rare. • Usual triggers include exposure to cold, stress and smoking. • Any body extremity may suffer, but the hands are most commonly involved. • In a given extremity, one, several or all fingers may be affected. • Some inter-individual variation exists, with hyperhidrosis as an occasional concomitant finding, and colour changes being sometimes subtle or inexistent. • Episode duration ranges from minutes to hours. • In between attacks examination may not reveal any abnormal findings.
3.2.1.4 Diagnosis 3.2.1.2 Epidemiology/Aetiology • The mechanisms behind the syndrome remain to be established. • Some patients exposed to the use of high-frequency vibrating tools (such as pneumatic hammers or chainsaws) or to repetitive motion (typing or piano playing) may develop Raynaud’s syndrome associated with diffuse arterial obstruction in the hand [4]. • Females are more frequently affected than males, and the condition seems to afflict 20–30% of persons living in cool climates [5].
Recommended European Standard Diagnostic Steps of Investigation Diagnostic evaluation should be directed towards possible coexisting conditions (occurring in up to 70% of patients with Raynaud’s syndrome) (Table 3.2.1): • neurological • connective tissue • haematological conditions • endocrine conditions • exposure to repetitive trauma • vasospastic drugs (e.g. ergots, clonidine, ciclosporin) • arterial obstructions either by peripheral emboli or Buerger’s disease.
238
3.2 Vasospastic Disorders of the Upper Extremities
Fig. 3.2.1 Raynaud’s syndrome pallor phase, affecting the distal index
In all patients with significant symptoms, a baseline laboratory evaluation should probably be obtained: • complete blood count with sedimentation rate • chemistry profile • hand X-rays • rheumatoid factor • antinuclear antibody • anti-DNA antibody • hepatitis B markers
• serum protein electrophoresis • complement C3 and C4 • cryoglobulins.
Additional Useful Diagnostic Steps of Investigation • Digital plethysmography with waveform analysis and digital blood pressure analysis allow differentia-
3.2.1 Raynaud’s Syndrome
Table 3.2.1 Conditions associated with Raynaud’s syndrome Connective tissue disorders Scleroderma Systemic lupus erythematosus Rheumatoid arthritis Sjögren’s syndrome Reiter’s syndrome CREST syndrome Polyarteritis Polymyositis Mixed connective tissue disorders Arterial diseases Atherosclerosis Peripheral emboli Buerger’s disease Takayasu’s arteritis Giant cell arteritis Endocrine diseases Hypothyroidism Graves’ disease Addison’s disease Cushing’s disease Carcinoid syndrome Phaeochromocytoma Haematological alterations Paraproteinemia Polycythaemia Cryofibrinogenemia, cryoglobulins, cold agglutinins Leukaemia Myeloid metaplasia Myeloma Drugs or toxin exposure Ergots Beta blockers Bromocriptine Cytotoxics Clonidine Ciclosporin Interferons Vinyl chloride Infections Hepatitis B Helicobacter pylori Parvovirus B19 Compression Thoracic outlet syndrome Carpal tunnel syndrome
tion between vasospastic and obstructive conditions. Documenting a digital blood pressure measurement 10 mmHg or more below brachial pressure indicates digital obstruction. • Arteriography should probably be kept to patients with unilateral disease in whom a high suspicion of proximal arterial disease exists; namely, stenosis or aneurysm which could behave as a source of emboli.
3.2.1.5 Therapy Recommended European Standard Therapeutic Steps • Proper explanation towards eviction of the triggering factor is probably the mainstay of treatment. Emotional stress-induced episodes may require psycho-active drugs or psychiatric counselling. • Calcium channel blockers (nifedipine, diltiazem) have largely replaced sympathetic blockers in Raynaud’s syndrome management, although the addition of prazosin may be of some benefit. • Pentoxifylline, captopril and losartan may also be valuable options. • Patients with digital ulceration (a sure sign of obstruction, ruling out mere vasospasm) pose an especially difficult therapeutic challenge. • Ulcerations occur in about half of patients with Raynaud’s syndrome associated with digital obstruction, and they recur in approximately 50% of them. • Conservative management includes soap and water scrubbing and directed antibiotics. • Surgical debridement should be kept to a minimum, and digital amputation must be contemplated only as a last resort option.
Additional Useful Therapeutic Options • Prostaglandin E and I2 infusions have been studied with promising results [2]. • Thoracic sympathectomy, extensively used in the past, is at least controversial nowadays, since symptoms generally recur after an initial improvement (typically after a 6-month period).
239
240
3.2 Vasospastic Disorders of the Upper Extremities
3.2.2 Hyperhidrosis 3.2.2.1 Definition • Hyperhidrosis lacks a precise definition but can be described as sweating in excess of that required for normal thermoregulation.
3.2.2.2 Epidemiology/Aetiology • Hyperhidrosis is a benign condition, but extremely disabling from a social standpoint. • Estimated prevalence is 1% in the western world.
Primary Hyperhidrosis • Primary hyperhidrosis occurs in the absence of any known structural abnormality of the eccrine glands, sympathetic nerves, or ganglia. • It typically presents in childhood or adolescence and the incidence is slightly higher in women than in men. • The observed familial tendency to increased sweating can be related to a genetic basis.
Secondary Hyperhidrosis • Secondary hyperhidrosis is rare and tends to be a more generalized symptom with sweating involving most body parts. • It is typically associated with endocrine diseases (including hyperthyroidism, phaeochromocytoma, diabetes or obesity), menopausal changes, but also occurs with malignancy and psychiatric disorders. • Prescribed medication can also cause generalized sweating as a side-effect: gonadorelin analogues and tricyclic antidepressants are good examples. • Secondary hyperhidrosis can also be iatrogenic: nerve injury may cause localized sweating in the area surrounding its cutaneous distribution. • The treatment for secondary hyperhidrosis must be directed to the underlying cause.
3.2.2.3 Symptoms • Primary hyperhidrosis affects the palms, axillae, plantar surfaces, face and neck, and torso in decreasing frequency, but also in different combinations. • Areas of involvement are usually symmetrical. • The condition is typically absent during sleep, and classic symptoms of Raynaud’s syndrome are usually not present. • The excessive sweating may be episodic, continuous or seasonal and can be exacerbated or precipitated by thermal, gustatory, or emotional stimuli specific to the individual patient. • Although sweating may be more intense during hot weather, climate is not considered a major causal factor. • The clinical picture is usually so clear-cut that extensive investigation is not required. • It is not a severe, life-threatening disease, but represents an extremely uncomfortable situation. • This discomfort can be seen in a great number of routine activities, leading to significant unease, embarrassment and shame, severely compromising the affective, professional and social life of those affected. • Socially and economically disabling symptoms occur particularly in palmar hyperhidrosis. Copious palmar sweating (Fig. 3.2.2) causes difficulty in social contact, writing, manual activities, car driving and handling objects, among others. • Sweaty feet, besides the discomfort they produce, render the use of sandals or even barefoot walking difficult. • Axillary hyperhidrosis dampens and stains clothes in addition to embarrassing their wearers, who usually wear only black or white clothes. • Craniofacial hyperhidrosis intensely embarrasses those who present it, by drawing attention to them and at the same time making them feel insecure, afraid and lacking in confidence. In a significant number of cases this insecurity is aggravated by the lack of importance given to the patient’s complaint (both by relatives and even by the attending physicians), diagnosis failure and a succession of previously proposed ineffective measures.
3.2.2 Hyperhidrosis
Fig. 3.2.2 Palmar hyperhidrosis
3.2.2.4 Treatment
Conservative Therapy
• A number of treatment options have been described for the control of primary hyperhidrosis [8]. • Specific therapies must be tailored to a patient’s individual requirement, to gain maximum symptomatic improvement with minimum invasiveness and sideeffects. • Many controversies exist in the selection of treatment because there are no good randomized controlled trials comparing one treatment modality with another. • Specific treatments target specific parts of the neuroendocrine pathway at: the thoracic sympathetic chain, axonal conduction, axon–sweat gland synapse, glandular production of sweat and passage of sweat to the skin surface.
• Aluminium-based antiperspirants occlude sweat pores to prevent sweat from reaching the skin surface and are mostly used for axillary symptoms. Many patients cannot tolerate the rashes, stinging sensations and local irritation of strong antiperspirants and discontinue their use within a short time. • Iontophoresis prevents sweat production within the gland. This treatment involves immersion of the sweating area in a solution, and the use of low-intensity electrical current from a D/C generator to drive charged ions in the skin. Most patients find iontophoresis time-consuming and inefficient. Multiple weekly sessions are necessary and its application to body parts other than volar surfaces is very difficult. This method
241
242
3.2 Vasospastic Disorders of the Upper Extremities
should not be used in pregnancy or in the presence of cardiac pacemakers and metal implants. • Cholinergic inhibitor (anticholinergic) therapy blocks neurotransmitter receptor sites on the sweat gland to stop sweat production. These drugs, such as glycopyrrolate, may be administered orally and are the only systemic treatment in use in hyperhidrosis. The widespread anticholinergic side-effects limit patient compliance with these drugs. • Botulinum A toxin–haemagglutin complex, administered by multiple local intradermal injection, disables neurotransmission to prevent acetylcholine release at the axonal synapse with the sweat gland. It is mostly used for axillary hyperhidrosis but problems include pain at the site of administration, lack of consensus regarding method and dosage and the temporary nature of the results. Antibody formation to the toxin can limit the long-term efficacy of botulinum toxin treatment and the induced local muscle group paralysis presents a serious problem that limits its usage in the hands. • Hypnosis, psychotherapy and psychopharmacologic therapies may help some patients to accept living with hyperhidrosis.
and groins, usually very well tolerated by most of them, provided they have been informed before surgery. The association between the extent of sympathectomy and the occurrence and severity of compensatory sweating after TES is controversial [6]. Other rare complications are Horner’s syndrome, pneumothorax, pleuritic chest pain, gustatory sweating, haemothorax, intercosto-brachial neuralgia, chylothorax and recurrence of hyperhidrosis. In very rare instances, eccrine glands may be congenitally absent in some areas of the body. For patients thus affected, compensatory localized sweating is the only means of cutaneous thermoregulation and sympathectomy is therefore inappropriate.
3.2.3 Acrocyanosis 3.2.3.1 Definition • Acrocyanosis is a disorder characterized by continuous bluish discoloration of the digits of the hands and, less frequently, of the feet [10, 11].
3.2.3.2 Epidemiology/Aetiology Surgery The gold standard for treatment of palmar hyperhidrosis has long been recognized as thoracic sympathectomy (satisfactory control of sweating is up to 95%) [15]. Though originally carried out as an open procedure (cervical or thoracic), a minimally invasive thoracoscopic approach is now used to interrupt the sympathetic chain (usually T2 and T3 ganglia). Transthoracic endoscopic sympathectomy (TES) is usually performed via one or two chest portals per hemithorax (usually 10 and 5 mm) and is associated with negligible scarring. Current technical controversies include anterolateral versus posterior approach in the prone position, diathermy coagulation of the sympathetic chain versus scissor dissection/excision, and sympathetic chain transection versus surgical clip application [3]. The effects are usually instantaneous, with patients leaving the hospital within 24 h. TES is undoubtedly effective, with complete and durable improvement for palmar, axillary and facial hyperhidrosis. Curiously enough, successful upper limb treatment may also be associated with improved pedal symptoms. Compensatory hyperhidrosis is the commonest complication of TES, with affected patients presenting increased sweating of the trunk
• Acrocyanosis is encountered more frequently in women and typically occurs in young adults (15–40 years). • It may be found in up to 20% of women with anorexia nervosa. • Current pathophysiological hypotheses remain insufficient but suggest dysfunction of the sympathetic nervous system with resultant abnormal and continuous vasospasm in small cutaneous arterioles, causing compensatory dilation of the capillaries and postcapillary venules. • The resultant decrease in blood flow and an increase in oxygen extraction are thought to produce cyanosis.
3.2.3.3 Symptoms • Acrocyanosis presents with a continuous bluish discoloration of the digits of the hands and, less frequently, of the feet [10, 11]. • There is a symmetrical distribution of this condition and patients refer to a sensation of coolness in the affected areas.
3.2.5 Cold Hypersensitivity
• The involved extremities are cool, often sweaty, with arterial pulses present, and there may be slight swelling of the digits. • This disorder is distinguished from Raynaud’s syndrome as it occurs on a persistent basis, rather than being episodic, and is generally devoid of other features associated with Raynaud’s syndrome including pain. • Patients with acrocyanosis do not routinely have blanching and there is proximal extension beyond the digits to involve the hands or feet. • Other areas such as the forehead, nose, cheeks, earlobes, elbows and knees may be also involved. • The discoloration and coolness are worse in cold weather but are present even in warm weather. • These symptoms may intensify during cold exposure and hyperaemia with rubor may be seen on rewarming. • The condition is usually benign with extremely good prognosis, and skin ulceration or loss of digital tissue is extremely rare.
3.2.3.4 Therapy Treatment consists of: • avoidance of exposure to cold • dressing warmly and wearing gloves. Pharmacological intervention with sympatholytic agents to produce symptomatic relief is rarely necessary.
3.2.4 Livedo Reticularis 3.2.4.1 Definition • This condition is characterized by persistent mottled or reticulated reddish blue discoloration of the skin, which is most marked on exposure to cold, but it is often present continuously, regardless of the existing environmental temperature [10].
• It is thought to be caused by the random spasm of cutaneous arterioles with secondary dilatation of associated capillaries and the creation of arteriovenous fistulas at the capillary level. • Livedo reticularis has been described in association with conditions such as periarteritis nodosa, lupus erythematosus, dermatomyositis and cholesterol emboli. This is particularly true for the rare patients with associated pain or skin ulceration (mostly digital), who should be screened for the presence of an underlying disease.
3.2.4.3 Symptoms • As mentioned above, livedo reticularis presents with a persistent mottled or reticulated reddish blue discoloration of the skin, which is most marked on exposure to cold, but it is often present continuously, regardless of the existing environmental temperature [10]. • The lower legs (Fig. 3.2.3) and feet are most often affected with symmetrical distribution. • Involvement of the hands and arms is less common, and the trunk is rarely affected, unless the lower extremities are also involved.
3.2.4.4 Therapy • Primary livedo reticularis is a benign condition, and no treatment is indicated other than avoidance of cold. These patients rarely complain of discomfort or pain but remain concerned about the appearance. After reassurance that it is a benign situation and not a grave illness, it is often accepted and the vague presenting features disappear, leaving behind only the cosmetic significance. • Those patients with livedo reticularis in whom an associated condition exists, surgical sympathectomy can be considered, although results are variable.
3.2.5 Cold Hypersensitivity
3.2.4.2 Epidemiology/Aetiology
3.2.5.1 Definition
• Livedo reticularis is quite common, presents at any age, without gender preference and is often confused with Raynaud’s syndrome.
• Patients exhibit sensitivity of a digit, hand or entire extremity that is exposed to cold repeatedly [10].
243
244
3.2 Vasospastic Disorders of the Upper Extremities
Fig. 3.2.3 Livedo reticularis in the lower limbs
• This is particularly true of, and may be seen after recovery from, prior frostbite. Minor frostbite most likely occurred during childhood. • Many patients, however, present this clinical picture with no previous history of frostbite.
3.2.5.2 Symptoms • These patients display a bluish discoloration of the skin in the exposed area and often complain of severe burning, which may last for hours or days, even with mild cold exposure. • The pain can be similar to that seen in a complex regional pain syndrome, and some authors consider this problem a variant of causalgia.
• The affected areas are predictable, repetitive and seldom symmetrical.
3.2.5.3 Therapy • The treatment of this condition mainly involves avoiding cold exposure, and dressing warmly. The basics of protection from cold exposure include warm gloves and footwear during cold weather. • Avoidance of any tobacco use is also advisable. • The use of drugs that diminish sympathetic neuromuscular transmission, such as nifedipine, or of new calcium-entry blocking agents is controversial with no proven good results.
3.2.6 Complex Regional Pain Syndrome
• If attacks are frequent and uncontrolled, surgical sympathectomy may provide lasting relief, and results are comparable to those achieved with posttraumatic pain syndromes.
3.2.6 Complex Regional Pain Syndrome
(including myocardial infarction, thrombophlebitis, or stroke) have been implicated as CRPS causes. • Several explanatory theories have been advanced, but none has been widely accepted. • Nevertheless, sympathetic involvement in pain mediation has been ruled out as one of the strict inclusion criteria for CRPS.
3.2.6.1 Synonyms
3.2.6.4 Symptoms
• Reflex sympathetic dystrophy, causalgia, traumatic dystrophy, algodystrophy, Sudeck’s atrophy.
• Unexpectedly intense pain in the affected extremity, as opposed to what would be expected considering the initial event, is the hallmark of CRPS. Diffuse, with a burning character, the pain has to be inconsistent with a peripheral nerve distribution. Emotional stress may exacerbate it [14]. • Other sensory changes of the pain-affected region may include allodynia and hyperesthesia. • Skin temperature and coloration changes may vary from red and warm to cold and blue. • Sudation may be augmented, diminished or unaffected. • Skin, hair and nails may suffer trophic changes. • The affected extremity may also present with peripheral oedema. • Tremor and loss of strength of the affected muscle groups have also been reported. • Importantly, CRPS is to be defined on clinical grounds solely, thus no diagnostic tests are adequate [14]. • A dramatic response to sympathetic blockade is a major backup for a CRSP suspicion. Sham blockades (using saline) may be essayed in doubtful responses.
3.2.6.2 Definition • First described in 1864 as a burning pain after major nerve injury [7], causalgia has ever since been an evolving concept. • Several analogous painful syndromes of different causes used to be referred to as mimocausalgia (mimicking causalgia). • Dozens of terms have been used to name this group of conditions, including traumatic dystrophy, algodystrophy and Sudeck’s atrophy, with emphasis being put on different specificities. • Since 1993, a new consensus nomenclature has been adopted: complex regional pain syndrome (CRPS) types I and II [13]. • Type I CRPS, previously referred to as reflex sympathetic dystrophy, develops after a noxious event, is not limited to a single peripheral nerve territory and is disproportionate to the inciting episode. At some point, symptoms include oedema, skin blood flow or sudomotor changes, pain, allodynia or hyperalgesia. • Type II CRPS, previously referred to as causalgia, basically coincides in every aspect with type I CRPS, but occurs after a nerve injury. The syndrome is excluded in the presence of any condition that could explain the clinical findings (nerve entrapment, peripheral neuritis or any other diagnosis more definitive than CRPS).
3.2.6.3 Aetiology • A number of traumatic (ranging from crush trauma to apparently benign sprains) and non-traumatic injuries
3.2.6.5 Therapy Precocious recognition and treatment (pain relief and active mobilization of the extremity) produce the more satisfying results. • Pain management should be attempted with “directeffect” drugs, such as phenytoin, amitriptyline, carbamazepine and baclofen. • Nifedipine and phenoxybenzamine have also been used with some success, especially in the early stages. • Physical therapy and occupational therapy have been reported as useful [9]. Time should not be wasted with conservative measures if these prove ineffective after a few attempts.
245
246
3.2 Vasospastic Disorders of the Upper Extremities
• Sympathetic blockade should be essayed, sometimes producing long-lasting relief or even complete pain remission. • Surgical sympathectomy (now performable via a thoracoscopic route) produces the more impressive results in patients with a previous favourable response to a sympathetic blockade with local anaesthetic [1]. References 1. AbuRahma AF, Robinson PA, Powell M, Bastug D, Boland JP (1994) Sympathectomy for reflex sympathetic dystrophy: factors affecting outcome. Ann Vasc Surg 8:372–379 2. Clifford PC, Martin MF, Dieppe PA, Sheddon EJ, Baird RN (1983) Prostaglandin E1 infusion for small vessel arterial ischemia. J Cardiovasc Surg 24:503–508 3. Doblas M, Gutierrez R, Fontcuberta J, Orgaz A, Lopez P, Criado E (2003) Thoracodorsal sympathectomy for severe hyperhidrosis: posterior bilateral versus unilateral staged sympathectomy. Ann Vasc Surg 17:97–102 4. Heslop J, Coggon D, Acheson ED (1983) The prevalence of intermittent digital ischemia (Raynaud’s phenomenon) in a general practice. J R Coll Gen Pract 33b:85 5. James PB, Galloway RW (1975) Arteriography of the hand in men exposed to vibration. In: Taylor W, Pelmear PL (eds) Vibration white finger in industry. Academic Press, London, p 31 6. Leseche G, Castier Y, Thabut G, Petit MD, Combes M, Cerceau O, Besnard M (2003) Endoscopic transthoracic sympathectomy for upper limb hyperhidrosis: limited sympathectomy does not reduce postoperative compensatory sweating. J Vasc Surg 37:124–128 7. Mitchell SW, Morehouse GR, Keen WW (1864) Gunshot wounds and other injuries of nerves. Lippincott, Philadelphia
8. Nyamekye IK (2004) Current therapeutic options for treating primary hyperhidrosis. Eur J Vasc Endovasc Surg 27:571–576 9. Oerlemans HM, Oostendorp RA, de Boo T, van der Laan L, Severens JL, Goris JA (2000) Adjuvant physical therapy versus occupational therapy in patients with reflex sympathetic dystrophy/complex regional pain syndrome type I. Arch Phys Med Rehabil 81:49–56 10. Patman RD, Shutze WP (1995) Vasospastic disorders. In: Dean R, Yao J, Brewster D (eds) Current diagnosis and treatment in vascular surgery, 1st edn. Appleton and Lange, Norwalk, pp 160–171 11. Planchon B, Becker F, Carpentier PH, Lazareth I, Le Devehat C, Levesque H, Pereon Y, Pistorius MA, Vayssairat M; French Cooperative Group on Acrocyanosis (French National Microcirculation Society) (2001) Acrocyanosis: changing concepts and nosological limitations. J Mal Vasc 26:5–15 12. Raynaud M (1888) On local asphyxia and symmetrical gangrene of the extremities. In: Selected monographs. New Sydenham Society, London 13. Stanton-Hicks M, Janig W, Hassenbusch S, Haddox JD, Boas R, Wilson P (1995) Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain 63:127–133 14. Wilson PR (1996) Diagnostic algorithm for complex regional pain syndromes. In: Janig W, Stanton-Hicks M (eds) Reflex sympathetic dystrophy: a reappraisal. IASP Press, Seattle, pp 93–105 15. Young O, Neary P, Keaveny TV, Mehigan D, Sheehan S (2003) Evaluation of the impact of transthoracic endoscopic sympathectomy on patients with palmar hyperhidrosis. Eur J Vasc Endovasc Surg 26:673–676
247
3.3 Thoracic Outlet Syndrome Jean-Baptiste Ricco, Jérôme Cau, Christophe Marchand, Jean-Michel Cormier
3.3.1 Definition • Thoracic outlet syndrome (TOS) describes a variety of symptoms caused by compression of the brachial plexus or subclavian vessels at the thoracic outlet. • In the majority of cases, symptoms are neurological with pain and weakness resulting from C8 or T1 root compression. • Arterial or venous symptoms resulting from compression are uncommon accounting for 5% of cases in a large published series [13].
3.3.2 Neurogenic Thoracic Outlet Compression Syndrome (N-TOCS) 3.3.2.1 Epidemiology/Aetiology • The neurovascular bundle may be compressed between the first rib and the clavicle as a result of a low lying shoulder girdle or from loss of muscle tone. • Other anatomical factors include congenital fibromuscular bands crossing the thoracic outlet which tent up the brachial plexus, and abnormalities or hypertrophy of the scalene muscles. • Bony lesions may also be the cause including: cervical ribs, a broad first rib and fracture or exostoses of the first rib or clavicle [15]. • The scalene triangle is the commonest site of nerve compression. It contains the brachial plexus and the subclavian artery. • N-TOCS probably represents a repetitive stress injury as there are well-defined at-risk occupations, e.g. typists, and sports, e.g. swimming. • Most patients with N-TOCS are in the 25- to 45-yearold group and 70% of them are women.
3.3.2.2 Symptoms • Arm pain, paraesthesia and weakness with involvement of all nerves of the brachial plexus or with specific patterns related to the upper plexus (median nerve) or lower plexus (ulnar nerve).
3.3.2.3 Clinical Examination • Vascular assessment of the upper limb should include the thoracic outlet. • Palpation and auscultation of the supraclavicular region may help to detect a cervical rib, a subclavian stenosis or aneurysm. • The arm pulses should be examined with the arm placed in the neutral position and then in abduction and external rotation (surrender position) to detect arterial thoracic outlet compression (TOCS). • Pulse palpation is important and must include the axillary, brachial, radial and ulnar pulses. • The blood pressure should be measured in both arms, preferably using a hand-held Doppler. A difference of more than 15% is abnormal. Examination of hand ischaemia is not complete unless an Allen test is performed: • The examiner compresses the radial and ulnar arteries at the wrist. • The subject is then asked to clench their fist in order to empty blood out of the hand. • The radial artery is then released and the hand is observed for return of colour. • The test is then repeated for the ulnar artery. • The test is normal if refilling of the hand is complete within less than 10 s. • Any portion of the hand that does not blush is an indication of incomplete continuity of the palmar arch. • The nail folds should be examined for infarcts and splinter haemorrhages.
248
3.3 Thoracic Outlet Syndrome
3.3.2.4 Diagnosis • Positive findings of N-TOCS on clinical examination include supraclavicular tenderness and paraesthesia in the ipsilateral upper extremity in response to pressure over the scalene muscles. • Rotating the head and tilting the head away from the involved side often produces radiating pain in the upper arm. • Abducting the arm to 90° in external rotation often reproduces the symptoms. • Diagnostic tests include a scalene muscle block: a good response to this test correlates well with successful surgical decompression [1]. • Neurophysiology testing is helpful in excluding other sites of nerve compression, e.g. carpal tunnel syndrome. There is a reduction in the sensory action potential of the medial cutaneous nerve of the forearm, prolonged F wave conduction and the electromyograph (EMG) shows motor unit drop out in the thenar muscles. • Duplex scanning is a useful surrogate marker, if it shows arterial compression in the stress position. • Cervical spine films may detect cervical or abnormal first ribs but will not detect non-bony causes of compression. • MR scanning is more useful for excluding cervical disc lesions than confirming N-TOCS.
3.3.2.5 Treatment Conservative Treatment • Therapy for N-TOCS should always begin with non operative treatment including neck stretching, postural exercises and physiotherapy. • Patients should avoid, if possible, heavy lifting and working with the arm above the shoulder level. • Conservative treatment should be continued for several months. The majority of patients will improve significantly and will not require surgery.
Surgical Treatment • Indications for surgery include failure of conservative therapy after several months and persisting disabling symptoms that interfere with work and activities of daily living.
• The goal of surgery for N-TOCS is to decompress the brachial plexus. • Transaxillary first rib resection is the most common operation performed for N-TOCS [13].
TransaxillaryResection of the First Rib
This technique described by Roos [13] is indicated for neurogenic complications of TOCS and can be summarized as follows: • The patient is placed in lateral position leaving the arm free. • The assistant elevates the shoulder by applying upward traction on the upper arm. • This manoeuvre opens up the costoclavicular space and pulls the neurovascular bundle away from the first rib. • A horizontal skin incision is made at the lower border of the axillary line over the third rib (Fig. 3.3.1). • From here the dissection extends proximally toward the apex of the axilla. • The intercostal nerve emerging from the second intercostal space should be preserved. The fascial roof of the axilla is opened to expose the anterior portion of the first rib. Scalenus anterior is separated from the artery with right angle forceps and sectioned at its attachment to the first rib (Fig. 3.3.2). • The tendon of the subclavius muscle is divided with care because of its close relation with the subclavian vein. • The scalenus medius is then pushed off the rib using a blunt elevator. • The intercostal muscles are similarly detached from the lower part of the rib and the pleura is dropped back from the operative zone. • The rib is then sectioned at the chondrocostal junction and maintained by bone-holding forceps to distance it from the neurovascular bundle (Fig. 3.3.3). • With the arm elevated, the T1 root is identified at the neck of the first rib. • The T1 root is displaced medially with care and an angled rib shear is set as far posteriorly as possible. • The rib is then sectioned. This section is completed to within 1 or 2 cm of the vertebral transverse process using rongeurs. • The stump must be smooth since sharp bony spicules may lacerate the plexus. • Any remaining fibrous bands around the plexus or vessels should be resected.
3.3.2 Neurogenic Thoracic Outlet Compression Syndrome (N-TOCS)
Fig. 3.3.1 Transaxillary resection of the first rib. Operative position and skin incision. The neurovascular bundle is pulled away from the first rib by traction on the arm
• In the same way, the scalenus anterior is pulled down between the subclavian vessels and resected. • Serum saline is then injected in the wound to be sure that the pleura is intact. • The wound is closed in the usual way with a closed suction drainage.
rib shear or by retraction can be responsible for this complication. To avoid this complication, the T1 root should always be in view during posterior rib manipulation.
Other Operative Techniques for N-TOCS Complications of Transaxillary Rib Resection
• Complications of transaxillary rib resection include subclavian vein or artery injury, extra-pleural haematoma or brachial plexus injury. • The most serious complication is brachial plexus injury. Traction of the arm, damage of T1 root by the
Other operative techniques for N-TOCS include a supraand infra-clavicular approach that will be described later on in this chapter. Axelrod et al. [1] reported the results of surgery in 170 patients operated for N-TOCS:
249
250
3.3 Thoracic Outlet Syndrome
Fig. 3.3.2 Transaxillary resection of the first rib. Exposure of the first rib, scalene muscles and subclavian-axillary vessels. Detachment of the scalenus anterior, medius and subclavius muscles from the first rib
Fig. 3.3.3 Transaxillary resection of the first rib. Exposure of the first rib. The rib has been disarticulated at the chondrocostal junction. T1 root is protected by a retractor. Extraperiostal resection of the first rib is completed
• No major operative complication occurred in these patients who underwent decompression. • Only 11% of patients experienced minor complications, most commonly the need for chest tube placement as the result of pneumothorax. • At short-term follow-up (10 months), most patients had improved pain levels (80%) and range of motion (82%). However, at long-term follow-up (47 months), residual symptoms were present in 65% of patients,
and 35% took medication for pain. Nonetheless, 64% said they were satisfied with the result. Lepantalo et al. [9] performed a long-term follow-up after first rib resection (average: 6.1 years): • The examiners were independent from the surgeons. • One month postoperatively, 77% were found to be improved whereas at long-term follow-up this frequency was only 37%.
3.3.3 Arterial Thoracic Outlet Compression Syndrome (A-TOCS)
Controversy still exists concerning surgical treatment of N-TOCS and a randomized study of thoracic outlet surgery versus conservative treatment is lacking in this indication.
3.3.3 Arterial Thoracic Outlet Compression Syndrome (A-TOCS)
3.3.3.2 Symptoms • Most emboli are small and localized in the hand vessels with pallor, paraesthesia and coldness suggestive of Raynaud’s syndrome. • If unrecognized, severe digital ischaemia with gangrene may occur.
3.3.3.3 Investigations/Examination 3.3.3.1 Epidemiology/Aetiology • Arterial complications are often associated with bony abnormalities including a complete cervical rib and fracture callus of the first rib or clavicle. • The initial arterial lesion is a fibrotic thickening with intimal damage and post-stenotic dilation, leading to aneurysmal degeneration with mural thrombus and the risk of embolization (Fig. 3.3.4).
• Early recognition of this condition is essential and a Duplex scan should be done for all patients with unilateral Raynaud’s syndrome and asymptomatic patients with cervical bruit. • Loss of the radial pulse during Adson’s manoeuvre (abduction and external rotation of the shoulder) is not very reliable as it is found in as many as 50% of normal subjects. • The arteriographic changes may be obvious, but may sometimes be minimal with moderate dilation beyond a bony abnormality at the thoracic outlet, and radiological evidence of distal embolization. • Subclavian stenosis is not always evident on anteroposterior view and oblique stress views are often necessary.
3.3.3.4 Treatment Surgical Management
Fig. 3.3.4 Anatomy of a cervical rib with compression of the subclavian-axillary artery and post-stenotic aneurysm with mural thrombus and distal embolization. (From Clagett [2])
• The transaxillary approach previously described, largely used for isolated rib resection in the presence of neurological syndromes, does not offer satisfactory exposure of the subclavian-axillary artery and is contraindicated in the management of arterial complications. • The transclavicular approach allows wide exposure of the supraclavicular and axillary region. • Resection of the mid-part of the clavicle has a low incidence of cosmetic and functional impairment. • However, because the same surgical procedure can be done without dividing the clavicle using a combined supra-clavicular and infra-clavicular approach, the only indications for clavicular resection are arterial complications due to malunion or hypertrophic callus of the clavicle.
251
252
3.3 Thoracic Outlet Syndrome
Combined Supra-clavicular and Infra-clavicular Approach • The combined supra-clavicular and infra-clavicular approach [5] offers complete exposure, which we also recommend for N-TOCS.
• The infra-clavicular dissection is commenced first with an S-shaped incision. Pectoralis major is detached from the upper sternum and clavicle (Fig. 3.3.5). • Pectoralis minor is then sectioned and the clavipectoral fascia opened to expose the subclavius and the anterior segment of the two first ribs.
Fig. 3.3.5 Combined supra- and infra-clavicular approach for first rib resection. Skin incision and section of the pectoralis major from the clavicle
Fig. 3.3.6 Combined supra- and infra-clavicular approach for first rib resection. Exposure of the axillary vessels. The axillary vessels are held aside with a retractor to show the first rib and insertion of the scalenus anterior. The infra-clavicular dissection end with detachment of the intercostal muscles from the first rib. The anterior portion of the rib will be removed and the first rib stump will be shortened via the supraclavicular exposure not shown here
3.3.3 Arterial Thoracic Outlet Compression Syndrome (A-TOCS)
• The subclavius is resected and the artery and the axillary vein are then freed behind the clavicle. • Via a supraclavicular part of this incision, the clavicular head of the sternomastoid and the external jugular vein are divided to expose the scalenus anterior and the phrenic nerve. • The scalenus anterior is then sectioned near the first rib. • The subclavian artery and vein are freed (Fig. 3.3.6). • The intercostal muscles are detached from the lower border of the first rib and the rib is disarticulated at the costochondral junction. • The rib is then sectioned without attempting to reach the posterior segment. • Access of the rib stump is achieved via the supra-clavicular exposure by reflecting the brachial plexus laterally and the artery medially.
• The scalenus medius is then detached from the first rib and, after protecting the T1 root, the rib is sectioned near the transverse process. • If a complete cervical rib is present, the tip is disarticulated via infra-clavicular exposure, the remaining part being removed above the clavicle with the stump of the first rib. • In patients with aneurysm or post-stenotic dilation secondary to first rib or cervical rib, there is often a sufficient length of artery to permit resection of the arterial lesion and direct anastomosis (Fig. 3.3.7). • When arterial lesions are more extensive, graft replacement is required using greater saphenous vein, or PTFE if no vein is available. • Intraoperative angiography is recommended in all cases.
Fig. 3.3.7 Combined supra- and infra-clavicular approach for first rib resection with post-stenotic aneurysm. Exposure of the subclavian and axillary vessels. Depending on the extent of arterial resection, end-to-end anastomosis or graft replacement is done
253
254
3.3 Thoracic Outlet Syndrome
• In patients with recent distal embolic event a catheter embolectomy should be attempted through a transverse brachial arteriotomy and if ineffective through a radial or ulnar arteriotomy at the wrist using a no.°2 Fogarty catheter, local thrombolysis being an option in these small arteries. • If embolectomy is impossible, a distal by-pass using the greater or the lesser saphenous vein may be needed in an attempt to revascularize one the forearm arteries including the interosseous artery. • Additional sympathectomy may also be considered when there is extensive long-standing distal embolic occlusion. • Difficulty in clearing the distal arterial bed accounts for the incomplete revascularization observed in advanced cases with disabling ischaemic sequelae. • Arterial reconstruction and first rib or cervical rib resection is indicated in all patients with arterial complications of thoracic outlet syndrome.
3.3.4 A Case Apart: Primary Subclavian– Axillary Vein Thrombosis 3.3.4.1 Epidemiology/Aetiology • Spontaneous or effort-related thrombosis in a fit young patient is known as Paget–Schroetter syndrome (PSS) – the first cases being published separately by these two authors over a century ago. • Hughes, who in 1949 collected 320 cases and recognized the distinct entity, coined the eponym. • As the indications for central venous access have increased, so has the incidence of catheter-related subclavian–axillary vein thrombosis (SVT) [14]. • Acute deep vein thrombosis (DVT) of the upper limb has many causes. The treatment and prognosis depend on the specific cause. • SVT can be divided in two groups: primary and secondary. • Primary SVT (PSS) is due to an anatomical venous compression in the thoracic outlet during exercise (VTOCS) and comprises about 25% of all cases. • Secondary SVT is the result of multiple aetiological factors, although in most series central venous catheters dominate this category (40% of all cases of SVT). • SVT is responsible for 1–4% of all deep venous thrombosis.
• Monreal et al. [12] reported a 15% incidence of pulmonary emboli in 30 consecutive patients with SVT that were investigated with ventilation-perfusion scanning.
3.3.4.2 Primary SVT Symptoms • Hurlbert and Rutherford [6], in a review of the literature, reported a 2:1 ratio of males to females with an average age of 30 years for patients with primary SVT. • Primary SVT represents only 3.5% of all cases of TOCS. • Venous thrombosis is seen three times more frequently on the right than on the left venous system, but bilateral venous compression also occurs frequently. • Thrombosis is believed to be caused by repetitive trauma from compression. • Virtually every patient had some degree of upper extremity swelling associated with pain that worsens with exertion. • Some patients may have cyanosis of the arm. • Unlike lower extremity DVT, symptoms in the upper extremity are more related to venous obstruction than reflux. • Venous outflow through the collateral vessels is limited, resulting in venous hypertension, swelling and even venous claudication. • Venous gangrene is an extremely rare complication of SVT.
Investigations/Examination/Diagnosis • Clinically the arm may be swollen and cyanosed with dilated shoulder girdle collateral veins. • Duplex is the first-line investigation of choice and has a sensitivity of 94% and a specificity of 96% compared with venography [7]. • Magnetic resonance angiography (MRA) has poor sensitivity for nonocclusive thrombi and short segment occlusion. • Computed tomography (CT) has been used to diagnose upper extremity DVT but its specificity and sensitivity are undetermined. • Venography is still considered as the reference in evaluating SVT. The basilic vein is the preferred site for injection, with the arm abducted at 30°. The cephalic
3.3.4 A Case Apart: Primary Subclavian–Axillary Vein Thrombosis
vein is not used because it joins directly with the subclavian vein and using this site means you may miss an axillary vein thrombosis.
Treatment • For many years, treatment of SVT relied on rest and elevation of the upper limb with anticoagulant therapy. However, the morbidity associated with this conservative treatment is high. • More recently, investigators have realized that many patients with SVT have compression at the thoracic outlet. • It has become accepted that treatment of primary upper extremity DVT requires: (1) restoration of patency and (2) removal of extrinsic compression.
• Waiting too long risks rethrombosis, whereas operating immediately risks bleeding due to the thrombolytic agent. • In TOS with subclavian–axillary vein thrombosis, it seems logical to recommend an early complete treatment with thrombolysis and first rib resection [18]. • Specific problems may arise in some patients after thrombolysis. In a small group, no residual lesion or compression is seen on positional venography after thrombolysis. In these cases, anticoagulation therapy is recommended without thoracic outlet decompression. • In other patients, intrinsic stenosis is seen on venography after thrombolysis. In these cases operative vein by-pass or patch angioplasty with first rib resection is needed and should be done in the days after thrombolysis because the risk of rethrombosis appears to be quite high.
Open Thrombectomy
• Initially, in patients with primary SVT, subclavian vein patency was restored by open thrombectomy associated with first rib resection [3]. Although now supplanted by thrombolysis, open thrombectomy has proved effective and should be considered in patients with contraindications or failure of thrombolysis therapy.
Thrombolytic Therapy and Thoracic Outlet Decompression
• Thrombolytic therapy produces less morbidity than open thrombectomy in primary SVT, but carries poor long-term outcome if not combined with thoracic outlet decompression. • Catheter-directed techniques of thrombolysis allow for immediate venous evaluation and assessment of extrinsic compression with positional venography after thrombolysis [10]. • However, Sheeran et al. [17] have shown that recanalization of the vein by thrombolysis without decompression of the thoracic outlet is not adequate, with 55% of patients remaining symptomatic. • In contrast, Machleder [11] reported the success of this combined treatment with 86% of 36 patients becoming asymptomatic. • The appropriate time interval between thrombolysis and thoracic outlet decompression is still under discussion. Machleder waited 3 months whereas Lee et al. [8] recommended immediate first rib resection within 4 days after thrombolysis.
Percutaneous Balloon Angioplasty and Decompression
• Recently, percutaneous balloon angioplasty with or without stenting has been suggested. • The results of this technique without thoracic outlet decompression are poor with a 1-year primary patency of 35% [4]. • Obviously, this technique does not obviate the need for surgery because thoracic outlet decompression is still required. • Even after thoracic outlet decompression, some venous stenoses are resistant to dilation or present intrinsic elastic recoil. • Various types of stents were used to treat residual stenoses, but acceptable results were seen only in patients who had thoracic outlet decompression. • In addition, venous stents underneath the clavicle are known to fracture. • The long-term patency rate of stenting in primary SVT plus thoracic outlet compression is unknown. As surgery is always needed for thoracic outlet decompression, it seems logical to repair the subclavian vein with patch angioplasty or short autogenous by-pass [16].
Open Thrombectomy and Vein Transposition
In many patients seen more than 10 days after the onset of primary upper limb DVT, thrombolysis fails. Most of these patients should be treated conservatively with anti-
255
256
3.3 Thoracic Outlet Syndrome
coagulation unless the occlusion is short. In these cases, open thrombectomy with vein reconstruction and first rib resection can be recommended with acceptable results. The technique used is internal jugular vein transposition or cephalic vein by-pass with a temporary arteriovenous fistula. Prosthetic by-pass has shown inferior results in this location.
3.3.5 Summary Main points of this chapter are : • Controversy concerning diagnosis and treatment of neurogenic thoracic outlet compression syndrome. • Emphasis concerning the value of a combined supraand infra-clavicular approach for first rib resection and arterial by-pass in patients with arterial thoracic outlet compression syndrome. • Value of early thrombolytic therapy in patients with primary subclavian vein thrombosis combined with thoracic outlet surgical decompression. References 1. Axelrod DA, Proctor MC, Geisser ME, Roth RS, Greenfield LJ (2001) Outcomes after surgery for thoracic outlet syndrome. J Vasc Surg 33:1220–1225 2. Clagett GP (2000) Upper extremity aneurysms. In: Rutherford RB (ed) Vascular surgery, 5th edn, Saunders, Philadelphia, p 1359 3. DeWeese JA, Adams JT, Gaiser DL (1970) Subclavian venous thrombectomy. Circulation 42:158–163 4. Glanz S, Gordon DH, Lipkowitz GS, Butt KM, Hong J, Sclafani SJ (1988) Axillary and subclavian vein stenosis. Percutaneous angioplasty. Radiology 168:371–373 5. Hempel GK, Rusher AH Jr, Wheeler CG, Hunt DG, Bukhari HI (1981) Supraclavicular resection of the first rib for thoracic outlet syndrome. Am J Surg 141:213–215 6. Hurlbert SN, Rutherford RB (2000) Subclavian-axillary vein thrombosis. In: Rutherford RB (ed) Vascular surgery, 5th edn. Saunders, Philadelphia, pp 1208–1221
7. Koksoy C, Kuzu A, Kutlay J, Erden I, Ozcan H, Ergin K (1995) The diagnostic value of colour doppler ultrasound in central venous catheter related thrombosis. Clin Radiol 50:687–689 8. Lee MC, Grassi CJ, Belkin M, Mannick JA, Whittemore AD, Donaldson MC (1998) Early operative intervention following thrombolytic therapy for primary subclavian vein thrombosis. An effective treatment approach. J Vasc Surg 27:1101–1108 9. Lepantalo M, Lindgren KA, Leino E, Lindfors O, von Smitten K, Nuutinen E, Totterman S (1989) Long-term outcome after resection of the first rib for thoracic outlet syndrome. Br J Surg 76:1255–1256 10. Lokanathan R, Salvian AJ, Chen JC, Morris C, Taylor DC, Hsiang YN (2001) Outcome after thrombolysis and selective thoracic outlet decompression for primary axillary vein thrombosis. J Vasc Surg 33:783–788 11. Machleder HI (1993) Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg 17:305–317 12. Monreal M, Lafoz E, Ruiz J et al (1991) Upper extremity deep venous thrombosis and pulmonary embolism. Chest 99:280–283 13. Roos DB (1984) Thoracic outlet and carpal tunnel syndrome. In Rutherford RB (ed) Vascular surgery, 2nd edn. Saunders, Philadelphia, pp 708–724 14. Rutherford RB, Hurlbert SN (1996) Primary subclavian-axillary vein thrombosis. Consensus and commentary. Cardiovasc Surg 4:420–423 15. Sanders RJ, Haug CE (1991) Thoracic outlet syndrome: a common sequela of neck injuries. Lippincott, Philadelphia, p 93 16. Sanders RJ, Cooper MA (1995) Surgical management of subclavian vein obstruction, including six cases of subclavian vein bypass. Surgery 118:856–863 17. Sheeran SR, Hallisey MJ, Murphy TP, Faberman RS, Sherman S (1997) Local thrombolytic therapy as part of a multidisciplinary approach to acute axillo-subclavian vein thrombosis (Paget-Schroetter syndrome). J Vasc Interv Radiol 8:253–260 18. Urschel HC, Razzuk MA (2000) Paget-Schroetter syndrome: what is the best management? Ann Thorac Surg 69:1663–1669
257
3.4 Traumatic Injury of Upper Extremity Arteries Josef Klocker, Gustav Fraedrich
3.4.1 Epidemiology • The incidence of vascular trauma in general, and of upper extremity artery and vein lesions in particular, is unknown. • Possible reasons for lack of data are: (1) death of individuals before arriving at the hospital, or before initiation of vascular repair; (2) failed diagnosis of blood vessel injury; (3) inadequate nationwide data collection; and (4) national vascular registries based on data about procedures instead of underlying diagnosis. • In a retrospective analysis, 3.3% of patients with upper extremity injuries admitted to a level I trauma centre in the USA were diagnosed to have concomitant arterial trauma [34]. • In patients with shoulder and elbow dislocations, symptomatic arterial injuries were present in 0.97% (axillary artery) and 0.47% (brachial artery), respectively [43]. • The anatomical distribution of vascular injuries from published European studies or vascular registries was recently summarized: the relative frequency of upper extremity arterial injuries was 33%, almost half of them being located in the brachial artery [13].
• Penetrating traumas are characterized by limited damage within a limited area and few accompanying lesions. • Today, the incidence of penetrating injuries in most European countries is low.
3.4.2.2 Blunt Trauma • Today the main emphasis in the management of vascular trauma has shifted towards blunt and iatrogenic injuries [13]. • The mechanisms of injury give important information on resulting lesions. • Blunt traumas usually result in vessel thrombosis, which is frequently caused by stretching of the artery, partial or complete intimal and/or medial disruption, leaving the highly thrombogenic tunica externa to maintain temporary vessel continuity. • Blunt vascular injuries are usually more critical than penetrating traumas due to associated fractures and dislocations, and concomitant injuries to nerves and muscles, as well as delayed therapy because of initial misinterpretation of the injury. • Therefore, blunt trauma leads to a significantly higher rate of disability [6, 14, 19, 25, 46, 47].
3.4.2 Aetiology 3.4.3 Diagnosis • Trauma to the extremities falls into two basic categories, penetrating and blunt. • Both lead to different types of vascular injuries and different ultimate outcome [52].
3.4.2.1 Penetrating Trauma • The mechanisms of injury give important information on resulting lesions.
3.4.3.1 Recommended European Standard Diagnostic Steps of Investigation The clinical presentation of arterial injuries varies widely. The majority of extremity arterial injuries are clinically occult, frequently leading to delayed diagnosis. First assessment of patients should be standardized. • Initial clinical investigation has to include checking for distal pulses, sensory and motor function, swell-
258
3.4 Traumatic Injury of Upper Extremity Arteries
•
•
•
•
•
ing, colour and temperature of the skin, and delayed capillary refill. Physical examination alone is inaccurate in excluding a vascular injury [26]. The presence of palpable distal extremity pulses does not sufficiently exclude a proximal arterial injury [12, 31, 52]. It is recommended to calculate radial and ulnar systolic Doppler pressure indices (wrist-brachial index, WBI) comparing the injured and the uninjured contralateral extremities [52]. It was shown that patients with normal clinical findings and minimum Doppler pressure indices no lower than 1.00 (defined as the lower of the two indices at the wrist) are very unlikely to have clinically significant arterial injury [23, 39, 50]. Noteworthy, in Weaver’s study, only 9 of 104 “normal” patients had (upper or lower) extremity arterial injuries as diagnosed by angiography, and none of them required therapeutic intervention [50]. Therefore, patients with normal extremity pulse examination and a minimal WBI of 1.00 or more do not require routine angiography. Diagnostic arteriography is considered the gold standard in diagnosis of extremity arterial injuries. Injured limbs associated with distal pulse deficit and/or a minimal WBI less than 1.00 should routinely undergo selective arteriography [3, 37]. Alternatively, colour flow Duplex (CFD) ultrasound has been suggested [20, 22, 28] and both the sensitivity and specificity of CFD were shown to be equal to or higher than 95% [7, 15]. CFD is particularly sensitive in the diagnosis and follow-up of floating intraluminal intimal tears or the haemodynamic relevance of local stenoses. Arteriography and/or CFD ultrasound can be used as first-line imaging modality depending on the availability of experienced investigators and equipment. In addition, helical computed tomographic arteriography (CTA) was reported as an initial diagnostic method in patients with suspected arterial injuries [41, 42]. CTA sensitivity was 95.1%, and specificity was 98.7%. It was concluded that CTA is an effective tool for the evaluation of medical and surgical emergencies [30]. A minority of patients present with obvious clinical evidence of arterial injury such as: pulsatile external bleeding, rapidly expanding haematoma, or an ischaemic limb. Those patients may undergo immediate surgical exploration in the operating room without previous diagnostic testing.
3.4.4 Therapy • Arterial injuries in an upper extremity are generally a less demanding problem than in the lower limb. • Unless active bleeding is present, limb injuries are less urgent than injuries to the trunk, head or neck. • Except for the subclavian and axillary arteries, lifethreatening haemorrhages in the upper limb are infrequent, and, because of better collateral flow, even ischaemic upper extremities tend to remain viable.
3.4.4.1 Conservative Therapy • Nonoperative management of clinically asymptomatic arterial injuries is controversial [51]. • Conservative treatment was shown to be feasible and safe in patients suffering from injuries with intact distal circulation in the presence of an adherent or downstream protrusion of intimal flaps or short (<5 mm) arterial wall disruption with intimal defects and pseudoaneurysms [10, 16, 17, 44, 52].
3.4.4.2 Endovascular Therapy • Endovascular management may be considered in single patients to occlude bleeding vessels and/or arteriovenous fistulae particularly in remote anatomical sites [11, 27, 32, 52].
3.4.4.3 Surgery Operative management of extremity arterial injuries is based on: • Control of blood loss. • Early revascularization.
Control of Blood Loss • Frequently, vascular injuries in extremities are associated with limb fractures. • In such patients, external fixation performed rapidly prior to vascular repair appears to be preferable due to its technical simplicity and low infection risk.
3.4.5 Prognosis
• Exposure of the artery can best be achieved using routine access for vascular repair, and in our opinion, when planning the approach, concessions to trauma surgeons should be avoided. • After proximal and distal control of the artery, the site of injury is inspected. Alternatively, especially in the case of subclavian and axillary artery injuries, endoluminal balloon occlusion can be used. • After exposure of the injured segment, the distal and proximal intraluminal thrombus is removed and heparinized saline solution is instilled. • Systemic anticoagulation using heparin can be initiated if not contraindicated.
Revascularization Points to note about surgical repair of extremity arterial injuries: • It is principally dependent on the severity and extent of damage. • Intimal dissections without disruption of the artery can undergo repair by lateral suture patch angioplasty. • If the injured arterial segments are excised, the adjacent normal arterial walls are sutured directly if a tension-free end-to-end anastomosis can be performed. • Otherwise, interposition grafts or, when associated soft-tissue injury is extensive, by-pass grafts are indicated. • Use of autologous vein grafts (greater or smaller saphenous vein and cephalic vein) from uninjured limbs is recommended whenever available [4, 21, 36]. • Completion arteriography is required in order to visualize arterial run-off, and to document initial technical success of revascularization.
Amputation • One of the most difficult decisions in the treatment of individuals with injuries of upper extremity arteries is whether and when to amputate [38]. • It is noteworthy that vascular injuries of the extremities remain the most important cause of limb amputations. • In polytraumatized patients, the pro and cons of reconstruction of injured upper extremity arteries have
to be calculated carefully, and decisions have to follow the rule “life before limb”. • Therefore, for unstable and multiply injured trauma patients or patients with extensive soft-tissue damage primary amputation should be considered. • However, in contrast to the concept of early amputation previously suggested in patients with severe combined vascular and neural injuries, Manord and co-workers [25] described significant improvement of initial disability after treatment, and final outcome could not be predicted on the basis of initial clinical presentation. • Nevertheless, nerve repairs still do have poor outcome and modern prosthetics may provide a better ultimate solution for some of these patients [19, 31, 33, 35, 46], even though most of the patients use prosthetics solely for cosmetic purposes [5, 9, 48].
Nerve Repair • There is considerable controversy regarding the timing of nerve repair in patients with severe vascular and neural injury [2, 40, 45]. • Both emergency and delayed nerve repair were performed in a large series of patients with complex upper extremity trauma [6, 14, 24, 25]. • According to Terzis and co-workers [45], if restoration of blood supply is necessary, it is wise to perform plexus exploration to determine the extent and level of nerve lesions. • There may be two major advantages of primary repair: (1) an end-to-end repair can be performed before retraction of the nerve stumps and (2) difficulties arising from residual scar tissue during a delayed procedure can be avoided.
3.4.5 Prognosis • Perioperative and procedure-related death due to upper extremity trauma is rare, and limb loss after reconstruction can be avoided in most patients [1, 18, 29, 47]. • Functional results after upper extremity vascular trauma mainly depend on the presence and severity of concomitant neurological injury.
259
260
3.4 Traumatic Injury of Upper Extremity Arteries
• When compared to penetrating trauma, blunt trauma is more frequently associated with neurological and orthopaedic injuries, and leads to a significantly higher rate of disability [6, 8, 14, 19, 25, 29, 31, 46, 47, 49]. References 1. Adinolfi MF, Hardin WD, O´Connell RC, Kerstein MD (1983) Amputations after vascular trauma in civilians. South Med J 76:1241–1243 2. Alnot J (1995) Traumatic brachial plexus lesions in the adult: indications and results. Hand Clin 11:623–631 3. Applebaum R, Yellin AE, Weaver FA, Oberg J, Pentecost M (1990) Role of routine arteriography in blunt lower-extremity trauma. Am J Surg 160:221–224 4. Bastounis E, Pikoulis E, Leppäniemi AK, Michail P, Alexiou D (1998) Revascularization of the limbs using vein grafts after vascular injuries. Injury 29:105–108 5. Beasley RW, de Bese GM (1986) Upper limb amputations and prostheses. Orthop Clin North Am 17:395–405 6. Brown KR, Jean-Claude J, Seabrook GR, Towne JB, Cambria RA (2001) Determinates of functional disability after complex upper extremity trauma. Ann Vasc Surg 15:43–48 7. Bynoe RP, Miles WS, Bell RM, Greenwold DR, Sessions G, Haynes JL, Rush DS (1991) Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg 14:346–352 8. Cikrit DF, Dalsing MC, Bryant BJ, Lalka SG, Sawchuk AP, Schulz JE (1990) An experience with upper-extremity vascular trauma. Am J Surg 160:229–233 9. Datta D, Kingston J, Ronald J (1989) Myoelectric prostheses for below-elbow amputees: the Trent experience. Int Disabil Stud 11:167–170 10. Dennis JW, Frykberg ER, Veldenz HC, Huffman S, Menawat SS (1998) Validation of nonoperative management of occult vascular injuries and accuracy of physical examination alone in penetrating extremity trauma: 5- to 10-year follow up. J Trauma 44:243–252 11. Dinkel HP, Eckstein FS, Triller J, Do DD (2002) Emergent axillary artery stent-graft placement for massive hemorrhage from an avulsed subscapular artery. J Endovasc Ther 9:129–133 12. Drapanas T, Hewitt RL, Weichert RF 3rd, Smith AD (1970) Civilian vascular injuries: a critical appraisal of three decades of management. Ann Surg 172:351–360 13. Fingerhut A, Leppaniemi AK, Androulakis GA, Archodovassilis F, Bouillon B, Cavina E et al (2002) The European experience with vascular injuries. Surg Clin North Am 82:175–188
14. Fitridge RA, Raptis S, Miller JH, Faris I (1994) Upper extremity arterial injuries: experience at the Royal Adelaide Hospital, 1969 to 1991. J Vasc Surg 20:941–946 15. Fry WR, Smith RS, Sayers DV, Henderson VJ, Morabito DJ, Tsoi EK et al (1993) The success of duplex ultrasonographic scanning in diagnosis of extremity vascular proximity trauma. Arch Surg 128:1368–1372 16. Frykberg ER (1995) Advances in the diagnosis and treatment of extremity vascular trauma. Surg Clin North Am 75:207–223 17. Frykberg ER, Vines FS, Alexander RH (1989) The natural history of clinically occult arterial injuries: a prospective evaluation. J Trauma 29:577–583 18. Hammond DC, Gould JS, Hanel DP (1992) Management of acute and chronic vascular injuries to the arm and forearm. Indications and technique. Hand Clin 8:453–463 19. Hardin WD, O´Connell RC, Adinolfi MF, Kerstein MD (1985) Traumatic arterial injuries of the upper extremity: determinants of disability. Am J Surg 150:266–270 20. Johansen K, Lynch K, Paun M, Copass MK (1991) Non-invasive vascular tests reliably exclude occult arterial trauma in injured extremities. J Trauma 31:515–522 21. Keen RR, Meyer JP, Durham JR, Eldrup-Jorgensen J, Flanigan P, Schwarcz TH et al (1991) Autogenous vein graft repair of injured extremity arteries: early and late results with 134 consecutive patients. J Vasc Surg 13:664–668 22. Knudson MM, Lewis FR, Atkinson K, Neuhaus A (1993) The role of duplex ultrasound arterial imaging in patients with penetrating extremity trauma. Arch Surg 128:1033–1037 23. Lynch K, Johansen K (1991) Can Doppler pressure measurement replace “exclusion” arteriography in the diagnosis of occult extremity arterial trauma? Ann Surg 214:737–741 24. Magalon G, Bordeaux J, Legre R, Aubert JP (1988) Emergency versus delayed repair of severe brachial plexus injuries. Clin Orthop 237:32–35 25. Manord JD, Garrard CL, Kline DG, Sternbergh WC 3rd, Money SR (1998) Management of severe proximal vascular and neural injury of the upper extremity. J Vasc Surg 27:43–49 26. McCormick TM, Burch BH (1979) Routine angiographic evaluation of neck and upper extremity injuries. J Trauma 19:384–387 27. McNeese S, Finck E, Yellin AE (1980) Definitive treatment of selected vascular injuries and post-traumatic arteriovenous fistulas by arteriographic embolization. Am J Surg 140:252–259 28. Meissner M, Paun M, Johansen K (1991) Duplex scanning for arterial trauma. Am J Surg 161:552–555
References
29. Myers SI, Harward TRS, Maher DP, Melissinos EG, Lowry PA (1990) Complex upper extremity vascular trauma in an urban population. J Vasc Surg 12:305–309 30. Novelline RA, Rhea JT, Rao PM, Stuk JL (1999) Helical CT in emergency radiology. Radiology 213:321–339 31. Orcutt MB, Levine BA, Gaskill HV, Sirinek KR (1986) Civilian vascular trauma of the upper extremity. J Trauma 26:63–67 32. Parodi JC, Schonholz C, Ferreira LM, Bergan J (1999) Endovascular stent-graft treatment of traumatic arterial lesions. Ann Vasc Surg 13:121–129 33. Peacock JB, Proctor HJ (1977) Factors limiting extremity function following vascular injury. J Trauma 17:532–535 34. Pillai L, Luchette FA, Romano KS, Ricotta JJ (1997) Upperextremity arterial injury. Am Surg 63:224–227 35. Pretre R, Hoffmeyer P, Bednarkiewicz M, Kursteiner K, Faidutti B (1994) Blunt injury to the subclavian or axillary artery. J Am Coll Surg 179:295–298 36. Razmadze A (1999) Vascular injuries of the limbs: a fifteen-year Georgian experience. Eur J Vasc Endovasc Surg 18:235–239 37. Reid JD, Weigelt JA, Thal ER, Francis H 3rd (1988) Assessment of proximity of a wound to major vascular structures as an indication for arteriography. Arch Surg 123:942–946 38. Roessler MS, Wisner DH, Holcroft JW (1991) The mangled extremity. When to amputate? Arch Surg 126:1243–1249 39. Schwartz MR, Weaver FA, Bauer M, Siegel A, Yellin AE (1993) Refining the indications for arteriography in penetrating extremity trauma: a prospective analysis. J Vasc Surg 17:116–122 40. Sedel L (1988) Repair of severe traction lesions of the brachial plexus. Clin Orthop 237:32–35 41. Soto JA, Munera F, Cardoso N, Guarin O, Medina S (1999) Diagnostic performance of helical CT angiography in trauma to large arteries of the extremities. J Comput Assist Tomogr 23:188–196
42. Soto JA, Munera F, Morales C, Lopera JE, Holguin D, Guarin O et al (2001) Focal arterial injuries of the proximal extremities: helical CT arteriography as the initial method of diagnosis. Radiology 218:188–194 43. Sparks SR, DeLaRosa J, Bergan JJ, Hoyt DB, Owens EL (2000) Arterial injury in uncomplicated upper extremity dislocations. Ann Vasc Surg 14:110–113 44. Stain SC, Yellin AE, Weaver FA, Pentecost MJ (1989) Selective management of nonocclusive arterial injuries. Arch Surg 124:1136–1141 45. Terzis JK, Vekris MD, Soucacos PN (2000) Brachial plexus. In: Russell RC (ed) Plastic surgery, 1st edn. Mosby, St. Louis, pp 2075–2101 46. Thompson PN, Chang BB, Shah DM, Darling RC 3rd, Leather RP (1993) Outcome following blunt vascular trauma of the upper extremity. Cardiovasc Surg 1:248–250 47. van der Sluis CK, Kucey DS, Brenneman FD, Hunter GA, Maggisano R, ten Duis HJ (1997) Long-term outcomes after upper limb arterial injuries. Can J Surg 40:265–270 48. van Lunteren A, van Lunteren-Gerritsen GH, Stassen HG, Zuithoff MJ (1983) A field evaluation of arm prostheses for unilateral amputees. Prosthet Orthot Int 7:141–151 49. Visser PA, Hermreck AS, Pierce GE, Thomas JH, Hardin CA (1980) Prognosis of nerve injuries incurred during acute trauma to peripheral arteries. Am J Surg 140:596–599 50. Weaver FA, Yellin AE, Bauer M, Oberg J, Ghalambor N, Emmanuel RP et al (1990) Is arterial proximity a valid indication for arteriography in penetrating extremity trauma? A prospective analysis. Arch Surg 125:1256–1260 51. Weaver FA, Yellin AE (1993) Regarding: complications of missed arterial injuries. J Vasc Surg 18:1077–1078 52. Weaver FA, Papanicolaou G, Yellin AE (1996) Difficult peripheral vascular injuries. Surg Clin North Am 76:843–859
261
Thoracic Aorta
265
4.1 Thoracoabdominal Aneurysms S.A. Black, M.J. Brooks, J.H.N. Wolfe
4.1.1 Definition • A thoracoabdominal aortic aneurysm is defined as a dilatation of the aorta involving the origins of the coeliac, superior mesenteric or renal arteries. • Crawford’s classification system is universally accepted (Fig. 4.1.1). • Aneurysms arising proximal to the left subclavian or ending proximal to the level of the diaphragm should be classified as arch or descending thoracic aneurysms and are outside of the scope of this chapter. • It is important to differentiate operations performed electively from those performed for acute dissection and free rupture, as mortality in these latter patients is higher.
4.1.2 Epidemiology/Aetiology • Rupture of thoracoabdominal aortic aneurysms of less than 4 cm diameter is uncommon. • In a follow-up study of 1600 patients the mean rate of aneurysm expansion was 1 mm per year and the risk of aneurysm rupture became significant when the aortic diameters exceeded 6 cm [19]. • The rate of expansion and size at which rupture occurs are consistent with past studies [7, 12, 18, 27]. • Conservative management of thoracoabdominal aortic aneurysms of greater than 6 cm diameter has a poor prognosis: survival is as low as 40% at 1 year and 7% at 5 years [2, 8, 11].
Fig. 4.1.1 Safi’s modification of Crawford classification of thoracoabdominal aortic aneurysms [39]
266
4.1 Thoracoabdominal Aneurysms
4.1.3 Investigations 4.1.3.1 Imaging • Imaging allows planning of the surgical approach and is essential if endovascular intervention is considered. • All patients with thoracoabdominal aortic aneurysms should undergo fine-slice contrast-enhanced spiral CT to define the aneurysm diameter, extent, side branch anatomy, presence of intimal dissection flaps and wall thickness (Fig. 4.1.2). • Identification of aortic dissection is particularly important as surgery may be technically difficult, endovascular repair impossible, and the risk of paraplegia increased. • Selective intercostal angiography has been proposed to locate the important arterial supply to the spinal cord, but this investigation has a morbidity (anterior spinal artery emboli) and is not widely practised [28, 50]. • Magnetic resonance angiography may, in the future, provide a noninvasive technique to provide this information. We obtain an aortic angiogram to accurately assess the aneurysm neck and identify visceral-origin, particularly renal, stenoses in our patients.
4.1.3.2 Additional Investigations • Coronary artery disease, left ventricular hypertrophy, chronic obstructive pulmonary disease, cerebrovascular and renovascular disease are common in these patients, who present at an older age than patients undergoing infra-renal aortic surgery. • The detection of occult cardiac disease may be particularly important as a proximal aortic cross-clamp induces significant myocardial ischaemia and left ventricular strain. • Dobutamine stress echocardiography followed by an aggressive approach to coronary revascularization has reduced mortality in our patients [22]. • One-third of patients in a small prospective study of routine coronary angiography (n=40) had haemodynamically significant coronary artery lesions [6]. Twelve of these patients underwent staged coronary revascularization, with no patient suffering a peri-operative cardiac event.
Fig. 4.1.2 CT reconstruction of a Crawford type II thoracoabdominal aortic aneurysm
• Spirometry is performed on all patients to identify those who will benefit from preoperative physiotherapy, bronchodilator therapy and occasionally elective tracheostomy. • We encourage cessation of smoking 3 months prior to operation. • The serum creatinine level is an important predictor of outcome [3, 5]. We use the serum creatinine, a radionucleotide excretion renogram (MAG III scan) and aortic angiogram to screen for renal disease.
4.1.4 Treatment
4.1.4 Treatment 4.1.4.1 Operative Repair • Making decisions on whom and when to operate, and the guidance given to patients constitute a vital component of their surgical management. • As experience has increased it has become possible to recognize patients at increased risk from elective surgery (Table 4.1.1). • Preoperative assessment may also reduce the risk of surgery by pre-optimization or indication that a lesser procedure should be performed (i.e. repairing only the most at-risk segment of a complex aneurysm).
4.1.4.2 Open Surgery: Operative Technique • The patient is placed supine on the operating table with the left side of the chest elevated and the left arm suspended in an arm gutter. • A skin incision is made over the sixth rib from the mid-axillary line anteriorly to the midline. • This incision is then continued inferiorly to below the level of the umbilicus. • The sixth rib is excised, the left pleural and peritoneal cavities are opened, and the diaphragm is partially divided radially. • In the repair of the least extensive (type IV) aneurysms, we limit the incision to the abdomen alone [4, 21].
• The abdominal aneurysm component and major aortic side branches are exposed by medial visceral rotation including the spleen, colon and left kidney (retroperitoneal dissection starting from the posterior-lateral parietal peritoneal attachment; Fig. 4.1.3). • Thoracic exposure is achieved by dissection of the mediastinum. • Once the aneurysm has been adequately exposed, healthy aorta is dissected out proximally and distally, aortic cross-clamps are applied, the aneurysm sac is opened, and surgical reconstruction is performed using a prosthetic graft. • The graft is sutured end-to-end to healthy proximal aorta, and one or more windows are cut in the graft for side-to-side anastomosis to patches of native aorta containing the origins of visceral and renal arteries. • Side grafts of 8 mm diameter dacron are used for reimplantation of the intercostal arteries.
4.1.4.3 Open Surgery: Adjuvant Techniques Left Heart By-pass • Left heart (atrio-femoral) by-pass is the most frequently used technique to maintain distal perfusion during these operations. • An afferent limb is placed through a purse-string suture in the left atrial appendage. • An efferent limb is placed into the left femoral artery via a short arteriotomy.
Table 4.1.1 Preoperative risk factors predicative of patient outcome [6, 9, 45] Pre-operative risk factor
Svensson et al. [45]ª
Coselli et al. [9]b
Brooks et al. [6]c
Crawford type II (III)
2.54 (1.5–4.4)
2.06 (1.2–3.4)
3.32 (1.6–6.9)
Age
1.05 (1.0–1.1)
1.06 (1.0–1.1)
Renal impairment
1.20 (1.1–1.3)
3.23 (1.9–5.7)
Coronary artery disease
1.66 (1.1–2.5)
ns
Chronic lung disease
1.57 (1.1–2.3)
ns
Aneurysm symptoms
ns
Systemic hypertension
ns
2.47 (1.3–4.7) ns
a 1446 patients, OR 30-day death as a function of interval-scaled variables b 1108 patients, risk model, OR in-hospital or 30 day deaths c
272 patients, response on factors, OR in-hospital death
ns 2.97 (1.6–5.4) ns 4.72 (2.4–9.5) ns 2.17 (1.2–4.1)
267
268
4.1 Thoracoabdominal Aneurysms
• In the absence of spinal cord monitoring (see below), flow is adjusted to achieve a mean perfusion pressure of 70 mmHg while maintaining normal proximal arterial pressure and venous filling. • There has been no randomized control study of left heart by-pass. • The authors of large case series recommend its use in patients undergoing Crawford type I, II and III repairs based on a reduction in both mortality and paraplegia rates when compared to historical controls [24, 40, 42, 45, 49]. • It is generally accepted that left heart by-pass is unnecessary for the repair of Crawford type IV aneurysms in which the cross-clamp time can be kept short by including the lower intercostal and visceral artery origins in an oblique, end-to-end, proximal anastomosis.
Selective Visceral Perfusion • This technique is a modification of atrio-femoral bypass in which the visceral and renal arteries are perfused directly using selective catheters. • The additional benefit of this intervention, which carries the risks of side branch embolization or dissection, is unproven. • In a small prospective nonrandomized study of the technique blood loss increased and no renal protection was observed [31]. • Achieving adequate flow rates through small distal catheters appears to have been the problem. • There are, however, pragmatic advantages to maintaining perfusion and excellent results have been achieved which incorporate this technique [26].
Hypothermic Circulatory Arrest • Hypothermic circulatory arrest with complete heart by-pass is routine in aortic root and arch surgery. • Moderate hypothermia (33–35°C) is preferred for thoracoabdominal aortic aneurysm repair and appears effective in protecting the kidneys and spinal cord during aortic cross-clamp placement [46]. • Results from an American vascular unit where hypothermic cardiopulmonary by-pass and circulatory arrest have been used routinely for 17 years (211 patients) suggest that mortality (7.1%) and paraplegia rates (2.9%) are equivalent to other techniques but
that respiratory function is compromised, with 24% of patients ventilated at 48 h [29, 30].
Spinal Cord Protection • Paraplegia is the most feared complication of these operations and contributes significant morbidity and mortality. • In our early experience neurological events occurred in 21% of patients undergoing Crawford type II repairs without adjuncts, with rates as high as 41% reported by other centres [22, 31]. • The mechanism of cord injury is multifactorial: the pre-existing cord blood supply, cerebrospinal fluid (CSF) pressure and ischaemia/reperfusion insult are all important. • In addition to the techniques discussed below pharmacological agents (naloxone, thiopentone and steroids), minimizing cord ischaemia time and the use of regional or systemic cooling may be important in protecting the spinal cord. • We rely on the natural hypothermia of the surgery and have been unsuccessful with local spinal cord cooling.
Intercostal Re-implantation
• Re-attachment of major intercostals from T9 to T12 appears important for spinal cord perfusion. • Most reports suggest that back-bleeding intercostals identified intraoperatively should be re-implanted using 8-mm jump grafts off the aortic prosthesis in at least half of patients [38, 41, 43]. • Intercostal re-implantation has been shown to return sensory and motor-evoked potentials to normal and avoid paraplegia [24, 26]. • Re-implantation may protect against late-onset paraplegia.
CSFDrainage
• In animal studies continuous CSF drainage has been shown to reduce the incidence of paraplegia when a high aortic cross-clamp is applied [20, 32, 44]. • The three randomized trials of CSF drainage in humans are shown in Table 4.1.2. • Crawford’s study has been criticized, as a maximum 50 ml of CSF was withdrawn and the catheter removed at the end of the procedure.
4.1.5 Endovascular Intervention
• The two other randomized studies both show benefit from CSF drainage. • Our own experience and published cases show that CSF drainage can reverse late-onset paraplegia [1]. • Subdural haemorrhage and bacterial meningitis have both been reported following CSF drainage. • The risk of a complication is reduced by careful control of the CSF pressure and prompt removal of the catheter. • The role of CSF drainage in patients undergoing Crawford type III repairs has not been defined. • Based on the trial data we use CSF drains in all patients undergoing Crawford type I, II or III repairs whether by an open or combined endovascular approach.
SpinalCord Monitoring
• Somatosensory-evoked potentials (sSEPs) are well established for monitoring the sensory tracts in the posterior columns of the spinal cord. • The blood supply of the dorsal columns is different from that of the anterio-lateral horns that control motor function. • This difference may, in part, explain the poor reported sensitivity and specificity of sSEPS in predicting postoperative paraplegia. • Motor-evoked potentials (MEPs) elicited using transcranial stimulation can only be monitored while the patient is under general anaesthesia. • In 52 consecutive patients with Crawford type I and II aneurysms, MEPs detected cord ischaemia within 2 min, and intercostal reattachment or an increase in systolic pressure was effective at restoring MEP potentials [26]. • Changes in sSEPS and MEPs have been separately compared in 56 consecutive patients undergoing thoracoabdominal aortic aneurysm repair [34]. • A significant time lag was observed in sSEPs (2–34 min) and false-positives were common.
4.1.5 Endovascular Intervention • The increasing use of endovascular stents for the treatment of thoracic aortic aneurysms has shown significant early promise, with several centres publishing encouraging early results of a procedure that reduces morbidity [16, 17]. • Endovascular treatment is attractive as it avoids the thoracotomy, extensive tissue dissection and the supra-coeliac aortic cross-clamp necessary for open repair. • However, treatment of aneurysmal disease of the aorta with endovascular stents was limited by involvement of the origins of the visceral and renal arteries in more extensive disease. • Combining endovascular stenting with an open abdominal procedure has increased the scope of endovascular treatment [37, 48]. • In the future, developments in branched stent grafts may allow an entirely endovascular approach but this is currently in the early stages of development although fenestrated grafts have a role in juxtarenal aneurysm and some type I thoracoabdominal aneurysms.
4.1.5.1 Visceral Hybrid Procedure • The principle of this operation is the retrograde revascularization of the visceral and renal arteries via an abdominal approach to allow the use of endovascular stent grafts to exclude Crawford type I, II and III thoracoabdominal aortic aneurysm in their entirety. • Open repair with a subcostal incision is preferred for Crawford type IV aneurysms. • The safety and durability of using retrograde by-pass grafts to supply the coeliac, superior mesenteric and renal arteries is controversial. The majority of such bypasses have been performed for chronic mesenteric
Table 4.1.2 Randomized controlled trials of CSF drainage during Crawford type II and III thoracoabdominal aortic aneurysm repair [10, 13, 47] Author
n
Crawford et al. [13]
100
Svensson et al. [47]
33
Coselli et al. [10]
No drain
(%)
CSF drain
(%)
Significance
17/49
35%
14/51
28%
ns
7/16
44%
2/17
12%
P<0.05
9/69
13%
2/76
3%
P=0.03
269
270
4.1 Thoracoabdominal Aneurysms
Fig. 4.1.3 Intraoperative picture showing the exposure achieved by a retroperitoneal dissection and medial visceral rotation
ischaemia and renal artery stenosis. Graft patency in these patients is acceptable [33, 35]. • It must also be remembered that patients with aneurysmal disease rarely have aortic side branch stenoses except at the vessel origins and have reduced life expectancy from comorbid conditions.
•
•
Preoperative Planning
•
• In order to successfully exclude an aneurysm, it is accepted that at least 2–3 cm of nonaneurysmal aorta is required in which to deploy the stent to achieve adequate fixation [15]. • In thoracoabdominal aortic aneurysms both the proximal and distal landing zones may prove problematic: it is safe to cover the origin of the left subclavian artery as
•
the arm is well co-lateralized and elderly right-handed patients rarely complain of symptoms [14, 23]. In younger patients, such as those with Marfan’s, or left-handed patients it may be necessary to perform a left common carotid to left subclavian by-pass graft. The proximal landing zone can be taken into the aortic arch if a right common carotid to left common carotid and subclavian cross-over graft is performed. We term the reconstruction of the upper limb and head vessels combined with endovascular stenting of an aneurysm an “arch hybrid” (these techniques are particular useful when a type I endoleak is present following a “visceral hybrid” procedure). In most endovascular aortic procedures the distal landing zone is less of a concern as the graft can seal in the iliac arteries.
4.1.6 Outcome
• For a visceral hybrid repair sufficient lower abdominal aorta or iliac arteries must be left uncovered to allow the anastomosis of the retrograde by-pass. • In our experience, one-quarter of these patients have had a past repair of the infra-renal abdominal aorta. • This graft provides a safe distal landing zone for the stent graft and take-off point for the retrograde bypass. • In the absence of a previous repair and with no healthy infra-renal aorta, it may be necessary to sew in an infra-renal tube or bifurcated graft to act as a distal landing zone. • In our experience very few patients have an hourglasstype aneurysm appearance to allow for this to be performed; therefore, in the majority, the common iliac arteries will need to be employed for take-off of the revascularization grafts. • This necessitates landing the stent grafts as near to the bifurcation of the aorta as possible to minimize the risk of distal type I endoleak. • In these complex patients the operation plan varies with each patient and must be carefully tailored to the individual.
Operative Procedure • The procedure is performed under general and epidural anaesthesia with the patient in a supine position. • Spinal drainage, cell salvage and rapid infusers are additionally employed. • Cardiac function during the procedure is monitored using transoesophageal echocardiography. • The abdominal aorta and iliac arteries, coeliac axis, superior mesenteric artery and origins of both renal arteries are exposed via a transperitoneal approach. • Simultaneously a branched graft is constructed for the retrograde revascularization of the aortic side branches; in the majority of cases an inverted 14-mm by 7-mm Dacron graft with two additional 8-mm sidepipes attached is used. • Following heparin administration the branched graft is anastomosed to either a pre-existing or a newly inserted infra-renal aortic graft, the distal aorta, or the proximal iliac arteries. • In our opinion it is preferable not to take all four revascularization limbs off one common iliac artery although this is sometimes necessary. Preferably separate grafts (i.e. 14-mm by 7-mm branched grafts) should be taken off each common iliac artery.
• The graft to the coeliac axis is tunnelled retroperitoneally anterior to the pancreas and anastomosed end-toside to the origin of the hepatic artery. • The graft to the superior mesenteric artery is anastomosed proximally to avoid ligating the middle colic branch and lies as a loose “Lazy C” curve so that it does not kink when the small bowel is returned to the abdomen Fig. 4.1.4. • The renal arteries are sequentially anastomosed in an end-to-side fashion, with the graft to the right renal artery tunnelled through the base of the small bowel mesentery. • The origins of these arteries are ligated on completion of the anastomosis, and this should be performed with a strong silk suture, to ensure a lasting seal to prevent type II endoleaks. • Doppler signals are checked in each by-pass graft in turn to ensure satisfactory flow exists. • The ischaemia time is usually 10–15 min for each anastomosis. • Following completion of the retrograde by-pass a suitable access site is chosen for endovascular stent deployment usually via a 10-mm side-pipe sewn onto the retrograde by-pass. • Alternatively the femoral or iliac arteries can be used but this increases the risk of dissection (many of these patients have a previous dissection or Marfan’s syndrome). • A catheter is also introduced percutaneously on the contralateral limb to allow flush angiography during and after stent placement. • The stent grafts can then be deployed sequentially to completely exclude the aneurysm. • In this way the entire aorta from the left subclavian origin to the bifurcation can be excluded, leaving the viscera and renals perfused from the proximal iliac arteries (Fig. 4.1.5).
4.1.6 Outcome • The advent of endovascular techniques has focused attention on the long-term outcome of patients undergoing open aneurysm repair; in infra-renal abdominal aortic aneurysm repair, endovascular techniques have already been shown to have better short-term outcome than open repair [25].
271
272
4.1 Thoracoabdominal Aneurysms
Fig. 4.1.4 Superior mesenteric artery (SMA) anastomosis demonstrating “Lazy C” curve
• Our early experience of the “visceral hybrid” approach to thoracoabdominal aortic aneurysm repair suggests that the same will be true of these operations. • The fact that patients undergoing thoracoabdominal aortic aneurysm repair are often elderly, have significant comorbidities and may have aneurysmal aortic segments left untreated has raised the question of the long-term survival of these patients after surgery. • The long-term outcome of patients in whom we have performed open repair is a 65% 5-year and 57% 10year survival. • Late deaths, most not aneurysm related, are unsurprising; more worrying is a recent quality of life analysis in which one-third of patients who underwent elective repair and two-thirds who underwent emergency repair were found to be dead or requiring institutionalized care at 1 year [36].
4.1.7 Summary and Conclusions • There have been significant advances in the management of patients with thoracoabdominal aortic aneurysms. • Improved understanding of the natural history of the disease and patient selection improves patient outcome and avoids futile operations. This is particularly true in emergency surgery. • Many of the adjuvant techniques to protect against visceral, renal and spinal cord ischaemia and reperfusion are now well established and allow specialist centres to report impressive results. • The advent of endovascular technologies, both our current “hybrid” approach and future branched stent grafts, suggest that the short-term outcome for these patients may soon be improved further.
References
References
Fig. 4.1.5 Completed visceral hybrid procedure showing the stented aorta and retrograde grafts to the coeliac, superior mesenteric and renal arteries
• In the immediate future we will continue to perform a hybrid procedure in preference to an open repair in appropriate cases. • It is gratifying that we are now considering the quality of life after these major and complex vascular procedures when once all that was considered was survival, even if that meant a patient suffering the catastrophic complication of paraplegia.
1. Ackerman LL, Traynelis VC (2002) Treatment of delayedonset neurological deficit after aortic surgery with lumbar cerebrospinal fluid drainage. Neurosurgery 51(6):1414– 1421; discussion 1421–1422 2. Bickerstaff LK, Pairolero PC et al (1982) Thoracic aortic aneurysms: a population-based study. Surgery 92(6):1103–1108 3. Bicknell CD, Cowan AR et al (2003) Renal dysfunction and prolonged visceral ischaemia increase mortality rate after suprarenal aneurysm repair. Br J Surg 90(9):1142–1146 4. Brooks MJ, Bradbury A et al (1999) Elective repair of type IV thoraco-abdominal aortic aneurysms; experience of a subcostal (transabdominal) approach. Eur J Vasc Endovasc Surg 18(4):290–293 5. Brooks MJ, Kerle M et al (2000) Thoracoabdominal aortic aneurysm: evaluation of pre-operative assessment in 257 elective repairs [abstract]. Association of Surgeons, Cardiff 6. Brooks MJ, Mayet J et al (2000) Routine coronary angiography in a consecutive series of patients undergoing thoracoabdominal aneurysm repair. Eur J Vasc Surg 21:437–444 7. Cambria RA, Gloviczki P et al (1995) Outcome and expansion rate of 57 thoracoabdominal aortic aneurysms managed nonoperatively. Am J Surg 170:213–217 8. Coselli JS, de Figueiredo LF (1997) Natural history of descending and thoracoabdominal aortic aneurysms. J Card Surg 12 [2 Suppl]:285–289; discussion 289–291 9. Coselli JS, LeMaire SA et al (2000) Mortality and paraplegia after thoracoabdominal aortic aneurysm repair: a risk factor analysis. Ann Thorac Surg 69(2):409–414 10. Coselli JS, Lemaire SA et al (2002) Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. J Vasc Surg 35(4):631–639 11. Crawford ES, Crawford JL et al (1986) Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg 3(3):389–404 12. Crawford ES, Hess KR et al (1991) Ruptured aneurysm of the descending thoracic and thoracoabdominal aorta. Analysis according to size and treatment. Ann Surg 213(5):417– 425; discussion 425–426 13. Crawford ES, Svensson LG et al (1991) A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg 13(1):36–45; discussion 45–46 14. Criado FJ, Barnatan MF et al (2002) Technical strategies to expand stent-graft applicability in the aortic arch and proximal descending thoracic aorta. J Endovasc Ther 9 [Suppl 2]: II32–II38
273
274
4.1 Thoracoabdominal Aneurysms
15. Criado FJ, Clark NS et al (2002) Stent graft repair in the aortic arch and descending thoracic aorta: a 4 year experience. J Vasc Surg 36:1121–1128 16. Dake MD, Miller DC et al (1994) Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 331(26):1729–1734 17. Dake MD, Miller DC et al (1998) The first generation of endovascular stent-grafts for patients with aneurysms of the descending thoracic aorta. J Thorac Cardiovasc Surg 116(5):689–703; discussion 703–704 18. Dapunt OK, Galla JD et al (1994) The natural history of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 107:1323–1333 19. Elefteriades JA (2002) Natural history of thoracic aortic aneurysms: indications for surgery and surgical versus nonsurgical risks. Ann Thorac Surg 74(5):S1877–S1880; discussion S1892–S1898 20. Elmore JR, Gloviczki P et al (1992) Spinal cord injury in experimental thoracic aortic occlusion: investigation of combined methods of protection. J Vasc Surg 15(5):789–798; discussion 798–799 21. Gilling-Smith GL, Wolfe JH (1995) Transabdominal repair of type IV thoraco-abdominal aortic aneurysms [see comments]. Eur J Vasc Endovasc Surg 9(1):112–113 22. Gilling-Smith GL, Worswick L et al (1995) Surgical repair of thoracoabdominal aortic aneurysm:10 years’ experience. Br J Surg 82(5):624–629 23. Gorich J, Asquan Y et al (2002) Initial experience with intentional stent-graft coverage of the subclavian artery during endovascular thoracic aortic repairs. J Endovasc Ther 9 [Suppl II]:II39–II43 24. Grabitz K, Sandmann W et al (1996) The risk of ischemic spinal cord injury in patients undergoing graft replacement for thoracoabdominal aortic aneurysms. J Vasc Surg 23(2):230–240 25. Greenhalgh RM, Brown LC et al (2004) Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1) 30-day operative mortality results: randomised controlled trial. Lancet 364(9437):843–848 26. Jacobs M, Meylaerts SA et al (1999) Strategies to prevent neurologic deficit based on motor-evoked potentials in type I and II thoracoabdominal aortic aneurysm repair. J Vasc Surg 29(1):48–57; discussion 57–59 27. Juvonen T, Ergin M et al (1997) Prospective study of the natural history of thoracic aortic aneurysms. Ann Thorac Surg 63:1533–1545
28. Kieffer E, Richard T et al (1989) Preoperative spinal cord arteriography in aneurysmal disease of the descending thoracic and thoracoabdominal aorta: preliminary results in 45 patients. Ann Vasc Surg 3(1):34–46 29. Kouchoukos NT, Masetti P et al (2002) Hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 74(5):S1885–S1887; discussion S1892–S1898 30. Kouchoukos NT, Masetti P et al (2003) Hypothermic cardiopulmonary bypass and circulatory arrest in the management of extensive thoracic and thoracoabdominal aortic aneurysms. Semin Thorac Cardiovasc Surg 15(4):333–339 31. Leijdekkers VJ, Wirds JW et al (1999) The visceral perfusion system and distal bypass during thoracoabdominal aneurysm surgery: an alternative for physiological blood flow? Cardiovasc Surg 7(2):219–224 32. McCullough JL, Hollier LH et al (1988) Paraplegia after thoracic aortic occlusion: influence of cerebrospinal fluid drainage. Experimental and early clinical results. J Vasc Surg 7(1):153–160 33. McMillan WD, McCarthy WJ et al (1995) Mesenteric artery bypass: objective patency determination. J Vasc Surg 21(5):729–740; discussion 740–741 34. Meylaerts SA, Jacobs MJ et al (1999) Comparison of transcranial motor evoked potentials and somatosensory evoked potentials during thoracoabdominal aortic aneurysm repair. Ann Surg 230(6):742–749 35. Moawad J, McKinsey JF et al (1997) Current results of surgical therapy for chronic mesenteric ischemia. Arch Surg 132(6):613–618; discussion 618–619 36. Rectenwald JE, Huber TS et al (2002) Functional outcome after thoracoabdominal aortic aneurysm repair. J Vasc Surg 35(4):640–647 37. Rimmer J, Wolfe JH (2003) Type III thoracoabdominal aortic aneurysm repair: a combined surgical and endovascular approach. Eur J Vasc Endovasc Surg 26(6):677–679 38. Ross SD, Kron IL et al (1999) Preservation of intercostal arteries during thoracoabdominal aortic aneurysm surgery: a retrospective study. J Thorac Cardiovasc Surg 118(1):17–25 39. Safi HJ (1999) How I do it: thoracoabdominal aortic aneurysm graft replacement. Cardiovasc Surg 7(6):607–613 40. Safi HJ, Miller CC 3rd et al (2003) Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair: ten years of organ protection. Ann Surg 238(3):372–380; discussion 380–381 41. Schepens MA, Vermeulen FE et al (1999) Impact of left heart bypass on the results of thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 67(6):1963–1967; discussion 1979–1980
References
42. Schepens M, Dossche K et al (2004) Introduction of adjuncts and their influence on changing results in 402 consecutive thoracoabdominal aortic aneurysm repairs. Eur J Cardiothorac Surg 25(5):701–707 43. Svensson LG (1999) An approach to spinal cord protection during descending or thoracoabdominal aortic repairs. Ann Thorac Surg 67(6):1935–1936; discussion 1953–1958 44. Svensson LG, Klepp P et al (1986) Spinal cord anatomy of the baboon – comparison with man and implications for spinal cord blood flow during thoracic aortic cross-clamping. S Afr J Surg 24(1):32–34 45. Svensson LG, Crawford ES et al (1993) Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 17(2):357–368; discussion 368–370 46. Svensson LG, Hess KR et al (1994) Influence of segmental arteries extent and atriofemoral bypass on postoperative paraplegia after thoracoabdominal aortic operations. J Vasc Surg 20(2):255–262
47. Svensson LG, Hess KR et al (1998) Reduction of neurologic injury after high-risk thoracoabdominal aortic operation. Ann Thorac Surg 66(1):132–138 48. Szmidt J, Rowinski O et al (2004) Simultaneous endovascular exclusion of thoracic aortic aneurysm with open abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg 28(4):442–448 49. von Segesser LK, Killer I et al (1993) Improved distal circulatory support for repair of descending thoracic aortic aneurysms. Ann Thorac Surg 56:1373–1380 50. Williams GM, Perler BA et al (1991) Angiographic localization of spinal cord blood supply and its relationship to postoperative paraplegia. J Vasc Surg 13(1):23–33; discussion 33–35
275
277
4.2 Aortic Dissection Csaba Dzsinich
4.2.1 Definition • Aortic/arterial dissection means intramural haemorrhage arising in most cases through an intimal lesion. • It leads to the separation of wall components and false lumen formation. • In certain cases multiple formations of false lumen may develop.
4.2.2 Epidemiology • Between 10 and 40 cases annually per one million population [19]. • Recent developments of accurate diagnostic tools have resulted in a higher number of aortic dissections being recognized. • These data would be higher if sudden death patients without diagnosis [18] and aortic dissection in children were included. • A typical occurrence in a young adult arises from congenital aortic wall weakness. • A typical occurrence in the sixth decade or beyond is in atherosclerotic individuals. • Isolated abdominal aortic dissection may also happen, but this is a rare condition [16]. • The rapidly spreading use of high-resolution imaging modalities may reveal more and more aortic dissections in living patients [29].
4.2.3 Aetiology 4.2.3.1 Association with Atherosclerotic Disease • The vast majority of aortic dissections are related to atherosclerotic intimae ulceration or rupture of
intimae associated with hypertension in patients of older age [33].
4.2.3.2 Association with Genetic Disease/ Congenital Malformations • Others having a genetically determined wall weakness of the aorta are also prone to incur dissection in a younger period of life. These diseases are: • Marfan’s syndrome – various types of defect of fibrillin synthesis • Turner’s syndrome • Idiopathic necrosis of the media (Gsell–Erdheim) • Ehlers–Danlos syndrome – cystic degeneration of the media, etc. [8]. • Certain congenital malformations are more frequently associated with dissection, such as the bicuspid aortic valve, annuloaortic ectasia and aortic coarctation with poststenotic dilatation [5, 36].
4.2.3.3 Association with Trauma • Indirect trauma of the isthmic aorta may also cause localized dissection and false aneurysm. • In recent times invasive diagnostic angiographies due to catheter passage through the diseased aorta, as well as stenting, stent graft placements and intra-aortic balloon pumping have played an increasing role in iatrogenic aortic dissections [5].
4.2.3.4 Other Associations • Inflammatory diseases may also be complicated with dissection, as in several cases of luetic or giant cell aortitis. • Some cases during pregnancy have also been reported.
278
4.2 Aortic Dissection
4.2.3.5 Localization
DeBakey
• Primary tear of the intima occurs at the ascending aorta in 64%, and at the proximal descending aorta in 22%. • An aortic arch intimal lesion may be found in 10% of cases and isolated abdominal aortic dissection in 4% of cases. • Furthermore, intramural haemorrhage following separation of layers without an intimal tear has been documented in 10–15% of patients [22]. • Very different figures for involved aortic segments and side branches have been found in other reports. In 450 autopsies Hirst and Gore [23] found the origin in one-third of cases at the ascending and in two-thirds at the descending aorta. In this group of patient material, 302 extended to a long segment, and in 129 the visceral and renal arteries were also involved [23].
• Type I – intimal tear at the ascending aorta, long segmental extension • Type II – intimal tear at the ascending aorta, with localized aneurysm formation • Type IIIa – intimal tear at the isthmic part, with localized aneurysm formation • Type IIIb – intimal tear at the isthmic part, with long segmental extension [13].
4.2.3.6 Classification
European Society for Cardiology Task Force on Aortic Dissection
For didactic and practical reasons two classifications are used in clinical practice: DeBakey and Stanford.
Fig. 4.2.1 Digital subtraction angiography (DSA). Type A (DeBakey type I) aortic dissection. Entry point above the aortic valve. Extension to the descending aorta
Stanford • Stanford A – all dissections starting at the ascending aorta • Stanford B – dissections are located at the descending aorta [27] (Figs. 4.2.1–4.2.13).
The European Society for Cardiology proposed a new classification based on Task Force on Aortic Dissection: • Type I – Classical aortic dissection • Type II – Intramural haemorrhage • Type III – Subtle/discrete aortic dissection • Type IV – Plaque rupture, ulceration • Type V – Traumatic/iatrogenic dissection [16].
Fig. 4.2.2 DSA. Type A (DeBakey type II) aortic dissection localized at the ascending aorta with huge regurgitation
4.2.3 Aetiology
Obviously these arbitrary classifications do not cover all the very variable forms of aortic dissection, but they help orientation in the pathomorphology of this disease and also decision-making on treatment tactics.
Fig. 4.2.3 Type A (DeBakey type II) aortic dissection localized at the ascending aorta with involvement of the innominate and common carotid arteries
Fig. 4.2.4 Type A aortic dissection. Huge false and compromised true lumen at the aortic arch with refenestration
4.2.3.7 Factors Determining Extension of Dissection Biomechanical properties determining the extent and progression of aortic dissection include: • Quality and resistance of the aortic layers • Kinetic energy of the bloodstream • Cohesion force between wall components • Tension within the false lumen.
Fig. 4.2.5 Type B (DeBakey type IIIa) aortic dissection. Posttraumatic false aneurysm. DSA imaging during stent graft placement
Fig. 4.2.6 Type B (DeBakey type IIIa) aortic dissection. Contrast-enhanced CT scan
279
280
4.2 Aortic Dissection
Fig. 4.2.7 DSA of a type B (DeBakey type IIIb) aortic dissection
Fig. 4.2.8 CT angiography (CTA) of a type B (DeBakey type IIIb) aortic dissection. Moderate aneurysm formation and long segmental extension is visible in a Marfan’s patient. The left subclavian artery is compromised by a subintimal clot
Fig. 4.2.9 CTA of a type B (DeBakey type IIIb) aortic dissection. Moderate aneurysm formation and long segmental extension is visible in a Marfan’s patient in a virtual 3D reconstruction
Fig. 4.2.10 CTA of a type B (DeBakey type IIIb) aortic dissection and long segmental extension. No aneurysm developed at the tear site
4.2.3 Aetiology
Fig. 4.2.11 DSA of a type B (DeBakey type IIIb) aortic dissection. Moderate aneurysm formation and long segmental extension
Fig. 4.2.12 CTA of a type B (DeBakey type IIIb) aortic dissection. Moderate aneurysm formation and long segmental extension. The false lumen runs in spiral form around the depressed true one
Local Aneurysm Formation • If the external aortic layers are weak and the cohesion force between layers is strong, a local aneurysm formation is expected. • Its progression depends on the kinetic energy of the bloodstream entering the subintimal space and on the tension within the false lumen. • The higher these are, the faster the aneurysm formation, finally leading to rupture.
Long Segmental Aneurysm Formation
Fig. 4.2.13 Contrast-enhanced horizontal section CT scan of a long segmental aortic dissection
• If the cohesion force between layers is frail, a long segmental extension may occur. • The higher the energy of the bloodstream and the higher the tension within the false lumen, most probably the longer the dissection. • Furthermore, the stronger the forces are in the false lumen, the wider the gap between the intimal column and the external aortic layer.
281
282
4.2 Aortic Dissection
• The dissection can run down to the aortic bifurcation and even beyond to the bifurcation of the femoral artery. • A spiral route of false lumen is typical if moderate forces are working, but in extreme situations circumferential detachment of the intima and severe compression of the true lumen may occur (Figs. 4.2.6–4.2.13).
Refenestration • In the case of diseased or weak intima, higher tension in the false lumen may result in the occurrence of refenestration. • This re-entry of the bloodstream at a fortunate site – without involvement of vital side branches – may save the patient’s life, because decreased tension may prevent further extension of the dissection in both the longitudinal and horizontal directions.
4.2.4 Symptoms 4.2.4.1 Stanford Type A • Acute stabbing chest pain with cervical radiation or back pain running down along the vertebral column is typical of this form of proximal dissection. • The initial symptoms may be similar to acute myocardial infarction. • In cases without coronary involvement, ECG and/or lack of troponin release can bring attention to dissection. • In patients with disturbed coronary circulation the opportunity to utilize this option for diagnosis remains uncertain. • Other diseases to differentiate include pleuritis, intercostal neuralgia, herpes zoster, spondylogenic pain, gastritis, cholecystitis, reflux oesophagitis, pulmonary embolism and expansion of thoracic aneurysms. • Compression of the central veins may cause cyanosis of the neck and head. • Valvular incompetence or coronary insufficiency could lead to different levels of cardiac arrhythmias and depressed cardiac function such as collapse or shock. • If rupture occurs in adjacent cavities or the mediastinum, the rapid development of shock results in sudden or early death.
• Further progress of the central dissection may produce uneven pulsation of radial then carotid arteries and related brain symptoms with different levels of consciousness or coma. • If hemispherical or focal cerebral hypoperfusion occurs, neurological signs are frequently accompanied by a difference in the pupils. • Right then left arm ischaemia may also develop during the evolution of type A dissection. • These symptoms may change if refenestration occurs and compression by the subintimal tension decreases and the true lumen reopens. • In type A dissection distal organs or lower extremities are affected in 10–15% of cases. Refenestration can cause these symptoms to change or even return to normal clinical status. • The presence of unstable, loosened intimal flaps may mask indications of impending vascular failure. In particular, the functioning of hidden visceral organs does not ensure intact morphology. For example, if urine output decreases or fails, or abdominal/lumbar pain is present, acute renal or bowel ischaemia is likely to be encountered. These signs, in most patients, indicate a very dangerous or hopeless situation. • Auscultation over the heart or supra-aortic trunks by detection of bruit, valvular incompetence and regurgitation may contribute to the physical diagnosis of dissection. If a pericardial tamponade is present, the widened cardiac contours and silent cardiac sounds are valuable physical signs.
4.2.4.2 Stanford Type B • Isthmic dissection may produce sudden back, lumbar or abdominal pain similar to electric shock, but in other cases no symptoms escort this severe disease. • In symptomless patients, chronic sequelae such as aneurysm formation can be revealed by chance during screening or checkups for other reasons. • Type B dissections with proximal rebound seldom produce neurological symptoms, but compression of the left subclavian artery may cause a difference of blood pressure at the arms, or even acute upper limb ischaemia. • Local aneurysm expansion due to traction of the recurrent laryngeal nerve may produce palsy of the vocal cords and hoarseness. Compression of the bronchus can reduce ventilation.
4.2.5 Complications
• The rapid growth of the aneurysm can be complicated by rupture in the left pleural cavity, lung, bronchus or mediastinum. Rupture is the main cause of death. • In long segmental type B dissections, oliguria, anuria, intractable hypertension, abdominal pain, or bloody stools may call attention to severe damage to side branches. • Different levels of paraparesis or paraplegia indicate spinal cord ischaemia due to disruption of main radicular artery or arteries. • If spontaneous re-entry takes place at the thoracic level, double lumen circulation does not disturb distal organ blood supply and provides a good chance of survival after transient, moderate or minimal symptoms. • If within the distal false lumen high pressure persists, the distal aneurysm may expand and even rupture at the thoracic or abdominal level causing life-threatening haemorrhage. • A more typical occurrence is refenestration near to the aortic bifurcation reducing tension of the false lumen; this may lead to recurrence of organ function because relief of side branch lumen compression allows organ perfusion to increase. • Reappearing femoral pulsation suggests refenestration. This beneficial but misleading change of peripheral symptoms does not guarantee normalization of circulation in the visceral and/or renal arteries. • Ischaemic complications of these organs are responsible for a fatal outcome in two-thirds of the mortality rate in the acute phase – in both medically and surgically treated groups [7, 14, 23]. • Disturbed circulation of these territories may lead to late complications in survivors, such as renovascular hypertension or dyspragia.
4.2.5 Complications 4.2.5.1 Type A
• Raised subintimal tension, which may compromise or tear coronary orifices (Fig. 4.2.2) and may lead to myocardial ischaemia. • Rapid extension of a false aneurysm, which may compromise the vicinity and may rupture into the pericardium (70%) or mediastinum.
Antegrade Complications • Dissections running into the aortic arch and supra-aortic trunks alter pulsation at the supra-aortic trunks. • Ischaemia of the brain and/or upper extremity (first right then left side). • Further extension to the descending aorta and more distally to involve spinal, visceral, renal and iliac arteries.
4.2.5.2 Type B Retrograde Complications • If cohesion between distal aortic layers is strong, the tension within the freshly created false aneurysm may detach the intima at the distal or even more proximal aortic arch, affecting the circulation of the left subclavian, and sometimes of the carotid artery. • This rebound seldom extends to the innominate artery.
Local Complications • • • •
Expanding aneurysm Compression of trachea/bronchus, upper lobe of lung Traction of recurrent laryngeal nerve Rupture into the pleural cavity, airways, lung, mediastinum.
Local Complications Antegrade Complications Local complications in localized forms of ascending aortic dissection include: • Sudden dilatation of the aortic root, which may lead to rupture of the suspension of the aortic valves causing acute insufficiency.
• Distal progression without damage of side branches • Distal progression with refenestration at sites that have no significant sequelae • Distal progression with side branch (spinal, visceral, renal iliac) involvement (Figs. 4.2.7–4.2.17).
283
284
4.2 Aortic Dissection
Fig. 4.2.14 Lateral view of a long segmental aortic dissection. Thoracoabdominal aortic level. Periorificial subintimal compression of the coeliac trunk and superior mesenteric artery is seen
Fig. 4.2.15 Sagittal view of a long segmental aortic dissection. Thoracoabdominal aortic level. Periorificial subintimal compression of the coeliac trunk and superior mesenteric artery is shown
Fig. 4.2.16 DSA. Sagittal view of a long segmental aortic dissection. The abdominal aorta and the right iliac artery are also dissected. Periorificial subintimal compression of the left iliac artery is clearly visible
Fig. 4.2.17 MRA of a long segmental aortic dissection. The abdominal aorta, the renal arteries and the right iliac artery are also dissected
4.2.6 Diagnosis/Investigation
Forms of Side Branch Damage Following Dissection • Periorificial intimal separation • Subintimal haematoma with lumen compression • Partial intimal rupture of side branches with unstable distal morphology • Complete disruption of the intimal cone with decreased organ circulation • Distal arterial occlusion and acute organ failure (Figs. 4.2.18–4.2.28).
4.2.6 Diagnosis/Investigation 4.2.6.1 Recommended European Standard Diagnostic Steps of Investigation If the patient’s history, symptoms, signs and physical examination reveal the smallest suspicion of acute aortic dissection, immediate noninvasive or invasive investigations are needed to confirm the diagnosis [4, 5, 16, 21, 29, 38]. • Chest x-ray may show a widening of the mediastinum, heart contours and motility, as well as pleural or pericardial fluid accumulation. • ECG gives signs of myocardial ischaemia or pericardial fluids. • Echocardiography is one of the most valuable diagnostic tools for detecting type A dissection at the ascending aorta, visualizing its morphological sequelae such as entry point, floating dissected intimal membrane, as well as true and false lumens. It also depicts aneurysm expansion, damage to the aortic valve, regurgitation pressure gradients, pericardial tamponade and escorting myocardial movements and other valvular competences. As a bedside method it is suitable for following the changes during further development of dissection. • Carotid Duplex scanning helps to estimate depressed flow of the supra-aortic trunks. • Transoesophageal echography provides even more insight into cardiac, ascending and proximal descending aortic lesions. Black windows for this method are the dome of the aortic arch and thoracoabdominal aorta. This method needs more expertise and cooperation with the anaesthetist for introduction of the probe, but makes intraoperative control possible. • Abdominal ultrasound helps to visualize the abdominal aorta and iliac arteries, but it is less sensitive at the
upper abdominal aorta especially in obese patients. Gadolinium improves the accuracy of all ultrasound investigations. • Peripheral Doppler flowmetry and pressure measurements reveal numerical differences at the extremities. • Contrast-enhanced CAT scan, 3D reconstruction of pictures and MRA visualize all details of aortic and side branch morphological damage at very high accuracy. These methods also provide information about organ perfusion or manifest tissue injuries of the brain, kidney and surrounding compartments.
4.2.6.2 Additional Useful Diagnostic Procedures • Digital subtraction angiography (DSA) as a purely diagnostic method has a somewhat declining role since the above, less invasive, imaging modalities have been introduced. However, there is no doubt that this technique depicts the luminal changes in the aorta and also in the side branches more accurately than other methods do. Further benefit of this diagnostic tool is the use of catheter refenestration or stent/stent graft placement, which in a developing new trend can be done in selected patients during the same procedure. • Intravascular ultrasound is an invasive procedure that extends diagnostic opportunities to enable accurate measurement of the aortic lumen and the condition of intimal flaps around orifices. • Laboratory tests are not specific, but may show anaemia, the release of myocardial enzymes, urine content, renal insufficiency and indirect signs of transmural bowel necrosis.
4.2.6.3 Clinical Judgement The question that should be answered expeditiously during the clinical evaluation is whether an aortic dissection is responsible for the patient’s symptoms. If yes, ascertain: • Site of intimal tear • Extent of dissection • Signs of expanding aneurysm • Signs of contained or free rupture alongside the dissected aorta • Signs of side branch lesions • Signs of unstable and impending side branch morphology
285
286
4.2 Aortic Dissection
Fig. 4.2.18a–c Morphology of side branch damage caused by aortic dissection. a Subintimal haemorrhagic cuff with lumen compression. b Partial tear of orificial intima causing unstable circulation. c Complete disconnection of the intimal cone from the distal lumen with immediate danger of occlusion by loosened intima or thrombi
Fig. 4.2.19 DSA of a long segmental aortic dissection. The thoracoabdominal aorta, the visceral and renal arteries are also dissected. Periorificial subintimal compression of the left renal is clearly visible
Fig. 4.2.20 CT scan of a long segmental aortic dissection. Periorificial subintimal compression of the coeliac trunk
4.2.6 Diagnosis/Investigation
Fig. 4.2.21 CT scan of a long segmental aortic dissection. The dissected membrane runs into the superior mesenteric artery (SMA)
Fig. 4.2.22 CTA scan of a long segmental aortic dissection. Lateral view. The coeliac trunk is supplied from the false lumen and the SMA from the true lumen
Fig. 4.2.23 CTA scan of a long segmental aortic dissection. Lateral view. Severe subintimal compression of the SMA
Fig. 4.2.24 DSA of a long segmental aortic dissection. Severe damage of both renal arteries
287
288
4.2 Aortic Dissection
Fig. 4.2.25 DSA of a long segmental aortic dissection. The right renal artery is dissected. The kidney shows inequal density confirming disturbed circulation
Fig. 4.2.26 DSA of a long segmental aortic dissection. The orifice of the left renal artery is completely torn out, but the circulation of the kidneys seems to be equalized
Fig. 4.2.27 DSA of a subacute long segmental aortic dissection. The orifice of the left renal artery is completely torn out. The density of the kidneys is inequal
Fig. 4.2.28 CTA of a long segmental aortic dissection. Double artery of the right kidney is shown. The cranial artery is patent and perfused from the false lumen; the distal artery is patent and perfused from the true lumen
4.2.8 Therapy
• Signs of manifest ischaemic organ failure: • recent myocardial and/or brain infarction, upper extremity ischaemia • spinal, visceral, renal and lower extremity ischaemia • Accompanying acute diseases that have an impact on the timing and method of treatment • Aortic regurgitation • Acute left ventricle insufficiency/pulmonary oedema • Accompanying chronic disease of the aorta: • congenital malformation • chronic thoracic or abdominal aneurysm • chronic occlusive disease of the aorta and side branches • General condition of the patient, other risk factors.
4.2.7 Prognosis of Acute or Subacute Aortic Dissection Without Treatment • Large autopsy studies confirm that one-third of patients with aortic dissection die within 1 day; one-half of them within 48 h, two-thirds during the first week and 80–90% within the first month. • The leading cause of death is rupture of the false aneurysm (80%) and the second most frequent cause is the organ ischaemia in both types. • Twenty percent of patients die before reaching hospital. • Only 15% of dissected patients were correctly diagnosed before death [16, 26].
4.2.8 Therapy 4.2.8.1 Treatment of Type A Aortic Dissection Emergency repair of the proximal aorta is mandatory at an expert cardiovascular surgical unit. Aims are to: • prevent death due to rupture of the aneurysm • halt the progression of dissection • re-establish the coronary circulation • re-establish aortic valve function • re-establish aortic and side branch perfusion at the arch and at the distal thoracoabdominal aorta. These interventions need cardiopulmonary by-pass. Retrograde arterial perfusion is hazardous, because dis-
section may be complicated by the perfusion of the false lumen leading to unexpected sequelae [10, 17]. The most useful technique is artificial arterial circulation via the right subclavian or axillary artery with cannulation of both the inferior and superior vena cavae (IVC and SVS). This method with antegrade perfusion of the true lumen to brain and body in combination with moderate hypothermia permits up to 40–45 min of cardiac arrest if extended replacement of the aortic arch is necessary as Kazui proposed [25].
Types of Aortic Replacements • • • •
Ascending aorta Extension to the proximal arch [1] Extension to the entire arch Extension to the entire aortic arch with elephant trunk procedure [3].
Types of Re-establishment of Aortic Valve Function • • • •
Annuloplasty [34] Valve-sparing operation [12] Biological valve replacement Mechanical valve replacement.
Types of Re-establishment of Coronary Circulation • Direct implantation of coronary arteries into an aortic graft [2] • Interposition of graft between an aortic graft and the coronary arteries [6] • Aortic graft–coronary by-pass. Use of the glue and “sandwich” technique with Teflon strips between the dissected layers is useful for reinforcing weakened aortic layers [16]. The individual combination of the above interventions should be adapted to the morphology of the dissection and the timing of the operation to the clinical feature. In a small (3–4%) subgroup of type A dissections proximal reconstruction does not reconstitute distal organ circulation sufficiently – or the blood content of a large false lumen due to perfusion of the true one may compromise the orifices of important side branches [23]. This condition needs re-evaluation at the distal aorta after a proximal procedure. If an unstable morphology is pres-
289
290
4.2 Aortic Dissection
ent – apart from the short ischaemic tolerance time of affected organs – prophylactic reconstruction is indicated. Manifest organ failure in most patients excludes the restitution of histological and functional integrity. The mortality rate of surgery for type A dissections is still very high, about 10–15% within 30 days [37].
4.2.8.2 Treatment of Type B Aortic Dissection • While type A dissections are treated by cardiac surgeons, type B dissections fall under the territory of cardiologists and vascular surgeons. • Attempts to replace a dissected aorta at the intimal tear site (entry point) with a short interposition graft led to similar disappointing results, due to renal (50–70%) and visceral (88%) ischaemic complications in long segmental forms [7, 14]. • In the overwhelming majority of patients hypotensive medical therapy yielded better final outcomes and reduced average mortality to 14%. • This method is widely accepted as first-choice treatment in patients with type B dissections [16].
Circumstances Under Which Intervention Should be Taken into Consideration If, in spite of hypotensive treatment: • A progressive, expanding aneurysm develops • Increasing transmural bleeding or rupture presents • There is persisting, back, lumbar or abdominal pain • There is decreasing urine output, increasing creatinine level • There is depressed organ perfusion due to a compromised true lumen • There is lower limb ischaemia.
Types of Intervention in the Case of Type B Aortic Dissection Artificial Refenestration and Tension Decompression
• Encouraged by earlier experiences with symptomfree aortic dissections and dissections that refenestrated at a fortunate site that did not affect major side branches. • Involves artificial refenestration and decompression of tension within the false lumen.
• Subrenal surgical refenestration was recommended by Gurin [20]. • Incidental refenestration during diagnostic catheter angiography with sudden relief of symptoms also supported this idea [15]. • Unfortunately subrenal refenestration does not prevent renal and visceral complications, but it does reestablish lower limb circulation. • Due to organ failure the mortality rate remained as high as 30–35%. • Pararenal refenestration controls renal perfusion, but visceral circulation remains uncertain; however, by using this method, the mortality decreased to 15% [31]. • Catheter refenestration at the infrarenal aorta may re-establish lower limb circulation, but leaves visceral and renal perfusion unsettled. If the orifices of these are not seriously damaged, decompression of the periorificial haematoma leads to the return of normal flow. • Perforation of dissected membranes at major side branches and stenting are the latest attempts to reopen them by endovascular means, reducing surgical trauma [11, 39].
Thoracoabdominal Refenestration • This type of surgery in a selected subgroup of patients is indicated if no major aneurysm is present at the tear site, but dangerous distal side branch morphology is present. • Through left thoracophrenolaparotomy along the 7th or 8th intercostal space and pararectal line, the thoracoabdominal aorta can be dissected. • The removal of the dissected intimal membrane leaves double lumen at the thoracic aorta, decreases tension of the false lumen, creates a common cavity at the visceral segment providing direct circulation to all organs and prevents further acute progress. • Fixation of the periorificial dissected intima and removal of loosened flaps stop further dissection of side branches. • Infrarenal intimal fixation is not necessary if refenestration at the bifurcation provides stable circulation for the limbs. • If no re-entry is present the distal intima should be fixed by suture, glue, sandwich technique or by stent placement if the gap is small.
4.2.8 Therapy
• In the case of a large false lumen under tension, graft replacement in the subrenal position may be indicated. • This more proximal refenestration has achieved a further reduction of the mortality rate to 4.5% [14, 15] (Figs. 4.2.29–4.2.38).
Fig. 4.2.29 Thoracoabdominal exposure of the aorta. Note the bluish discoloration of the intramural haematoma caused by dissection
Fig. 4.2.30 Schematic view of the thoracoabdominal dissected aorta
Fig. 4.2.31 Thoracoabdominal exposure of the aorta. Through longitudinal aortotomy the dissection is visible. Note the dissected right renal orifice
Fig. 4.2.32 Schematic view of the thoracoabdominal dissected aorta after aortotomy
291
292
4.2 Aortic Dissection
Fig. 4.2.33 Thoracoabdominal exposure of the aorta. Through longitudinal aortotomy the dissection is visible. The coeliac trunk, SMA and right renal artery are controlled by balloons. The dissected membrane from the lower thoracic segment down to the subrenal aorta has been removed. The double lumen remains in the proximal aorta
Fig. 4.2.34 The removed intima. The torn out orifices are presented
Fig. 4.2.35 After removal of all loosened intimal fibres the dissected edge has been fixed by sutures around the orifices and distally. A common cavity has been created, providing direct perfusion to all visceral and renal branches
Fig. 4.2.36 The drawing demonstrates the situation after endarterectomy and intimal fixation
4.2.8 Therapy
Fig. 4.2.37 After having completed endarterectomy and intimal fixation the aortotomy is closed by running suture
Fig. 4.2.38 The final situation after endarterectomy is shown
Surgical Graft Repair
• Inserting an endograft under pressure into an aorta with a weak wall, as in Marfan’s patients, presumably increases the risk of perforation, endoleaks or dislodgement and even retrograde or anterograde dissection. • The advantage of this modality seems to be obvious in atherosclerotic and traumatic dissections of the isthmus segment [16, 30, 32]. • In a recent development, stent graft placement at the tear site with complementary branch stenting may achieve further improvement of results [35]. • The need for intervention at both sites simultaneously is uncommon (Fig. 4.2.40).
• Surgical replacement of the proximal descending aorta in acute/subacute cases of localized dissection with graft interposition was the method of choice for a long time, especially for expanding or ruptured traumatic dissections. • This procedure requires left thoracotomy in the fifth intercostal space. • The clamp and go technique or femoro-femoral, atriofemoral by-pass or Gott shunt can be used with the patient normothermic, in combination with other spinal cord protective methods to prevent paraplegia during clamping [16, 24] (Fig. 4.2.39). • If a wide dissected gap is present, closure of the distal false lumen may press blood or clot content into the periorificial subintimal space causing secondary severe damage such as spinal cord ischaemic injury and renal or bowel necrosis in the acute phase, or produce chronic stenosis of the affected arteries. • The smaller the false lumen the smaller the risk of these complications. • Fixation of the intimal flap and closure of the entry point by stent graft placement reduces the surgical risk remarkably, but the same possible consequences should be taken in consideration.
Complications Follow-up of all dissected patients is mandatory. Possible late complications related to earlier aortic dissection are: • repeated dissection either proximally or distally • chronic aneurysm formation (see Chapter 4.1, “Thoracoabdominal aneurysms”) • chronic reduction of organ perfusion (renal/visceral chronic ischaemia). Recognizing late complications in time by the use of less invasive imaging modalities, such as MR or CAT scan,
293
294
4.2 Aortic Dissection
Fig. 4.2.39 Intraoperative photos of an expanding isthmic dissecting aneurysm treated by open surgery. The arrow shows the entry and the subintimal haematoma within the false lumen. An interposition graft was used
Fig. 4.2.40 Stent graft placement into the isthmic aorta for expanding subacute traumatic dissection
may help to prevent late mortality. In these patients more interventions are expected in different, or the same, segments of the aorta [9, 28]. In genetically determined dis-
eases, screening should also be extended to family members. In these cases chromosomal investigations may confirm the diagnosis [16] (Figs. 4.2.41–4.2.44).
4.2.8 Therapy
Fig. 4.2.41 DSA. In a young Marfan’s patient 3 years after replacement of the dissected ascending aorta, dilatation of the aortic root and acute long segmental type B dissection has occurred
Fig. 4.2.42 CTA of chronic type II thoracoabdominal aneurysm formation after aortic dissection
Fig. 4.2.43 CTA of a chronic coeliac trunk stenosis caused by an old aortic dissection
Fig. 4.2.44 CTA of a chronic left renal artery stenosis caused by an old aortic dissection
295
296
4.2 Aortic Dissection
References 1. Bachet J (2004) Complete replacement of the aortic root and ascending aorta: techniques and results. In: Chiesa R, Melissano G (eds) Aortic surgery. The first edition of the Congress Aortic Surgery “How to do it”. 17–18 December 2004, Milan, pp 19–21 2. Bentall HH, DeBono A (1968) A technique for complete replacement of the ascending aorta. Thorax 23:338–339 3. Borst HG, Walterbusch G, Schaps D (1983) Extensive aortic replacement using “elephant trunk” prosthesis. J Thorac Cardiovasc Surg 31:37–40 4. Buck TH Gorge G, Hunold P, Erbel R (1998) Three-dimensional imaging in aortic disease by lighthouse transesophageal echocardiography using intravascular ultrasound catheters. J Am Soc Echocardiogr 11:243–258 5. Burks JM, Illes RW, Keating EC, Lubbe WJ (1998) Ascending aortic aneurysm and dissection in young adults with bicuspid aortic valve: implications for echocardiographic surveillance. Clin Cardiol 21:439–443 6. Cabrol C, Pavie A, Gandjbakhch I et al (1981) Complete replacement of the ascending aorta with reimplantation of the coronary arteries. A new surgical approach. J Thorac Cardiovasc Surg 81:309–315 7. Cambria RP, Brewster DC, Gertler J et al (1988) Vascular complications associated with aortic dissections. J Vasc Surg 7:199–209 8. Coady M, Davies R, Roberts M et al (1999) Familial patterns of thoracic aortic aneurysms. Arch Surg 134:361–367 9. Coselli JS (2004) Morbidity and morbidity after extent II thoracoabdominal aortic aneurysm repair. In: Chiesa R, Melissano G (eds) Aortic surgery. The first edition of the Congress Aortic Surgery “How to do it“. 17–18 December 2004, Milan, pp 120–134 10. Coselli JS, Buket S, Djukanovic B (1995) Aortic arch operations: current treatment and results. Ann Thorac Surg 9:19–27 11. Cowling MG, Redwood D, Buckenham TM (1995) Case report: critical limb ischemia due to aortic dissection relieved by percutaneous transfemoral fenestration. Clin Radiol 50:654–657 12. David TE, Feindel CM (1992) An aortic valve-sparing operation for patients with aortic incompetence and aneurysm of ascending aorta. J Thorac Cardiovasc Surg 103:617–621 13. DeBakey ME, McCollum CH, Crawford ES et al (1982) Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 92:1118–1134 14. Dzsinich C (2002) Thoracoabdominal endoaortectomy in case of type B aortic dissection. Acta Chir Belg 102:307–312
15. Elefteriades JA,Hammond GL, Gusberg RJ, Kopf GS, Baldwin JC (1990) Fenestration revisited: a safe and effective procedure for descending aortic dissection. Arch Surg 125:786–790 16. Erbel R, Alfonso F, Boileau C et al (2001) Diagnosis and management of aortic dissection. Task force report. Eur Heart J 22:1642–1681 17. Ergin MA, Galla JD, Lansman SL, Quitana C, Bodian C, Griepp R (1994) Hypothermic circulatory arrest in operations of the thoracic aorta: determinants of operative mortality and neurologic outcome. J Thorac Cardiovasc Surg 107:788–799 18. Fowkes FG, Macintyre CC, Ruckley CV (1989) Increasing incidence of aortic aneurysms in England and Wales. Br Med J 298:33–35 19. Fuster V, Halperin JL (1994) Aortic dissection: a medical perspective. J Cardiol Surg 9:713–728 20. Gurin D, Bulmer JW, Derby R (1935) Dissecting aneurysm of the aorta. Diagnosis and operative relief of acute aortic obstruction due to this cause. NY State J Med 35:1200–1202 21. Hayashi K, Meany TF, Zelch JV, Tarar R (1974) Aortographic analysis of aortic dissection. Am J Roentgenol Radium Ther Nucl Med 122:769–782 22. Heberer G, Reidemeister JC (1974) In: HebererG, Rau G, Schoop W (eds) Aneurysmen und Elongationen der Arterien in Angiologie. Thieme, Stuttgart, pp 569–570 23. Hirst AE, Gore I (1983) The etiology and pathology of aortic dissection. In: Doroghazi RM, Slater EE (eds) Aortic dissection. McGraw-Hill, New York, p 193 24. Jacobs M (2004) Surgical treatment of type B aortic dissections. In: Chiesa R, Melissano G (eds) Aortic surgery. The first edition of the Congress Aortic Surgery “How to do it“. 17–18 December 2004, Milan, pp 66–69 25. Kazui T, Kimura N, Komatsu S (1995) Surgical treatment of aortic arch aneurysms using selective cerebral perfusion: experience with 100 patients. Eur J Cardiothorac Surg 9:491–495 26. Mészáros I, Morocz J, Szlávi J et al (2000) Epidemiology and clinicopathology of aortic dissection. Chest 117:1271–1278 27. Miller DC (1983) Surgical management of aortic dissections: indications, perioperative management, and longterm results. In: Doroghazi RM, Slater EE (eds) Aortic dissection. McGraw-Hill, New York, p 193 28. Neufang KF, Theissen P, Deider S, Sechtem U (1989) Thoracic aorta dissection – the place of MRT and CT in the follow up after prosthetic aortic replacement. Fortschr Röntgenstr 151:659–665
References
29. Nienaber CA, Spielmann RP, von Kodolitsch Y et al (1992) Diagnosis of thoracic aortic dissection. Magnetic resonance imaging versus transesophageal echocardiography. Circulation 85:434–447 30. Nienaber CA, Fattori R, Lund G et al (1999) Nonsurgical reconstruction of thoracic aortic dissection by stent graft placement. N Engl J Med 340:1539–1545 31. Panetton JM, Swee HTHE, Cherry KJ et al (2000) Aortic fenestration for acute or chronic aortic dissection: an uncommon but effective procedure. J Vasc Surg 32:711–721 32. Riambau V (2004) Endovascular treatment of acute type B aortic dissection. In: Chiesa R, Melissano G (eds) Aortic surgery. The first edition of the Congress Aortic Surgery “How to do it”. 17–18 December 2004, Milan, , pp 75–77 33. Sarris GE, Miller DC (1989) Peripheral vascular manifestations in acute aortic dissections. In: Rutherford RB (ed) Vascular surgery. Saunders, Philadelphia, pp 942–951 34. Sarsam MA, Yacoub M (1993) Remodeling of the aortic valve annulus. J Thorac Cardiovasc Surg 105:435–438
35. Slonim SM, Nyman U, Semba CP et al (1996) Aortic dissection percutaneous management of ischemic complications with endovascular stents and balloon fenestration. J Vasc Surg 23:241–251 36. Vitiello R, McCrindle BW, Nykanen D, Freedom RM, Benson LN (1998) Complications associated with pediatric cardiac catheterisation. J Am Coll Cardiol 32:1433–1440 37. Westaby S, Saito S, Katsumata T (2002) Acute type A dissection conservative methods provides consistently low mortality. Ann Thorac Surg 73:701–703 38. White RD, Lipton MJ, Higgins CB et al (1986) Noninvasive evaluation of suspected thoracic aortic disease by contrast enhanced computed tomography. Am J Cardiol 57:282–290 39. Williams DM, Brothers TE, Messina LM (1990) Relief of mesenteric ischemia in type III aortic dissection with percutaneous fenestration of the aortic septum. Radiology 174:450–452
297
299
4.3 Trauma of the Thoracic Aorta A. Nevelsteen, K. Daenens, I. Fourneau
4.3.1 Introduction • Thoracic aortic trauma is a relatively rare but catastrophic event. • It may be secondary to several mechanisms: it can be seen after penetrating or iatrogenic trauma. • The most frequent cause however is blunt trauma and this chapter will focus on this specific aetiological mechanism. • Most of the patients have suffered automobile-related trauma and the associated mortality remains enormous. • Therefore, thoracic aortic trauma is identified in the advanced trauma life support (ATLS) franchise as one of the eight “life-threatening chest injuries” in the socalled secondary survey. • Diagnosis is based on clinical suspicion and technical examinations such as spiral computed tomography, angiography and transoesophageal echocardiography. • Classic treatment consists of open surgery, but endovascular stent-grafting is becoming more and more popular.
4.3.2 Epidemiology • The true incidence of blunt thoracic aortic trauma remains unclear. • It is certainly a relatively rare event with around two cases per million inhabitants per year, which means that even large trauma centres will see only two to three cases a year.
4.3.2.1 Automobile-related Incidences • Recent studies show that in the US and Canada around 7500–8000 victims die of this condition each year,
which in the majority of cases is the result of an automotive accident [13]. This corresponds with 5–16% of motoring fatalities in North America. The majority of blunt aortic trauma cases are seen in patients aged from 20 to 30. • Males predominate in a 9:1 sex ratio. • There is a direct relation to the impact of the trauma: Greendyke [20] reported a 27% incidence in those who were ejected from a vehicle versus a 12% incidence in those who were not. Pate et al. [45] found that associated injuries were present in more than 90% of patients with blunt thoracic aortic trauma and that 24% of patients needed a major operation before treatment of the aortic trauma.
4.3.2.2 Blunt Thoracic Trauma • Although the majority of cases are seen after automotive accidents, there are indications that blunt thoracic aortic trauma is also responsible for over 10% of pedestrian fatalities. • Brundage et al. [5] reported on a study of 220 pedestrian fatalities over a 6-year period in the USA. Twentyeight (12.7%) had blunt thoracic aortic trauma. Overall there were 30 cases of aortic trauma, of which 80% died at the scene of the accident. Only two pedestrians survived after adequate treatment of the injuries, giving an overall mortality of 93%. • The incidence of aortic trauma might even be the highest amongst passengers involved in aircraft accidents. Mason [33] indicated an incidence as high as 43%, and some others have also indicated an incidence of 39% in light aircraft fatalities. • Apart from this, blunt thoracic aortic trauma might also be seen in other scenarios such as motorcyclists, fall victims, patients being struck by a falling tree or more exceptionally in an individual being covered by silt during a cave-in [13, 16, 43].
300
4.3 Trauma of the Thoracic Aorta
4.3.2.3 Outcome • Taking into account the severity of the injury, it is no surprise that most of the victims die at the scene of the accident. • Parmley et al. [43] reported as early as in 1958 on a combined autopsy and clinical study of 275 cases of thoracic aortic trauma: only 38 (13%) survived the initial insult. • The majority of the initial survivors died within 15 days after the accident and ultimately only two patients survived their injuries. • Among others, Dunn and Williams [12], who reported an 80% mortality rate at the scene of the accident, confirmed these data. • From 20% of the patients that reach the hospital alive, it has been suggested that – without appropriate treatment – only 70% will survive for more than 6 h, 40– 50% will die within 24 h and 90% within 4 months [23]. • Richens et al. [50] presented a major study regarding the incidence and prognosis of blunt aortic trauma in 2003. These investigators reported on a total of 8285 vehicles carrying 14,435 occupants, which were involved in 7067 accidents. There were 613 fatalities and 130 (21%) had blunt traumatic aortic rupture. The scene survival rate for blunt aortic trauma was 9% and the overall mortality rate 98%. They documented also that the use of an airbag or seat belts does not elimi-
nate the risk and that aortic trauma can also occur in low severity impacts, particularly in side impact. • Others have also stressed thoracic aortic injuries as a consequence of side impact [3].
4.3.3 Aetiology 4.3.3.1 Anatomy • The aortic isthmus is cited traditionally as the classical site of thoracic aortic trauma. • This is particularly true in clinical reports, where trauma of the aortic isthmus covers over 90% of the cases versus a 6% incidence at the ascending aorta. • In autopsy studies, trauma of the ascending aorta might, however, be seen in up to one-quarter of cases (Fig. 4.3.1). • Trauma of the aortic arch or the distal descending aorta is quite infrequent. • Single rupture is the typical mode of presentation, although multiple tears in the same individual have been described [36]. • In addition, blunt thoracic aortic trauma in combination with trauma of one of the great intrathoracic vessels is reported in 1–3% of cases. • Typical trauma consists of a transverse tear in the wall of the aorta. Depending on the severity of the impact,
Fig. 4.3.1 Distribution of aortic lesions following blunt chest trauma.
4.3.4 Symptoms
• Lundewall [30] performed a series of experiments with isolated strips of aorta free of adventitia. He found out that the isthmus was only two-thirds as strong as the ascending aorta. The descending aorta was of intermediate strength.
Fig. 4.3.2a,b Thoracic aortic trauma – typical lesions. a Transverse tear; b complete transection with pseudoaneurysm formation
the tear may involve only the aortic intima, extending or not into the medial layer. Here the adventitia might be strong enough to prevent catastrophic haemorrhage and – if not treated – pseudoaneurysm formation and rupture might be seen in the long term (Fig. 4.3.2). • As an alternative, blood may be forced between the layers of the aortic wall leading to aortic dissection and eventually to distal hypoperfusion. • Complete transection of the aorta is usually fatal, but there are reports in the literature on individuals who survived long enough to allow adequate treatment [43].
4.3.3.2 Mechanism of Pathology The exact mechanism of blunt thoracic aortic trauma remains debated. One of the oldest theories implies sudden stretching of the aorta [51]: • This theory is based on the predominance of trauma at the aortic isthmus and the observation that, during a deceleration injury, the heart, the ascending aorta and the transverse arch continue to move forward while the isthmus and the descending aorta remain fixed by their posterior attachments. • In addition, there is evidence that the aorta is inherently weaker at the isthmus.
A rapid increase of intravascular pressure has been implied as a second aetiological factor: • Kroell et al. [27] investigated the increase in arterial pressure of cadaver aortas during impacts on the chest. • Their findings suggest that the increase in arterial pressure during a vehicle impact may be significant enough to cause aortic disruption. • The pressure required might be as low as 580 mmHg or as high as 2500 mmHg. • In addition, it is suspected that, during a vehicle impact, the aorta might become occluded at its passage through the diaphragm. This in turn leads to a highpressure wave resulting in a “water-hammer” effect [48]. Finally, another hypothesis involves the osseous pinch theory: • Here it is proposed that aortic rupture occurs when the aorta is pinched between the spine and the anterior bony thorax during chest compression caused by abrupt deceleration [8]. • In this regard, Voight and Wifert [60] pointed out that in the case of sternal fracture, the lower portion is displaced upwards and backwards. • Here the mediastinum and the ascending aorta are forced superiorly. • This movement puts tensile strength on the proximal descending aorta and rupture might occur at its fixed point at the level of the ligamentum arteriosum. Based on all these theories, it is logical to suppose that blunt thoracic aortic trauma might arise under several conditions, such as crushing or deceleration/acceleration. At this moment however it is not yet possible to determine the exact primary mechanism [49].
4.3.4 Symptoms Symptoms on admission are most often related to concomitant injuries. In a series of 54 patients, all had other
301
302
4.3 Trauma of the Thoracic Aorta
serious injuries – 17% neurological, 60% abdominal, 35% pelvic fracture and 65% fracture elsewhere – distracting attention away from the chest injury [10]. It has also been reported that 30% of the patients with aortic trauma will have no external signs of chest injury on presentation [43]. Finally there is no single physical finding or combination of findings that is typical for aortic trauma. Duhaylongsod et al. [11] reviewed the English-language surgical literature from 1970 to 1990 and presented data on 1188 patients among 59 reports. The mean age was 32.4 years (range 4.5–81 years) with a male:female ratio of 5:1. Motor vehicle occupants were involved in 75%, motorcyclists in 15.7%, pedestrians in 7.4% and falls from a height in 2.8% of the cases. The most common presenting symptoms were: • Chest pain (76%) • Dyspnoea (56%) • Loss of consciousness or coma (36.8%) • Hypotension (25.9%). No patient had a complete negative physical examination and each presented with at least one associated injury. Classically cited associated findings pointing to the diagnosis of aortic trauma include: • Multiple rib fractures • Fractures of first and second rib • Fractured sternum • Pulse deficits • Interscapular systolic murmur • Blood in the carotid or subclavian sheath • Hoarseness or voice change without laryngeal injury • Superior vena cava syndrome [64]. However, their incidence varies considerably among different series. The same is true for the so-called typical acute coarctation syndrome characterized by: • hypertension in the upper limbs and • a difference in pulse amplitude between the arms and the legs, which was described in 1973 by Symbas et al. [56] (Fig. 4.3.3).
4.3.5 Diagnosis • Thoracic aortic injury is often overwhelmed by the presence of concomitant serious injuries. • In addition there are few typical clinical symptoms, indicating that a high index of clinical suspicion remains
Fig. 4.3.3 Acute coarctation syndrome following thoracic aortic trauma: angiographic appearance
the most important factor leading to the diagnosis of thoracic aortic rupture. • Taking into account the pathogenesis, thoracic aortic trauma should be suspected after any fall from more than three storeys or in any motor vehicle accident at speeds in excess of 60 km/h. • Additional circumstances such as severe associated injuries or the death of other automobile occupants should alert the physician.
4.3.5.1 Recommended European Standard Diagnostic Steps of Investigation Because of the lack of typical clinical signs, diagnosis has to be made by technical examination including: • chest radiography • spiral CT
4.3.5 Diagnosis
• transoesophageal echocardiography and, eventually, • angiography. Magnetic resonance imaging and intravascular ultrasound might become important in the future, but are not yet validated.
Chest radiography • Routine chest radiography remains an important step in the evaluation of any trauma victim. • A chest radiograph was indeed already recognized in the 1980s by ATLS as part of the trauma series, necessary during the primary survey assessment of each trauma patient. • The most frequently reported sign in relation to aortic trauma is undoubtedly widening of the mediastinum (Fig. 4.3.4). • Mediastinal widening is indeed a reliable sign of thoracic aortic trauma. • A panel of radiologists and surgeons blinded to outcome correctly interpreted mediastinal widening in 89% of patients with aortic trauma [21]. • Although a widening of the mediastinum might be documented in 50–90% of cases, the specificity is quite low (10%), as is the positive predictive value (10%) [13].
Fig. 4.3.4 Chest radiograph in a patient with thoracic aortic trauma. Note widening of the mediastinum
• Moreover, it has also been recognized that positioning and inspiration, which may be very difficult to standardize in the trauma setting, play a major role in the interpretation of mediastinal widening. • In order to improve the diagnostic value of chest radiography, Woodring [65] studied 52 articles for a total of 652 patients. He looked not only for a widened mediastinum but also for other mediastinal abnormalities, such as abnormal aortic outline, opacification of the aortopulmonary window, downward displacement of the left mainstem bronchus and deviation of the trachea to the right of the midline. Even then, he found that some 7% of the patients had a completely normal mediastinum on their initial chest radiographs. • Therefore, chest radiography cannot be used as the sole test for diagnosing or excluding aortic injury.
Angiography • Angiography is traditionally cited as the gold standard in the diagnosis of thoracic aortic trauma. • Digital subtraction angiography (DSA) is preferred and intravenous examinations should be avoided because it produces poor-quality studies in one-third of cases. • When performed adequately, intra-arterial DSA can detect thoracic aortic injury with a sensitivity of 95– 99% and a specificity of 94–100% [39]. • False-positive results are most frequently related to a prominent ductus diverticulum or large ulcerated atheromas just distally to the left subclavian artery [18]. • False-negative results may be due to incomplete series, misinterpretation or inadequate projections (Fig. 4.3.5). • Left anterior oblique projections (15–20°) should be included in every examination in order to avoid missing the diagnosis! • Thoracic aortic injury might present itself angiographically most frequently as an intimal irregularity or filling defect caused by an intimal flap. • Pseudoaneurysm formation is demonstrated by contained extravasation of contrast outside the aortic lumen (Fig. 4.3.6). • Apart from the high sensitivity and specificity, aortography is also capable of showing associated lesions of the supra-aortic vessels. In addition, endovascular stent-grafting can follow it immediately.
303
304
4.3 Trauma of the Thoracic Aorta
Fig. 4.3.5a,b Angiography after blunt thoracic trauma. a Lesion at aortic isthmus was considered to be ductus diverticulum. b Angiography after 2 years showed typical pseudoaneurysm formation
• The major disadvantage of angiography is that it is time consuming and the patient must be transferred for a prolonged period to the vascular suite. In addition, it is invasive and it requires iodinated contrast material. • Although there are no reports on the guidewire/catheter penetrating the injured aortic wall, full rupture of the aorta has been reported after high volume dye injection [14].
• •
Computed Tomography (CT) • • Conventional CT was welcomed at the end of the 1980s as an alternative to angiography in the diagnosis of thoracic aortic rupture. • Although initial reports were very enthusiastic, the relatively high incidence of both false-negative and false-positive findings indicated that conventional CT was merely a screening and not a diagnostic tool [47]. • Helical or spiral CT was introduced in the mid 1990s and Gavant et al. [17] were among the first to report superior results. They compared spiral CT and angiography in a series of 127 patients with abnormalities on
•
•
spiral CT. On this basis they documented that spiral CT showed 100% sensitivity and 82% specificity in the detection of aortic injury. These data were subsequently confirmed in some other studies [63]. Scaglione et al. [53] defined in 2001 “direct and indirect” signs of thoracic aortic trauma on spiral CT. Direct signs are indicative of aortic trauma and include intimal flap, pseudoaneurysm, contour irregularity, lumen abnormality and extravasation of contrast material (Fig. 4.3.7). Isolated mediastinal haematoma is considered as an indirect sign. Based on 1419 examinations they concluded that patients with direct signs on spiral CT do not need any other diagnostic investigation to confirm the diagnosis. Furthermore aortic injury is invariably associated with mediastinal haematoma. In cases of isolated mediastinal haematoma other possible sources of bleeding should be considered. Spiral CT has a lot of advantages over angiography: it is indeed fast, minimally invasive and readily available in most large trauma centres. When adequately performed, it has a sensitivity of 100% and a specificity of
4.3.5 Diagnosis
Fig. 4.3.6a,b Typical angiographic findings in thoracic aortic trauma: a partial and b diffuse pseudoaneurysm formation
Fig. 4.3.7a,b Direct signs of thoracic aortic trauma as seen on spiral CT: intimal flap (a); extravasation of contrast (b); note also mediastinal haematoma
99%. In addition, it is capable of documenting associated cardiopulmonary injuries. • There is still the disadvantage of the need for intravenous contrast, but on the other hand it can be used as the final diagnostic test on which definite treatment
– whether open surgery or endovascular stent-grafting – can be planned. • Spiral CT has therefore virtually completely replaced angiography as a diagnostic tool in most trauma centres.
305
306
4.3 Trauma of the Thoracic Aorta
Transoesophageal Echocardiography (TEE) • TEE has certainly some theoretical advantages over both angiography and spiral CT (Fig. 4.3.8): it is minimally invasive, it avoids contrast and it saves time because it can be performed in the emergency room. • It has economic benefits and in addition it can also detect concomitant cardiac injuries such as pericardial effusions, valvular and blunt myocardial injury. • On the other hand, its use in trauma patients might be limited, because it is contraindicated in patients with cervical spine injuries and patients with potential airway problems [4]. • The major disadvantage is the fact that it is extremely operator-dependent. • This might explain the disparity between results published from different authors: • Vignon et al. compared TEE and CT in a series of 110 consecutive patients with severe blunt chest trauma of whom 17 had vascular injury [59]. • The documented diagnostic accuracy was as follows (TEE vs. CT): sensitivity (93% vs. 73%), specificity (100% vs. 100%), negative predictive value (99% vs. 73%) and positive predictive value (100% vs. 100%). • Buckmeister et al. [6] have published similar excellent results. • Saletta et al. [52], on the other hand, reviewed TEE as the “sole” diagnostic modality in 114 consecutive patients with possible aortic trauma. They documented a sensitivity of only 63% and a specificity of 84%. • In addition, two patients in whom the correct diagnosis was delayed died from massive aortic injury. • Although in some centres with extensive experience some surgeons are willing to operate on the basis of a positive TEE only [19], larger prospective studies are needed and thus far TEE has not yet become the standard of care in the diagnosis of blunt thoracic aortic trauma.
4.3.6 Therapy Fig. 4.3.8a,b Transoesophageal echocardiographic findings in thoracic aortic trauma: a intimal flap (arrow) and pseudoaneurysm; b corresponding angiography
4.3.6.1 Surgery Traumatic aortic rupture has traditionally been characterized as a surgical emergency.
4.3.6 Therapy
Delayed Repair Some authors who described excellent results with delayed repair have challenged this aggressive attitude in recent years [22, 57]: • Pierangeli et al. [46] compared 21 patients (group I) who underwent immediate repair with another group of 29 patients (group II) who underwent intensive medical treatment and delayed repair. • The operative mortality in group I was 19% and three patients developed paraplegia. • One patient in group II died of aortic rupture 8 h after the trauma. • The others were operated with no deaths and no major complications. • Although there is no consensus and the discussion might become less important in the light of endovascular repair, it might be agreed that delayed treatment with intensive medical therapy can be justified if: i. the patient is haemodynamically stable without evidence of thoracic haemorrhage, ii. the patient is considered at high risk because of craniocerebral or cardiopulmonary reasons and/or iii. the diagnosis is made more than 24 h after the accident. • On the other hand, it is agreed that treatment should be planned – also in stable patients – as soon as it can be performed under safe conditions.
Repair Techniques The first successful repair of thoracic traumatic rupture was reported as early as in 1959 [44]. The surgical approach is dictated by the location of the aortic tear. Median sternotomy is used for lesions of the ascending aorta. Anterior thoracotomy is rarely used. In urgent cases, it might provide rapid access to the mediastinum. Since most lesions are located at the aortic isthmus, posterolateral thoracotomy is most frequently the approach of choice: • The patient is placed in right decubitus and an incision made, extending from behind the medial border of the scapula below its tip and then anteriorly to the anterior axillary line. • A split-lumen tube allows selective collapse of the left lung and the thorax is usually entered along the fifth rib.
• The aortic arch is approached and clamped between the left common carotid and the subclavian artery. • The distal clamp is placed as high as possible. • Options for repair include simple suture or prosthetic graft insertion. • Simple suture repair is possible with a partial laceration or a small disruption. • It has the advantage of the speed with which it can be performed, the absence of a prosthetic graft and the decreased risk of infection. • Nevertheless in most series, simple suture repair is possible in only 20% of cases and prosthetic (Dacron) graft interposition is the method of choice in most cases (Fig. 4.3.9).
Choice of Technique • Controversy continues about the optimal technique for repair because of concern about proximal hypertension and distal hypotension with the possibility of spinal cord ischaemia and the potential for lower limb paralysis. • There are still strong advocates of the simple clamp and repair method, particularly in urgent situations. • Techniques for distal perfusion include the use of passive shunts, partial or complete cardiopulmonary bypass and left heart by-pass (Biomedicus, Eden Prairie, Minn.). • Passive shunts are now avoided completely because of the lack of control. • Cardiopulmonary by-pass has also fallen largely into disfavour because of the need for systemic anticoagulation, which risks widespread haemorrhage in a patient with multi-system trauma. • Therefore, left heart by-pass (left atrium to femoral artery by-pass) is favoured in most centres. • The disadvantage is that it does not incorporate a heat exchanger and is dependent on adequate pulmonary function for oxygenation. • It offers however several advantages over cardiopulmonary by-pass: (1) it does not require systemic anticoagulation, (2) it deprimes itself automatically if air enters, therefore effectively reducing the risk of systemic embolization, (3) it is flow dependent and will decrease flow if inflow is obstructed and (4) it is resistance dependent, which means that it will stop pumping if excessively high pressures in the outflow are present.
307
308
4.3 Trauma of the Thoracic Aorta
Fig. 4.3.9a,b Dacron graft interposition for thoracic aortic rupture (a); (b) peri-operative view
Results • The results of open surgery are not only dependent on the operative technique but also and maybe primarily on the nature of the associated lesions, which means that the mortality and morbidity rates are quite high. • Von Oppell presented in 1994 a meta-analysis on the mortality and paraplegia rates after surgery for traumatic aortic rupture [61]. Eighty-seven articles published between 1974 and 1992 were included, totalling 1428 patients (Table 4.3.1). The overall mortality was 15.3%, ranging from 11.9% when active distal perfusion was used to 18.2% in the group with distal perfusion by cardiopulmonary by-pass (P<0.01). The paraplegia rate was 19% with the clamp and repair method and came down to below 3% with active distal perfusion (P<0.00001).
• More recent results of open surgery in relation to the operative technique are summarized in Tables 4.3.2– 4.3.4. • When compared with the data from von Oppell [61], it appears that there has not been much progress with
Table 4.3.1 Operative results of surgery for traumatic aortic rupture [61] Mortality (%) Paraplegia (%) Overall (n=1428)
15.3
9.9
Clamp and repair (n=443) 16
19
Passive shunt (n=424)
12.3
11.1
With heparin (n=490)
18.2
2.4
Without heparin (n=71)
11.9
1.7
Active shunt (n=561)
4.3.6 Therapy
Table 4.3.2 Contemporary results of open surgery with clamp and repair method Author
Number of patients
Mortality n (%)
Paraplegia n (%)ª
Magissano et al. (1995) [31]
32
5 (16)
1 (3.7)
Sweeney et al. (1997) [55]
71
9 (13)
1 (2)
Fabian et al. (1997) [13]
73
11 (15)
12 (16.4) 10 (24)
Attar et al. (1999) [2]
54
12 (22)
Tatou et al. (2000) [58]
69
NS
4 (5.7)
Carter et al. (2001) [7]
44
16 (36)
7 (25)
Jahromi et al. (2001) [24]
21
2 (10)
3 (16)
Kwon et al. (2002) [28]
14
5 (36)
0
Personal experience
15
2 (13)
3 (23)
393
62 (19)
41 (6.4)
Total a Related to surviving patients
Table 4.3.3 Contemporary results of open surgery with cardiopulmonary by-pass Author
Number of patients
Mortality n (%)
Paraplegia n (%)ª
Fabian et al. (1997) [13]
39
5 (12.8)
3 (7.7)
Gammie et al. (1998) [16]
10
1 (10)
0
Attar et al. (1999) [2]
43
7 (16)
0
Langanay et al. (2002) [29]
48
9 (18)
1 (2.6)
Jamieson et al. (2002) [25]
42
5 (12)
0
Nishimoto et al. (2003) [38]
12
0
0
8
0
0
Amabile et al. (2004) [1] Total
202
27 (13.4)
4 (2.3)
a Related to surviving patients
regard to the operative mortality, which remains primarily determined by the presence of concomitant injuries. • The paraplegia rate has come down to 6.4% in the clamp and repair group, but remains relatively high when compared with distal perfusion techniques.
4.3.6.2 Endovascular Approach Endovascular repair (stent-grafting) has emerged in recent years as an attractive alternative to open surgery [9].
Advantages It has indeed several advantages: • There is no need for a lengthy open operation with significant blood loss and cross clamping of the aorta. • Patients with pulmonary contusions do not always tolerate single-lung ventilation. • Because of its minimal invasive character, endovascular repair may even be performed under local anaesthesia. • The aortic lesion is usually well localized which means that a short graft will suffice, therefore also minimizing the risk for paraplegia.
309
310
4.3 Trauma of the Thoracic Aorta
Table 4.3.4 Contemporary results of open surgery with left heart by-pass Author
Number of patients
Mortality n (%) 10 (14.5)
Paraplegia n (%)a
Fabian et al. (1997) [13]
69
2 (3.4)
Gammie et al. (1998) [16]
14
1 (7)
0
Carter et al. (2001) [7]
47
6 (12.8)
0
Kwon et al. (2002) [28]
17
4 (24)
2 (15)
Symbas et al. (2002) [57]
19
5 (26)
0
Amabile et al. (2004) [1]
2
0
0
24
1 (4)
0
192
27 (13)
Personal experience Total
4 (2.4)
a Related to surviving patients
Fig. 4.3.10a,b Endovascular repair of thoracic aortic trauma: a calibrated angiography; b status post endoprosthesis covering the left subclavian artery
4.3.6 Therapy
Fig. 4.3.11a,b Evolution after endovascular repair of thoracic aortic trauma: a preoperative CT scan demonstrating intimal flap and mediastinal haematoma; b CT scan 3 years after stent-grafting: disappearance of intimal flap and mediastinal haematoma
Points to Note
Outcome
• The predominant localization of the rupture next to the left subclavian artery means that in some cases the origin of the left subclavian artery has to be covered in order to create a sufficient proximal sealing zone (Fig. 4.3.10). • It has however been shown that this can be done without major consequences [9]. • In the rare case of arm ischaemia, a reconstruction can be done later on. • We have now covered the subclavian artery in over 15 cases (atherosclerotic aneurysms and aortic dissections included) and only one patient needed a subsequent carotid subclavian transposition after 3 months. • A major contraindication for covering the subclavian artery is the presence of a left-sided mammary-to-coronary arterial by-pass. • In addition, there are exceptional anomalies of the circle of Willis, where the basilar artery is completely dependent on a dominant left vertebral artery. This is the reason why we always perform an angiography of the cerebral circulation before covering the subclavian artery. • Apart from this, it is admitted that these procedures should be reserved for centres fully equipped for emergency endovascular grafting and that the long-term behaviour of these endografts is not yet completely documented (Fig. 4.3.11).
• Endovascular reconstruction has certainly been met with enthusiasm and over the last 5 years there have been at least 12 papers presenting more than 5 cases (Table 4.3.5). • In these series, all grafts were deployed successfully and there were no early conversions. • The overall mortality (9.7%) is quite high, which might be explained by the fact that virtually all deaths were due to concomitant injuries. • One patient however died because of rupture of the ascending aorta on postoperative day 6 [15]. • Paraplegia has not been reported. • With the exception of the report by Melnitchouk et al. [35], the mean follow-up in these series does not exceed 2 years. • Seven graft-related complications are mentioned in four papers [26, 32, 37, 62]. These include four persistent endoleaks, of which two were treated conservatively and another two by placement of a second graft. • In the series of Morishita et al. [37], two patients were converted to open repair while another one underwent redo stent-grafting because of stent failure. • Although these results are encouraging, larger series and longer follow-up are needed before endovascular repair can be advocated as the method of choice in blunt aortic trauma, particularly in younger patients.
311
312
4.3 Trauma of the Thoracic Aorta
Table 4.3.5 Endovascular reconstruction for thoracic aortic trauma Author Fujikawa et al. (2001) [15]
Number of patients
Technical success (%) Mortality n (%)
Paraplegia n (%)ª
6
100
1 (16.6)
0
Orend et al. (2002) [40]
11
100
1 (9)
0
Orford et al. (2003) [41]
9
100
1 (11)
0
Marty-Ane et al. (2003) [32] Karmy-Jones et al. (2003) [26] Ott et al. (2004) [42]
9
100
0
0
11
100
3 (27)
0
6
100
0
0
Amabile et al. (2004) [1]
9
100
0
0
Wellons et al. (2004) [62]
9
100
1 (11)
0
Morishita et al. (2004) [37]
18
100
3 (17)
0
Meites et al. (2004) [34]
13
100
0
0
Melnitchouk et al. (2004) [35]
15
100
1 (6.6)
0
Scheinert et al. (2004) [54]
10
100
0
0
Personal experience
11
100
1 (9)
0
137
100
12 (9.7)
0
Total a Related to surviving patients
References 1. Amabile P, Collart F, Gariboldi V et al (2004) Surgical versus endovascular treatment of traumatic aortic rupture. J Vasc Surg 40:873–879 2. Attar S, Cardarelli MG, Downing SW et al (1999) Traumatic aortic rupture: recent outcome with regard to neurologic deficit. Ann Thorac Surg 67:959–965 3. Ben-Menachem Y (1993) Rupture of the thoracic aorta by broadside impacts in road traffic and other collisions: further angiographic observations and preliminary autopsy findings. J Trauma 35:363–367 4. Ben-Menachem Y (1997) Assessment of blunt aorto-brachiocephalic trauma: should angiography be supplanted by transesophageal echocardiography? J Trauma 42:969–972 5. Brundage SI, Harruff R, Jurkovich GJ et al (1998) The epidemiology of thoracic aortic injuries in pedestrians. J Trauma 43:1010–1014 6. Buckmeister MJ, Kearney PA, Johnson SB et al (1994) Further experience with transesophageal echocardiography in the evaluation of thoracic aortic injury. J Trauma 37:989–995 7. Carter Y, Meissner M, Bulger E et al (2001) Anatomical considerations in the surgical management of blunt thoracic injury. J Vasc Surg 34:628–633
8. Crass JR, Cohen AM, Motta AO et al (1990) A proposed new mechanism of traumatic aortic rupture: the osseous pinch. Radiology 176:645–649 9. Daenen G, Maleux G, Daenens K et al (2003) Thoracic aortic endoprosthesis: the final countdown for open surgery after traumatic aortic rupture. Ann Vasc Surg 17:185–191 10. Downing SW, Sperling JS, Mirvis SE et al (2001) Experience with spiral computed tomography as the sole diagnostic method for traumatic aortic rupture. Ann Thorac Surg 72:495–502 11. Duhaylongsod FG, Glower DD, Wolfe WG (1992) Acute traumatic aneurysm: the Duke experience from 1970 to 1990. J Vasc Surg 15:331–342 12. Dunn JA, Williams RG (1996) Occult ascending aortic rupture in the presence of an airbag. Ann Thorac Surg 62:577–578 13. Fabian TC, Richardson JD, Croce MA et al (1997) Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma. J Trauma 42:374–380 14. Fisher RG, Hadlack F, Ben-Menachem Y (1981) Laceration of the thoracic and brachiocephalic arteries by blunt trauma. Radiol Clin North Am 19:91–110
References
15. Fujikawa T, Yukioka T, Ishimura S et al (2001) Endovascular stent grafting for the treatment of blunt thoracic aortic injury. J Trauma 50:223–229 16. Gammie SJ, Shah AS, Hattler BG et al (1998) Traumatic aortic rupture: diagnosis and management. Ann Thorac Surg 66:1295–1300 17. Gavant ML, Menke PG, Fabian T et al (1995) Blunt traumatic aortic rupture: detection with helical CT of the chest. Radiology 197:125–133 18. Goodman PC, Jeffrey RB, Minagi H et al (1982) Angiographic evaluation of the ductus diverticulum. Cardiovasc Intervent Radiol 5:1–4 19. Greenberg MD, Rosen CL (1999) Evaluation of the patients with blunt chest trauma: an evidence based approach. Emerg Med Clin North Am 17:41–62 20. Greendyke RM (1966) Traumatic rupture of the aorta. Special references to automobile accidents. J Am Med Assoc 195:527–531 21. Gundry SR, Burney RE, Mackenzie JR et al (1983) Assessment of mediastinal widening associated with traumatic rupture of the aorta. J Trauma 22:293–299 22. Hemmila MR, Arabi S, Rowe SA et al (2004) Delayed repair for blunt thoracic aortic injury: is it really equivalent to early repair? J Trauma 56:13–23 23. Hunt JP, Baker CC, Lentz CW et al (1996) Thoracic aorta injuries: management and outcome of 144 patients. J Trauma 40:547–556 24. Jahromi AS, Kazemi K, Safar HA et al (2001) Traumatic rupture of the thoracic aorta: cohort study and systematic review. J Vasc Surg 34:1029–1034 25. Jamieson WR, Janusz MT, Gudas VM et al (2002) Traumatic rupture of the thoracic aorta: third decade of experience. Am J Surg 183:571–575 26. Karmy-Jones R, Hoffer E, Meissner MH et al (2003) Endovascular stent grafts and aortic rupture: a case series. J Trauma 55:805–810 27. Kroell C, Schnieder D, Nahum A (1974) Impact tolerance and response of the human thorax. In: 18th Stapp Car Crash Conference, Society of Automotive Engineers, Warrendale, Pa. 28. Kwon CC, Gill IS, Fallon WF et al (2002) Delayed operative intervention in the management of traumatic thoracic aortic rupture. Ann Thorac Surg 74:S1888–S1891 29. Langanay T, Verhoye JP, Corbineau H et al (2002) Surgical treatment of acute traumatic rupture of the thoracic aorta: a timing reappraisal? Eur J Cardiothorac Surg 21:282–287 30. Lundewall J (1964) The mechanics of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 62:34–36
31. Magissano R, Nathens A, Alexandrova NA et al (1995) Traumatic rupture of the thoracic aorta: should one always operate immediately? Ann Vasc Surg 9:44–52 32. Marty-Ane CH, Berthet JP, Branchereau P et al (2003) Endovascular repair for acute traumatic rupture of the thoracic aorta. Ann Thorac Surg 75:1803–1807 33. Mason JK (1978) The aircraft accident as an example of a major disaster. In: Mason JK (ed) The pathology of violent injury. Edward Arnold, London, pp 56–74 34. Meites G, Conil C, Rousseau H et al (2004) Indication of endovascular stent grafts for traumatic rupture of the thoracic aorta. Ann Fr Anesth Reanim 23:700–703 35. Melnitchouk S, Pfammatter Th, Kadner A et al (2004) Emergency stent-graft placement for hemorrhage control in acute thoracic aortic rupture. Eur J Cardiothorac Surg 25(6):1032–1038 36. Moar JJ (1985) Traumatic rupture of the thoracic aorta. An autopsy and histopathological study. S Afr Med J 67:383–385 37. Morishita K, Kurimoto Y, Kawaharada N et al (2004) Descending thoracic aortic rupture: role of endovascular stentgraft. Ann Thorac Surg 78:1630–1634 38. Nishimoto M, Fukumoto H, Nishimoto Y et al (2003) Surgical treatment of traumatic thoracic aortic rupture. Jpn J Thorac Cardiovasc Surg 51:138–143 39. O’Conor CE (2004) Diagnosing traumatic rupture of the thoracic aorta in the emergency department. Emerg Med J 21:414–419 40. Orend KH, Pamler R, Kapfer X et al (2002) Endovascular repair of traumatic descending aortic transection. J Endovasc Ther 9:573–578 41. Orford VP, Atkinson NR, Thomson K et al (2003) Blunt traumatic aortic transection: the endovascular experience. Ann Thorac Surg 75:106–111 42. Ott MC, Stewart TC, Lawlor DK et al (2004) Management of blunt thoracic aortic injuries: endovascular stents versus open repair. J Trauma 56:565–570 43. Parmley LF, Mattingly TW, Manion WC et al (1958) Nonpenetrating traumatic injury of the aorta. Circulation 17:1086–1101 44. Passaro E, Pace WG (1959) Traumatic rupture of the aorta. Surgery 46:787–791 45. Pate JW, Fabian TC, Walker WA (1995) Acute traumatic rupture of the aortic isthmus: repair with cardiopulmonary bypass. Ann Thorac Surg 59:90–99 46. Pierangeli A, Turinetto B, Galli R et al (2000) Delayed treatment of isthmic aortic rupture. Cardiovasc Surg 8:280–283 47. Raptopoulos V, Sheiman RG, Philips DE et al (1992) Traumatic aortic tear: screening with chest CT. Radiology 182:667–673
313
314
4.3 Trauma of the Thoracic Aorta
48. Ray G, Liu YK, Davids N (1975) Wall stress in curved aorta in blunt-chest trauma. In: Proceedings of the 28th Annual Conference on Engineering in Medicine and Biology, Alliance for Engineering in Medicine and Biology, 20–24 September, vol. 17, p 412 49. Richens D, Field M, Neale M et al (2002) The mechanism of injury in blunt traumatic rupture of the aorta. Eur J Cardiothorac Surg 21:288–293 50. Richens D, Kotidis K, Neale M et al (2003) Rupture of the aorta following road traffic accidents in the United Kingdom 1992–1999. The results of the co-operative crash injury study. Eur J Cardiothorac Surg 23:143–148 51. Rindfleish E (1893) Zur entstehung und heilung des Aneurysma dissecans Aortae. Virschow Arch Pathol Anat 374–378 52. Saletta S, Lederman E, Fein S et al (1995) Transoesophageal echocardiography for the initial evaluation of the widened mediastinum in trauma patients. J Trauma 39:137–142 53. Scaglione M, Pinto A, Pinto F et al (2001) Role of contrast-enhanced helical CT in the evaluation of acute thoracic aortic injuries after blunt chest trauma. Eur Radiol 11:2444–2448 54. Scheinert D, Krankenberg H, Schmidt A et al (2004) Endoluminal stent-graft placement for acute rupture of the descending aorta. Eur Heart J 25:694–700 55. Sweeney MS, Young DJ, Frazier OH et al (1997) Traumatic aortic transections: eight-year experience with the “clampsew” technique. Ann Thorac Surg 64:384–389 56. Symbas PN, Tyras DH, Ware RE et al (1973) Rupture of the aorta – a diagnostic triad. Ann Thorac Surg 15:405–410
57. Symbas PN, Sherman AJ, Silver JM et al (2002) Traumatic rupture of the aorta: immediate or delayed repair? Ann Surg 235:796–802 58. Tatou E, Steinmetz E, Jazayeri S et al (2000) Surgical outcome of traumatic rupture of the thoracic aorta. Ann Thorac Surg 69:70–73 59. Vignon P, Boncoeur MP, Francois B et al (2001) Comparison of multiplane transesophageal echocardiography and contrast-enhanced helical CT in the diagnosis of blunt traumatic cardiovascular injuries. Anesthesiology 94:615–622 60. Voight GE, Wifert K (1969) Mechanisms of injuries to unrestrained drivers in head-on collisions. In Proceedings of the 13th Stapp Car conference. Society of Automotive Engineers, New York, pp 295–313 61. Von Oppell UO, Dunne TT, De Groot MK et al (1994) Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg 58:585–593 62. Wellons ED, Milner R, Solis M et al (2004) Stent-graft repair of traumatic thoracic aortic disruptions. J Vasc Surg 40:1095–1100 63. Wicky S, Capasso P, Meuli R et al (1998) Spiral aortography: an efficient technique for the diagnosis of traumatic aortic injury. Eur Radiol 8:828–823 64. Wilson RF (1991) Thoracic vascular trauma. In: Bongard F, Wilson SE, Perry MO (eds) Vascular injuries in surgical practice. Appleton and Lange, Norwalk, p 107 65. Woodring JH (1990) The normal mediastinum in blunt traumatic rupture of the thoracic aorta and brachiocephalic arteries. J Emerg Med 8:467–476
Abdominal Aorta and Iliac Arteries
317
5.1 Abdominal Aortic Aneurysm (AAA) David Bergqvist, Martin Björck, Anders Wanhainen
5.1.1 Introduction Although problems and complications of aneurysm management have been recognized for nearly 4000 years, abdominal aortic aneurysm (AAA) was inaccessible to treatment until, in 1817, Sir Astley Cooper (1768–1841) made the first attempt to ligate the infrarenal aorta in a man with a leaking iliac aneurysm. The patient, however, succumbed 40 h after the operation. A variety of techniques to treat AAA were introduced in the nineteenth century but all unsuccessful. As well as different techniques of ligation or banding, endoaneurysmorrhaphy, and wrapping and wiring the sac were also tested. In the beginning of the twentieth century important steps were taken, one being the development of vascular grafts. Preserved homograft was used for treatment of coarctation of the aorta and during the 1950s aneurysmatic aortas were replaced with homografts, autologous veins and finally with synthetic prostheses. Knitted Dacron graft and the inlay technique leaving the aneurysmal sac in situ became the gold standard for AAA resection. Since 1986 [29], endovascular deployment of stent grafts has been increasingly used, and the technical development is so rapid that properly randomized evaluations are very difficult to perform.
5.1.2 Definition • The Greek word aneurynein means to widen. • AAA are true aneurysms (aneurysma verum), i.e. the aneurysmal wall is composed of all layers in the arterial wall (intima, media, adventitia). • The presence of clinically relevant aneurysms never used to be a problem: when detected through abdominal palpation or when ruptured, the aneurysm was often large and needed treatment anyhow.
• Definition of AAA has become important with the detection of small, not palpable aneurysms through increasing use of ultrasonography, CT, screening and in epidemiological research. • There is, however, no general agreement on how to define an AAA, with proposed definitions all being based on the diameter [7, 10, 15, 23, 30]. Some use the aneurysm diameter, some use the relation between aneurysm diameter and normal aortic diameter above the aneurysm or a combination of these. Others refer to an expected diameter and nomograms have been constructed to correct for body size, age and sex [22]. • From a practical point of view a diameter of ≥30 mm or 1.5 times larger than the suprarenal aortic diameter seems reasonable. • In recent studies, small aneurysms have been considered when the diameter is between 4.0 and 5.5 cm and large aneurysms above that [13, 19, 25].
5.1.3 Epidemiology/Aetiology Most patients with AAA start to develop their aneurysm at about 55 years of age [4]. The aneurysmal disease is probably multifactorial, and there is also the possibility that the aneurysm is a common response of the vessel wall to several disease processes (Fig. 5.1.1): • Evidence is accumulating that AAA is partly a genetically determined disease and that the strength of the aortic wall is predetermined in the individual person [11, 16]. • Defects in both elastin and type III collagen have been reported; elastin being important for keeping normal vascular dimensions and elasticity, while collagen is important for stability and tensile strength. Elastin degradation products have been suggested to indicate patients with an unstable aneurysm [18].
318
5.1 Abdominal Aortic Aneurysm (AAA)
Fig. 5.1.1 Schematic summary of causes and development of abdominal aortic aneurysm (AAA)
• Matrix metalloproteinases are proteolytic enzymes within the aneurysm wall and they may be important in the development of AAA. Proteolysis and inflammation are considered crucial factors for AAA expansion [21]. • The human abdominal aorta has fewer vasa vasorum than that of other mammals, especially the infrarenal part, and it has been speculated that a relative medial ischaemia could weaken the wall and eventually give rise to a dilatation. • Another possibility being discussed is chronic infection with Chlamydia pneumoniae [17].
5.1.3.1 Risk Factors • AAA is associated with having a first-degree relative with an AAA [28], increasing age, male sex, atherosclerotic disease and smoking [31]. • Chronic pulmonary disease and hypertension may also be associated with AAA.
• The more risk factors present, the higher is the prevalence of AAA [31]. • The disease process is complex with a strong possibility of a gene–environment interaction.
5.1.3.2 Prevalence • The most important factors determining the prevalence of AAA are sex and age (Fig. 5.1.2) [2]. • AAA in patients younger than 50–55 years of age usually is part of a well-defined disease entity such as Marfan’s syndrome, Ehlers–Danlos syndrome. • If the abdominal aorta is normal at 65 years of age, later aneurysmal development is rare, at least before the age of 75 [20]. • AAAs below 5.0–5.5 cm in diameter seldom rupture, and in a practical clinical setting the size-specific prevalence is important (Table 5.1.2). • The age-specific prevalence in the populations in Western Europe seems to have increased since the 1950s. In
5.1.3 Epidemiology/Aetiology
• In a population-based study from the city of Malmö, Sweden (autopsy rate of 89%), the incidence peaked at 112.7/100,000 men aged 80–89 years and 67.6/100,000 women aged 90 or above [2]. • Only around 15% of all AAAs detected at autopsy do rupture, which means that the absolute majority of patients with AAA die of other causes – mainly cardiovascular. • AAA is a cause of death in 1.5–2.0% of the male and 0.5–0.7% of the female population [9, 26]. • Also, after correcting for mortality in AAA rupture, the mortality is higher in patients with AAA than in a matched population, due to co-morbidity. Fig. 5.1.2 Prevalence of AAA related to age and sex. Data based on an autopsy study with an autopsy rate of 83%. From Bengtsson et al. [2]
Table 5.1.1 Prevalence of AAA among 73,451 American veterans aged 50–79 years. Ultrasonographic diagnosis Diameter (cm)
Prevalence (%)
3.0
4.6
4.0
1.4
5.0
0.5
5.5
0.3
6.0
0.2
7.0
0.1
8.0
0.03
From Lederle et al. [12]
men, after the age of 55 years the prevalence increases rapidly, peaking at about 80–85 years at about 6%. In women AAAs appear 10–15 years later and are 2–4 times less common than in men, although these figures depend on which definition of AAA is used. • The prevalence detected in ultrasonography screening studies is in good accordance with autopsy findings in populations with a high autopsy rate [2, 27, 32].
5.1.3.3 Incidence of AAA Rupture • The incidence of AAA rupture lies between 5 and 10 per 100,000 inhabitants per year.
5.1.3.4 Disease Progression • If an AAA is left without intervention it will expand gradually and will eventually rupture (Table 5.1.2). • The expansion rate is size dependent, with a higher rate in larger aneurysms. • Although the mathematical expansion rate follows an exponential function, with a rate of around 10% per year, there are great individual variations [3]. Some AAAs are stable in size, others expand rapidly, while others vary in expansion rate and pattern over time. Moreover, parts of the aneurysm may bulge locally, making the wall fragile. • Factors influencing the expansion pattern may differ from those initiating the disease. In addition to initial diameter, factors predictive of rapid expansion are age, smoking and hypertension [6, 8]. • Table 5.1.2 shows the risk of rupture in relation to aneurysmal size.
Table 5.1.2 Risk of rupture in relation to the diameter of an AAA Initial diameter (cm)
Risk of rupture (%) 1 year
5 years
4
1
15
5
3
20
6
9
30
7
25
50
8
40
75
319
320
5.1 Abdominal Aortic Aneurysm (AAA)
• In addition to AAA size, female sex, a positive family history, smoking, hypertension and chronic obstructive pulmonary disease contribute to an increased risk of rupture. • Local factors in the aneurysmal wall are probably important but less well known. • The presence of an intraluminal thrombus seems to be important in increasing the risk of rupture, whether it is due to a local enzymatic effect or local hypoxia. • Palpatory tenderness over the aneurysm is a warning sign of rupture.
5.1.3.5 Treatment • As most of the operations are prophylactic in asymptomatic patients with the aim of preventing rupture in the future, the intervention must not have a worse outcome than the natural course of the disease. • Three key variables have to be considered: (1) elective operative risk, (2) the risk of AAA rupture and (3) life expectancy. • Based on these factors the threshold diameter is estimated. As a practical rule of thumb, size can be used in the decision-making process on when to operate on patients with AAA. • In male patients the size is 5.0–5.5 cm, in females 0.5 cm less.
5.1.4 Symptoms The majority of aneurysms are asymptomatic and remain unknown until detected by chance, e.g. when the patient undergoes CT, pelvic or abdominal X-ray, urography, etc., for other reasons, or during surgery for other intraabdominal disorders. When symptomatic there may be various ways of presentation: • Pain, which may be vague and diffuse • Feeling of pulsations • Symptoms from neighbouring organs (pressure on ureters, duodenum, etc.) • Microembolism (sometimes macroembolism) • Thrombotic occlusion • Rupture • into the free abdominal cavity • retroperitoneally
• into the bowel (primary aortoenteric fistula) • into the vena cava, aortocaval fistula (or very rarely the iliac vein).
5.1.4.1 Expanding Aneurysm • A painful aneurysm without rupture is often called an expanding aneurysm or an AAA with impending rupture. • Emergency surgery in such patients will often show a glassy oedema retroperitoneally but without extraaortal blood, which obviously indicates that there is some form of retroperitoneal reaction. • In the majority of aneurysms there is an intra-aneurysmal thrombus, part of which can embolize, most frequently in the form of microemboli. • Acute thrombotic occlusion is rare and almost always seen when there is stenosing iliac or femoral disease compromising the outflow.
5.1.4.2 Inflammatory AAA • A special form of AAA is inflammatory (around 5% of all), where the aneurysmal wall is surrounded by a thick fibrotic and often hyperaemic capsula, sometimes involving the ureters and causing hydronephrosis, or the duodenum. • The patients often have diffuse abdominal pain and tenderness on palpation. • Sedimentation rate and C-reactive protein are usually very high.
5.1.4.3 Rupture • Rupture causes severe pain and often the clinical picture of hypovolaemia. • Whether or not the patient has been in shock has prognostic significance. • The patients may have microscopic haematuria and the most common differential diagnosis is ureterolithiasis. • Otherwise rupture of an AAA can simulate several acute diseases within the abdomen, the back or the breast and the pelvic region.
5.1.5 Diagnosis
• In elderly patients with acute breast, back or abdominal pain, rupture of an aortic aneurysm must be considered. • Rarely, the bleeding may stop and a false aneurysm develops (contained rupture), almost always followed by secondary rupture.
5.1.5 Diagnosis 5.1.5.1 Recommended European Standard Diagnostic Steps of Investigation Abdominal Palpation • When the investigator palpates an aneurysm the diagnosis is usually true but palpation to exclude an aneurysm is not reliable, especially if the patient is somewhat adipose, has a rigid abdomen or is in shock.
CT and MRI • Computerized tomography (especially spiral CT) and magnetic resonance imaging, especially when the respective angiographic modalities are included, give optimal information both regarding: (1) whether or not there is an AAA and (2) the diameter. • Important information is obtained on the amount of thrombus, the relation to other organs and arterial and venous anatomy, especially concerning renal and iliac vessels. • When planning endovascular stent graft treatment specific information is necessary on the extent of the AAA, the length of the aortic neck (i.e. the distance to the renal arteries), exact aortic diameter, the angle between the aorta and the aneurysm and the diameter of the iliac arteries.
Ultrasonography • In experienced hands ultrasonography can give the same information as CT. • It is the method which is of interest in screening situations because it is relatively cheap, rapid and available. • When following the expansion rate of an aneurysm it is the method of choice.
• Modern intravascular ultrasound will probably be of help during placement of endovascular stent grafts in the future.
5.1.5.2 Aspects on Screening As AAA is a potentially fatal disease and as most patients with an AAA are unaware of it, screening should be an attractive alternative with intervention in selected cases. As already shown, the prevalence of AAA of a size that prompts discussion of intervention does not motivate general screening. According to the World Health Organization (WHO), screening is a medical investigation that does not arise from a person’s request for advice on specific complaints. The following basic criteria should be fulfilled [33]: • The disease is an important health problem. AAA causes 1% of all deaths and in elderly males it may cause as many as 2% of all deaths. • There is a generally accepted treatment. The gold standard is surgical treatment with intraluminal graft replacement with a peri-operative mortality of less than 5%. • Provisions for diagnosis and treatment are available. The screening strategy may affect the demand for resources. To screen men once at the age of 65 years could be handled nowadays. • The disease must have a detectable latent stage. The risk of aneurysm rupture is in proportion to the aneurysm size. Most screening-detected AAAs are small and have a low risk of rupture. • A suitable screening method must be available. The screening method should not only show a high diagnostic accuracy but should also be rapid, inexpensive and safe. Ultrasonography is a noninvasive test that fulfils these criteria. • The screening method must be accepted by the target population. Ultrasonography has proven to be well accepted in several population-based screening studies. The attendance rate is often above 75%. • The natural course of the disease must be known. The most important factors predicting rupture are aneurysm diameter and expansion rate. AAAs less than 55 mm have a low risk of rupture. • The policy for treatment of the disease must be clear. The UK Small Aneurysm Trial [25] and the ADAM study [12] have demonstrated the safety with surveillance until the AAA diameter reaches 55 mm.
321
322
5.1 Abdominal Aortic Aneurysm (AAA)
• The cost-effectiveness of a screening programme must be reasonable. Most previous studies have found screening 65-year-old men to be cost-effective. There are, however, only a few prospective studies concerning cost-effectiveness, and they all have a short follow-up. • The treatment of the disease should favour prognosis of patients. Elective surgery in appropriately selected individuals will prevent rupture, and long-term survival after successful AAA repair is only slightly shorter compared to the general aged-matched population.
rysmal sac, often as a straight graft from below the renal arteries to the aortic bifurcation. • When the bifurcation is heavily calcified or where there are aneurysms in the iliac arteries, a bifurcation graft is used, either (and preferably) to the iliac arteries or (if needed) to the femoral. • It is important to preserve circulation in at least one internal iliac artery to avoid colonic ischaemia and hip claudication.
5.1.6.2 Endovascular Aortic Repair (EVAR) In a screening programme, whichever group of individuals is selected, there would be detection of a high proportion of small AAAs where intervention is not indicated but regular follow-up is necessary to be able to intervene when a certain aneurysmal size is reached. Today there are some large-scale studies clearly indicating screenings to decrease the rupture rate in the population [1, 14, 24, 32]. Screening 65-year-old men for AAA seems cost-effective, while screening younger men with a re-screening could be equally cost-effective with the advantage of more life years gained. The trade-off between high AAA prevalence and lower life expectancy in high-risk groups, such as smokers and persons with angina pectoris or claudication, eliminates most of the expected additional benefits of screening these groups selectively. Male firstdegree relatives have a very high prevalence of AAA and should be offered an ultrasonic investigation.
5.1.6 Therapy There are so far no conservative treatment options inhibiting the expansion of a AAA, although there have been and are ongoing trials on β-blockade and antibiotics, especially against Chlamydia. At an aneurysmal size of more than 5.0–5.5 cm in diameter intervention should be contemplated, perhaps 0.5 cm smaller in females. Although the proportion of AAAs treated endovascularly is increasing, open surgery still dominates and is the method that has given reliable long-term results.
5.1.6.1 Open Surgery • In open surgery, a synthetic graft [polyester or polytetrafluoroethylene (PTFE)] is placed within the aneu-
• In endovascular aortic repair (EVAR) the graft is introduced by the femoral artery route and fixed to the aorta and the iliac arteries with metallic stents. • This procedure is made with coordinated surgical and radiology expertise. • Most frequently various modular graft systems are used. • The technical development of devices is rapid and new generation systems are introduced so rapidly that performing proper controlled studies is difficult.
5.1.6.3 Rupture and Reconstruction • If rupture is suspected and especially if the patient is hypovolaemic immediate reconstruction is important. • The first and vital step is aortic clamping proximal to the aneurysm to avoid further blood loss. • The reconstruction is performed as in elective cases and it is important to make it as rapid and simple as possible. • Ruptured AAAs can also be treated endovascularly and this is a step forward. • When comparing results from different techniques of treating patients with ruptured AAAs one must also consider those who were not operated on and those who died during diagnostic work-up. • It must, however, be remembered that with increasing numbers of patients being reconstructed endovascularly, the ones needing open surgery are usually the most difficult and demanding ones technically, and this fact puts special emphasis on practical education of vascular surgeons and probably also makes centralization necessary.
References
5.1.6.4 Outcome • After elective surgery the 30-day mortality is below 5%, but it increases to around 40% if there was a rupture and the patient was in shock. • Surviving the first postoperative month, however, gives both groups an expected survival that is only somewhat lower than that of a matched “normal” population. • After endovascular treatment the immediate postoperative mortality seems somewhat lower than after open surgery but large-scale long-term results are still awaited. • So far there seems definitively to be a need for more complementary procedures after endovascular repair (see below).
5.1.7 Possible Complications of Surgery
• Migration because of poor stent fixation or widening of the aortic neck. Many of those complications need re-interventions, either open or with a new endovascular procedure.
5.1.8 Practical Recommendations • AAAs with a diameter of >5 cm in males and >4.5 cm in females should be referred to a vascular surgeon for interventional evaluation. • AAAs between 4.0 and 5.0 cm are followed every 6 months with ultrasonography and smaller ones are followed yearly. • AAAs with symptoms or complications should always be evaluated by a vascular surgeon. References
• The most common postoperative complications after AAA surgery are myocardial infarction, renal insufficiency and ischaemia of the left colon. To avoid the latter at least one internal iliac artery should be saved or revascularized [5]. • Graft infection and secondary aortoenteric fistula are feared long-term complications seen in around 1%. Morbidity and mortality are high. In patients with an aortic graft and gastrointestinal bleeding a fistula must be suspected until otherwise proven. • Pseudoaneurysm in anastomotic locations is more common after aneurysm surgery than after surgery for occlusive disease, indicating a decreased wall strength and stability in aneurysmatic arteries. The most common location is in the groin area, pointing to the possible role of infection. • When preaortic nerve plexa are injured during open surgery sexual dysfunction may be a complication, most frequently as retrograde ejaculation. Specific complications after endovascular intervention for an AAA are: • Endoleakage, which may occur in anastomoses, in connections in cases of modular graft systems, because of back bleeding arteries into the aneurysmal sac or because of a defect in the graft material. • Endotension, which is increased pressure within the aneurysmal sac in spite of no back bleeding. • Graft limb occlusion because of kinking between modules.
1. Ashton HA, Buxton MJ, Day NE, Kim LG, Marteau TM, Scott RA, Thompson SG, Walker NM (2002) The Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet 360:1531–1539 2. Bengtsson H, Bergqvist D, Sternby N (1992) Increasing prevalence of aortic abdominal aneurysms – an autopsybased study. Eur J Surg 158:19–23 3. Bengtsson H, Nilsson P, Bergqvist D (1993) Natural history of abdominal aortic aneurysm detected by screening. Br J Surg 80:718–720 4. Bengtsson H, Sonesson B, Bergqvist D (1996) Incidence and prevalence of abdominal aortic aneurysms, estimated by necropsy studies and population screening by ultrasound. Ann N Y Acad Sci 800:1–24 5. Bjorck M, Troeng T, Bergqvist D (1997) Risk factors for intestinal ischaemia after aortoiliac surgery: a combined cohort and case-control study of 2824 operations. Eur J Vasc Endovasc Surg 13:531–539 6. Chang JB, Stein TA, Liu JP, Dunn ME (1997) Risk factors associated with rapid growth of small abdominal aortic aneurysms. Surgery 121:117–122 7. Collin J, Araujo L, Walton J, Lindsell D (1988) Oxford screening programme for abdominal aortic aneurysm in men aged 65 to 74 years. Lancet 2:613–615 8. Cronenwett JL, Sargent SK, Wall MH, Hawkes ML, Freeman DH, Dain BJ, Cure JK, Walsh DB, Zwolak RM, McDaniel MD, et al (1990) Variables that affect the expansion rate and outcome of small abdominal aortic aneurysms. J Vasc Surg 11:260–269
323
324
5.1 Abdominal Aortic Aneurysm (AAA)
9. Earnshaw JJ, Shaw E, Whyman MR, Poskitt KR, Heather BP (2004) Screening for abdominal aortic aneurysms in men. BMJ 328:1122–1124 10. Johnston KW, Rutherford RB, Tilson MD, Shah DM, Hollier L, Stanley JC (1991) Suggested standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg 13:452–458 11. Kuivaniemi H, Tromp G, Prockop DJ (1991) Genetic causes of aortic aneurysms. Unlearning at least part of what the textbooks say. J Clin Invest 88:1441–1444 12. Lederle F, Johnson G, Wilson S, Chute E, Littooy F, Bandyk D, Krupsky W, Barone G, Acher C, Ballard DJ (1997) Prevalence and associations of abdominal aortic aneurysm detected through screening. Ann Intern Med 126:441–449 13. Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN, Acher CW, Ballard DJ, Messina LM, Gordon IL, Chute EP, Krupski WC, Busuttil SJ, Barone GW, Sparks S, Graham LM, Rapp JH, Makaroun MS, Moneta GL, Cambria RA, Makhoul RG, Eton D, Ansel HJ, Freischlag JA, Bandyk D (2002) Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med 346:1437–1444 14. Lindholt JS, Juul S, Fasting H, Henneberg EW (2002) Hospital costs and benefits of screening for abdominal aortic aneurysms. Results from a randomised population screening trial. Eur J Vasc Endovasc Surg 23:55–60 15. McGregor JC, Pollock JG, Anton HC (1975) The value of ultrasonography in the diagnosis of abdominal aortic aneurysm. Scott Med J 20:133–137 16. Menashi S, Campa JS, Greenhalgh RM, Powell JT (1987) Collagen in abdominal aortic aneurysm: typing, content, and degradation. J Vasc Surg 6:578–582 17. Petersen E, Boman J, Persson K, Arnerlov C, Wadell G, Juto P, Eriksson A, Dahlen G, Angquist KA (1998) Chlamydia pneumoniae in human abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 15:138–142 18. Petersen E, Gineitis A, Wagberg F, Angquist KA (2001) Serum levels of elastin-derived peptides in patients with ruptured and asymptomatic abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 22:48–52 19. Powell JT, Greenhalgh RM (2003) Clinical practice. Small abdominal aortic aneurysms. N Engl J Med 348:1895–1901 20. Scott RA, Vardulaki KA, Walker NM, Day NE, Duffy SW, Ashton HA (2001) The long-term benefits of a single scan for abdominal aortic aneurysm (AAA) at age 65. Eur J Vasc Endovasc Surg 21:535–540
21. Shah PK (1997) Inflammation, metalloproteinases, and increased proteolysis: an emerging pathophysiological paradigm in aortic aneurysm. Circulation 96:2115–2117 22. Sonesson B, Lanne T, Hansen F, Sandgren T (1994) Infrarenal aortic diameter in the healthy person. Eur J Vasc Surg 8:89–95 23. Sterpetti AV, Schultz RD, Feldhaus RJ, Cheng SE, Peetz DJ Jr (1987) Factors influencing enlargement rate of small abdominal aortic aneurysms. J Surg Res 43:211–219 24. Swedenborg J, Bjorck M, Wanhainen A, Bergqvist D (2003) Screening for abdominal aortic aneurysm saves lives at a reasonable cost. Lakartidningen 100:1886–1891 25. The UK Small Aneurysm Trial Participants (1998) Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet 352:1649–1655 26. Vardulaki KA, Prevost TC, Walker NM, Day NE, Wilmink AB, Quick CR, Ashton HA, Scott RA (1998) Growth rates and risk of rupture of abdominal aortic aneurysms. Br J Surg 85:1674–1680 27. Vardulaki KA, Prevost TC, Walker NM, Day NE, Wilmink AB, Quick CR, Ashton HA, Scott RA (1999) Incidence among men of asymptomatic abdominal aortic aneurysms: estimates from 500 screen detected cases. J Med Screen 6:50–54 28. van Vlijmen-van Keulen CJ, Vahl AC, Hennekam RC, Rauwerda JA, Pals G (2003) Genetic linkage of candidate genes in families with abdominal aortic aneurysms? Eur J Vasc Endovasc Surg 26:205–210 29. Volodos NL, Shekhanin VE, Karpovich IP, Troian VI, Gur’ev Iu A (1986) A self-fixing synthetic blood vessel endoprosthesis. Vestn Khir Im I I Grek 137:123–125 30. Wanhainen A, Bjorck M, Boman K, Rutegard J, Bergqvist D (2001) Influence of diagnostic criteria on the prevalence of abdominal aortic aneurysm. J Vasc Surg 34:229–235 31. Wanhainen A, Rosen C, Rutegard J, Bergqvist D, Bjorck M (2004) Low quality of life prior to screening for abdominal aortic aneurysm: a possible risk factor for negative mental effects. Ann Vasc Surg 18:287–293 32. Wilmink TB, Quick CR, Hubbard CS, Day NE (1999) The influence of screening on the incidence of ruptured abdominal aortic aneurysms. J Vasc Surg 30:203–208 33. Wilson J, Jungner Y (1968) Principles and practice of screening of disease. WHO, Geneva, Public Health Paper no. 34
325
5.2 Treatment Options for Abdominal Aortic Aneurysm (AAA) David Bergqvist, Martin Björck, Christer Ljungman, Rickard Nyman, Anders Wanhainen
5.2.1 Introduction This chapter will focus on how to deal with AAA from a practical point of view and also give hints on how to correct some of the complications that may occur. The two principal options to treat AAA are by: (1) open repair or (2) endovascular aneurysm repair (EVAR). Both can be used irrespective of whether the AAA is ruptured or treated electively, although the experience on EVAR in the case of rupture so far is limited. A third option, laparoscopic repair, can still be considered as non-established, and its role remains to be seen. It will not be further discussed in this chapter. Today there are no pharmacological means to treat AAA or reduce expansions, although β-blockade and antibiotics have been tried. A better understanding of the cause of AAA may, however, lead to other treatment options in the future.
5.2.2 Open Repair There are basically three ways to approach the aorta: 1. Through a long midline transperitoneal incision. 2. Through a transverse left subcostal incision, transperitoneally. The problem is to reach the iliac arteries and a small extraperitoneal help incision may be needed. 3. Through a left transverse or paramedian, laterally curved, incision with retroperitoneal dissection and medial rotation of the abdominal viscera. The left kidney can be left in situ or included in the medial rotation. This is to be preferred in cases of hostile abdomen and in cases with suprarenal extension of the aneurysm. It could also be preferable in patients who are morbidly obese.
One advantage of the intraperitoneal approaches is that the abdominal cavity can be investigated for potential co-morbidities, the patients often being of an age where malignancies are not rare and AAA shares important risk factors with malignancies, such as smoking. The posterior peritoneum is incised a couple of centimetres left of the duodenum, which is mobilized to the right. The inferior mesenteric vein is preferably divided to avoid becoming torn and injured later during the procedure. The next landmark is the left renal vein traversing in front of the aorta, but it is important to know that in around 1% of the population the left renal vein is retroaortic. Proximal dissection in such a case in search of the vein, which will not be found, may lead to dangerous contact with the superior mesenteric artery. The location of the left renal vein should be looked for at preoperative CT or MR investigations. The aneurysmal neck is secured, below the renal arteries in the vast majority of cases, and preparation is made for clamping. In elective cases we often prefer transverse clamping. Especially where the distance to the renal arteries is short, such a manoeuvre simplifies performing the anastomosis. When dissecting the left lateral part of the neck it is important to know that often a lumbar vein approaches the renal vein here. It should be avoided or preferably ligated. Sometimes it is necessary also to ligate the gonadal vein. However, if for some reason the left renal vein must be divided, this can be done only if there are enough outflow alternatives from the kidney (gonadal and adrenal veins), and the division should be placed close to the inferior caval vein. If not, the renal vein must be reconstructed. Where to place the distal control depends on the extent of the aneurysm. Wherever the optimal location is, during the dissection the following points are important: • Do not manipulate or massage the aneurysm because of the risk of embolization of intra-aneurysmal thrombosis, which can lead to trash feet or colonic ischaemia, secondary to embolism to the internal iliac arteries.
326
5.2 Treatment Options for Abdominal Aortic Aneurysm (AAA)
• Be careful not to divide structures in the aortic bifurcation region, especially on the left side, because of the risk of postoperative sexual dysfunction, especially retrograde ejaculation, if autonomic nerves are damaged. • Avoid ligating the inferior mesenteric artery as it can be difficult to exactly localize its origin, with the risk that important collaterals are divided, increasing the risk of postoperative colonic ischaemia. If the inferior mesenteric artery is patent the best solution is to oversew it from within the aneurysmal sack, when it has been opened. • Avoid encircling the iliac arteries, especially near the aortic and iliac bifurcation, because of the very close and sometimes adherent relation to the iliac veins, with the risk of severe venous bleeding that is not easily controlled (Blakemore’s angle of sorrow). A sagittal clamp is preferable, but if that is difficult it may be safer with intraluminal control with balloon catheters, after proximal clamping and opening of the aneurysm. Before clamping, some 5000 IU of heparin is given, perhaps not so much to avoid thrombosis as to avoid serious coronary complications [3]. After clamping, the aneurysmal sack is opened longitudinally. In cases of inflammatory aneurysms or rupture, where anatomical landmarks are not perfectly clear, it is important to open the aneurysm to the left to avoid injury to the duodenum. Otherwise opening to the right is preferable, to save collaterals to the inferior mesenteric artery. Having opened the aneurysm, thrombotic material is removed and bleeding sources are suture ligated (lumbar arteries, inferior mesenteric artery). This should be made with big stitches to rapidly obtain haemostasis, to not lose tempo and to avoid prolonging cross-clamping unnecessarily. An automatic retractor may help to hold the aneurysm sack open when suturing the graft. There are various types of grafts made from polyester or polytetrafluoroethylene (PTFE). Their porosity means that knitted untreated polyester grafts must be pre-clotted, resulting in fibrin in the pores, otherwise there will be uncontrollable bleeding. Today, however, the majority of grafts are sealed with albumin, collagen or gelatin. PTFE grafts are tight. The graft is sutured into the aneurysm with an inlay technique, that is the anterior half of the aorta is transected and the back of the aortic wall is used as a ridge where the sutures are placed. If the aneurysm extends into the iliac arteries or the bifurcation is heavily calcified, a bifurcation graft is inserted but in some 70% of cases a straight graft can be used. When a bifurcated
graft is used it is important to maintain the waist short to avoid kinking of the iliac limbs. It is also important to keep at least one of the internal iliac arteries patent to prevent colonic ischaemia and gluteal claudication. Before declamping there must be close cooperation with the anaesthetist to ensure that the patient is optimally volume substituted to avoid declamping hypotension, which at worst may lead to myocardial infarction, cardiac insufficiency and hypoperfusion of vital organs, i.e. kidneys and brain. The principles of repair of ruptured AAAs are similar but the procedure is often more difficult because of a large haematoma and deranged anatomy. To improve prognosis it is important to make the operations speedy, safe and simple. In the case of rupture the most rapid approach is to place the proximal clamp in the sagittal direction or, if the haematoma makes orientation difficult, to make a temporary supracoeliac clamp through the diaphragmatic crura. It is important to move this proximal clamp infrarenally as fast as possible to shorten visceral ischaemia. To speed up the procedure a straight graft should be used whenever possible. The development of declamping hypotension could be deleterious in patients with a rupture, where there often has been prolonged hypotension or even shock prior to surgery. In patients with rupture it is also important to make a Fogarty manoeuvre in the legs as often there is thrombotic material, which otherwise may lead to postoperative ischaemia. There are some situations where special considerations should be taken: • Hostile abdomen (previous extensive surgery, stomas, previous radiation, intra-abdominal infection). A retroperitoneal approach should be contemplated. • Inflammatory aneurysm may be suspected where the aneurysm is tender, the erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) level is high and CT shows a thickened, well-vascularized wall. Difficult dissection can be foreseen and a retroperitoneal approach may be preferred. Intraluminal balloon catheter control distally is recommended. Duodenum and ureters are often densely adherent to the fibrotic tissue. • Kidney anomalies, especially horseshoe kidney. Renal artery abnormalities are almost always present with renal arteries originating from the distal aorta or even the iliac arteries. This should be evaluated preoperatively. Sometimes renal arteries originate from the aneurysm and they must usually be reimplanted into the graft.
5.2.3 Endovascular Repair
• Aneurysm without intra-aneurysmal thrombus on CT, MR or ultrasonography. A haemostatic defect must be excluded to avoid unnecessary bleeding. The haemostatic defect may be pharmacologically or disease induced. • Venous anomalies. Retroaortic left renal vein has already been mentioned. The vena cava can be left-sided or duplicated in 1–2% of cases. • Aorto-caval fistula. A rupture into the caval vein leads to an AV shunt that will dominate the symptomatology. A midline incision is preferred to avoid cutting veins, with increased pressure causing troublesome bleeding. It is important not to press or squeeze the aneurysm during the dissection, which could cause a pulmonary embolism, eventually fatal. There should be no attempt to isolate the fistula from outside the aneurysm. Instead it should be oversewn from within the aneurysmal sack, once it has been opened. • Ehlers-Danlos syndrome type IV (EDS) is an autosomal-dominant inherited connective tissue disorder. Rupture of vessels, with or without aneurysm formation, is common. Surgery may be extremely hazardous and should as far as possible be avoided. Most important is to suspect the condition. A history of easy bruising and complication at previous surgery, together with increased joint mobility and skin elasticity, may lead to the diagnosis, which can be confirmed by a skin biopsy. In the case of AAA repair, a non-traumatic technique is important. The aneurysmal neck should be divided and pledgets or a short graft placed outside the neck should be used as external support.
5.2.2.1 Complications The immediate complications which need surgical corrections are: • Distal embolization, which may be solved with the use of a Fogarty balloon catheter but in rare cases the distal microvasculature may be occluded. Low doses of local thrombolytic agents may be tried, sometimes with success. Tissue plasminogen activator (t-PA) is preferred because of its short half-life. • Ischaemia of the left colon. When this is suspected clinically (general deterioration, peritonitis, sepsis, increased creatinine, early passage of stools, passage of bloody stools) in combination with ischaemic findings in the left colon at colonoscopy, laparotomy is indicated and the gangrenous bowel should be resected, often as a Hartmann’s procedure.
• Abdominal compartment syndrome occurs in 5– 19% after operation for a ruptured AAA. Decompression laparotomy may be life-saving. In the long run, complications of immediate surgical interest are: • Graft infection, most frequently seen if a bifurcation graft was anastomosed in the groin, where the diagnosis is rather obvious. More difficult to diagnose is a graft infection when the graft is hidden retroperitoneally. CT or MR is often diagnostic. When there is a graft infection the therapeutic principle is graft removal and extra-anatomical reconstruction (axillobifemoral graft). In special situations (i.e. elderly fragile patients, low virulent infection) less radical solutions may be used: in situ reconstruction with vein, antibiotic-coated or silver-coated grafts or even partial graft removal with reconstruction being improvised. • Pseudoaneurysm. Again the dominating location is the groin. If infection can be excluded as the cause of the pseudoaneurysm a local reconstruction may be tried. • Aortoenteric fistula. This is a disastrous complication that must be suspected in every patient with an aortic graft who presents with gastrointestinal bleeding. This complication should be dealt with as indicated above regarding infection. In addition the intestinal defect must be closed. Also after successful treatment recurrence is not rare. Especially feared is blow-out of the sutured aortic stump.
5.2.3 Endovascular Repair It is only some 15 years since this development started and during this period technical modifications have come and gone, and intermediate and some long-term results of larger series of patients have just begun to be reported. The first randomized studies have been published showing beneficial short-term results compared to patients treated with open surgery [2]. To be accepted for endovascular treatment the preoperative investigation must be more detailed than before open surgery since the choice of a correct graft system is of utmost importance for success. The proportion of AAAs suitable for endovascular repair varies and the exact selection criteria have yet to be defined and moreover are evolving. Today suitability for vascular repair has to do with:
327
328
5.2 Treatment Options for Abdominal Aortic Aneurysm (AAA)
• the endovascular graft system chosen • individual patient anatomy • nonanatomical factors in individual patients. There has been a reluctance to use endovascular treatment in younger individuals because of scarce information on long-term results. On the other hand, there has been a tendency to try endovascular repair in patients where open surgery has been considered too risky (so called compassionate cases). Today there are three basic technical solutions used for endovascular repair: tube graft (very rarely needed or possible), bifurcated modular graft or aortoiliac or aortofemoral graft on one side combined with a contralateral iliac occlusion device and an open femoro-femoral crossover graft. The preoperative evaluation is based on a high-quality contrast-enhanced spiral CT investigation with 3- to 6-mm cuts, which is often enough to decide on how to proceed and which graft system to use. Sometimes further information is obtained through MRA or conventional angiography. The basic anatomical criteria for endovascular repair to be considered are: • The dimension and quality of the proximal neck. The distance to the renal arteries should not be less than 15 mm, the neck should be cylindrical and not conical, it should be less than 30 mm in diameter and should be thrombus free. Usually the stent graft is somewhat oversized compared with the neck diameter (around 10%). • The angle between the neck and the aneurysm, which is a result of the elongation often seen in aneurysmatic aortas. Angles greater than 60° are generally considered to exclude the possibility of endovascular repair. • Quality of the distal landing zone, almost always the iliac arteries. Difficulties can be foreseen in cases of tortuosity (>90°), dilatation (>20 mm), severe calcification or the presence of thrombotic material. • Quality of access arteries, i.e. the femoral arteries. They must be of a calibre that allows the passage of the introducer sheath (8–10 mm) and the tortuosity must be limited. • Arterial anatomy. Aberrant renal arteries may arise from the aneurysm and would be sacrificed using endovascular repair, which otherwise would be suitable. Sacrificing both internal iliac arteries may cause colonic ischaemia and gluteal claudication. Today there are several commercially available stent graft systems, the graft body being made of polyester or
PTFE. There are several stent types, the majority today with barbs or hooks to assure secure fixation of the stent to the aortic wall. On the market there are both self-expandable and balloon-expandable stents. In the majority of aneurysms an industry-made modular device is used. The advantage with modular systems is greater flexibility regarding size and modifications during the procedure. It is our opinion that optimal treatment is arrived at when there is a close cooperation between the interventional radiologist and the vascular surgeon. The treatment is preferably performed in a hybrid operating room with good equipment both for the radiological part of the procedure and for open surgery. Motivations for having an operating room environment are: • To have optimally sterile conditions • To have the possibility of performing open surgery simultaneously. Such procedures could be a femorofemoral crossover by-pass, obtaining open access to a tortuous iliac artery through an extraperitoneal approach, or repair of iatrogenically injured femoral or iliac arteries. • To rapidly convert the procedure to open surgery in cases of emergency (bleeding or occlusion with acute ischaemia).
5.2.3.1 Complications Complications in need of open surgery or endovascular treatment are: • Endoleakage. Depending on the type of endoleak, there are several treatment options: embolization of leaking arteries, endoscopic ligation of backbleeding inferior mesenteric artery or lumbar arteries, new stent grafts, cuffs or extensions covering modular or anastomotic leakage, open surgery. • Migration. One important factor causing migration is the spontaneous widening of the aortic neck over time. Migration can lead to a type I endoleak. Using stents with hooks and barbs this is a decreasing problem. Loosening of the proximal fixation may be solved with a new stent but when there is total loss of fixation, open surgery is required. • Graft limb occlusion can have several causes and represents varying degrees of emergency. The highest risk is seen with unsupported grafts. With this background there are many potential solutions: thrombolysis or thrombectomy followed by correction of the morphological cause, again with endovascular or open surgi-
References
cal procedures. Surgical thrombectomy may be less attractive because of risk of dislodging the graft. • Aneurysmal rupture often needs open surgical reconstruction, but the course is rarely as dramatic as with primary rupture. Risk of rupture has been estimated to around 1–1.5% per year. With new generation devices there seems to have been a decreasing trend in risk of rupture. An updated review on complications of endovascular aneurysm repair and how to manage them has recently been published [1].
References 1. Eskandari MK, Matsumura JS (2004) Complications of endovascular aortic aneurysm repair: significance and management. Semin Vasc Surg 17:261 2. Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson SG (2004) Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomised controlled trial. Lancet 364:843–848 3. Thompson JF, Mullee MA, Bell PR, Campbell WB, Chant AD, Darke SG, et al (1996) Intraoperative heparinisation, blood loss and myocardial infarction during aortic aneurysm surgery: a Joint Vascular Research Group study. Eur J Vasc Endovasc Surg 12:86–90
329
331
5.3 Inflammatory Aneurysms of the Abdominal Aorta A. Nevelsteen, K. Daenens, I. Fourneau
5.3.1 Introduction • The indications of abdominal aortic aneurysm repair have been well defined in the UK Small Aneurysm Trial [52]. • Elective reconstruction can be offered with an acceptable morbidity and mortality rate. • Occasionally however, the vascular surgeon is confronted with certain pathological or anatomical variants, which may increase the risk of the operation. • In this chapter a distinct pathological and anatomical entity is described, namely the inflammatory aneurysm of the abdominal aorta, which is characterized by a very thick wall and a dense fibrotic reaction enveloping the aneurysm and the surrounding structures, leading to ureteral and even caval vein obstruction in a significant percentage of the cases.
improved markedly after the operation and an intravenous pyelogram (IVP) at 2 months was normal. In 1972, Walker et al. [59] presented a landmark paper where they described their experience in 19 patients with this kind of disease, representing 10% of their total series of abdominal aortic aneurysms. Rupture was noted in three patients and the overall operative mortality rate was 19%. They emphasized the hazards of separating adjacent retroperitoneal structures from their surfaces and were the first to coin the term “inflammatory aneurysm”. This historical paper was soon followed by numerous other observations [19, 37, 43]. Therefore, inflammatory abdominal aneurysm emerged as a distinct clinical and pathological entity describing these aneurysms characterized by a very thick wall as they are encased by an excessive, whitish hard fibrotic inflammatory mass (“porcelain aneurysm”), creating dense adhesions to adjacent structures and eventually involving the ureters and/or the caval vein (Figs. 5.3.1, 5.3.2).
5.3.2 Definition James reported in 1935 on a patient dying of uraemia secondary to obstruction of both ureters in an inflammatory reaction around a large abdominal aortic aneurysm [27]. In 1955, DeWeerd et al. treated a patient with bilateral ureteral obstruction, severe hydronephrosis and a large abdominal aortic aneurysm [14]. The aneurysm was left alone and the ureteral obstruction was handled by bilateral nephrostomy followed by bilateral ureterolysis. They reported good renal function and patient survival at 15 months postoperatively. A few months later, Shumacker and Garrett [44] managed a similar patient by combined aneurysm replacement and ureterolysis. The patient had a 10-cm aortic aneurysm involving both common iliac arteries, which was replaced by a bifurcation graft. At operation, they found that the jejunum and sigmoid colon was firmly adherent to a thick inflammatory mass that surrounded the aneurysm. The patient’s renal function
Fig. 5.3.1 Operative view demonstrating inflammatory aneurysm (porcelain aneurysm) with dense adhesions to the duodenum
332
5.3 Inflammatory Aneurysms of the Abdominal Aorta
Fig. 5.3.2 Operative view after incision of inflammatory aneurysm. Note the 15-mm-thick aortic wall (arrow)
5.3.3 Epidemiology • Inflammatory aneurysms are considered to be quite rare and their incidence in the literature varies between 1.1% and 9.5% of all aneurysms. • Crawford et al. [12] report an incidence of 1.1%, but he focused only on patients with acute symptoms. • Pennell et al. [38] from the Mayo Clinics described 127 cases in a series of 2816 patients undergoing repair for abdominal aortic aneurysms, giving an incidence of 4.5%. This is in agreement with a multicentre study in Sweden including 98 cases [31].
• Sterpetti et al. [47] documented an incidence of 6.2%, while the authors of this chapter published a series of 110 patients, out of a total of 1440 abdominal aortic aneurysms (7.6% incidence) [29]. • Ureteral involvement is noticed most frequently: the authors identified 23 patients (21%) with uni- or bilateral associated hydronephrosis [29]. Five of them presented with acute anuria and six with renal insufficiency (Fig. 5.3.3). This is confirmed by the reports of Sterpetti et al. [47] and Lindblad et al. [31], who also reported entrapment of the ureters in 20% and 19% of the patients, respectively. • Involvement of other adjacent organs is rarely mentioned. • Venous compression is reported anecdotally. Houle and Ellwood [26] described a patient with pitting oedema due to caval vein compression from an inflammatory aneurysm. Braxton et al. [8] mentioned bilateral lower extremity oedema as the presenting sign. The authors observed one patient with associated thrombosis of the caval vein [29]. This was also reported by Kashyap et al. [28]. • Duodenal problems occur even more rarely and are described as an isolated case by Torella et al. [54]. • Finally, the fibrotic process does not always limit itself to the infrarenal aorta. • Thoracic or thoracoabdominal inflammatory aneurysms have been mentioned by both Crawford et al. [12] and Pennell et al. [38]. • The first report on an inflammatory aneurysm of the ascending aorta was published in 1994 [11]. Since then another four cases have been described [42].
Fig. 5.3.3 Excretory urography: terminal hydronephrosis due to ureteral entrapment by inflammatory aneurysm
5.3.5 Symptoms
• More recently, Dorigo et al. [15] also documented an isolated inflammatory aneurysm of the superior mesenteric artery.
5.3.4 Aetiology The aetiology of inflammatory aortic aneurysms remains unknown. There are several theories and all have their own advocates. • Walker suggested a kind of reaction towards intraluminal thrombi [59]. • Subclinical retroperitoneal leakage of blood has been implied [21]. This hypothesis has been rejected because haemosiderin-laden macrophages are rarely found in the retroperitoneal fibrosis. Other historical hypotheses include: • Compression of lymphatic vessels with stasis, oedema and secondary fibrosis [32]. • Allergic reaction towards some medicaments such as methysergide [20].
5.3.4.1 Extension of Inflammation • Several specialists argue that the characteristic inflammatory process represents merely an extension of the inflammation observed in nonspecific (atherosclerotic) aneurysms [12]. • What has been documented very well indeed is that a chronic inflammatory infiltrate occupying the aortic adventitia occurs in both nonspecific and inflammatory aneurysms [41]. • The difference is found in the intensity and the extent of the process, which is much greater in inflammatory aneurysms. • Proponents of this theory stress the fact that the inflammatory process is always greatest at the site of the aneurysm and that the inflammation subsides in both the aneurysm wall and the retroperitoneal region following graft insertion [4]. • However, why some patients respond with a greater intensity and extent of this inflammatory process remains enigmatic. • An autoimmune reaction towards an insoluble oxidized lipoprotein (ceroid) in the atheromatous wall has been suggested but not definitely proved [33].
5.3.4.2 Infection • Tanaka et al. reported in 1992 a possible role of human cytomegalovirus in the pathogenesis of inflammatory aortic diseases [49]. • They also showed by means of DNA polymerase chain reaction that either herpes simplex virus or cytomegalovirus was present more frequently in inflammatory (29% or 86%, respectively) and atherosclerotic aneurysms (27% or 65%) than in normal aortic tissues (6% or 31%, respectively) [50]. • They suggested that the human herpes viruses might play various roles in the pathogenicity of aortic diseases, in particular that replicating infections of the cytomegalovirus might potentially cause the formation of inflammatory aneurysms.
5.3.4.3 Autoimmune Disease • Abdominal aortic aneurysms have been described in patients with various autoimmune diseases, but Haug et al. [22] were recently the first to show a higher incidence of autoimmune diseases in patients with inflammatory aneurysms compared with matched control subjects with noninflammatory aneurysm. • In a series of 31 patients with inflammatory aneurysms, 6 patients (19%) had an autoimmune disease compared with none of the control subjects (P=0.0017). • Three patients had rheumatoid arthritis, two patients had systemic lupus erythematosus and one had giant cell arteritis. • The relatively high incidence of autoimmune disease is in accordance with other reports showing a genetic risk determinant mapped to the human leukocyte antigen (HLA) molecule in patients with inflammatory aneurysms [39, 40]. • Further research however is necessary to explore whether inflammatory aneurysms might be a separate entity with a role of antigen binding in the origin of the disease.
5.3.5 Symptoms Most reports confirm that an inflammatory aneurysm is much more likely to be associated with clinical symptoms than nonspecific aneurysms. According to the literature,
333
334
5.3 Inflammatory Aneurysms of the Abdominal Aorta
as much as 80% of the patients have suffered from symptoms, particularly abdominal or back pain, prior to operation [29, 31, 38, 47]. This abdominal pain may be so striking that some authors state that an inflammatory aneurysm is characterized by severe abdominal pain in the absence of rupture [12]. In addition, approximately 20% of the patients experience a significant weight loss in the months prior to the diagnosis. Laboratory tests may show an elevated erythrocyte sedimentation rate in up to 90% of the patients [36], which makes: • The combination of abdominal pain, weight loss and elevated sedimentation rate quite characteristic of the presence of an inflammatory aneurysm [12]. • Colic pain might be the presenting symptom in cases of ureteral involvement and the combination of hydronephrosis and aortic aneurysm should alert the physician. • Venous hypertension at the lower limbs as a result of caval vein compression is rarely seen [8, 28].
5.3.5.1 Literature • In 1996 Nitecki et al. [36] presented a series of 29 consecutive patients with an inflammatory aneurysm, who were matched in a case-control fashion to a group of 58 patients with noninflammatory aneurysms. • The two groups had comparable characteristics of age, gender and cardiovascular risk factors.
• Patients with inflammatory aneurysms were significantly more symptomatic than those with noninflammatory aneurysms (93% vs. 9%, P<0.001), were more likely to have a family history of aneurysms (17% vs. 1.5%, P=0.007) and tended to be current smokers (45% vs. 24%, P=0.049). • An elevated erythrocyte sedimentation rate was documented in 89% of the inflammatory series, compared with only 11% in the noninflammatory series (P<0.00001). • In addition, inflammatory aneurysms were significantly larger than noninflammatory aneurysms at presentation (6.8 cm vs. 5.9 cm, P<0.05). • The same findings were reported in a second case– control study, presented by Bonamigo et al. [6].
5.3.5.2 Rupture • It has been said that patients with inflammatory aneurysms are well protected from rupture by the excessively thickened wall. • The posterolateral wall is however frequently not involved in the inflammation, and rupture (particularly at the posterior site) has been reported in 5–20% of the reported cases [31, 59] (Fig. 5.3.4). • The incidence in the authors’ own experience is 12% [29]. • In addition, there are indications that the risk of aortic fistula is higher in inflammatory aneurysms. • Tambyraja et al. [48] presented a series of 24 ruptured inflammatory aneurysms, which was compared with a contemporary series of 273 noninflammatory ruptured aneurysms. • The incidence of aortic fistula was 21% in the inflammatory group, versus 1% in the noninflammatory series. Eighty percent of the fistulas were to the caval vein and, according to Calligaro et al. [9], this reflects an increased predisposition for posterior rather than anterior rupture, as a result of anterior fibrosis and thickening.
5.3.6 Diagnosis
Fig. 5.3.4 Spiral CT indicating inflammatory aortic aneurysm with contained rupture at the posterior site (arrow)
• In earlier reports, inflammatory aneurysms were seen most frequently as an unpleasant surprise peri-operatively.
5.3.6 Diagnosis
Fig. 5.3.5a,b Excretory urography: a medial deviation of the ureters in the case of an inflammatory aneurysm; b lateral ureteral deviation by nonspecific aneurysm
• In the series of Pennell, the diagnosis was made preoperatively in only 21 patients (16.5%) [38]. Thanks to increased familiarity and better imaging techniques, this has increased in recent series to nearly 90%. • Clinical symptoms can point in the direction of inflammatory aneurysms, but a definite diagnosis can only be made with technical examinations, and spiral CT scan is the reference. • Plain abdominal X-ray and angiography might indicate at best the presence of aneurysm but do not add to the exact diagnosis. • Excretory urography was used in older studies and might indicate medial deviation of the ureters or ureteral obstruction, which is suggestive for the diagnosis in around 30% of cases [12] (Fig. 5.3.5).
5.3.6.1 Recommended European Standard Diagnostic Steps of Investigation Ultrasonography • Ultrasonography has been advocated since it might show a sonolucent halo anteriorly and laterally with clear definition of the aortic wall posterior to this [23]. • Pennell [38] reported that preoperative diagnosis with ultrasound was possible in 13.5% of cases. • A retrospective review of the ultrasounds revealed diagnostic findings of inflammatory aneurysm in 60% of the sonograms, indicating the importance of familiarity with and awareness of this condition.
Spiral CT • Spiral CT is the examination of choice in the preoperative diagnosis of inflammatory aneurysms. • Although the sensitivity and the specificity of CT scan was relatively low in earlier studies, this has increased,
335
336
5.3 Inflammatory Aneurysms of the Abdominal Aorta
Fig. 5.3.6 Spiral CT scan demonstrating the characteristic four layers of an inflammatory aneurysm
•
•
• •
•
•
after the reports of Vint [57] and the introduction of spiral CT scan, to well over 90%. The typical image of an inflammatory aneurysm is composed of four layers: i. the lumen of the aorta ii. the surrounding thrombus that is not enhanced with intravenous contrast iii. the calcified aortic wall and iv. most important, a para-aortic retroperitoneal soft tissue mass that can be enhanced by intravenous contrast (Fig. 5.3.6). Intravenous contrast is essential in order to avoid confusion with a leaking aneurysm and a retroperitoneal haematoma [1]. CT scan has a lot of advantages: it is minimally invasive and it provides the correct diagnosis. It will show the extent of peri-aortic fibrosis. This is most frequently limited to the infrarenal aorta and the common iliac arteries, but sometimes it extends well above the renal arteries. In addition, CT is capable of demonstrating ureteral entrapment, hydronephrosis, concomitant involvement of the caval vein and surrounding structures. Nevertheless, familiarity with and awareness of the pathology remain crucial. Even over the last 2 years, the authors of this chapter admitted two patients after exploratory operation elsewhere. The operation was abandoned because of “unsuspected” findings of periaortic fibrosis and exposure difficulties, which in retrospect was clearly shown on the preoperative CT.
5.3.7 Therapy • Although the rate of rupture of inflammatory aneurysms is still debated, there is general agreement that inflammatory aneurysms should be handled the same way as nonspecific aneurysms [16, 24]. • Corticosteroids have been shown to be effective in reducing the retroperitoneal fibrosis [4], but they do not alter the evolution of the aneurysm itself. • Most specialists have also abandoned the preoperative use of corticosteroid therapy, because if it really reduces the peri-aortic fibrous reaction, it might also elevate the tendency to rupture [47].
5.3.7.1 Surgery • The peri-aortic fibrosis and the dense adhesions to adjacent organs turn surgery for inflammatory aneurysms into a technical challenge. • In early experiences, surgeons attempted extensive adhesiolysis of the peri-aneurysmal adhesions, which resulted in catastrophic complications. The operation was abandoned quite frequently and the patients were deemed inoperable. • Of the 30 patients presented by Crawford et al. [12], 10 had undergone previous exploratory operation elsewhere.
5.3.7 Therapy
• In the authors’ experience, presented in 1997, the incidence was still 3% [29].
Technical Aspects In 1978, Goldstone et al. [19] described the importance of a modified surgical approach to the inflammatory aneurysm, which remains the gold standard, even today. These modifications include: • Minimal dissection of tissues adjacent to the aneurysm.
• Clamping of the aorta well above the duodenum – liberal use of supracoeliac clamping. • Minimal dissection to obtain distal control – use of occlusion balloon catheter instead of clamping. • Graft insertion with the inclusion technique. As advocated by Fiorani et al. [17] and Todd and DeRose [53], the authors of this chapter also favour the left extraperitoneal approach. On CT it is indeed clear that the amount of fibrosis is frequently far less pronounced on the left posterolateral aspect of the aneurysm than on the anterior wall (Fig. 5.3.7). Therefore, a retroperitoneal approach will facilitate dissection and clamping
Fig. 5.3.7a,b Inflammatory aneurysm: spiral CT (a) shows peri-aortic fibrosis (arrow) predominantly located at the right side. Patient was successfully operated on by the left retroperitoneal approach despite the presence of the left caval vein (b)
337
338
5.3 Inflammatory Aneurysms of the Abdominal Aorta
of the aorta. Problems with adjacent organs, particularly the duodenum, are also less likely. A disadvantage of this approach might be that reconstruction of the right iliac artery can be quite difficult. However, in the rare case that tunnelling of the graft is impossible, this can be solved by a crossover graft.
in 14 patients, resulted in the disappearance of hydronephrosis and stabilization or improvement of renal function. • The conclusion was that inflammatory aneurysms involving the ureters and compressing the urinary structures respond well to aneurysmal resection only without a urological procedure.
Mortality Postoperative Retroperitoneal Fibrosis • With these techniques, Crawford et al. [12] reported an operative mortality rate of 3%. • Pennell et al. [38] reviewed a 30-year experience with surgery for inflammatory aneurysms and showed that the operative mortality rate improved in each decade: from 1955 to 1964 the operative mortality rate was 12.5%; from 1965 to 1974, 8.3%; and from 1975 to 1984 it decreased further to 4.2%. • The mortality rate for elective reconstruction in our experience before 1997 was 5.1% [29]. • This has decreased to 3.5% in recent years, indicating that the actual mortality rates are identical or very close to those encountered in the repair of atherosclerotic aneurysms.
Ureteral Involvement • There is still no consensus regarding treatment of concomitant ureteral obstruction. • Most surgeons have left extensive surgical ureterolysis. • Some advocate ureteral stenting while others propose no treatment at all [12]. • The authors have performed ureterolysis on 21 occasions in 14 patients [29]. Normal function was observed in 18 and restenosis in 3 ureters. Eight patients for a total of 11 ureters were handled by simple ureteral stenting. The stents were removed between 3 and 6 months postoperatively and normal function was observed in ten cases. • Arroyo et al. [2] subsequently confirmed the efficiency of simple ureteral stenting. • On the other hand, both Crawford et al. [12] and Pennell et al. [38] reported excellent results without any treatment at all. • Speziale et al. [45] presented in 2001 a series of 19 patients with inflammatory aneurysm and concomitant hydronephrosis. Simple aneurysmectomy, performed
• The postoperative course of the retroperitoneal fibrosis remains another point of controversy. • It is traditionally stated in older studies that the fibrosis virtually always subsides after open surgery [12, 38]. • This has however been challenged by more recently reported CT observations. • Stella reported in 1993 on a series of 19 patients who were assessed by CT scan preoperatively and postoperatively [46]. Complete postoperative regression was observed in nine cases (47.3%), partial regression in four (21%) while stable lesions was observed in the remaining six patients (31.7%). • When related to the histological findings, it appeared that complete regression was observed when high cell density and a cell:fibrosis ratio >1 was found. In contrast, little or no regression occurred when a low cell density and a cell:fibrosis ratio <1 was found. • These data were subsequently confirmed by Von Fritschen et al. [58]. These investigators indicated complete regression in only 23% of the patients, partial regression in 35%, stable fibrosis in 38% but also progression of peri-aortic fibrosis in 4% (1 patient). • So it seems that the postoperative evolution of the peri-aortic fibrosis is not always as benign as previously described [5, 18, 36].
5.3.7.2 Endovascular Treatment • As is the case for nonspecific aneurysms, endovascular repair might represent an attractive alternative treatment for inflammatory aneurysms, particularly taking into account the technical difficulties encountered during open surgery.
5.3.7 Therapy
Literature • The first experience of the authors of this chapter was published in 1999 [34]. It concerned a 64-yearold male who presented with anuria due to bilateral ureteral entrapment in the presence of an inflammatory aneurysm. He was handled by bilateral ureteral stenting and insertion of a Stentor (Min Tec, Freeport, Bahamas) endoprosthesis. Postoperatively, there was regression of the peri-aortic fibrosis and the ureteral stents were removed at 6 months. Actually the patient is alive and doing fine. • The authors’ experience was updated in 2002 and 2003 [13, 35] and actually we have a series of 10 patients. These patients received different kinds of endografts and the technical success rate was 100%. The mean fol-
low-up is now more than 36 months: all patients are alive and there were two graft-related complications. One patient developed claudication because of graft limb stenosis, while another one presented with unilateral graft limb thrombosis, 26 months after repair. • Lange et al. [30] reviewed the experience as reported in the Eurostar database. They compared 52 cases of inflammatory aneurysms to 4236 patients with nonspecific aneurysms. Patients in the inflammatory group tended to be younger (P<0.05) and there were more current smokers. Hypertension and cardiopulmonary disease was seen less frequently (P<0.05). There were no differences with regard to early technical success, postoperative mortality or early conversion. Cumulative outcome rates at 3 years also showed no differences between the two groups.
Fig. 5.3.8a,b Inflammatory aneurysm: preoperative spiral CT (a): patient was admitted with anuria due to bilateral ureter entrapment. Treatment consisted of bilateral ureteral stent and endovascular aneurysm repair, resulting in regression of peri-aortic fibrosis. Ureteral stents were removed after 6 months. Spiral CT at 6 years (b) shows partial aneurysm reduction and virtually complete regression of peri-aortic fibrosis (maximum aneurysm diameter not shown)
339
340
5.3 Inflammatory Aneurysms of the Abdominal Aorta
Fig. 5.3.9a,b Inflammatory aneurysm. a Preoperative CT scan – no hydronephrosis. Treatment consisted of endografting. b Postoperative CT scan at 6 months: no regression of peri-aortic fibrosis and development of left hydronephrosis (arrow)
Peri-aortic Fibrosis and Renal Consequences • Despite these results, there remains concern with regard to the evolution of the peri-aortic fibrosis and the renal consequences. • Hinchliffe et al. [25] observed no progression of retroperitoneal fibrosis and no renal complications in a series of 14 patients. • Based on CT, the authors noticed postoperative progression in 20% of the patients; complete or partial regression was also noted in 20% each, while the periaortic fibrosis did not change in 40% of the patients. • In the authors’ series, five patients had concomitant hydronephrosis (unilateral n=2; bilateral n=3). Treatment consisted of ureteral stenting in seven occasions and hydronephrosis could be cured in four cases (57%) (Fig. 5.3.8). Two patients (three ureters – 43%) still have a ureteral stent in place after 5 and 6 years, respectively. Finally one patient did not receive a stent and the hydronephrosis persists after 3 years. In addi-
•
• • •
tion, two patients developed unilateral hydronephrosis during follow-up while another one underwent a unilateral nephrectomy (Fig. 5.3.9). Review of the literature with regard to the evolution of the peri-aortic fibrosis reveals data for a total of 33 patients [3, 7, 10, 25, 35, 51, 55, 56]: the fibrosis remained unchanged in 50% of the patients, complete or partial regression was noticed in 12.5% and 25%, respectively, while progression was seen in 12.5% of the cases. Ureteral entrapment is reported in the literature in 17 patients totalling 24 kidneys [7, 10, 25, 35, 51]. Resolution of hydronephrosis was observed in 50% of the cases. In addition, postoperative hydronephrosis was documented in 5 (33%) out of 15 patients without preoperative involvement [3, 25, 35, 55].
Based on these observations, it can only be concluded that endovascular repair of inflammatory aneurysms is feasible and safe from a technical point of view. The
References
patients however need to be followed carefully not only with regard to endograft complications but also with regard to the postoperative course of peri-aortic fibrosis and ureteral entrapment. At this moment the evolution of the peri-aortic fibrosis after endovascular repair seems difficult to predict. There are however indications that it might be even less favourable than after open repair. References 1. Aiello MR, Cohen WN (1980) Inflammatory aneurysm of the abdominal aorta. J Comput Assist Tomogr 4:265–267 2. Arroyo A, Rodriguez J, Port J et al (2003) Management and course of hydronephrosis secondary to inflammatory aneurysms of the abdominal aorta. Ann Vasc Surg 17:481–485 3. Barrett JA, Wells IP, Roobottom CA et al (2001) Progression of peri-aortic fibrosis despite endovascular repair of an inflammatory aneurysm. Eur J Vasc Endovasc Surg 21:567–568 4. Baskerville PA, Blakeny CG, Young AE et al (1983) The diagnosis and treatment of peri-aortic fibrosis (“inflammatory” aneurysms). Br J Surg 15:381–385 5. Bitsch M, Norgaard HH, Roder O et al (1997) Inflammatory aortic aneurysms: regression of fibrosis after aneurysm surgery. Eur J Vasc Endovasc Surg 13:371–374 6. Bonamigo TP, Bianco C, Becker M et al (2002) Inflammatory aneurysms of the infra-renal abdominal aorta. A case– control study. Minerva Cardioangiol 50:253–258 7. Boyle JR, Thompson MM, Nasim A et al (1997) Endovascular repair of an inflammatory aneurysm. Eur J Vasc Endovasc Surg 13:328–329 8. Braxton JH, Salander JM, Gomez ER et al (1990) Inflammatory abdominal aortic aneurysm masquerading as occlusion of the inferior vena cava. J Vasc Surg 12:527–530 9. Calligaro KD, Savarese RP, DeLaurentis DA (1990) Unusual aspects of aorto-venous fistulas associated with ruptured abdominal aortic aneurysms. J Vasc Surg 12:586–590 10. Chuter T, Ivancev K, Malina M et al (1997) Inflammatory aneurysm treated by means of transfemoral endovascular graft insertion. J Vasc Interv Radiol 8:39–41 11. Connery CP, Descalzi ME, Kirshner R (1994) Inflammatory aneurysm of the ascending aorta: An unreported entity. J Cardiovasc Surg 35:33–34 12. Crawford JL, Stowe CL, Safi HJ et al (1985) Inflammatory aneurysms of the aorta. J Vasc Surg 2:113–124 13. Deleersnijder R, Daenens K, Fourneau I et al (2002) Endovascular repair of abdominal aortic aneurysms with special reference to concomitant ureteric obstruction. Eur J Vasc Endovasc Surg 24:146–149
14. DeWeerd JH, Ringer Jr MG, Pool TL et al (1955) Aortic aneurysm causing bilateral ureteral obstruction: report of a case. J Urol 74:78–81 15. Dorigo W, Pulli R, Innocenti AA et al (2004) Isolated inflammatory aneurysm of superior mesenteric artery: unexpected pathologic diagnosis. J Vasc Surg 39:903–905 16. Fiorani P, Bondanini S, Faraglia V et al (1986) Clinical and therapeutical evaluations of inflammatory aneurysms of the abdominal aorta. Int Angiol 5:49–53 17. Fiorani P, Faraglia V, Speziale F et al (1991) Extraperitoneal approach for repair of inflammatory abdominal aortic aneurysm. J Vasc Surg 13:692–697 18. Gigoni R, Borashi P, Cartei F et al (1996) Inflammatory aneurysm of the abdominal aorta: CT assessment of the postoperative course. Radiol Med (Torino) 92:213–217 19. Goldstone J, Malone JM, Moore WS (1978) Inflammatory aneurysms of the abdominal aorta. Surgery 83:425–430 20. Graham JR (1964) Methysergide for prevention of headache: experience in five hundred patients over three years. New Engl J Med 270:67–72 21. Hackett E (1958) Idiopathic retroperitoneal fibrosis: a condition involving the ureters, the aorta and the inferior vena cava. Br J Surg 46:3–9 22. Haug ES, Skomsvoll JF, Jacobsen G et al (2003) Inflammatory aortic aneurysm is associated with increased incidence of autoimmune disease. J Vasc Surg 38:492–497 23. Henry LG, Doust B, Korns ME et al (1978) Abdominal aortic aneurysms and retroperitoneal fibrosis. Ultrasonic diagnosis and treatment. Arch Surg 113:1456–1460 24. Hill J, Charlesworth D (1988) Inflammatory abdominal aortic aneurysms: a report of thirty-seven cases. Ann Vasc Surg 2:352–357 25. Hinchliffe RJ, Macierewicz JA, Hopkinson BR (2002) Endovascular repair of inflammatory abdominal aortic aneurysms. J Endovasc Ther 9:277–281 26. Houle BJC, Ellwood RA (1982) Retroperitoneal fibrosis from aortic aneurysm causing vena cava obstruction: a case report. Angiology 33:64–66 27. James TGI (1935) Uremia due to aneurysm of the abdominal aorta. Br J Urol 7:157 28. Kashyap VS, Fang R, Fitzpatrick CM et al (2003) Caval and ureteral obstruction secondary to an inflammatory abdominal aortic aneurysm. J Vasc Surg 38:1416–1421 29. Lacquet JP, Lacroix H, Nevelsteen A (1997) Inflammatory abdominal aortic aneurysms. A retrospective study of 110 cases. Acta Chir Belg 97:286–292 30. Lange C, Hobo R, Myhre HO et al (2004) Results of endovascular repair of inflammatory aneurysms. XVIII Annual Meeting of the European Society for Vascular Surgery, Innsbruck, Austria
341
342
5.3 Inflammatory Aneurysms of the Abdominal Aorta
31. Lindblad B, Almgren B, Bergqvist D et al (1991) Abdominal aortic aneurysm with perianeurysmal fibrosis: experience from 11 Swedish vascular centers. J Vasc Surg 13:231–239 32. Mathisen W, Holta AL (1966) Idiopathic retroperitoneal fibrosis. Surg Gynecol Obstet 122:1278–1282 33. Mitchinson MJ (1986) Retroperitoneal fibrosis revisited. Arch Pathol Lab Med 110:784–786 34. Nevelsteen A, Lacroix H, Stockx L et al (1999) Inflammatory abdominal aortic aneurysm and bilateral complete ureteral obstruction: treatment by endovascular graft and bilateral ureteric stenting. Ann Vasc Surg 13:222–224 35. Nevelsteen A, Maleux G, Daenens K et al (2003) Inflammatory aneurysms: are they a good indication for endovascular for endovascular reconstruction? In: Becquemin JP, Loisance D, Watelet J (eds) Controversies and update in vascular and cardiovascular surgery. Edizioni Minerva Medica, Turin, pp 68–73 36. Nitecki SS, Hallett JW, Stanson AW et al (1996) Inflammatory abdominal aortic aneurysms: a case–control study. J Vasc Surg 23:860–869 37. Olcott IV C, Holcroft JW, Stoney RJ et al (1978) Unusual problems of abdominal aortic aneurysms. Am J Surg 135:426–431 38. Pennell RC, Hollier LH, Lie JT et al (1985) Inflammatory abdominal aortic aneurysms: a thirty-year review. J Vasc Surg 2:859–869 39. Rasmussen TE, Hallett JW, Metzger RLM (1997) Genetic risk factors in inflammatory abdominal aortic aneurysms: polymorphic residue 70 in the HLA-DR B1 gene as a key genetic element. J Vasc Surg 25:356–364 40. Rasmussen TE, Hallett JW, Schulte S et al (2001) Genetic similarity in inflammatory and degenerative abdominal aortic aneurysms: a study of human leukocyte antigen class II risk genes. J Vasc Surg 34:84–89 41. Rose AG, Dent DM (1981) Inflammatory variant of abdominal atherosclerotic aneurysm. Arch Pathol Lab Med 105:409–413 42. Roth M, Schonburg M, Klovekorn WP et al (2001) Inflammatory aneurysm of the ascending aorta. Eur J Cardiothorac Surg 19:214 43. Sethia B, Darke SG (1983) Abdominal aortic aneurysm with retroperitoneal fibrosis and ureteric entrapment. Br J Surg 70:434–436 44. Shumacker HB Jr, Garrett R (1955) Obstructive uropathy from abdominal aortic aneurysm. Surg Gynecol Obstet 100:458–761
45. Speziale F, Sbarigia E, Grossi R et al (2001) Inflammatory aneurysm of the abdominal aorta involving the ureters: is combined treatment really necessary? J Urol 165:27–31 46. Stella A, Gargioulo M, Faggioli GL et al (1993) Postoperative course of inflammatory abdominal aortic aneurysms. Ann Vasc Surg 7:229–238 47. Sterpetti AV, Hunter WJ, Feldhaus RJ et al (1989) Inflammatory aneurysms of the abdominal aorta: incidence, pathologic and etiologic considerations. J Vasc Surg 9:643–650 48. Tambyraja AL, Murie JA, Chalmers RTA (2004) Ruptured inflammatory abdominal aortic aneurysms: insights on clinical management and outcome. J Vasc Surg 39:400–403 49. Tanaka S, Toh Y, Mori R et al (1992) Possible role of cytomegalovirus in the pathogenesis of inflammatory aortic diseases. J Vasc Surg 16:274–279 50. Tanaka S, Komori K, Okadome K et al (1994) Detection of active cytomegalovirus infection in inflammatory aneurysms with RNA polymerase chain reaction. J Vasc Surg 20:235–243 51. Teruya TH, Abou-Zamzam AM, Ballard JL (2001) Inflammatory abdominal aortic aneurysm treated by endovascular stent grafting: a case report. Vasc Surg 35:391–395 52. The UK Small Aneurysm Trial Participants (1998) Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet 21:1949–1655 53. Todd GJ, DeRose JJ (1995) Retroperitoneal approach for repair of inflammatory aneurysms. Ann Vasc Surg 9:525–534 54. Torella M, De Santo LS, Della Corte A et al (2003) Extensive retroperitoneal fibrosis with duodenal and ureteral obstruction associated with giant inflammatory aneurysm of abdominal aorta. Tex Heart Inst J 30:311–313 55. Vallabhaneni SR, McWilliams RG, Anbarasu A et al (2001) Peri-aneurysmal fibrosis: a relative contra-indication to endovascular repair. Eur J Vasc Endovasc Surg 22:535–541 56. Villareal RP, Howell MH, Krajcer Z (2000) Regression of inflammatory abdominal aortic aneurysm. Tex Heart Inst J 27:146–149 57. Vint VC (1980) Aortic perianeurysmal fibrosis: CT density enhancement and ureteral obstruction. AJR 134:570–580 58. Von Fritschen U, Malzfeld E, Clasen A et al (1999) Inflammatory abdominal aortic aneurysm: a postoperative course of retroperitoneal fibrosis. J Vasc Surg 30:1090–1098 59. Walker DI, Bloor K, Williams G et al (1972) Inflammatory aneurysms of the abdominal aorta. Br J Surg 59:609–614
343
5.4 Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms Kiriakos Ktenidis, Stefan Schulte, Dimitrios Kiskinis, Svante Horsch
5.4.1 Introduction Aortic aneurysms and treatment thereof continue to challenge the vascular surgeon. The natural history of aneurysms has been well documented, and the indication for treatment extensively discussed [56]. The goal of treatment is to prevent aneurysm rupture and distal embolization. It is well known that aneurysm size is the most important criterion determining the main risk, namely rupture. Arterial hypertension is the second most important parameter that influences this risk, according to Laplace’s law (tension on the wall is produced by the product of pressure and radius). As experience has accumulated, the durability of open surgical therapy, which was introduced over 50 years ago, has also been well documented [29]. In contrast, there are very few data on the long-term durability of endovascular aneurysm repair (EVAR), which was introduced as a new approach about 15 years ago [45]. Indeed major advances in EVAR have been made. It is understood that the key to successful stent grafting with durable results is careful patient selection based on clearly defined anatomical parameters. Without doubt, vascular anatomy and morphology determine EVAR suitability and the graft configuration that promises to give the best possible result for the patient [13, 14, 23, 32, 38, 46]. In daily practice, it is not uncommon to have aneurysm patients with difficult anatomy and morphology, which mainly includes short aneurysm neck, conical necks, thrombus at the sealing zone, as well as elongated and calcified pathoanatomy. These cases represent technically challenging cases for endovascular repair. In addition, aortic aneurysms that involve the supra-aortic arteries or the visceral arteries are per se difficult and challenging for the application of endovascular therapy. Other challenging cases include patients with aorto-oesophageal, bronchial or aorto-enteric fistulas, inflammatory or mycotic aortic aneurysms and abdominal aortic aneurysm (AAA) associated with horseshoe kidney. In all these cases the
EVAR procedure is frequently associated with intra- and post-procedural problems and, if EVAR is not avoidable, special considerations must be made in order to avoid severe or catastrophic complications for the patient.
5.4.2 Universally Challenging Situations 5.4.2.1 Vascular Access Morphology Vascular access problem is a primary consideration in the decision to treat aortic aneurysms endoluminally. The inaccessibility of the aorto-iliac axis is one of the main technical limitation factors for EVAR, more frequent for thoracic than for AAAs. For the thoracic aorta, currently available endografts have an inner diameter of between 20 and 24 French (Fr) and an outer diameter of 22–26 Fr. Considering that 1 mm is equivalent to 3 Fr, the usual delivery system has an outer diameter of 7–9 mm and needs analogous-sized access arteries [15, 26, 35]. Therefore, vascular access assessment must be carefully performed preoperatively by means of detailed anatomical studies based on spiral CT with 3D reconstruction (Fig. 5.4.1). If necessary, special vascular access must be anticipated using prosthetic conduits inserted in the common iliac artery and infrarenal aorta. Some authors propose that, in very special cases, the access could be gained through the descending aorta (thorascopically assisted), the ascending aorta (via thoracotomy) or directly through the common carotid artery [7, 12, 16]. In cases of elongated and/or calcified access arteries, the kink resistance and flexibility of the delivery system play an eminent role in facilitating insertion [35, 40].
5.4.2.2 Aortic Aneurysm Configuration Many patients may remain unsuitable for EVAR on the basis of their having an unfavourable aortic aneurysm
344
5.4 Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms
Fig. 5.4.1 This 3D reconstruction of the aorta and iliac arteries was performed on a patient with a thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm (AAA). Despite bilaterally palpable femoral pulses, the accessibility to the thoracic aorta is significantly reduced by the elongated iliac arteries
configuration. Inadequate aneurysm neck is a common cause for EVAR rejection. On the other hand, the neck is a key factor for successful application of EVAR and is responsible for endograft fixation and sealing of the aneurysmal sac. The measurement of neck length and diameter must be calculated exactly, and the evaluation of morphology is equally important.
Aneurysm Neck Diameter In general, the diameter of the implanted graft has to be bigger than the real aortic neck diameter in order to achieve sufficient fixation at the attachment zone. For most systems the upsizing of the stent graft is such that it has to be 10–15 % greater than the outer wall-to-outer wall diameter for thoracic and AAAs. Upsizing in the
treatment of aortic dissection is less important and currently not recommended to exceed 10% [2, 3, 17, 18, 21]. Aneurysms with a large aortic neck diameter [> 28 for AAA or > 38 mm for thoracic aortic aneurysm (TAA)] may continue to enlarge despite primary sufficient sealing at the landing zone, but this is not clear because it is difficult to find out whether the aortic wall in this position is stable or aneurysmal [6]. The endografting of TAAs with commercially available stent grafts is only possible in patients with an aortic neck diameter of between 30 and 40 mm [36].
Aneurysm Neck Length In order to establish adequate proximal fixation, the proximal aortic neck length is an important parameter
5.4.2 Universally Challenging Situations
that determines the long-term result at the sealing zones. The minimum length accepted for most EVAR applicants is over 15 mm for AAA and 20 mm for TAA [36, 39].
Angulated Aneurysm Neck The angulated aneurysm neck is an essential parameter that directly influences accurate graft deployment at the proximal landing zone. However, if it is also short, thrombosed or calcified, an angulated neck may influence whether there is sufficient sealing of the aneurysm sac and stent graft fixation during the long-term followup. The degree of aortic arch angulation is also an important anatomical feature that has to be considered when selecting patients for graft surgery [13, 14, 23, 46]. In the thoracic aortic position, severe neck angulation is a challenge independent of the other neck characteristics. In an angulated aortic arch, it is difficult to insert the delivery system and special modifications and tricks have to be used in order to facilitate the insertion. The use of an extra stiff guidewire, which builds a loop inside the ascending aorta, is the standard technique for placing the delivery system into a mild or moderately elongated aortic arch. The through-and-through brachial wire technique is more efficient for inserting the sheath into an extremely angulated aortic arch. Flexible sheaths and graft are made and help to achieve successful graft deployment in this position. Pre-curved sheaths are very useful for patients with severe aortic arch angulation [23, 40, 46]. Regarding AAAs, the incidence and prevalence of aortic neck angulation depend on its definition. According to Carpenter [13] angulations are classified in three categories: (1) less then 30°, (2) 30–60° and (3) greater than 60°. Mild angulations (<30°) are frequent in AAA patients, while
Fig. 5.4.2 Angulated neck in axial CT scan and in 3D reconstruction format
moderate angulations (30–60°) are described in 25% of patients with AAA [13, 54]. Severe angulations (>60°) at the aortic neck are present in less than 10% of AAA cases (Fig. 5.4.2). In these cases, Carpenter recommends open repair surgery as long as the patients are medically fit. In any case EVAR for such patients demands a long neck length and endograft with suprarenal fixation and high radial force [13].
Conical Aneurysm Neck A further morphological parameter that is a challenge for EVAR is a conical neck. The definition of conical aortic neck differs greatly, from the very simple Blum’s definition (cone-shaped, divergent walls from proximal to distal) to the very sophisticated Albertini’s “neck coefficient”, which is calculated by the following formula: D=arctan [(D3–D1)/l]·180/π, where D is the diameter and l is neck length [8]. The conical aortic neck is a challenge to all aspects of EVAR, which is contraindicated if there are other negative morphological parameters of the aneurysm neck [8, 41, 54]. Balloon-expandable stent grafts, such as the Edwards Lifepath® Stentgraft System (no longer commercially available), have been used successfully in such cases [49], while stent grafts such as the Endologix PowerLink® System and the Cook Zenith® Trifab System, which combine suprarenal fixation and axial stabilization sitting on the bifurcation, may be used as an alternative in those patients unfit for surgery.
Calcified Stenotic Aneurysm Neck Calcifications and stenotic lesions at the proximal and distal landing zone are particular considerations for device selection and upsizing. These are commonly associated with thrombus, and/or elongations, and therefore a challenging situation for EVAR [48]. As an additional problem, stenotic lesion in the iliac axis may provide access difficulties. For adequate fixation in a stenotic aneurysm neck, stent grafts with a high radial force are recommended in order to resist the recoil effect [10]. Balloon-expandable stent grafts such as the Lifepath® system used to be used successfully in such cases [48]. Today, in the era of self-expandable stent graft systems, EVAR for such cases must include modelling of the stent graft with high-pressure balloons or additional implantation of Palmaz stents in the stenotic neck area. In cases of bilateral aorto-iliac lesions the kissing balloon or kissing stent
345
346
5.4 Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms
Fig. 5.4.3 Due to the challenging anatomy localized on the right iliac axis, aorto-uniiliac endografting and crossover by-pass procedures are required. Occluder implantation in the right common iliac artery is shown
technique must be considered [48]. Aorto-uniiliac grafts are uniquely suited in cases of challenging anatomy at the aortic bifurcation (too short to anchor the tube graft and too narrow to accommodate the limbs) and/or one of the iliac arteries (occluded, stenosed or/and kinked) (Fig. 5.4.3).
Elongated Aortic Aneurysms Aortic aneurysms are frequently associated with severe elongations and angulations. In these cases the endovascular devices are not easy to push upwards and to handle during the deployment. Intra- and post-procedural problems are not rare. The curved delivery system is under tension and graft deployment may be problematic [11, 39, 40]. This usually arises in aortic arch or descending aortic aneurysms that have c- or s-shaped elongations (Fig. 5.4.4). This occurrence is further worsened if the
stent graft is deployed by the pull-back technique such as in Medtronic Talent®, Endomed Endofit® and Cook TX1/ TX2® stent graft systems. The use of flexible and kink-resistant devices with a long profile tip is essential. Some authors recommend heating the stiff dilatators (Endofit® stent graft system) in boiling water in order to make them more soft and flexible [40]. For the implantation of TAG/ Excluder® devices, there is no need to pass a sheath for descending aorta and aortic arch aneurysms (Fig. 5.4.4). Pre-curved devices are developed in order to make deployment of the graft easier in the aortic arch. The decrease of systemic blood pressure minimizes further the risk of intra-procedural dislocation [24, 25]. The use of stiff guidewires in various modifications is necessary and helps to neutralize some angulations or elongations, but increases the risk of distal embolization. Systemic heparinization and the careful use of catheter and guidewires are therefore very important for minimizing such risk [30]. If two stent grafts or more are necessary to cover
5.4.3 Special Challenging Situations
Fig. 5.4.4 This case demonstrates double descending aortic aneurysms (3D reconstruction) with s-shaped elongation. Only very flexible devices are able to treat such cases. An Excluder™ stent graft device was used and adequate exclusion of aneurysms was achieved
the aneurysmal area, disconnection of the graft during the follow-up can occur. Long overlap between the grafts placed using the trombone technique is recommended. A graft-to-graft overlapping zone of more 50 mm is the current recommendation [19, 35, 39].
5.4.3 Special Challenging Situations 5.4.3.1 The Case of Aortic Arch Aneurysm Aneurysms of the aortic arch and descending aorta involving the aortic arch are the most challenging EVAR application in the thoracic position. This difficult location is frequently associated with deployment problems caused by the curved configuration of the aorta and its high flow rate. In most cases it is necessary to carry out additional open surgical procedures [37, 57]. Extra-anatomic or intra-thoracic revascularization procedures are necessary if partial or complete covering of the aortic arch is planned (Fig. 5.4.5). Ostial coverage of the left subclavian artery (LSA) is frequent. The risks associated with LSA coverage are left arm ischaemia, vertebrobasilar insufficiency/stroke and type II endoleak via retrograde flow in the LSA [3]. The decision to cover the LSA ostium
remains controversial. While some specialists deem that covering is only indicated in emergency cases [2, 28, 51], others accept that routine covering is required in order to achieve sufficient graft fixation, and only see an indication for revascularization in symptomatic patients [3, 11, 19, 21, 31, 50]. LSA ostium coverage is absolutely contraindicated in left internal mammary artery (LIMA) bypass patients (after or planned), in haemodialysis patients and in patients with known arterial disease in the left upper extremity. Accidental over-stenting of the left carotid artery (LCA) and/or brachiocephalic artery (BCA) is rarely described and its incidence is between 1.5% and 2.0% in experienced endovascular centres [44, 53]. The risk of accidental coverage is increased in patients with a short neck combined with a very angulated aortic arch [2, 3, 19, 28, 31, 50, 51, 57].
5.4.3.2 The Case of Aortic Dissection The pathophysiology, management and prognosis of aortic dissection are different from those of aortic aneurysm. Untreated aortic dissection has a high mortality [4]. Recently, a consensus has evolved regarding the acceptable management of aortic dissections. For the acute Stanford type A dissection immediate surgery is recom-
347
348
5.4 Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms
Fig. 5.4.5a–f Endovascular aneurysm repair (EVAR) for TAA with involvement of supra-aortic arteries – hybrid management. a, b Intraoperative angiography before and after stent graft placement. c, d CT scan before and after stent graft placement. e, f 3D CT reconstruction 1 and 6 months (after subclavian artery transposition) after endografting
5.4.3 Special Challenging Situations
mended, whereas the management of acute Stanford type B dissection depends on its clinical manifestation [42]. Surgical intervention is only indicated in cases of impending rupture, visceral and lower limb ischaemia, therapy-resistant hypertension and continued pain [27]. EVAR has emerged as a less invasive alternative technique for the management of complicated aortic type B dissection. EVAR significantly reduces the morbidity and mortality rates in comparison to open repair [43]. The choice of stent graft is particularly important for patients with aortic dissection. It is recommended to implant stent grafts with high flexibility and low rigidity. Customized stent grafts should be used when covering up to 20 cm of the dissected aorta [33]. In order to avoid retrograde aortic dissection, the placement of stent grafts with bare stents, hooks and barbs should be avoided. The graft oversizing should not exceed 8–10 % of the aortic diameter. Retrograde dissections are reported in up to 10% of dissection patients after EVAR [39]. The placement of stent graft in the true lumen is not simple and demands transoesophageal echocardiography (TEE) monitoring and/
or intravascular ultrasonography (IVUS) application. If it does not occur spontaneously, sufficient refenestration of the false lumen percutaneously is technically challenging.
5.4.3.3 The Case of Aortic Bronchial and Enteric Fistula Aorto-bronchial and aorto-enteric fistulas are rare but serious complications, which can develop from an aneurysm of the descending thoracic or abdominal aorta. The leading symptom is haemorrhage into the target organ: bronchus (haemoptysis) or bowel (haematemesis, melena). Conventional surgery via thoracotomy or laparotomy is a risky procedure. EVAR of such potentially infected fistulas is an attractive alternative with excellent primary results (Fig. 5.4.6). Most authors postulate a good prognosis, but in cases of superinfection the risk of recurrence is increased; therefore, close surveillance of the patient is strongly recommended [1, 9, 52].
Fig. 5.4.6 EVAR for complicated aortic type B dissection (rupture of thoracic aorta, visceral and renal ischaemia, occlusion of right iliac axis) – hybrid management (figure continued on the following page)
349
350
5.4 Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms
Fig. 5.4.6 (continued) EVAR for complicated aortic type B dissection (rupture of thoracic aorta, visceral and renal ischaemia, occlusion of right iliac axis) – hybrid management
5.4.3.4 Other Challenging Cases for EVAR The introduction of fenestrated and branched grafts into clinical practice has overcome many of the problems associated with the most challenging aneurysm cases, namely thoraco-abdominal and suprarenal aortic aneurysms. Customization is absolute necessary for the successful application of fenestrated and branched grafts. This technique is a very promising solution, but until now the use of such grafts has been limited to a few centres for clinical evaluation [5, 34, 54, 58]. In the same way this technique
may provide a solution when aneurysmal disease has extended into the iliac bifurcation [55] and in AAA associated with horseshoe-shaped kidney (Fig. 5.4.7).
5.4.4 Conclusion A preoperative accurate assessment of aneurysm morphology is vital. It is estimated that the majority of aortic aneurysms are treatable with current endovascular tech-
References
Fig. 5.4.7 This case demonstrates an infrarenal aortic aneurysm in a patient with horseshoe-shaped kidney: 3D reconstruction and CTA imaging
nology. Adverse anatomical features are frequently present and increase the risk of postoperative complications. They are responsible for most of the unexpected and unforeseen intra-procedural challenges. Thoracic aortic aneurysms and dissections are commonly associated with challenging anatomical and morphological features and therefore need an experienced endovascular team with complete knowledge of the technology. For AAA an inadequate proximal aneurysm neck is the most common challenging factor and requires deployment of the graft as close as possible to the renal arteries and the use of stent graft systems with bare stents, hooks and barbs. Challenging anatomy localized on one iliac axis demands aorto-uniiliac endografting and a crossover by-pass procedure. In cases of involvement of supra-aortic arteries and visceral arteries in the aneurysmal area, fenestrated and branched grafts are a promising solution, but until now the use of such grafts has been limited to very few centres for clinical evaluation. Postoperative regular surveillance of endovascularly treated aneurysms is essential and absolutely unavoidable, particularly in cases of challenging anatomy.
References 1. Algaba Caldéron A, Jara Chinarro B, Abad Fernandez A, Isidoro Navarrete O, Ramos Martos A, Juretschke Moragues MA (2005) Recurrent hemoptysis secondary to an aortobronchial fistula. Arch Bronconeumol 41:352–354 2. Alric P, Berthet JP, Branchereau P, Veerapen R, Marty-Ane CH (2002) Endovascular repair for acute rupture of the descending thoracic aorta. J Endovasc Ther 9 [Suppl 2]: II51–II59 3. Alric P, Berthet JP, Branchereau P, Veerapen R, Albertin J, Marty-Ane C (2005) Aortic neck problems during EVAR. In: Branchereau A, Jacobs M (eds) Unexpected challenges in vascular surgery. Blackwell, Oxford, pp 73–85 4. Anagnostopoulos CE, Prabhakar MJ, Kittle CF (1972) Aortic dissections and dissecting aneurysms. Am J Cardiol 30:263–273 5. Anderson JL (2004) Fenestrated and branch aortic stent grafts. Endovasc Today Suppl, June, pp 3–6 6. Beebe HG (2003) Lessons learned from aortic aneurysm stent graft failure; observations from several perspectives. Semin Vasc Surg 16:129–138 7. Bernier PL, Turcotte R, Normand JP, Dagenais F (2004) Video-assisted mini-thoracotomy for thoracic stent-graft implantation: a novel vascular access for endovascular repair. Endovasc Ther 11:180–182
351
352
5.4 Technically Challenging Cases for Endovascular Repair of Aortic Aneurysms
8. Blum U, Hauer M, Pfammatter T, Voshage G (2001) Percutaneous endoprosthesis for treatment of aortic aneurysms. World J Surg 25:347–354 9. Bockler D, Schumacher H, Schwarzbach M, Ockert S, Rotert H, Allenberg JR (2004) Endoluminal stent-graft repair of aortobronchial fistulas: bridging or definitive long-term solution? J Endovasc Ther 11:41–48 10. Boyle JR, Thompson MM, Clode-Baker EG, Green J, Bolia A, Fishwick G, Bell PR (1998) Torsion and kinking of unsupported aortic endografts: treatment by endovascular intervention. J Endovasc Surg 5:216–221 11. Burks JA Jr, Faries PL, Gravereaux EC, Hollier LH, Marin ML (2002) Endovascular repair of thoracic aortic aneurysms: stent-graft fixation across the aortic arch vessels. Ann Vasc Surg 16:24–28 12. Buth J, Penn O, Tielbeek A, Mersman M (1998) Combined approach to stent-graft treatment of an aortic arch aneurysm. J Endovasc Surg 5:329–332 13. Carpenter JP (2003) EVAR in angulated neck. Endovasc Today Suppl, May/June, pp 4–7 14. Carpenter JP, Baum RA, Barker CF, Golden MA, Mitchell ME, Velazquez OC, Fairman RM (2001) Impact of exclusion criteria on patient selection for endovascular abdominal aortic aneurysm repair. J Vasc Surg 34:1050–1054 15. Chabbert V, Otal P, Bouchard L, Soula P, Van TT, Kos X, Meites G, Claude C, Joffre F, Rousseau H (2003) Midterm outcomes of thoracic aortic stent-grafts: complications and imaging techniques. J Endovasc Ther 10:494–504 16. Chuter TA, Schneider DB, Reilly LM, Lobo EP, Messina LM (2003) Modular branched stent graft for endovascular repair of aortic arch aneurysm and dissection. J Vasc Surg 38:859–863 17. Criado FJ, Barnatan MF, Rizk Y, Clark NS, Wang CF (2002) Technical strategies to expand stent-graft applicability in the aortic arch and proximal descending thoracic aorta. J Endovasc Ther 9 [Suppl 2]:II32–II38 18. Criado FJ, Clark NS, Barnatan MF (2002) Stent graft repair in the aortic arch and descending thoracic aorta: a 4-year experience. J Vasc Surg 36:1121–1128 19. Criado FJ, Abul-Khoudoud OR, Domer GS, McKendrick C, Zuzga M, Clark NS, Monaghan K, Barnatan MF (2005) Endovascular repair of the thoracic aorta: lessons learned. Ann Thorac Surg 80:857–863 20. Czerny M, Fleck T, Zimpfer D, Kilo J, Sandner D, Cejna M, Lammer J, Wolner E, Grabenwoger M (2003) Combined repair of an aortic arch aneurysm by sequential transposition of the supra-aortic branches and endovascular stent-graft placement. J Thorac Cardiovasc Surg 126:916–918
21. Dake MD (2001) Endovascular stent-graft management of thoracic aortic diseases. Eur J Radiol 39:42–49 22. Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP (1994) Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 331:1729–1734 23. Demers P, Miller DC, Mitchell RS, Kee ST, Sze D, Razavi MK, Dake MD (2004) Midterm results of endovascular repair of descending thoracic aortic aneurysms with first-generation stent grafts. J Thorac Cardiovasc Surg 127:664–673 24. Diethrich EB (1996) A safe, simple alternative for pressure reduction during aortic endograft deployment. J Endovasc Surg 3:275 25. Dorros G, Cohn JM (1996) Adenosine-induced transient cardiac asystole enhances precise deployment of stentgrafts in the thoracic or abdominal aorta. J Endovasc Surg 3:270–272 26. Doss M, Balzer J, Martens S, Fieguth HG, Vogl T, Moritz A, Wimmer-Greinecker G (2003) Emergent endovascular interventions for contained rupture of thoracic aortic aneurysms. Heart Surg Forum 6:E133–E137 27. Fann JI, Smith JA, Miller DC, Mitchell RS, Moore KA, Grunkemeier G, Stinson EB, Oyer PE, Reitz BA, Shumway NE (1995) Surgical management of aortic dissection during a 30-year period. Circulation 92 [Suppl 9]:II113–II1121 28. Grabenwoger M, Fleck T, Czerny M, Hutschala D, Ehrlich M, Schoder M, Lammer J, Wolner E (2003) Endovascular stent graft placement in patients with acute thoracic aortic syndromes. Eur J Cardiothorac Surg 23:788–793 29. Hallett JW Jr (1997) Back to the future of vascular surgery – why certain procedures become obsolete. J Vasc Surg 25:791–795 30. Hamilton G (2005) Distal embolisation during aneurismal surgery: from blue toe syndrome to fatal stroke. In: Branchereau A, Jacobs M (eds) Unexpected challenges in vascular surgery. Blackwell, Oxford (UK), pp 15–22 31. Hausegger KA, Oberwalder P, Tiesenhausen K, Tauss J, Stanger O, Schedlbauer P, Deutschmann H, Rigler B (2001) Intentional left subclavian artery occlusion by thoracic aortic stent-grafts without surgical transposition. J Endovasc Ther 8:472–476 32. Hinchliffe RJ, Hopkinson BR (2002) Endovascular repair of abdominal aortic aneurysm: current status. J R Coll Surg Edinb 47:523–527 33. Ince H, Rehders TC, Kische S, Petzsch M Nienaber CA (2005) Thoracic type B dissection: endovascular options. In: Greenhalgh RM (ed) Towards vascular and endovascular consensus. BIBA, London, pp 118–126
References
34. Inoue K, Hosokawa H, Iwase T, Sato M, Yoshida Y, Ueno K, Tsubokawa A, Tanaka A, Tamaki S, Suzuki T (1999) Aortic arch reconstruction by transluminally placed endovascular branched stent graft. Circulation 100 [Suppl 19]: II316–II321 35. Ivancev K (2004) Descending thoracic endovascular grafting into 2005. Endovasc Today Suppl, June, pp 15–17 36. Ivancev K, Vallabhaneni SR, Dias NV, Malina M, Sonesson B (2005) Atherosclerotic descending thoracic aneurysms: endovascular option. In: Greenhalgh RM (ed) Towards vascular and endovascular consensus. BIBA, London, pp 139–144 37. Kato N, Shimono T, Hirano T, Mizumoto T, Ishida M, Fujii H, Yada I, Takeda K (2002) Aortic arch aneurysms: treatment with extra-anatomical bypass and endovascular stentgrafting. Cardiovasc Intervent Radiol 25:419–422 38. Laheij RJ, Buth J, Harris PL, Moll FL, Stelter WJ, Verhoeven EL (2000) Need for secondary interventions after endovascular repair of abdominal aortic aneurysms. Intermediateterm follow-up results of a European collaborative registry (EUROSTAR). Br J Surg 87:1666–1673 39. Leville C, Greenberg R (2005) Challenges in endovascular thoracic aneurysm repair. In: Branchereau A, Jacobs M (eds) Unexpected challenges in vascular surgery. Blackwell, Oxford, pp 15–22 40. Malina M, Sonesson B, Ivancev K (2005) Aortic neck problems during EVAR. In: Branchereau A, Jacobs M (eds) Unexpected challenges in vascular surgery. Blackwell, Oxford, pp 73–85 41. May J, White GH, Yu W, Ly CN, Waugh R, Stephen MS, Arulchelvam M, Harris JP (1998) Concurrent comparison of endoluminal versus open repair in the treatment of abdominal aortic aneurysms: analysis of 303 patients by life table method. J Vasc Surg 27:213–221 42. Miller DC, Stinson EB, Oyer PE, Rossiter SJ, Reitz BA, Griepp RB, Shumway NE (1979) Operative treatment of aortic dissections. Experience with 125 patients over a sixteenyear period. J Thorac Cardiovasc Surg 78:365–382 43. Nienaber CA, Fattori R, Lund G, Dieckmann C, Wolf W, von Kodolitsch Y,Nicolas V, Pierangeli A (1999) Nonsurgical reconstruction of thoracic aortic dissection by stentgraft placement. N Engl J Med 340:1539–1545 44. Orend KH, Scharrer-Pamler R, Kapfer X, Kotsis T, Gorich J, Sunder-Plassmann L (2003) Endovascular treatment in diseases of the descending thoracic aorta: 6-year results of a single center. J Vasc Surg 37:91–99
45. Parodi JC, Palmaz JC, Barone HD (1991) Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 5:491–499 46. Pasic M, Bergs P, Knollmann F, Zipfel B, Muller P, Hofmann M, Hetzer R (2002) Delayed retrograde aortic dissection after endovascular stenting of the descending thoracic aorta. J Vasc Surg 36:184–186 47. Peeters P, Jürgen V, Deloose K (2003) EVAR patients with challenging iliac arteries. Endovasc Today Suppl, May/June, pp 16–19 48. Raithel D (2003) Stenotic proximal and distal aortic necks. Endovasc Today Suppl, May/June, pp 12–15 49. Riambau V (2003) EVAR in conical neck. Endovasc Today Suppl, May/June, pp 8–11 50. Rousseau H, Bolduc JP, Dambrin C, Marcheix B, Canevet G, Otal P (2005) Stent-graft repair of thoracic aortic aneurysms. Tech Vasc Interv Radiol 8:61–72 51. Saccani S, Nicolini F, Beghi C, Marcato C, Uccelli M, Larini P, Budillon AM, Agostinelli A, Gherli T (2002) Thoracic aortic stents: a combined solution for complex cases. Eur J Vasc Endovasc Surg 24:423–427 52. Saratzis A, Saratzis N, Fillipou D, Melas N, Kiskinis D (2005) Endovascular stent-graft repair of an aortobronchial fistula: case report and review of the literature. Eur J Vasc Endovasc Surg 30:223 53. Schumacher H, Bockler D, Bardenheuer H, Hansmann J, Allenberg JR (2003) Endovascular aortic arch reconstruction with supra-aortic transposition for symptomatic contained rupture and dissection: early experience in 8 highrisk patients. J Endovasc Ther 10:1066–1074 54. Stanley BM, Semmens JB, Lawrence-Brown MM, Goodman MA, Hartley DE (2001) Fenestration in endovascular grafts for aortic aneurysm repair: new horizons for preserving blood flow in branch vessels. J Endovasc Ther 8:16–24 55. Stelter WJ (2004) Endovascular iliac bifurcation grafting. Endovasc Today Suppl, June, pp 13–14 56. Szilagyi DE, Elliott JP, Smith RF (1972) Clinical fate of the patient with asymptomatic abdominal aortic aneurysm and unfit for surgical treatment. Arch Surg 104:600–606 57. Tse LW, MacKenzie KS, Montreuil B, Obrand DI, Steinmetz OK (2004) The proximal landing zone in endovascular repair of the thoracic aorta. Ann Vasc Surg 18:178–185 58. Verhoeven EL, Zeebregts CJ, Kapma MR, Tielliu IF, Prins TR, van den Dungen JJ (2005) Fenestrated and branched endovascular techniques for thoraco-abdominal aneurysm repair. J Cardiovasc Surg (Torino) 46:131–140
353
355
5.5 Aortoiliac Occlusive Disease Domenico Palombo, Simone Mambrini, Gianmarco de Donato
5.5.1 Basics The infrarenal aorta and its branches supply a very large anatomical area which includes the walls of the inferior part of the abdomen, the walls of the pelvis, the descending colon, the viscera of the pelvis, the reproductive organs and the inferior limbs. For this reason, acute infrarenal aortic occlusion is a catastrophic event. In contrast, chronic obstructive aortoiliac disease can be asymptomatic. It depends on how quickly the disease develops, its extent and the development of collateral circulation. Indeed, the branches of the aortoiliac artery develop a large anastomotic, parietal, visceral and parieto-visceral circulation. This is fundamental in the context of the physiopathology of aortoiliac obstructive disease. The major anastomotic parietal circulation includes: • The epigastric system, consisting of: superior epigastric artery, intercostal arteries, diaphragmatic arteries, lumbar arteries, inferior epigastric artery, superficial epigastric artery. It connects the subclavian artery, the descending thoracic aorta and the abdominal aorta with the external iliac artery (EIA) and the common femoral artery (CFA). • The iliolumbar system, consisting of: inferior intercostal arteries, lumbar arteries, middle sacral artery, lateral sacral artery, iliolumbar artery, superior and inferior gluteal arteries and the deep circumflex iliac artery. It connects the descending thoracic aorta and the abdominal aorta with the hypogastric artery and the EIA. • The gluteal-obturator system, consisting of: superior and inferior gluteal arteries, obturator artery, medial and lateral circumflex femoris arteries, first perforans artery. It connects the hypogastric artery with the common femoral and/or profunda femoris arteries.
The major anastomotic visceral circulation includes: • Riolan’s arch and Drummond’s marginal arch, which connects the superior mesenteric with the inferior mesenteric arteries. • In the male, the internal pudendal system, comprising: spermatic artery, internal pudendal artery, external pudendal arteries; it connects the abdominal aorta with the hypogastric artery and the CFA. • In the female, the utero-ovarian system, comprising: ovarian artery, uterine artery, vesico-umbilical artery, inferior vesical artery; it connects the abdominal aorta with the hypogastric artery. The viscero-parietal circulation: • Directly consists of the haemorrhoidal plexus, composed of: the superior haemorrhoidal artery (branch of the inferior mesenteric artery), the middle and inferior haemorrhoidal arteries (branches of the internal pudendal arteries) and the middle sacral artery. • Indirectly consists of multiple connections among the previous anastomosis.
5.5.2 Synonyms • Aortoiliac occlusive disease (AIOD) • Leriche’s syndrome (LS) • Small aortic syndrome (SAS).
5.5.3 Definition AIOD includes: • Chronic clinical syndrome, due to stenosis or occlusion of the infrarenal aorta and/or iliac arteries (unior bilateral).
356
5.5 Aortoiliac Occlusive Disease
• Acute clinical syndrome, due to thrombosis of the infrarenal aorta and/or iliac arteries, or to embolic occlusion of the aortic bifurcation or iliac bifurcation.
5.5.3.1 Morphological Features in the Chronic Forms AIOD is classified, according to Brewster [6], as follows: • Type I: lesions limited to the infrarenal aorta and common iliac artery (CIA) (5–10%); its clinical equivalent is LS, characterized by intermittent claudication of the inferior limbs, no femoral pulse and, in the male, sexual dysfunction (50–80%) with impotence in 30–50% of patients. • Type II: lesions extend into the EIA (25%); in this case claudication is frequently disabling. • Type III: lesions extend into infra-inguinal arteries (65%); in this case symptoms can be rest pain and/or tissue loss. In 5–10% of patients, the infrarenal aorta, iliac and femoral arteries are very small (juxtarenal aorta <13.2 mm; distal aorta <10.3 mm; common femoral artery <5 mm). This feature is defined as small aortic syndrome (SAS) [9]. Iliac stenosis or occlusion is associated with pulselessness or pulse reduction of the ipsilateral femoral artery and with peripheral ischaemia with claudication, rest pain, or tissue loss related to the condition of the distal vessels. In 2000 a TransAtlantic Inter-Society Consensus (TASC) [25] classified the iliac arterial lesions as follows:
Type A • Single stenosis <3 cm of the CIA or EIA (uni- or bilateral).
Type B • Single stenosis 3–10 cm in length, not extending into the CFA. • Total of two stenoses <5 cm long in the CIA and/or in the EIA and not extending into the CFA. • Unilateral CIA occlusion.
Type C • Bilateral 5- to 10-cm-long stenoses of the CIA or EIA, not extending into the CFA. • Unilateral EIA occlusion, not extending into the CFA. • Unilateral EIA stenosis extending into the CFA. • Bilateral CIA occlusion.
Type D • Diffuse, multiple unilateral stenosis involving the CIA, EIA and CFA (usually >10 cm). • Unilateral occlusion involving both common and external iliac arteries. • Bilateral EIA occlusion. • Diffuse disease involving the aorta and both iliac arteries. • Iliac stenosis in a patient with an abdominal aortic aneurysm or other lesions requiring aortic or iliac surgery. This classification is actually currently being revised. A more recent classification was proposed by the American Heart Association (AHA) in 2003 [20]. It classified the focal aortic and the iliac lesions as follows:
Focal Aortic Lesions • Category 1: short segment stenosis of the infrarenal abdominal aorta (<2 cm) with minimal atherosclerotic disease of the aorta otherwise. • Category 2: medium-length stenosis of the infrarenal abdominal aorta (2–4 cm) with mild atherosclerotic disease of the aorta otherwise. • Category 3: long segment (>4 cm) stenosis of the infrarenal abdominal aorta, or aortic stenosis with atheroembolic disease (blue toe syndrome), or medium-length stenosis of the infrarenal abdominal aorta (2–4 cm) with moderate to severe atherosclerosis of the aorta otherwise. • Category 4: aortic occlusion or aortic stenosis associated with an abdominal aortic aneurysm.
5.5.5 Aetiology
Iliac Lesions • Category 1: stenosis is <3 cm in length and concentric and noncalcified. • Category 2: stenosis is 3–5 cm in length or calcified and eccentric but <3 cm in length. • Category 3: stenosis is 5–10 cm in length or occlusion is <5 cm in length after thrombolytic therapy with chronic symptoms. • Category 4: stenosis is >10 cm in length, or occlusion is >5 cm in length after thrombolytic therapy and with chronic symptoms, or there is extensive bilateral aortoiliac atherosclerotic disease, or the lesion is an iliac stenosis in a patient with abdominal aortic aneurysm or another lesion requiring aortic or iliac surgery.
5.5.4 Epidemiology • The infrarenal abdominal aorta and the iliac arteries are the sites most commonly affected by atherosclerosis in patients with ischaemic peripheral atherosclerotic disease [10]. • The true prevalence of AIOD is unknown because it is frequently asymptomatic. • Chronic occlusion of the infrarenal aorta (Fig. 5.5.1) is rare – reported in only 0.15% of autopsies [23]. In contrast, asymptomatic stenosis and chronic aortoiliac occlusion are present in about 55% of patients affected by symptomatic pathology of the coronary circulation [18]. • In addition, surgical or endovascular treatment of AIOD represents about 48% of all inferior limb revascularizations [17]. This percentage rises to 55% when patients younger than 40 years old are considered [22]. • Patients with type I lesions are usually relatively young, heavy smokers and present a minor prevalence of diabetes and hypertension. Among them a hyperlipidaemia is frequent and there is no difference between male and female gender. • SAS is more common in women, usually about 50 years old, heavy smokers, with high aortic bifurcation and a history of surgical or post-radiation premature menopause. • Patients with type II and type III lesions are older (>60 years old), usually diabetic and hypertensive and have multilevel atherosclerotic disease (cerebral artery, coronary and visceral artery).
Fig. 5.5.1 Chronic juxtarenal aortic occlusion
• Males are involved sixfold more frequently than females.
5.5.5 Aetiology • Ninety percent of chronic AIOD depends on atherosclerosis; its risk factors are well known (diabetes mellitus and impaired glucose tolerance, smoking, hypertension, hyperlipidaemia, hyperhomocysteinaemia). • The remaining cases depend on atypical aortic coarctation, due to arteritis (particularly Takayasu’s disease) or fibromuscular dysplasia. • Acute AIOD is rare and about 12-fold less frequent than chronic disease [8]. Its causes are embolism (10%) and thrombosis (90%) [4]. • Usually the source of embolism is cardiac because of atrial fibrillation, recent myocardial infarct, valvulopathy, or myxoma. • Thrombotic AIOD may depend on pre-existing atherosclerotic lesions (80%), hypercoagulable state (13%) and acute occlusion of small aortic aneurysms (7%). • Traumatic aetiology is reported but very infrequent.
357
358
5.5 Aortoiliac Occlusive Disease
• Thrombosis of underlying atherosclerotic plaques is precipitated by a low-flow state caused by dehydration (poor intake of fluid, aggressive diuresis, or third space fluid loss) or cardiac decompensation (congestive heart failure, acute myocardial infarct, or sudden intractable arrhythmias). • In the subgroup of patients with hypercoagulable state the causes can be hereditary hypercoagulable states [factor V Leiden mutation (activated protein C or APC resistance); protein C deficiency; protein S deficiency; antithrombin deficiency; dysfibrinogenaemia; prothrombin mutation] or acquired hypercoagulable states [antiphospholipid syndrome; cancer-associated thrombosis (Trousseau’s syndrome); inflammatory bowel disease; antithrombin deficiency due to lowprotein states – protein-losing enteropathy, nephrotic syndrome, malnutrition; hyperhomocysteinaemia due to folic acid or vitamin B12 deficiency].
5.5.6 Symptoms 5.5.6.1 Chronic AIOD • All clinical stages of the well-known Leriche–Fontaine’s classification (stage one: asymptomatic patient; stage two: claudication; stage three: rest pain; stage four: tissue loss) can be present.
Intermittent Claudication • Intermittent claudication of the inferior limbs is the most common symptom. • Typically it involves the gluteus, the hip and the proximal regions of the thigh. • It allows a walking range that is stereotyped in a single patient, but variable from patient to patient, even when the lesions are similar. • In cases of monoiliac stenosis or chronic occlusion, claudication involves the ipsilateral inferior limb. • In cases of bilateral iliac or aortoiliac lesions (Fig. 5.5.2), claudication is bilateral, but usually asymmetrical because of the frequent prevalence of disease in one limb. • In type II and especially type III AIOD, claudication involves the entire inferior limb, while it is proximal in patients with type I lesions.
Fig. 5.5.2 Chronic right iliac artery occlusion with contralateral stenosis
Sexual Dysfunction • Occurs in 50–80% of males, with impotence in 30– 50% of cases.
Rest Pain • Rest pain is absent in patients with type I or II lesions, whereas it can be present in those with type III lesions. • In this last case peripheral tissue loss, such as ischaemic ulcer and gangrene, can be present too. • In type I and II AIOD, tissue loss is rare and depends on microembolism (blue toe syndrome).
Abdominal Pain • Rarely, there is abdominal pain during walking, caused by mesenteric steal through Riolan’s arch,
5.5.7 Diagnosis
Drummond’s marginal arch, the inferior mesenteric artery and haemorrhoidal plexus (mesenteric steal syndrome).
5.5.6.2 Acute AIOD • Acute occlusion of the infrarenal aorta, with variable extension to iliac vessels, frequently gives severe symptoms. • Presentation includes acute bilateral limb ischaemia, with pallor or cyanosis, hypothermia and pain, and neurological deficits simulating acute spinal cord injuries, with paraesthesia, dysaesthesia, anaesthesia, paresis and paralysis. After 8–10 h of ischaemia, cyanotic marbling extends to the middle umbilical line. • Eight percent of the cases present with abdominal pain, an expression of bowel ischaemia; 4% of the cases show hypertensive crisis, followed by signs of acute renal failure due to renal artery thrombosis. • Rarely this presentation develops a rapid peroneal gangrene. • Patients with acute occlusion of the iliac axis generally develop acute ischaemic symptoms in the ipsilateral inferior limb.
5.5.7 Diagnosis 5.5.7.1 Recommended European Standard Inspection • Skin aspect (pallor, cyanosis, erythrocyanosis) in the clinostatic position and after maintaining the limb up (pallor appearance: Buerger’s sign) or in a downward position (cyanosis or erythrocyanosis appearance). • Skin and adnexa trophism (skin atrophy, thinning and translucent skin, hair bulb rarefaction, onychodystrophy, oedema, tissue loss). • Superficial venous refilling in the clinostatic position (empty superficial veins) and after maintaining the limb up (delayed venous refilling). • Muscular trophism (hypotrophy).
Palpation • Skin temperature (hypothermia and thermal gradient). • Abdomen (pulsatory mass). • Arterial pulse (hyposphygmia or pulseless). • Muscular tone (hypotone and hyposthenia).
Auscultation • Arterial bruits (abdominal and femoral) at rest and after exercise.
Femoral and Tibial (at the Ankle) Duplex Continuous Wave • Sound wave analysis (three-phase or biphasic versus monophasic, post-stenotic or post-obstructive, or demodulating pulse flow waveforms; absence of Duplex signal). • Ankle/brachial blood pressure index at rest and after standardized exercise (walking on treadmill at 3 km/h speed and 10% slope).
Aortoiliac and Infra-inguinal Echo Flow Duplex Scanning • Morphological analysis • Site and type of lesions: stenosis or occlusion, chronic (hyperechogenic thrombus) or recent (hypoechogenic thrombus with hyperechogenic areas). • Vascular wall features at the occlusion site: the presence of atheromatous lesions suggests thrombosis; the absence of parietal lesions suggests embolism. • Plaque aspect: irregular or ulcerated surface, calcification. • Lesion extent. • Haemodynamic study: spectral analysis of pulse flow waveforms at different levels to define: • Haemodynamic importance of stenosis: a peak systolic velocity (PSV) <200 cm/s and/or a PSV ratio (stenotic PSV divided by prestenotic or poststenotic PSV) <2.5 indicates <50% stenosis; a PSV ratio ≥2.5 indicates ≥50% stenosis; a PSV ratio ≥5.0 and an end-diastolic velocity (EDV) >40 cm/s indicate
359
360
5.5 Aortoiliac Occlusive Disease
≥75% stenosis; and an EDV >0 cm/s indicates stenosis of haemodynamic importance [12]. • Absence of flow at the site of the occlusion (stopped pulse flow waveforms upstream). • Quality of pulse flow waveforms afterwards.
•
Radiological Diagnostic Technique • Angiography (with possibility of endovascular treatment of lesions documented by Duplex scanning). • Three-dimensional angio-TC m.s. • Angio-MRI (in patients intolerant of radiological contrast medium or affected by severe chronic renal failure).
• •
5.5.7.2 Additional/Useful Diagnostic Procedures • • Level of glycaemia, triglyceridaemia, cholesterolaemia and homocysteinaemia, to evaluate corrigible atherosclerotic risk factors. • Definition of a hypercoagulable state with a blood sample being taken before the start of anticoagulant therapy in patients affected by aortic thrombosis. • Transthoracic echocardiogram (TTE) or transoesophageal echocardiogram (TEE) to evaluate the presence of residual embolus in the heart or in the proximal aorta (in patients with acute embolic occlusion), or to define ventricular function (especially in patients with aortic thrombosis). • Cardiologist evaluation of surgical elective patients, to stratify their cardiac risk and, if indicated, provocative tests (TTE or myocardial scintigraphy with stress, stress test) and/or coronarography. • Evaluation by a respiratory physician and spirometry of surgical elective patients to ameliorate their respiratory condition before the operation.
•
•
choice between conservative and invasive treatment must be considered on the basis of the risk:benefit ratio. Nevertheless, recently the development of endovascular procedures [percutaneous transluminal angioplasty (PTA) and stent] to the region of the aortoiliac artery has given very encouraging results and this technique has a significantly reduced the risk:benefit ratio compared to surgery. Accordingly, patients with subjective disabling claudication can be considered for endovascular treatment. When the procedure is not feasible due to the lesion’s features (TASC and AHA classification and related indications) or the presence of co-morbidity (severe chronic renal failure, radiological contrast medium intolerance), it is reasonable to treat the patient conservatively for a trial period and to resort to surgery if conservative treatment fails. The length of the trial period is defined case by case, considering age, co-morbidity, work necessity and the lifestyle of the patients as well as their response to conservative treatment. Obviously, if the walking range of the patient is seriously compromised (<50 m), the possibility of physical exercise (which is the most important phase of conservative treatment) drops and a direct surgical approach becomes necessary. Patients with AIOD responsible for peripheral embolism (aortic and/or iliac complicated plaques even if not haemodynamically important), or associated with acute or critical chronic ischaemia are always candidates for invasive treatment. Finally, an aortic juxtarenal occlusion is a surgical indication even if peripheral ischaemia is minor and stable, because of the risk of acute renal failure or bowel ischaemia due to the upward extension of the thrombosis if one is present.
5.5.8.1 Conservative Treatment 5.5.8 Treatment • Conservative treatment of aortoiliac lesions is indicated only in chronic forms and in asymptomatic patients or those without disabling claudication. Its goal is to control the progress of the disease and support the development of collateral circulation. • When the walking range is limiting the patient or erectile deficit in a sexually active male is present, the
Recommended European Standard • Correction of atherosclerotic risk factors: stopping smoking, pharmacological treatment of hypertension, diabetes, dyslipidaemia and hyperhomocysteinaemia. • Platelet inhibitors. • Daily physical exercise, planned on the basis of claudication severity.
5.5.8 Treatment
Additional Useful Therapeutic Strategies • Haemorrheological drugs.
5.5.8.2 Endovascular and Surgical Treatment Recommended European Indication on the Basis of Morphological Criteria Aortic Lesions
• Chronic aortic occlusion (AHA category 4 aortic lesions). Surgical treatment from the following options: aortobifemoral (Figs. 5.5.3, 5.5.4) or bilateral aortoiliac by-pass; uni- or bilateral thoraco-iliofemoral bypass in cases of a very calcified infrarenal aorta or very hostile abdomen; in patients at very high surgical risk, axillobifemoral by-pass. • Acute aortic thrombosis. Surgical treatment from the following options: aortobifemoral or bilateral aortoiliac by-pass; in the patient with cardiac failure, ax-
Fig. 5.5.3 Aortobifemoral by-pass graft: aortic anastomosis
illobifemoral by-pass; only limited reports regarding local fibrinolysis with subsequent PTA; there is no sufficient evidence to recommend this technique; in cases treated by endovascular technique, endoprosthetic exclusion of the pathological aortic segment is necessary in theory. • Acute aortic embolic occlusion. Surgical treatment: transfemoral or transaortic aortoiliac embolectomy. • Aortic stenosis: • AHA categories 1 and 2 aortic lesions. Endovascular treatment of choice: simple PTA and stent in infrarenal aorta when lesion is more than 10 mm from the aortic bifurcation; kissing balloon and kissing stent when aortic bifurcation is pathological. • Complicated and embolic aortic plaque (AHA category 3 aortic lesions). Surgical treatment of choice: transaortic endarterectomy or aortic exclusion and bilateral aortoiliac or aortobifemoral graft reconstruction; in the high-risk patient, exclusion of the pathological segment with an endoprosthesis
361
362
5.5 Aortoiliac Occlusive Disease
Fig. 5.5.4 Aortobifemoral by-pass graft: femoral anastomosis
can be considered where technically and clinically feasible (proximal point of the lesion at more than 15 mm from the renal arteries; distal point of the lesion at more than 10 mm from the aortic bifurcation; absence of polar renal arteries; in the case of a pervious inferior mesenteric artery, the absence of a significant stenosis in at least one hypogastric artery). • In the presence of diffuse infrarenal aortic stenosis (AHA category 3 aortic lesions). Surgical treatment of choice: in high-risk patients endovascular treatment can be considered.
Iliac Lesions
• Chronic iliac stenosis or occlusion: • TASC type A or AHA categories 1 and 2 iliac lesions: endovascular treatment of choice (Figs. 5.5.5, 5.5.6).
• TASC type D or AHA category 4 iliac lesions: surgical treatment of choice. • TASC type B iliac lesions: endovascular treatment is currently more often used, but in the absence of evidence for recommendation. • TASC type C iliac lesions: surgical treatment is currently used more often, but in the absence of evidence for recommendation. • AHA category 3 iliac lesions: endovascular treatment has a significantly lower chance of initial success or long-term benefit than surgical treatment. • Acute iliac thrombosis: surgical treatment of choice; iliofemoral or aortofemoral by-pass graft; in the patient at high surgical risk: femoro-femoral or axillofemoral by-pass graft; the reports regarding fibrinolysis with subsequent PTA are not sufficient to recommend this technique. • Acute iliac embolic occlusion: surgical treatment of choice; transfemoral embolectomy.
5.5.10 Prognosis
Fig. 5.5.5 Short-segment right common iliac artery stenosis Fig. 5.5.6 Result after PTA
5.5.9 Differential Diagnosis Although AIOD shows typical clinical features, differential diagnosis must to be made with regard to the following:
5.5.9.1 In the Case of Chronic AIOD • Degenerative disease of the lumbar column or hip; in these cases symptoms appear when the patients pass to the orthostatic position, they worsen with walking, and regress when the patients pass to the sitting position or lie down; spine or trochanter palpation often provokes local pain; rest pain, when present, does not involve the extremities. • Cauda equina syndrome and lumbar radiculopathy (compression by a herniated disk or reduction of the intervertebral space); in these cases the pain radiates along the sciatic nerve; Lasegue’s manoeuvre is positive. • Diabetic neuropathy: differential diagnosis is more difficult and Duplex scanning and angiography can be useful.
• Fibromyalgia syndrome and other muscle disease: generally, only proximal muscle groups are involved and the pain appears even at rest without foot involvement; frequently, the femoral pulse is sufficient for a correct diagnostic suspicion; in dubious cases, the ankle/brachial index (normal value >0.92) is a simple and rapid parameter for differential diagnosis, except in diabetic patients.
5.5.9.2 In the Case of Acute AIOD • Spinal cord ischaemia or compression; in these cases ischaemic signs are absent and infra-inguinal pulses are valid.
5.5.10 Prognosis • Patients with type I AIOD, asymptomatic without disabling claudication, have a good life expectancy if the risk factors are treated.
363
364
5.5 Aortoiliac Occlusive Disease
• On the other hand, patients with type II or III AIOD, symptomatic for disabling claudication or rest pain or tissue loss, have an associated reduction of life expectancy. The 5-, 10- and 15-year mortality rates from all causes are approximately 30%, 50%, and 70% respectively, in the case of claudication [5]. In cases of critical limb ischaemia the 2-year mortality rate is 31.6% [24], whereas the 95% of patients with ischaemic gangrene and the 80% of patients with rest pain die within 10 years [13]. • The results of endovascular procedures and surgical revascularization are excellent when the indication is correct in claudicant patients, with immediate recovery of symptoms. The primary patency rate at 1and 3-year follow-up increases to 95% for the PTA and stenting group, and to 100% for the aortofemoral by-pass group, with a peri-operative mortality rate of nearly zero in the endovascular group and very low in the surgical group (< 3%). • In the presence of multilevel disease, correction of inflow problems is sufficient in about 70–80% of patients whose symptoms of ischaemia are relieved. Nevertheless, in 20–30% of cases, subsequent or contemporary (10–15% of patients) peripheral revascularization is necessary. • Acute aortic occlusion, even when promptly diagnosed and treated by revascularization, has a poor outcome, with a high peri-operative mortality (14–100%), especially in patients with thrombosis, in whom the disease may represent either end-stage cardiovascular dysfunction or poorly understood derangement of coagulation homeostasis [4]. • In all cases, despite successful revascularization, reperfusion initiates a cascade of deleterious local and systemic phenomena, such as compartment syndrome, skeletal muscle necrosis, hypovolaemic shock, hyperkalaemia, acidosis, myoglobinaemia, pulmonary embolism, acute kidney failure, arrhythmias and in some cases multiorgan failure.
Anaesthesia • Local in the site of puncture with noninvasive monitoring of arterial pressure, cardiac frequency, electrocardiogram, oxygen saturation.
Angioplasty Technique Common femoral or axillary approach by percutaneous arterial puncture with Seldinger’s technique and introduction of a hydrophilic guidewire and an introducer catheter. 2. Progression of the guidewire, under radioscopy, as far as the abdominal aorta. 3. Introduction and progression of the arteriographic catheter (usually pig-tail) over the guidewire as far as the abdominal aorta under radioscopy. 4. Acquisition of arteriographic images with the digital subtraction technique. 5. Removal of the arteriographic catheter. 6. Introduction and progression of the operative catheter (balloon catheter) over the guidewire; the balloon is positioned, under radioscopy, across the lesion; an arteriographic map can facilitate the positioning. 7. Angioplasty: inflation of the balloon (for 60 s) under radioscopy by injection of contrast medium and saline at 50% (inflating pressure: 405–1723 kPa or 4–17 atm). 8. Deflation of the balloon and removal of its catheter under radioscopy. 9. Re-introduction and progression of the angiographic catheter over the guidewire as far as the abdominal aorta under radioscopy. 10. Acquisition of arteriographic images with the digital subtraction technique; if there is: • residual stenosis >30%, a gradient across the treated lesion of >10 mmHg or postangioplasty dissection, stenting is required; • a good morphological result, removal of devices and compression at the site of the puncture are required. 1.
5.5.11 Surgical and Endovascular Principle Stenting Technique 5.5.11.1 Aortoiliac Angioplasty and Stenting Background • Angiography suite or operating room.
Follow stages 1–10 above. 1. Removal of angiographic catheter. 2. Introduction and progression of operative catheter (sheath catheter with stent) over the guidewire; the
5.5.11 Surgical and Endovascular Principle
stent is positioned, under radioscopy, across the angioplasty site; an arteriographic map facilitates the positioning. 3. Deployment of stent: a. Self-expandable stent: usually in the case of long segment disease, tortuous iliac vessels, contralateral approach. b. Balloon-expandable stent: usually in the case of focal lesions, severely calcified lesions, lesions adjacent to the aortic bifurcation, recanalization of iliac obstructions. 4. Removal of sheath catheter under radioscopy. 5. Under angiographic control, removal of devices, and compression at the site of the puncture.
5.
6. 7.
8. 9.
Specific Cases • Recanalization of iliac obstruction: under radioscopy, the guidewire can pass through some obstructive iliac lesions by gently pushing against resistance to progression of the device; in these cases, subsequent deployment of a balloon-expandable stent is indicated. • Treatment of distal aortic stenosis or proximal and bilateral common iliac stenosis: the procedure necessitates a bilateral femoral approach as well as double and simultaneous iliac balloon angioplasty (kissing balloon); in the case of stent deployment (balloon-expandable stent), double and simultaneous iliac stenting (kissing stent) is also necessary; indeed, dilatation of only one iliac ostium can provoke contralateral compression and thrombosis. • Treatment of embolic and complicated plaque of the aorta: covered stents are employed; the procedures can be totally percutaneous or combined surgical and percutaneous; in the case of a combined procedure, the technique involves: 1. Surgical femoral approach through a groin incision (side A). 2. Contralateral common femoral approach (or axillary approach) by percutaneous arterial puncture with Seldinger’s technique and introduction of a hydrophilic guidewire and an introducer catheter (side B). 3. Progression of the guidewire as far as the abdominal aorta under radioscopic control. 4. Introduction and progression of an arteriographic catheter (usually pig-tail) over the guidewire as far as the abdominal aorta under radioscopic control.
10. 11.
12. 13.
14.
15.
Puncture of the common femoral artery, surgically prepared, and introduction of a second guidewire through a temporary introducer catheter; clamping with a tourniquet of the common femoral artery permits haemostasis. Acquisition of arteriographic images with the digital subtraction technique. Retrieval, under radioscopic control, of the guidewire and angiographic catheter, inserted from side B. Removal of the temporary introducer femoral catheter in side A. In side A, introduction and progression of the operative catheter (sheath catheter with endoprosthesis) over the guidewire; the covered stent is positioned, under radioscopic control, across the lesion in the infrarenal aorta; an arteriographic map facilitates the positioning. Deployment of an endoprosthesis. Retrieval, under radioscopic control, of the operative catheter and introduction and progression over the guidewire of a balloon catheter as far as the endoprosthesis. Angioplasty: balloon inflation with dilatation of the endoprosthesis and aortic lesion. Deflation of the balloon, and removal of its catheter under radioscopic control with femoral cross-clamping. Progression of the arteriographic catheter, inserted in side B, as far as the abdominal aorta and a final angiographic check as a control. Removal of the devices, with compression in side B, arteriography, declamping and suture of surgical access in side A.
5.5.11.1 Unilateral and Bilateral Aortofemoral By-pass Anaesthesia Narcosis and thoracic epidural catheter (blended anaesthesia for intraoperative and postoperative pain control) [2] with: • Blood recuperation. • Continuous invasive monitoring of arterial pressure (by radial, ulnar or brachial catheter), cardiac frequency, electrocardiogram, central venous pressure (by central venous catheter), oxygen saturation, di-
365
366
5.5 Aortoiliac Occlusive Disease
uresis (by bladder catheter), temperature and finally pulmonary wedge pressure and cardiac performance (by Swan Ganz catheter and/or TEE). • Use of fluid warming and forced-air warming systems to maintain normothermia [16]. • Use of centrifugal red blood cell washers for intraoperative autotransfusion to limit human bank blood infusion [21].
Specific Case: Juxtarenal Aortic Occlusion 1. This necessitates, through a midline or transverse lap-
2. 3.
Surgical Technique 1. 2.
3. 4.
5. 6. 7. 8. 9.
10. 11.
12. 13. 14.
Femoral approach: uni- or bilateral groin incision and exposure of femoral arteries. Abdominal approach: a. Midline or transverse laparotomy (minilaparotomy is preferable) and transperitoneal exposure of the infrarenal aorta (no evisceration is preferable). b. Left pararectal or Rob’s laparotomy and retroperitoneal exposure of the intrarenal aorta. Preparation of retroperitoneal tunnel (along the iliac axis as far as the femoral triangle). Aortic clamping: a. Double cross-clamping, or tangential clamping, and longitudinal aortotomy. b. Double cross-clamping, aortic section, possible suture of the distal aortic stump and removal of the distal aortic clamp. End-to-side or end-to-end anastomosis between the prosthesis and the aorta. Proximal cross-clamping of the prosthesis or prosthetic branches and removal of aortic clamp(s). Flushing and washing of the prosthesis or prosthetic branches with heparin solution. Tunnelling the prosthesis or prosthetic branches. Femoral cross-clamping and longitudinal arteriotomy (common femoral or profunda femoris) or section of the artery (with eventual ligature of proximal stump) and longitudinal arteriotomy on the distal stump. End-to-side or end-to-end anastomosis between the prosthesis and the femoral artery. Flushing and washing with heparin solution, completion of the anastomosis and sequential declamping. Control of haemostasis. One or more drains. Suture of surgical access.
4.
5. 6.
arotomy, the exposure not only of the infrarenal aorta, but also of the left renal vein, the renal arteries and the suprarenal aorta. After mobilization of the left renal vein, the suprarenal aorta and renal arteries are cross-clamped. The juxtarenal thrombus is removed through a large longitudinal infrarenal aortotomy or aortic section. After aortic and bilateral renal flushing, the infrarenal aorta is clamped and the clamps in the suprarenal aorta and renal arteries are removed. The proximal end-to-end prosthesis–aorta anastomosis is made. Finally, the distal aortic stump is sutured.
5.5.11.2 Unilateral or Bilateral Aortoiliac By-pass Anaesthesia • See Section 5.5.11.1.
Surgical Technique 1. Abdominal approach: a. In the case of bilateral aortoiliac by-pass, the tech-
nique is as follows: midline or transverse laparotomy and transperitoneal exposure of the infrarenal aorta and iliac arteries; when the distal sites of anastomosis are the external iliac arteries, the exposure of these vessels is obtained by an inframesosigmoid-colon route on the left, and by an infra-caecum route on the right. b. In the case of unilateral aortoiliac by-pass, an extraperitoneal route is possible through a pararectal or Rob’s laparotomy. 2. Aortic clamping: a. Double cross-clamping, or tangential clamping, and longitudinal aortotomy. b. Double cross-clamping, aortic section, possible suture of the distal aortic stump and removal of the distal aortic clamp. 3. End-to-side prosthesis–aorta anastomosis. 4. Proximal cross-clamping of the prosthesis or prosthetic branches and removal of aortic clamp(s).
5.5.11 Surgical and Endovascular Principle
5. Flushing and washing of the prosthesis or prosthetic 6.
7.
8.
9.
branches with heparin solution. In the case of distal anastomosis on the external iliac arteries, retroperitoneal tunnelling of prosthetic branches. Cross-clamping of pervious iliac arteries and longitudinal arteriotomy or section of the artery(ies) (with eventual ligature of the proximal stump). End-to-side or end-to-end anastomosis between the prosthesis and the common/external iliac or iliac bifurcation. See stages 11–14 of Section 5.5.11.1.
Surgical Technique 1. 2.
3.
4.
Specific Case: Juxtarenal Aortic Occlusion See “Specific Case: Juxtarenal Aortic Occlusion” above.
5.5.11.3 Aortic Exclusion and Bilateral Aortoiliac or Bilateral Aortofemoral Prosthetic Reconstruction Anaesthesia See Section 5.5.11.1.
Surgical Technique 1. Surgical approach: a. See stages 1, 2a and 3 of Section 5.5.11.1. b. See stage 1a of Section 5.5.11.2. 2. Double aortic cross-clamping. 3. Suture of the distal aortic stump and removal of the
distal aortic clamp. 4. End-to-end prosthesis–aorta anastomosis. 5. See stages 6–14 of Section 5.5.11.1 and stages 4–9 of Section 5.5.11.2.
5. 6. 7. 8. 9. 10.
5.5.11.4 Unilateral or Bilateral Thoracoiliofemoral By-pass Anaesthesia See “Anaesthesia” in Section 5.5.11.1; preferably endotracheal intubation is performed with a double lumen tube to facilitate aortic exposure by collapsing the left lung.
11. 12. 13. 14.
If the femoral approach is necessary: uni- or bilateral groin incision and exposure of femoral arteries. If the iliac approach is necessary: left and eventually right pararectal or Rob’s laparotomy and extraperitoneal exposure of iliac arteries. Thoracic approach: left anterolateral thoracotomy through the eighth intercostal space (the sixth to ninth are also adequate), deflation of the left lung, taking down or cutting the inferior pulmonary ligament, dissection of 7–8 cm of the mediastinic pleura, and exposure of the descending thoracic aorta. Thoraco-retroperitoneal and inguinal tunnel preparation: in the case of left groin incision, a left pararectal or Rob’s laparotomy is necessary with extraperitoneal exposure of the left iliac arteries; this retroperitoneal preparation is prolonged as follows: a. Upwards: lateral to the abdominal aorta, posterior to the left kidney as far as the insertion of the diaphragm on the ribs. b. Downwards (in cases of femoral revascularization): posterior to the left inguinal ligament as far as the femoral triangle. c. Medially: posterior to the pubis and rectal muscles and anterior to the bladder, in the space of Bogros, as far as the contralateral iliac artery or the left femoral triangle (passing behind the left inguinal ligament). d. Blunt dissection of the posteromedial costodiaphragmatic sulcus completes the pleuro-retroperitoneal tunnel. Tangential clamping of thoracic aorta and longitudinal aortotomy. End-to-side prosthesis–aorta anastomosis. Proximal cross-clamping of the prosthesis and removal of the aortic clamp. Prosthetic flushing and washing with heparin solution. Tunnelling of the prosthesis. See stages 9 and 10 of Section 5.5.11.1 and stages 7 and 8 of Section 5.5.11.2. Flushing, washing with heparin solution, completion of the anastomosis, and sequential declamping. Control of haemostasis. One or more pleuric, retroperitoneal and inguinal drains. Suture of surgical access.
367
368
5.5 Aortoiliac Occlusive Disease
5.5.11.5 Aortoiliac Endarterectomy
b. Midline umbilicus–pubic laparotomy and retro-
Anaesthesia See “Anaesthesia” in Section 5.5.11.1.
3. 4.
Surgical Technique
5.
Abdominal approach: midline or transverse laparotomy and transperitoneal exposure of infrarenal aorta and iliac arteries. 2. Cross-clamping of juxtarenal aorta, external iliac arteries and hypogastric arteries. 3. Large longitudinal arteriotomy in the infrarenal aorta, extended downstream in the proximal part of one common iliac artery. 4. Short longitudinal arteriotomies in the distal part of both common iliac arteries. 5. Cleavage and removal of the aortoiliac plaque. 6. Eventual distal fixation of endo-arterial layers by Kunlin’s stitches 7. Aortic and iliac arteriorraphy (with or without prosthetic patch) with flushing and washing with heparin solution after closing the iliac sutures. 8. Sequential declamping and control of haemostasis. 9. One or more drains. 10. Suture of surgical access.
6.
1.
7. 8. 9.
10. 11.
12. 13.
peritoneal or transperitoneal preparation of the iliac arteries. Preparation of retroinguinal tunnel. Iliac cross-clamping and longitudinal arteriotomy or section of the artery (with eventual ligature of the distal stump). End-to-side or end-to-end prosthesis–iliac anastomosis. Proximal cross-clamping of the prosthesis and removal of iliac clamp(s). Prosthetic flushing and washing with heparin solution. Tunnelling of the prosthesis. Cross-clamping of femoral arteries and longitudinal arteriotomy (common femoral or profunda femoris) or section of the artery (with eventual ligature of proximal stump). End-to-side or end-to-end prosthesis–femoral anastomosis. Flushing, washing with heparin solution, ending the suture, sequential declamping and control of haemostasis. One or more drains. Suture of surgical access.
5.5.11.7 Femoro-femoral Cross-over By-pass Anaesthesia
5.5.11.6 Iliofemoral By-pass Anaesthesia Narcosis or epidural catheter, with continuous invasive monitoring of arterial pressure (by radial, ulnar or brachial catheter), cardiac frequency, electrocardiogram, oxygen saturation, and diuresis (bladder catheter).
Narcosis or epidural catheter or single subarachnoid, with continuous invasive monitoring of arterial pressure (by radial, ulnar or brachial catheter), cardiac frequency, electrocardiogram, oxygen saturation and diuresis (bladder catheter).
Surgical Technique By-pass Technique 1. 2.
Femoral approach: groin incision and preparation of femoral arteries. Abdominal approach: a. Rob’s or mini-Rob’s laparotomy or pararectal laparotomy and retroperitoneal preparation of the iliac arteries.
1. 2.
Femoral approach: bilateral groin incision and exposure of femoral arteries. Preparation of tunnel: a. Retropubic tunnel is preferable; it passes posterior to the pubis and rectal muscles and anterior to the bladder in the retroperitoneal space of Bogros, then behind the contralateral inguinal ligament as far as the contralateral femoral triangle.
5.5.11 Surgical and Endovascular Principle
b. Subcutaneous tunnel passes in front of the ipsilat-
3. 4. 5. 6. 7. 8.
9. 10. 11. 12. 13.
eral inguinal ligament, rectal muscles and contralateral inguinal ligament as far as the contralateral femoral triangle. Donor femoral artery cross-clamping and longitudinal arteriotomy on the common femoral. End-to-side prosthesis–femoral anastomosis. Proximal cross-clamping of the prosthesis and removal of donor femoral artery clamps. Prosthetic flushing and washing with heparin solution. Tunnelling of the prosthesis. Cross-clamping of the pervious contralateral femoral arteries and longitudinal arteriotomy (common femoral or profunda femoris) or section of the artery (with eventual ligature of the proximal stump). End-to-side or end-to-end prosthesis–femoral anastomosis. Flushing, washing with heparin solution, ending the suture and sequential declamping. Control of haemostasis. One drain in each femoral triangle. Suture of surgical access.
5.5.11.8 Unilateral or Bilateral Axillofemoral By-pass Anaesthesia Narcosis with continuous invasive monitoring of arterial pressure (by radial, ulnar or brachial contralateral catheter), cardiac frequency, electrocardiogram, oxygen saturation and diuresis (bladder catheter).
inguinal ligament as far as the ipsilateral femoral triangle; in the case of axillobifemoral by-pass, another subcutaneous tunnel begins from the suprainguinal region and passes in front of the rectal muscles and contralateral inguinal ligament, as far as the contralateral femoral triangle. 4. Axillary artery cross-clamping. 5. End-to-side prosthesis–axillary anastomosis. 6. Proximal cross-clamping of the prosthesis and removal of axillary clamps. 7. Prosthetic flushing and washing with heparin solution. 8. Tunnelling of the prosthesis (usually bifurcated prostheses are employed). 9. See stages 9–12 of Section 5.5.11.1. 10. One drain in each femoral triangle and in the axillary cavity. 11. Suture of surgical access.
5.5.11.9 Retrograde Femoral Embolectomy Anaesthesia Local or epidural/subdural with noninvasive monitoring of arterial pressure, cardiac frequency, electrocardiogram, oxygen saturation; if there is the possibility of subsequent by-pass, follow the guidelines for anaesthesia in the appropriate section above.
Surgical Technique 1.
Surgical Technique 1. 2. 3.
Femoral approach: uni- or bilateral groin incision and exposure of femoral arteries. Axillary approach: subclavicular incision and exposure of axillary artery. Preparation of tunnel: through one or more short incisions in the lateral part of the thorax and abdomen, it begins from the axillary cavity, passes behind the pectoral muscle, descends into the subcutaneous tissue of the lateral part of the thorax and abdomen, as far as the ipsilateral suprainguinal region; from here the prosthetic tunnel proceeds in front of the
2.
3. 4.
Femoral approach: uni- or bilateral groin incision and exposure of femoral arteries. Cross-clamping of the femoral arteries; to prevent a contralateral iatrogenic embolization, simultaneous cross-clamping of bilateral femoral arteries is indicated, lasting until the end of the procedure, in cases of: a. Aortic embolization b. Uni- or bilateral embolic thrombus extending into the proximal common iliac artery. Uni- or bilateral longitudinal or transverse arteriotomy on the common femoral artery. Uni- or bilateral introduction and retrograde progression of a size 3, 4 and eventually 5 or 6 Fogarty catheter.
369
370
5.5 Aortoiliac Occlusive Disease
Fig. 5.5.7 Midline minilaparotomy
Uni- or bilateral inflation of a balloon and retraction of the Fogarty catheter with removal of the embolic thrombus. 6. Uni- or bilateral flushing, controlling the quality of the run-in. 7. Uni- or bilateral arteriorraphy, flushing, washing with heparin solution, ending the suture, and removal of vascular clamps. 8. Control of haemostasis. 9. Place a drain in the femoral triangle(s). 10. Suture of surgical access. 5.
5.5.11.10 New Surgical Trends Minimally Invasive Surgery • • • • •
This was proposed by Turnipseed [26]. Actually employed in aortoiliofemoral by-pass Reduced length of surgical incisions Mostly in the abdomen Midline minilaparotomy (median para-umbilical incision <10 cm) (Fig. 5.5.7).
Video-assisted Surgery • A hybrid of laparoscopic and conventional surgery, in which laparoscopic procedures are employed to minimize the surgical approach.
5.5.11 Surgical and Endovascular Principle
Fig. 5.5.8 Hand-Port system
• Since the first laparoscopically assisted aortobifemoral by-pass, performed by Dion in 1993 [15], several techniques have been proposed. • The most common techniques are the Hand-Port system, described by Kolvenbach [19] and Arous [3] (Fig. 5.5.8); the minimally invasive direct aortic surgery (MIDAS) reported by de Donato and Weber [11]; and the technique proposed by Alimi [1].
5.5.11.11 Aortobifemoral Video-assisted By-pass with Hand-Port System Anaesthesia See Section 5.5.11.1.
Surgical Technique Total Laparoscopic Surgery There are various techniques, such as: • Dion and Gracia’s technique [14]. • Coggia’s technique [7] which differs in the patient’s position, the site of trocar insertion and modality of exposing the aorta.
Surgical team consists of operative and assistant surgeons and laparoscopic surgeon: 1. Femoral approach: bilateral mini groin incisions and exposure of the femoral vessels. 2. Introduction of an infra-umbilical trocar and establishment of the pneumoperitoneum.
371
372
5.5 Aortoiliac Occlusive Disease
3. 4. 5.
6.
7. 8.
9.
10. 11.
12.
13. 14. 15.
Introduction through the infra-umbilical trocar of the endoscope. Introduction of two trocar ports at the intersection points between midclavicular and bisiliac lines. Midline supra-umbilical minilaparotomy (7 cm long); at section of the fascia the pneumoperitoneum is stopped. Placement of the Hand-Port System in the minilaparotomy; the Hand-Port System consists of: a. Base retractor component, which, when inflated, sits airtight in the abdominal incision. b. Bracelet and sleeve component, which, worn on the surgeon’s arm, maintains a seal between it and the base retractor, to prevent failure of the pneumoperitoneum. Re-establishment of the pneumoperitoneum. While the surgeon’s hand mobilizes the greater omentum, the small bowel and the retroperitoneal trances, the laparoscopic surgeon exposes the aorta from the level of the left renal vein to the aortic bifurcation. Preparation of tunnels: introduction of tunnelling clamps in each femoral triangle and progression of these along the ilio-femoral axis with hand assistance; introduction of rubber drains through each lateral trocar; by tunnelling clamps the rubber drains are tunnelled as far as each femoral triangle. Placing of a paddle retractor through the right trocar for retraction of the bowel. Interruption of the pneumoperitoneum, disconnection of the sleeve and removal of the laparoscopy instruments. Abdominal access through the base retractor component of the Hand-Port System: see stages 4–7 of Section 5.5.11.1. Tunnelling of prosthetic branches by the rubber drains. See stages 9–13 of Section 5.5.11.1. Removal of the base retractor component of the Hand-Port System and suture of surgical access.
5.5.11.12 Aortobifemoral Totally Laparoscopic By-pass with Coggia’s Technique Anaesthesia See Section 5.5.11.1.
Surgical Technique Patient’s position: dorsal decubitus with inflatable pillow placed behind the left flank (50° to 60° rotation of the abdomen); the pillow is inflated during the abdominal stages with maximal right rotation of the operative table (70° to 80° rotation of the abdomen). Surgical operators: operator in front of the patient’s abdomen, first assistant in front of the operator, second assistant on the right of the operating surgeon. 1. Establishment of the pneumoperitoneum. 2. Introduction of the endoscope on the left anterior axillary line, 3 cm below the costal margin. 3. Introduction of two trocars at the supra-umbilical and left paramedial level, for the insertion of operator instruments. 4. Introduction of one trocar under the xiphoid for insertion, at the beginning of the visceral endoretractor, followed by introduction of the proximal aortic clamp. 5. Introduction of one trocar 6 cm below the navel for the insertion of the distal aortic clamp. 6. Introduction of one trocar in the left inferior abdomen for the insertion of assistant instrumentation. 7. Incision of the posterior peritoneum in the left paracolic gutter up to the splenic flexure and dissection of Toldt’s fascia as far as the left renal vein. 8. Elevation and medial displacement of the left colon by an endoretractor inserted through the subxiphoid trocar. 9. In cases of prerenal access, placing of a traction suture through Gerota’s fascia, if the left kidney moves toward the median line; in cases of retrorenal access, incision of Gerota’s fascia and medial displacement of the left kidney and the spleen. 10. Deflation of the pillow, left rotation of the operative table, and deflation of pneumoperitoneum. 11. Bilateral groin mini-incision for dissection of the femoral arteries. 12. Re-inflation of the pillow, left rotation of the operative table, and re-inflation of the pneumoperitoneum. 13. Introduction of a vascular prosthesis into the abdomen, through one of the trocars; the prosthesis has distally ligated limbs. 14. Dissection of the anterior aspect of the right CIA (over 3–5 cm). 15. Tunnelling of the right limb of the graft by an aortic clamp introduced through the right groin incision
References
16.
17. 18.
19. 20.
21. 22. 23. 24. 25.
26. 27.
28.
and pushed in front of the ipsilateral iliofemoral axis, under endoscopic control. Removal of the endoretractor and insertion of a proximal aortic clamp through the infraxiphoid trocar; this clamp stabilizes the left mesocolon during the aortic anastomosis. Insertion of a distal aortic clamp through the infraumbilical trocar. Aortic cross-clamping: a. Longitudinal aortotomy and end-to-side prosthesis–aorta anastomosis. b. Aortic section, suture of the distal aortic stump with a mechanical stapler or polypropylene double running suture, and end-to-end prosthesis–aorta anastomosis. Aortic declamping and control of the suture. Tunnelling of the left limb of the prosthesis by an aortic clamp introduced through the left groin incision and pushed in front of the ipsilateral iliofemoral axis, under endoscopic control; at that stage, gas is sometimes lost through the left groin incision. Cross-clamping of the prosthetic limbs and section of the prosthesis-ligated segment. Washing of the graft limbs with heparin solution. Deflation of the pillow, left rotation of the operating table and deflation of the pneumoperitoneum. Distal prosthetic–femoral anastomosis (see stages 9–12 of Section 5.5.11.1). Re-inflation of the pillow, left rotation of the operating table, and re-inflation of the pneumoperitoneum with introduction of the endoretractor through the infraxiphoid trocar. Final laparoscopic control and insertion of drains under videoscopic assistance. Deflation of the pillow, left rotation of the operating table, deflation of the pneumoperitoneum, and removal of laparoscopic instruments and trocars. Suture of the surgical access.
3
4 5 6
7
8
9 10
11
12
13 14
15
16
References
17
1. Alimi YS, Hartung O, Valerio N, Juhan C (2001) Laparoscopic aorto-iliac surgery for aneurysm and occlusive disease: when should a minilaparotomy be performed? J Vasc Surg 33:469–475 2 Arena L, Di Sebastiano N, Russo L, Di Filippo A (1992) Alfentanyl and Midazolam in combined anaesthesia. Clinical evaluation. Minerva Anestesiol 58:369–373
18
19
Arous EJ, Nelson PR, Yood SM, Kelly JJ, Sandor A, Litwin DEM (2000) Hand-assisted laparoscopic aortobifemoral bypass grafting. J Vasc Surg 31:1142–1148 Babu SC, Shah PM, Nitahara J (1995) Acute aortic occlusion – factors that influence outcome. J Vasc Surg 21:567–575 Bloor K (1961) Natural history of arteriosclerosis of the lower extremities. Ann R Coll Surg Engl 28:36–52 Brewster DC (1991) Clinical and anatomic considerations for surgery in aortoiliac disease and results of surgical treatment. Circulation 83 [Suppl I]:I–42 Coggia M, Javerliat I, Di Centa I, Colacchio G, Leschi JP, Kitzis M, Goëau-Brissonière O (2004) Total laparoscopic bypass for aortoiliac occlusive lesions: 93-case experience. J Vasc Surg 40:899–906 Corson JD, Brewster DC, Darling RC (1982) Surgical management of infrarenal aortic occlusion. Surg Gynecol Obstet 153:369–372 Cronenwett JL, Davis JT Jr, Gooch JB (1980) Aortoiliac occlusive disease in women. Surgery 88:775 DeBakey ME, Lawrie GM, Glaeser DH (1985) Patterns of atherosclerosis and their surgical significance. Ann Surg 201:115 de Donato G, Weber G, de Donato G (2002) Minimally invasive or conventional aorto-bifemoral by-pass. A randomised study. Eur J Vasc Endovasc Surg 24:485–491 De Smet AAEA, Ermers EJM, Kitselaar PJEHM (1996) Duplex velocity characteristics of aortoiliac stenoses. J Vasc Surg 23:628–636 De Weese JA, Rob CG (1962) Autogenous vein graft ten years later. Surgery 6:775–784 Dion YM, Gracia CR (1997) A new technique for laparoscopic aortobifemoral grafting in occlusive aortoiliac disease. J Vasc Surg 26:685–692 Dion YM, Katkouda N, Rouleau C, Aucoin A (1993) Laparoscopically-assisted aortobifemoral bypass. Surg Laparosc Endosc 3:425–429 Elmore JR, Franklin DP, Youkey JR, Oren JW, Frey CM (1998) Normothermia is protective during infrarenal aortic surgery. J Vasc Surg 28:984–992 Jansen RMG, de Vries SO, Cullen KA, Donaldson MC, Hunink MGM (1998) Cost-identification analysis of revascularization procedures on patients with peripheral arterial occlusive disease. J Vasc Surg 28:617–623 Kafetzakis A, Giannoukas AD, Kochiadakis G, Igoumenidis N, Vlachonikolis IG, Tsetis D, Katsamouris A (2001) Occult aorto-iliac disease in patients with symptomatic coronary artery disease. Int Angiol 20:295–300 Kolvenbach R, Da Silva L, Deling O, Schwierz E (2000) Video-assisted aortic surgery. J Am Coll Surg 190:451–457
373
374
5.5 Aortoiliac Occlusive Disease
20 Pentecost MJ, Criqui MH, Dorros G, Glodstone J, Johnston KW, Martin EC, Ring EJ, Spies JB (2003) Guidelines for peripheral percutaneous transluminal angioplasty of the abdominal aorta and lower extremity vessels. J Vasc Interv Radiol 14:S495–S515 21 Shulman G (2000) Quality of processed blood for autotransfusion. J Extra Corpor Technol 32:11–19 22 Sise MJ, Shackford SR, Rowley WR, Pistone FJ (1989) Claudication in young adults: a frequently delayed diagnosis. J Vasc Surg 10:68–74 23 Starer F, Sutton D (1958) Aortic thrombosis. BMJ 1:1255–1263
24 The I.C.A.I. group (gruppo di studio dell’ischemia cronica critica degli arti inferiori) (1997) Long term mortality and its predicators in patients with critical leg ischaemia. Eur J Vasc Endovasc Surg 14:91–95 25 TransAtlantic Inter-Society Consensus (TASC) (2000) Management of peripheral arterial disease (PAD). Eur J Vasc Endovasc Surg 19 [Suppl A] 26 Turnipseed WD, Carr SC, Tefera G, Acher CW, Hoch JR (2001) Minimal incision aortic surgery. J Vasc Surg 34:47–53
375
5.6 Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures Jérôme Cau, Jean-Baptiste Ricco, Matthieu Guillou, Guillaume Febrer, Alexandre Lecis, Christophe Marchand
5.6.1 Introduction The use of minimally invasive laparoscopic techniques has expanded in recent years. As in other specialties, these techniques are becoming increasingly prevalent in vascular surgery. For aortic repair best results in terms of long-term patency are obtained by conventional surgery but its associated short-term morbidity and mortality have not changed in the last 10 years. This situation created an opening for endovascular techniques that are much less invasive but with less reliable long-term results. In addition to endovascular surgery, video-endoscopic aortic surgery has been proposed as an alternative to conventional open surgery and is considered by some as a veritable third solution. The advantages of minimally invasive surgery are shorter intensive care and hospital stay, quicker resumption of intestinal transit, requirement for less analgesic and fewer abdominal wall complications. But specialized training is required to master the procedure and to become acquainted with the coelioscopic practice necessary for laparoscopic suture.
Transperitoneal Route as Described by Alimi [2] The patient is placed in the dorsal decubitus position. The operating surgeon and first assistant stand on the left side of the table and the second assistant on the right. The procedure begins with a 10-mm peri-umbilical incision for placement of the viewing endoscope using the open-coelioscopy technique. The working trocars are placed along the same pararectal line in a triangular configuration with the viewing endoscope. The patient is then placed in the Trendelenburg position at 30° and the table is tilted 20° to the right so that the small intestinal loops fall into the top right corner of the abdomen. The dedicated laparoscopic retractor is then inserted to collect and maintain the loops on the right side. Aortic dissection is performed under laparoscopic guidance. The posterior parietal peritoneum is opened over the duodenojejunal angle medially to the inferior
5.6.2 Operative Procedures 5.6.2.1 Laparoscopy-Assisted Operative Procedures with Vascular Suturing by the Minimally Invasive Route In laparoscopy-assisted repair, dissection of the infrarenal aorta is done entirely under laparoscopic guidance and aortic suture is performed by minilaparotomy through the transperitoneal or retroperitoneal route. One of the main technical difficulties of laparoscopic procedures is achieving stable aortic exposure. Several teams have designed dedicated laparoscopic retractors to retain intestinal loops when using the transperitoneal approach [1, 3, 4].
Fig. 5.6.1 Alimi’s retractor allowing the dissection of the infrarenal aorta through a transperitoneal route. Patient in dorsal decubitus position. Small intestinal loops are maintained by the retractor
376
5.6 Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures
mesenteric vein. The duodenojejunal angle is released by sectioning the Treitz muscle. After identification of the left renal vein, the peri-aortic lymphatic tissue is incised using coagulating scissors and the anterior half of the circumference of the infrarenal aorta is exposed. At this time, the retractor (Fig. 5.6.1) can be lowered so as to obtain better exposure of the right anterior edge of the aorta. Distal dissection is continued to the mesenteric artery that is controlled. To facilitate tunnelling, the aortic bifurcation as well as the first 4 cm of the common iliac arteries are dissected on both sides. After systemic heparinization, proximal occlusion of the aorta is performed by applying an atraumatic clamp (DeBakey clamp, BBraun/Aesculap, Tuttlingen, Germany) through a 10-mm incision made under the xiphoid process. The distal clamp is placed on either the aorta or the common iliac arteries if there is extensive calcification of the distal aorta. A 6-cm or 8-cm minilaparotomy is performed after complete dissection of the infrarenal aorta and clamp placement. Exposure stays the same (trocars, retractors and clamps stay in place). The anastomosis is made using the conventional technique under visual control [1, 2]. The prosthetic branches are tunnelled anatomically and anastomosed on the femoral arteries after conventional exposure.
Retroperitoneal Route as Described by Edoga [6, 17] The patient is placed in the dorsal decubitus position with the trunk rotated 30° to the right by placing a bolster under the dorsolumbar region. The operating surgeon stands on the left side of the table, the assistant stands on the other side, and the instrumentalist stands beside the operating surgeon. Kolvenbach developed a video-assisted procedure called hand-assisted laparoscopic surgery (HALS), which permits surgeons to introduce their nondominant hand into the abdomen to assist videoscopic exposure and dissection. After establishing a pneumoperitoneum, a 6-cm subumbilical incision is made for placement of the hand access device (Handport, Smith and Nephew Surgical, Andover, Mass., USA) [3]. The viewing endoscope is placed under the umbilicus and two operating trocars are inserted in a triangular configuration in the right pararectal region. Dissection and exposure of the aorta are performed in the same way as described for the transperitoneal route except that it can be assisted by the hand in the peritoneum [20, 21]. The system is then withdrawn, a two-blade retractor is used to expose the aorta, and the anastomosis is performed via minilaparotomy.
The operation begins with a 15-cm vertical cutaneous incision in the left flank between the iliac crest and the 12th rib. After making a 30-mm incision in the aponeurosis of the superior oblique muscle and separating the muscle layers, retroperitoneal dissection is started using digital manipulation. A 10-mm balloon trocar is inserted in the incision to allow introduction of a 30° angled viewing endoscope. A preperitoneal distension balloon (OMS-PDBS2 Origin Medsystems, California, USA) can be helpful to initiate the retroperitoneal dissection plane. Carbon dioxide is progressively insufflated to establish a retro-pneumoperitoneum with a pressure of 13–15 mmHg. After terminating dissection using the endoscope, the two 10-mm operating trocars are placed in a triangular configuration under visual control. Reclining the retroperitoneal cavity requires special care due to the risk of tearing the peritoneum and causing pneumoperitoneum. Two additional 10-mm trocars are inserted, i.e. the first on the medioclavicular line at 5 cm from the inguinal ligament for introduction of an intestinal retractor and the second on the edge of the rib on the posterior axillary line for insertion of a suction catheter and later of the proximal aortic clamp. Vascular dissection begins with exposure of the left common iliac artery after locating the ureter. Dissection is continued until the left renal artery is identified after clipping the hemi-azygos-lumbar vein. Proximal aortic clamping is performed through the left subcostal trocar. Distal clamping is performed through the lower clamp above the left inguinal ligament. According to the technique described by Edoga [6] CO2 insufflation is stopped after placement of a wall-lifting device (Laparolift, Origin Medsystems, Menlo Park, Calif., USA) at the beginning of the dissection. If extensive pneumoperitoneum occurs, retroperitoneal dissection must be reduced, in which case exsufflation is necessary via a Palmer needle introduced transperitoneally at the level of the umbilicus. A 4-cm minilaparotomy centred on the trocar placed by the open coelioscopic technique is made between the anterosuperior iliac crest and the 12th rib. Proximal anastomosis is performed under visual control without changing laparoscopic exposure. Anastomosis may be made end-to-end or side-to-end. The branches of the prosthesis are tunnelled anatomically and anastomosed to the common femoral artery using the conventional technique. The advantage of the retroperitoneal approach is to eliminate contact with intestinal loops. However, dissection is more difficult because the operating space achieved in the retroperitoneal cavity is smaller than in the peritoneal cavity. In addition, the operating space in
5.6.3 Totally Laparoscopic Operative Procedures
the retroperitoneal cavity has a tendency to diminish because of gas diffusion in the peritoneal cavity during the procedure. This can become problematic since exsufflation using a Palmer needle is not always effective.
5.6.3 Totally Laparoscopic Operative Procedures To date four procedures have been described for achieving totally laparoscopic revascularization of the lower extremities from the infrarenal aorta. In these operative procedures the proximal aortic anastomosis is performed totally under laparoscopic guidance (endoanastomosis) [5, 8, 12, 24]: • Retrocolic or prerenal transperitoneal procedure • Combined transperitoneal and retroperitoneal procedure • Strict retroperitoneal procedure • Direct transperitoneal procedure.
5.6.3.1 Retrocolic or Prerenal Transperitoneal Procedure as Described by Coggia [8, 11] The transperitoneal procedure described by Coggia et al. involves exposure of the aorta by left prerenal colic dissection. This technique is similar to the one used for laparotomy. The patient is placed in the dorsal decubitus position with an inflatable bolster under the left flank. The left arm remains free and the right arm is placed on an arm-
Fig. 5.6.2 Trocars’ position for the retrocolic transperitoneal route. (1 30° angled viewing endoscope, 2 coagulating scissors needle holder, 3 blunt grasping forceps, 4 suction lavage system, 5 blunt grasping forceps distal clamp, 6 retractor-proximal clamp)
rest. The lower extremities are flexed at 30° and attached parallel to each other. Two supports must be placed on the right side of the thorax and flank in order to retain the patient when the table is tilted to the right (45°) and the bolster is inflated (35°). After these manoeuvres, i.e. tilting and inflation, the patient is in the complete right lateral decubitus position (Fig. 5.6.2). Using this installation technique, it is possible to change the patient from the right lateral decubitus position, used during exposure of the aorta, to the dorsal decubitus position, used during exposure of the femoral artery, simply by tilting the operating table. The operating surgeon and first assistant stand in front of the patient’s abdomen and the second assistant stands opposite the operating surgeon (Fig. 5.6.3). The 10-mm trocar is placed by the open coelioscopic technique on the left midaxillary line 3–4 cm below the chondrocostal junction. The other five trocars are introduced under visual control after establishing a pneumoperitoneum at a pressure of 15 mmHg. The two operating trocars are placed 6–7 cm apart on the left transrectal line parallel to the midline (trocar no. 2 scissors and needle holder and trocar no. 3 fenestrated forceps). The two trocars for the first assistant are introduced in the left iliac fossa and on the midline 5 cm from the pubis (trocar no. 4 suction catheter and trocar no. 5 fenestrated forceps followed by distal clamp). The last trocar is positioned on the midline 2 cm below the xiphoid process distal (trocar no. 6 proximal clamp) (Fig. 5.6.4).
Fig. 5.6.3 Patient in right lateral decubitus position for the retrocolic transperitoneal route. (1 Operating surgeon, 2 first assistant, 3 second assistant)
377
378
5.6 Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures
Fig. 5.6.4 Operative view: position of the operators and trocars for the retrocolic transperitoneal approach
The left laterocolic approach involves left colic dissection to achieve prerenal exposure of the aorta. The table is tilted as far as possible to the right (i.e. 45°) and the bolster is inflated to enhance the right lateral decubitus position by 30°. The Toldt fascia is incised from the left colic angle to the mesosigmoid to allow complete dissection of the left mesocolon. After identification of the genital vein, prerenal dissection is continued to the left renal vein, which is completely mobilized. With the patient in the right lateral decubitus position, the intestinal loops collect on the right side of the abdominal cavity (Fig. 5.6.5). Using transparietal sutures the mesocolon is attached to the abdominal wall so that it forms an apron, thus providing stable exposure of the aorta. In patients with large kidneys, transparietal sutures through the Gerota’s fascia can be used to hold the left kidney out of the operating field. The lymphatic tissue surrounding the aorta is opened using coagulating scissors to expose the infrarenal aorta. Use of a 30° or 45° angled viewing endoscope facilitates circumferential aortic visualization, which is necessary for proximal clamping. Mobilization of the renal vein is necessary to expose the inter-renal portion of the aorta. Exposure can be enlarged to include the suprarenal aorta by retropancreatic dissection. Dissection is extended to the common iliac artery after control of the inferior mesenteric artery. Unlike the left common iliac artery, the right common iliac artery is controlled over 3–5 cm. For exposure of the femoral arteries the table is untilted and
Fig. 5.6.5 Patient in right lateral decubitus with an inflated bolster. The left mesocolon has been dissected forming an apron on the intestinal loops. The 30° angled viewing endoscope shows the aorta
the bolster is deflated. After femoral exposure, the table is retilted to the right to allow introduction of the bifurcated prosthesis through one of the trocars. The right branch of the prosthesis is tunnelled in the anatomical position before making the proximal anastomosis. The left branch is closed and left in the abdomen to avoid the risk of gas loss if another tunnelling procedure is performed at this time. Proximal and distal aortic clamping is performed with laparoscopic clamps (B/Braun/Aesculap, Tuttlingen, Germany or Storz-France) introduced through trocar nos. 5 and 6 (Fig. 5.6.4). The anastomosis between the aorta and the prosthesis is made with two hemisutures using 3/0 polypropylene under total laparoscopic guidance. Suturing is performed using an 18-cm-long segment of 3/0 polypropylene suture with one end tied to a pledget to avoid having to tie the first knot. This technique reduces suture time and limits mechanical trauma during suture. As in traditional open surgery, either an end-to-side or an end-to-end anastomosis can be used for treatment of occlusive lesions. After performing longitudinal arteri-
5.6.3 Totally Laparoscopic Operative Procedures
Fig. 5.6.6 End-to-end totally coelioscopic aortic anastomosis with a polypropylene 3/0 running suture
Fig. 5.6.7 End-to-end totally coelioscopic aortic anastomosis. Closure of the distal stump of the aorta with a polypropylene 3/0 running suture
otomy using Potts scissors, the end-to-side anastomosis begins with a tacking suture on the heel of the prosthesis. Endoanastomosis begins with the left hemisuture using a segment of polypropylene tied to a pledget (Fig. 5.6.6). Hemisuturing is stopped at the toe of the prosthesis. The right hemisuture is made in a similar way. The two sutures are joined with knots tied laparoscopically. For end-to-end endoanastomosis the infrarenal aorta is transected with excision of a 3-cm aortic collar to close the distal aortic stump using a back-and-forth polypropylene 3/0 suture (Fig. 5.6.7). The left branch of the prosthesis is then tunnelled. Distal anastomoses on the common femoral arteries are performed conventionally with the patient in the dorsal decubitus position. After removing the clamp, haemostasis of the distal aortic stump and proximal anastomosis should be carefully checked. The mesocolon is repositioned under videoscopic control so as to isolate the prosthesis. It is not necessary to attach the mesocolon to the wall. Exsufflation of the pneumoperitoneum is performed through a Redon drain. Use of this retrocolic procedure resolves two important problems, i.e. achieving adequate exposure and operating space. The mesocolon and intestinal loops are maintained out of the operating field without retractors by positioning the patient in lateral decubitus. The intestinal loops are excluded from the operating field by the mesocolon, which acts as a peritoneal apron [16]. This
provides a stable operating space allowing high-quality coelioanastomosis. In thin patients or patients with a history of left renal or colonic surgery, it is better to use the left retrorenal retrocolic procedure [9]. Exposure of the aorta can be extended up to the coeliac region by continuing dissection using the partial mediovisceral rotation technique. Passage into the retrorenal plan allows even wider exposure of the coeliac region. Unlike the common iliac artery, the right iliac artery can be difficult to dissect. Exposure is achieved on the slant and the left mesocolon limits control to no more than 6 cm. Inexperienced surgeons may, at the beginning of their training, inflict peritoneal lesions during mobilization of the mesocolon in thin patients. These must be sutured immediately to avoid invasion of the operating field by the small intestine loops.
5.6.3.2 Combined Transperitoneal and Retroperitoneal Procedures The combined transperitoneal and retroperitoneal procedure presented here is described by Dion [12–15]. The main feature of the technique is creation of a peritoneal apron that retains the intestinal loops without reducing the size of the operating cavity. A 10-mm trocar is introduced at the level of the umbilicus to establish a pneumo-
379
380
5.6 Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures
peritoneum at a pressure of 15 mmHg. The patient is then placed in the Trendelenburg position at 10° with the table tilted to the right. As initially described by Dion, the technique involved distinct retroperitoneal and transperitoneal phases for dissection of the left parietal peritoneum, transposition to the right side of the midline, and attachment to the wall by three transparietal sutures to form a peritoneal apron. The technique was subsequently simplified [16] based on the retrocolic technique described by Coggia [8]. The procedure begins with an incision in the left parietal peritoneum about 8 cm anterolateral to the line of Toldt. The operating surgeon stands on the patient’s right during this phase of the procedure. Dissection is continued along the prerenal plane up to the renal vein. The infrarenal aorta proximal to the inferior mesenteric artery is then dissected. The surgeon moves to the patient’s left side to complete the procedure. The instruments are placed in their definitive position. The apron is then attached to the wall to keep the intestinal loops out of the operating field. The distal aorta and the two common iliac arteries are dissected. Creation of the peritoneal “apron” begins with an incision in the parietal peritoneum 3 cm above the left internal inguinal ring. Dissection is continued along the edge of the left large rectal muscle. The last two lateral pararectal trocars are placed. The vascular prosthesis is introduced into the retroperitoneal cavity and each limb of the prosthesis is tunnelled in the anatomical position to the femoral triangles before performing the proximal anastomosis. The aorta is then transected 15 mm below the proximal clamp and an end-to-end anastomosis is performed under laparoscopic guidance using two prolene 3-0 hemisutures. Distal anastomoses were performed on the common femoral artery using the conventional technique.
5.6.3.3 Retroperitoneal Operation The exclusively retroperitoneal technique was first described by Said [24] and later developed by Edoga [17], who associated minilaparotomy with vascular anastomosis. The retroperitoneal procedure is a suitable alternative when the transperitoneal procedure is contraindicated [19] (e.g. hostile abdomen and peritoneal adhesions) or when exposure of the common iliac artery is needed (e.g. iliofemoral by-pass). The patient is placed in the right lateral decubitus position as for the retrocolic transperitoneal procedure (see Section 5.6.2.1). The viewing endoscope is introduced
through a 15-mm incision above and medial to the iliac crest using the open retroperitoneoscopic technique with prior dissection of the retroperitoneal space using digital manipulation (see Section 5.6.2.2). The most important step is dissection of the retroperitoneum under videoscopic control. This dissection should be extended up to the midline level to avoid peritoneal tears. The main advantage of the retroperitoneal route is to exclude the visceral organs from the operating field albeit at the expense of a smaller working cavity. The risk of peritoneal tears is high if dissection is not performed carefully. This can lead to a reduction in the size of the operating cavity due to the pneumoperitoneum. In most cases, conversion to traditional open repair is necessary. Although it has been abandoned by most groups, the exclusively retroperitoneal procedure can be useful in special cases.
5.6.3.4 Direct Transperitoneal Procedure [7] Until now direct transperitoneal exposure of the aorta, as in traditional open surgery, has been difficult due to the lack of a retractor to retain the intestinal loops and achieve stable aortic exposure. Recently a simple and effective bowel retractor was proposed. This prototype consists of a net placed in a racket-like fashion between two 30-cm-long pre-shaped flexible steel rods attached to an operating handle. The net is used to gather up and retract the bowel loops (Fig. 5.6.8). The device is packed in a 10-cm-long, 1-cm-diameter sheath that passes easily through a 10-mm-diameter endoscopic trocar. Inside the sheath the two blades are in contact on their convex edge. When the operator pushes the handle in, the rods exit from the end of the sheath and assume their pre-defined “S” shape, thus deploying the net within the abdominal cavity. The exact shape of the retractor depends on the size of the net that determines how far the shafts can spread. After placement of the bowel retractor, the patient is repositioned in the total dorsal decubitus position. The retractor holds the bowel loops clear of the operating field throughout the procedure. As in conventional open surgery, exposure of the aorta begins by incision of the posterior parietal peritoneum and section of the ligament of Treitz. During this step the retractor is pushed towards the diaphragm so as to mobilize the duodenum. After division of the pre-aortic lymphatics and dissection of the left renal vein, the infrarenal aorta is visualized. Use of a 30° viewing endoscope greatly facilitates exposure of the infrarenal aorta and its branch-
5.6.4 Instrumentation
two rods back into the sheath. The net folds up automatically without further manipulation.
5.6.4 Instrumentation New instrumentation such as self-retaining retractor arms, video racks and specific vascular coelioscopic devices has contributed greatly to the development of minimally invasive and laparoscopic vascular surgery.
5.6.4.1 Standard Laparoscopic Instruments
Fig. 5.6.8 Self-expandable bowel retractor allowing totally coelioscopic, direct transperitoneal exposure of the aorta
es, including the inferior mesenteric artery and both common iliac arteries. After completing exposure, the proximal aortic clamp is introduced through the working channel and placed below the xiphoid appendix. The distal clamp is introduced through the suprapubic trocar. Aortic by-pass is performed according to the technique described by Coggia [8]. After dividing the aorta, proximal anastomosis is performed using two hemicircumferential running sutures. Femoral anastomoses are done through a conventional approach. After closing the posterior parietal peritoneum using a 3/0 resorbable suture, the retractor is removed by simply withdrawing the
Laparoscopic aortic repair requires the use of standard coelioscopic equipment as well as instruments designed specifically for vascular surgery. The basic set-up includes the following instrumentation: • 0–10 mm endoscope • 10-mm 30° angled viewing endoscope • cold light source • video rack with a triCDD monitor (for optimal image quality) • electronic insufflator • 10-mm open coelioscopic trocar • 6 × 10-mm trocars with valve to prevent CO2 loss • 3 × 5-mm blunt grasping forceps to hold digestive structures during dissection; these forceps must also be suitable for handling needles during endoanastomosis • coagulating scissors • right-angled coagulating hook or bipolar coagulation forceps • suction lavage system.
5.6.4.2 Specific Laparoscopic Instruments for Vascular Laparoscopy Specific laparoscopic instruments for vascular surgery include the following: • Potts laparoscopic scissors (Fig. 5.6.9) • Two releasable clamps (Clamps B/Braun) for occlusion of the iliac arteries (Fig. 5.6.10) • Two laparoscopic clamps with 10-mm DeBakey-type jaws and safety ratchet for proximal and distal aortic clamping (B/Braun-Aesculap or Storz-France) (Fig. 5.6.11)
381
382
5.6 Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures
Fig. 5.6.12 Curved jaws and axial handle needle holder for making totally coelioscopic aortic anastomosis
Fig. 5.6.9 Potts laparoscopic scissors (B/Braun-Aesculap)
• One needle holder with curved jaws (MicrofranceXomed) and axial handle used to fashion the endoanastomoses (Fig. 5.6.12) • Two 10-mm endoscopic retractors (Endoretract, Ethicon-France) • 3/0 gauge polypropylene suture for endoanastomoses and haemostasis • Endosuture material; the most suitable suture material for endoanastomosis is an 18-cm-long segment attached to a pledget to avoid having to tie the first knot.
5.6.5 Complications 5.6.5.1 Intraoperative Complications Vessel Lesions [2, 12] Fig. 5.6.10 Releasable clamps (B/Braun-Aesculap) for occlusion of the iliac arteries and inferior mesenteric artery
This is a common complication. Haemostasis can be difficult since the lumbar veins quickly retract behind the spine. Bleeding can be minimized by videoendoscopy with high insufflation pressure. Great care is necessary when exposing the lumbar veins.
Urethral Lesion [2, 6, 14] This complication can occur during dissection or tunnellization. The best preventive measure is constant careful visual control during both steps.
5.6.5.2 Early Postoperative Complications Retroperitoneal Haematoma [17, 24] Fig. 5.6.11 Aortic clamp with DeBakey-type jaws and safety ratchet (B/Braun-Aesculap) for proximal and distal aortic clamping
This frequent complication is due to excessive dissection of the retroperitoneal space and to insufficient hae-
5.6.6 Current Indications and Results
mostasis also in relation to the minimizing effects of the pneumoretroperitoneum on bleeding. Drainage of the retroperitoneal cavity should be performed in all cases. Haematoma is associated with an increase in postoperative pain and duration of hospitalization.
Occlusion of a Prosthetic Limb [2, 17, 20] This complication has been observed in most series. It is linked to the duration of clamping and to problems with purging and cleaning the limbs of the prosthesis. Tunnelling of the limbs is difficult to control and defects have led to a number of occlusions.
5.6.6 Current Indications and Results The indications for laparoscopically assisted and totally laparoscopic revascularization of the lower limbs from the aorta or common iliac artery are the same as those for conventional open revascularization. Revascularization using laparoscopic techniques should be limited to long, multiple lesions of the iliac arteries (TASC C, D) or after failure of endovascular treatment. Abdominal-pelvic CT-scan without contrast injection is necessary before minimally invasive and or laparoscopic revascularization to study the extent and location of aortic and iliac calcification. No prospective randomized trial has been carried out to compare minimally invasive, video-assisted and totally laparoscopic procedures. It is difficult to obtain data from reported series, because of technical differences: aortobifemoral by-pass, aortounifemoral by-pass, iliofemoral bypass for claudication or critical ischaemia. At the present time the main points of controversy between advocates of the video-assisted procedure and the total laparoscopic procedure involve the duration of clamping and the difficulty of performing vascular endoanastomosis.
The rate of conversion to open surgery for totally laparoscopic procedures has varied from 2.15% to 30% in various series (Table 5.6.1). The totally laparoscopic procedures always take longer than conventional surgery but the time decreases as a function of the operators’ training and experience. Mean clamping time in the different series has ranged from 1 h to 2 h with maximum times being associated with end-to-end anastomosis in totally laparoscopic procedures. Clamping time also decreases with experience but is still longer than in conventional surgery regardless of the minimally invasive technique used. Clamping times closest to those of conventional surgery have been achieved in video-assisted techniques but total procedures times are substantially longer due to the duration of laparoscopic dissection. In a retrospective study Edoga [17] compared postoperative recovery in patients undergoing laparoscopic and conventional revascularization. Findings showed that the duration of mechanical ventilation and intensive care was significantly shorter after laparoscopic revascularization. In agreement with other studies, Edoga also observed more rapid resumption of intestinal transit and a decreased the need for analgesics after laparoscopic revascularization. In addition to equipment specially adapted for vascular surgery, laparoscopic aortic revascularization requires training in coelioscopy, which is rarely included in vascular surgery training programmes. In our opinion coelioscopy courses should include training on a Pelvitrainer. Trainees should be able to perform end-to-end and endto-side anastomoses in less than 20 min. Most teams developing minimally invasive techniques or laparoscopic techniques have performed treatment of aortobifemoral by-pass first and then moved on to treatment of infrarenal aortic aneurysm, which still requires a great deal of experience [10, 23].
Table 5.6.1 Totally laparoscopic reconstruction of aortoiliac occlusive disease. Characteristics and results. Time in minutes Patients Barbera [4]
24
Dion [16]
10
Coggia [10]
93
Aortic clamping time
121 67.5
Operative time
Conversion to open surgery (%)
Mortality (%)
Morbidity (%)
261
16.6
0
300
30
0
30
4
4
240
2.15
?
Hospital stay (day) 8.6 ? 7
383
384
5.6 Aortobifemoral By-pass: Laparoscopy-Assisted and Totally Laparoscopic Operative Procedures
5.6.7 Conclusions Currently there are two competing methods of minimally invasive revascularization, i.e. video-assisted and totally laparoscopic procedures. For many surgeons, the best alternative to the mini-incision method is totally laparoscopic repair. With sufficient experience operators can achieve extensive control of the infrarenal and suprarenal aorta. However, the video-assisted method provides a good way to become familiar with the “total laparoscopic” technique. The totally laparoscopic approach provides a much larger operating field than the mini-incision method and allows complex procedures including repair of the visceral arteries [18]. The place of laparoscopic vascular surgery in relation to traditional open surgery and endovascular repair remains to be proved. The future of this technique is unknown and will depend mainly on training, which will allow surgeons to use the totally laparoscopic approach with acceptable clamping and procedure times. References 1. Alimi YS, Hartung O, Cavalero C, Brunet C, Bonnoit J, Juhan C (2000) Intestinal retractor for transperitoneal laparoscopic aortoiliac reconstruction: experimental study on human cadavers and initial clinical experience. Surg Endosc 14:915–919 2. Alimi YS, Hartung O, Valerio N, Juhan C (2001) Laparoscopic aortoiliac surgery for aneurysm and occlusive disease: when a minilaparotomy should be performed? J Vasc Surg 33:469–475 3. Arous EJ, Nelson PR, Yood SM, Kelly JJ, Sandor A, Litwin DE (2000) Hand-assisted laparoscopic aortobifemoral bypass grafting. J Vasc Surg 31:1142–1148 4. Barbera L, Mumme A, Metin S, Zumtobel V, Kemen M (1998) Operative results and outcome of twenty-four totally laparoscopic vascular procedures for aortoiliac occlusive disease. J Vasc Surg 28:136–142 5. Barbera L, Ludemann R, Grossefeld M, Welch L, Mumme A, Swanstrom L (2000) Newly designed retraction devices for intestine control during laparoscopic aortic surgery: a comparative study in an animal model. Surg Endosc 14:63–66 6. Castronuovo JJ Jr, James KV, Resnikoff M, McLean ER, Edoga JK (2000) Laparoscopic-assisted abdominal aortic aneurysmectomy. J Vasc Surg 32:224–233 7. Cau J, Ricco JB, Deelchand A, Berard X, Cau B, Costecalde M, Chaufour X, Barret F, Barret A, Bossavy JP (2005) Totally laparoscopic aortic repair: a new device for direct transperitoneal approach. J Vasc Surg 41:902–906
8. Coggia M, Bourriez A, Javerliat I, Goeau-Brissonniere O (2002) Totally laparoscopic aortobifemoral bypass: a new and simplified approach. Eur J Vasc Endovasc Surg 24:274–275 9. Coggia M, Di Centa I, Javerliat I, Colacchio G, Goeau-Brissonniere O (2004) Total laparoscopic aortic surgery: transperitoneal left retrorenal approach. Eur J Vasc Endovasc Surg 28:619–622 10. Coggia M, Javerliat I, Di Centa I, Colacchio G, Cerceau P, Kitzis M, Goeau-Brissonniere OA (2004) Total laparoscopic infrarenal aortic aneurysm repair: preliminary results. J Vasc Surg 40:448–454 11. Coggia M, Javerliat I, Di Centa I, Colacchio G, Leschi JP, Kitzis M, Goeau-Brissonniere OA (2004) Total laparoscopic bypass for aortoiliac occlusive lesions: 93-case experience. J Vasc Surg 40:899–906 12. Dion YM, Chin AK, Thompson TA (1995) Experimental laparoscopic aortobifemoral bypass. Surg Endosc 9:894–897 13. Dion YM, Gracia CR, Demalsy JC (1996) Laparoscopic aortic surgery. J Vasc Surg 23:539 14. Dion YM, Gracia CR, Estakhri M, Demalsy JC, Douville Y, Piccinini E, Stancanelli V (1998) Totally laparoscopic aortobifemoral bypass: a review of 10 patients. Surg Laparosc Endosc 8:165–170 15. Dion YM, Gracia CR, Ben El Kadi HH (2001) Totally laparoscopic abdominal aortic aneurysm repair. J Vasc Surg 33:181–185 16. Dion YM, Thaveau F, Fearn SJ (2003) Current modifications to totally laparoscopic «apron technique». J Vasc Surg 38:403–406 17. Edoga JK, Asgarian K, Singh D, James KV, Romanelli J, Merchant S, Romano D, Joostema B, Street J (1998) Laparoscopic surgery for abdominal aortic aneurysms. Technical elements of the procedure and a preliminary report of the first 22 patients. Surg Endosc 12:1064–1072 18. Javerliat I, Coggia M, Bourriez A, Di Centa I, Cerceau P, Goeau-Brissonniere OA (2004) Total laparoscopic aortomesenteric bypass. Vascular 12:126–129 19. Javerliat I, Coggia M, Centa ID, Dubosq F, Colacchio G, Leschi JP, Goeau-Brissonniere O (2005) Total videoscopic aortic surgery: left retroperitoneoscopic approach. Eur J Vasc Endovasc Surg 29:244–246 20. Kolvenbach R, Deling O, Schwierz E, Landers B (1998) Reducing the operative trauma in aortoiliac reconstructions – a prospective study to evaluate the role of video-assisted vascular surgery. Eur J Vasc Endovasc Surg 15:483–488 21. Kolvenbach R, Da Silva L, Deling O, Schwierz E (2000) Video-assisted aortic surgery. J Am Coll Surg 190:451–457
References
22. Kolvenbach R, Ceshire N, Pinter L, Da Silva L, Deling O, Kasper AS (2001) Laparoscopy-assisted aneurysm resection as a minimal invasive alternative in patients unsuitable for endovascular surgery. J Vasc Surg 34:216–221
23. Kolvenbach R, Schwierz E, Wasilljew S, Miloud A, Puerschel A, Pinter L (2004) Total laparoscopically and robotically assisted aortic aneurysm surgery: a critical evaluation. J Vasc Surg 39:771–776 24. Said S, Mall J, Peter F, Muller JM (1999) Laparoscopic aortofemoral bypass grafting: human cadaveric and initial clinical experiences. J Vasc Surg 29:639–648
385
387
5.7 Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair N.A. Saratzis, N. Melas, A. Saratzis, D.A. Kiskinis
5.7.1 Introduction Since the recent publication of EVAR Trial I [23] and DREAM [29], endovascular aneurysm repair (EVAR) has proven superior results versus open surgical repair concerning 30-day mortality and morbidity. It is now well enough established that EVAR is feasible, efficacious and has proven considerable benefits over conventional open surgery in many aspects; namely, duration of operation, blood loss, length of hospital and intensive care unit stay, quality of life (QOL) and 30-day mortality and morbidity [11, 14, 21, 23, 29, 30]. Moreover, midterm results of EVAR are sufficiently encouraging to justify the procedure, especially in high-risk patients [6, 11, 15, 17, 30, 40, 51, 63]. However, some publications have raised concerns about the long-term results of the procedure [4, 24, 26, 43, 62]. In some abdominal aortic aneurysms (AAA) or iliac aneurysms though, endografting with a bifurcated endoprosthesis is contraindicated due to anatomical restrictions, such as a narrow terminal aorta and an aneurismal, tortuous, narrow or calcified contralateral iliac artery [1, 9]. In these circumstances, aortouniiliac endograft and femoro-femoral crossover by-pass could overcome the limitations and be used to repair difficult AAAs in highrisk patients [13, 34, 40, 45, 49, 56, 61].
5.7.2 Definition A bifurcated endograft is a unibody or modular reversed Y-shaped stent graft that excludes an AAA intraluminally by gaining proximal sealing just below the renal arteries and distal sealing at each common iliac artery, following the internal native vascular axis. In contrast, an aortouniiliac (AUI) endograft is a conical (tapered) unibody stent graft with a gradually decreasing diameter from top to
bottom, which is attached proximally, as above, below the renal arteries, but distally it follows only one common iliac artery, excluding the opposite one from the in-flow. In order to avoid endoleak type II from the contralateral axis towards the sack, the contralateral common iliac artery must be obliterated with a short occluding stent graft (occluder). In order to provide blood flow to the contralateral femoral, external and internal iliac arteries, adjacent extra-anatomic femoro-femoral crossover by-pass should follow the procedure.
5.7.3 Indications Indications for EVAR using AUI endograft configuration are: • Narrow terminal aorta (diameter <15 mm), since in such a narrow space the contralateral leg of a bifurcated endograft would lack adequate space for safe deployment or its catheterization would be impossible. • Contralateral common iliac artery >90° from the longitudinal axis of the aneurysm [54], since this anatomy could cause kinking of the contralateral leg of a bifurcated endograft. • Heavily calcified contralateral iliac artery, which could cause difficulty in advancing and deploying the contralateral leg of a bifurcated endograft and probably lead to angulation-kinking of the leg. In contrast, the sheath of the occluder is usually smaller in diameter, enabling easier passage. • Narrow contralateral iliac artery (diameter <6 mm) or obstructed (for the same reason). • Concomitant ecstatic or frankly aneurismal common iliac arteries [21]. • Combination of the previous indications. • Conversion of bifurcated endograft to AUI due to impossible contralateral limb catheterization.
388
5.7 Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair
5.7.4 Contraindications Contraindications for AUI graft implantation, leading to abandonment of the endovascular approach, are: • Proximal neck <10 mm in length (device dependent) • Proximal neck >32 mm in diameter (device dependent) • Proximal neck thrombus >30% of the perimeter • Bilateral common iliac arteries <6 mm in diameter • Bilateral common iliac arteries >16 mm in diameter with indispensable internal iliac arteries (device dependent) • Excessive bilateral iliac artery tortuosity greater than 90° • Excessive bilateral iliac artery calcification • Indispensable inferior mesenteric artery (IMA) • General contraindications for every endovascular procedure: age <18 years, allergy to contrast medium, coagulopathy, pregnancy-lactation, creatinine level >1.7 mg/dl, groin infection and connective tissue disease. Moreover, whenever a bifurcated endograft is implantable, AUI should be avoided as it utilizes extra-anatomic by-pass.
5.7.5 Preoperative Management Preoperative abdominal intravenous (iv) contrast CT scan (aortography) with 3D reconstruction, including groin slices, is standard practice and should be assessed in order to determine the exact anatomical measurements of the proximal and distal landing zones (diameter, length), the aortic and iliac tortuosity and the inner diameters of the access vessels. All these elements assist proper preoperative management and are correlated to the criteria for endovascular repair of abdominal aortic aneurysms. If the creatinine level is above 1.7 mg/dl, then MR angiography (MRA) should be performed instead of contrast CT. Postoperative follow-up plain chest radiograms should be assessed for frame integrity and graft migration. Postoperative iv contrast CT scan should be compared to the preoperative scan in terms of sack diameter and volume, endoleak and kinking. If an endoleak is detected, digital subtraction angiography is the examination of choice to clarify the type.
5.7.6 Procedure Having the patient in the supine position on a radiolucent floating surgical table and in an operating room equipped with a portable C-arm, under regional or general anaesthesia, access is gained through longitudinal bilateral femoral incisions, using a standard technique. The ipsilateral common femoral artery (i.e. the artery from where the main AUI device will be inserted) is catheterized using a puncture Seldinger needle and an 8-Fr sheath is introduced. Heparin (100 IU/kg) is administered iv. Under fluoroscopy, a hydrophilic Terumo guidewire is advanced cephalad to track the iliac axis and well beyond the renal arteries. A guiding catheter is inserted over the Terumo and the latter is exchanged for a stiff 0.035 inch, 260-cm-long guidewire (Amplantz, medi-tech, Boston Scientific, USA). Using the same technique, the contralateral common femoral artery (meaning the artery from where the occluder will be inserted) is catheterized and the Terumo is advanced beyond the renal arteries. Over the Terumo a long (45 cm) 8-Fr Arrow (Arr International, USA) sheath is introduced over the wire. An initial angiogram (SUB) with 20 ml contrast medium confirms the exact anatomical position of the lower renal artery. From the ipsilateral short sheath additional 20 ml dye confirms the position of the ipsilateral internal iliac artery. The ipsilateral short sheath is removed and the 22-Fr introducing system with the preloaded covered endoprosthesis is advanced, under fluoroscopic guidance, over the aneurysm, so that the bare proximal stent is placed just above the lower renal artery. Upon withdrawal of the introducer sheath the endograft is deployed with the bare stent attached suprarenally, thus enhancing proximal fixation, while the first covered segment of the prosthesis is gaining its seal against the proximal neck, excluding the aneurysm. During deployment, angiography is performed from the contralateral axis through the Arrow sheath, which is withdrawn just below the neck inside the sack and the systemic blood pressure is lowered to a level of 90 mmHg, enhancing accurate positioning (Fig. 5.7.1). Distally the graft gains its seal against the ipsilateral common iliac artery in a nonaneurismal segment, except in some cases where the orifice of the ipsilateral hypogastric artery is involved in the aneurysm, so its occlusion is unavoidable, and the graft is distally attached to the external iliac artery, usually by interposing an extension. In some cases preoperative coil embolization of the aneurismal internal iliac artery
5.7.7 Results and Complications
Fig. 5.7.1 From left to right: initial angiogram (note the excessive left iliac tortuosity), aortouniiliac (AUI) deployment, completion angiogram (yellow arrow confirms renal artery patency, and red arrows absence of endoleak)
is obtained in order to avoid possible type II endoleak. For safer attachment in order to increase proximal and distal radial force, in selected cases balloon inflation at the attachment zones or at the overlapping zones should follow the procedure. Through the contralateral femoral artery, angiography (20 ml dye) reveals the position of the contralateral iliac axis. After removing the Arrow sheath, an 18-Fr introducing sheath is inserted and the “occluder” is advanced to the contralateral common iliac artery under fluoroscopy. Upon release of the occluder, by removing the sheath, the aneurysm sack is completely excluded. Angiography through the contralateral femoral artery confirms the absence of endoleak from the occluder. Completion angiogram (20 ml dye) from the ipsilateral axis should be performed to confirm the absence of endoleak, migration, stenosis, kinking or any other complication. Upon completion of the endovascular procedure, sheaths and wires are removed and an 8-mm or 10-mm PTFE graft with rings is sutured from the ipsilateral to the contralateral common femoral artery using a standard technique, to provide blood to the contralateral femoral, external and internal iliac arteries. Aspirin is administered from the same day, clopidogrel is added on the first postoperative day, then the patient is mobilized on the second postoperative day and a plain abdominal radiogram is performed to image the graft’s
integrity and position. The patient is usually released on the fourth postoperative day. Patients should be followed with abdominal CT, during postoperative months 1, 6 and 12 and annually thereafter for possible sack diameter/volume increase, endoleak, migration and kinking (Fig. 5.7.2).
5.7.7 Results and Complications In some AAAs, endografting with a bifurcated endoprosthesis is not feasible due to anatomical restrictions, such as a narrow terminal aorta and an aneurismal, tortuous, narrow or calcified contralateral iliac artery [1, 9]. In these circumstances, aortouniiliac endograft and femoro-femoral crossover by-pass have proven efficacy to overcome the limitations and repair difficult AAAs in high-risk patients [13, 34, 40, 45, 49, 56, 61]. In other words, EVAR with aortouniiliac endoprostheses extends the morphological range of aneurysms that can be treated endoluminally and is potentially a more rapid and simple operation than bifurcated endovascular repair [25]. This EVAR configuration was initially reported by May et al. [34], Parodi [44] and Marin et al. [33], with use of a balloon-expandable stent for proximal graft fixation and distal graft anastomosis to the iliac artery.
389
390
5.7 Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair
Fig. 5.7.2 Spiral CT – angiography during follow-up confirms absence of endoleak
Early reports suggested that only about 20% of patients with an AAA would be anatomically suitable for EVAR. Nowadays, applicability has been raised to 50– 60% or more of these patients, due to mechanical and design enhancements and technique evolvement [2, 3, 5, 59]. However, it has been estimated that approximately 50% of patients are excluded from EVAR because of “unsuitable” iliofemoral arteries [59]. If this disadvantageous iliac artery anatomy could be overcome, perhaps twothirds of patients would be potential candidates for EVAR if open repair is not considered optimal. Clouse et al. [15] mentions in his article that an aortouniiliac prosthesis combined with contralateral lower extremity revascularization with femoro-femoral crossover by-pass grafting could overcome many of these iliac limitations if one iliac system provides adequate access and a distal attachment zone. Recognized advantages to such a system include ease of device deployment, without rotational concerns, and no modular interface requirements and their potential pitfalls. Also, ease of use broadens EVAR applicability to patients with ruptured aneurysms [42]. Unique disadvantages of this repair include the potential drawbacks of femoro-femoral by-pass grafting, including poor late patency and infection, and development of thigh or buttock claudication when pelvic flow is disturbed by either ipsilateral or contralateral occlusion or alteration of the in-flow. Furthermore, occasional difficulties with therapeutic contralateral iliac system occlusion, e.g. endoleak, may occur.
5.7.8 Patency of the Femoro-femoral Crossover By-pass Some specialists were reluctant or even opposed to the technique, based on its possible disadvantages. They claimed that femoro-femoral crossover by-pass patency rates are quite poor, influencing the durability of the endograft, with probable tendency to thrombosis. Their speculation was based on various publications referring to femoro-femoral crossover by-pass 5-year patency rates ranging from 35% [46] to 92% [7, 16, 18, 19, 22, 28, 32, 37, 41, 47]. Moreover, they claimed the aortobifemoral by-pass is considered the “gold standard” for aortoiliac occlusive disease with patency rates that greatly exceed those of femoro-femoral by-pass [46, 47, 52, 53]. All these speculations, though, are strictly hypothetical, as AUI endografting with femoro-femoral crossover by-pass is usually applied to patients with aneurismal disease that do not present peripheral arterial obstructive disease (PAD). In addition to the occlusion of the superficial femoral artery [27, 46], poor run-off in the infrapopliteal arteries has been shown to negatively affect the patency of femoro-femoral crossover by-pass [20, 57]. Moreover, many publications about the patency rates of femorofemoral crossover by-pass as an adjunctive to AUI endografting report impressive patency, ranging from 91% at 3 years [25] to 99% at 4 years [31]. Similar results, with low morbidity and mortality and satisfactory patency
5.7.9 Local Wound Complications, Graft Infection and Morbidity
rates, have been published from various other authors [16, 40, 49, 56, 59, 60, 61]. Hinchliffe et al. [25] found that in all ten patients with femoro-femoral by-pass occlusion there was coexisting occlusion of the endovascular aortic stent graft. This means that the poor in-flow from the kinked or stenotic AUI graft caused the femoro-femoral graft thrombosis. The iliac limb of the endograft was deployed in the external iliac artery in five of these ten patients with grafts that subsequently became occluded. In a report of the failure of endovascular aortic limbs, there appeared to be improved patency in aortouniiliac grafts (97%) at 18 months compared with bifurcated grafts (90%); however, the results did not reach statistical significance [10]. Fully stented endograft limbs appear to offer improved patency over unsupported limbs, probably related to their kink resistance [10]. However, the current range of fully stented designs remains at risk of kinking in tortuous arteries. The risk remains over the long term because of alterations in stent position secondary to migration or possibly longitudinal shrinkage of the aneurysm sac. Bifurcated endografts may be susceptible to occlusion of one iliac limb when both limbs compete for space in the presence of a narrow distal aorta, which may compress one or other limb. Graft limb thrombosis was reported with bifurcated stent graft systems: 7% at a mean of 11 months of follow-up by Stelter et al. [55] and 5% at 7 months of follow-up by Faries et al. [21]. In Hinchliffes’ [25] study, in-flow problems leading to early graft occlusion were due to damage of the external iliac artery caused by the instrumentation, a low-flow state created by an unrecognized kink in the endograft, or deployment of the endograft in a narrow external iliac artery. Carroccio et al. [12] in their study of bifurcated endografts suggested that deployment of endografts in narrow external iliac arteries should be avoided. Occlusion of endografts extending into the external iliac arteries may be related to a number of factors, including: gross oversizing of grafts with inadequate deployment or crowding of graft material in the relatively narrow external iliac artery, low flow within a narrow external iliac artery, or kinking of the endograft at the angulation between the common and external iliac arteries. Late occlusions were primarily associated with caudal migration and endograft kinking [25]. Hinchliffe [25] found that there is no relationship between the incidence of complications and the type of graft material used for femoro-femoral by-pass, which corresponds to findings of a recent large prospective random-
ized study of Dacron and PTFE in aortofemoral by-pass grafts [48]. In conclusion, the patency rate of femoro-femoral bypass grafting for aneurismal disease is generally better than that reported for occlusive disease and comparable to that with open aortobifemoral or bifurcated endovascular repair of AAA over the medium and long term. In contrast to their use in iliac occlusive disease, the mode of graft failure appears to be related to problems of in-flow rather than run-off. Specifically, patency of the femorofemoral by-pass graft is ultimately related to performance of the aortouniiliac endograft. Occlusion of the crossover graft may be prevented in the peri-operative period by paying particular attention to avert damage to the donor external iliac artery or common femoral artery from arterial sheaths and guidewires, by preventing or treating the kinking of iliac limbs, and by not deploying endografts in narrow external iliac arteries [25].
5.7.9 Local Wound Complications, Graft Infection and Morbidity Local wound complications, e.g. haematoma, seroma and superficial wound infection, are not necessarily related to the femoro-femoral by-pass graft and can just as easily be related to dissection of the common femoral artery. Bifurcated devices may be expected to produce in the region of 8.4% local groin complications [21], similar to the 11% experienced in Hinchliffes’ cohort [25]. Yilmaz et al. [60] found that all wound or graft infections complicated femoral exposure through a longitudinal incision. Since changing to an oblique incision, they have performed 139 repairs without a single wound or graft infection [60]. It is interesting to note that infection of femoro-femoral by-pass grafts has not been associated with direct or indirect spread of infection to the endovascular graft [25]. In conclusion, peri-operative morbidity associated with aortouniiliac endovascular aneurysm repair and femoro-femoral crossover is similar to that reported with bifurcated endovascular stent grafts [25]. Nowadays, a variety of commercial AUI endografts have been approved for use in Europe and USA, including stainless steel Gianturco Z-stents or nitinol self-expanding stents, tapered, with or without a proximal bare
391
Endoleak
Rupture
Conversion
Endograft complications
Actuarial survival
30-day mortality rate
Primary technical success
11 (22%); 5 type I (3 pr, 2 dis); 6 type II
1
0%
98%
52.3% at discharge; 30.9% at 12 months; 28.6% at 36 months
2 (1.8%)
3
78.4 (at 2 years); 63.4 (at 4 years)
4.2%
113/121 (94.2%)
533
631 (±62)
Mean estimated blood loss (ml)
5.4 258
4 (±1.2)
Mean duration of surgery 223 (±8) (min)
Mean hospital stay (days)
5.4 (±0.9)
6.2
36.2 (±16.7)
22 Dacron; 28 PTFE (8 or 10 mm)
Fem-fem grafts utilized
EVT/Guidant
Mean AAA diameter (cm)
22 EVT/Guidant; 28 custom made
AUI endografts utilized
121
Mean follow-up (months) 15.8 (2.2–33)
51
Patients (n)
Rehring et al. [49] Clouse et al. [15]; Moore et al. [40] 110
Lipsitz et al. [31]
3
5 (16.7%)
3.5%
25 (83.3%)
500 (450–1500)
160 (90–480)
6 (4–9)
4 (1–13)
29 (1–68)
Modified Gianturco; Ancure; Talent; stent, Dacron graft custom made and Wallstent
30
Yusuf et al. [61]
Table 5.7.1 Results from six series of AUI endografting utilizing a femoro-femoral by-pass
165 (±56)
7.1 (5–12)
29
170 Dacron; 59 PTFE; 8 or 10 mm
Chuter, Nottingham-Malmo, Zenith
231
Hinchliffe et al. [25]
11 (7%)
83% at 12 months; 48% at 48 months
3.4%
100%
196 (±69)
6.2 (2.6–10.7)
24 (±16)
148
Yilmaz et al. [61]
392 5.7 Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair
1 (2%)
Ischemic colitis
3 (6%)
Superficial wound infection
98% primary; 100% secondary (16 months)
1 (2%)
Fem-fem graft thrombosis
Fem-fem crossover graft patency rates
2 (4%)
Arterial dissection/injury 0%
10
10
6 (3%)
10 (4%)
9 (4%)
0
10
Hinchliffe et al. [25]
95% primary; 99% 91% at 3 years; 83% at 5 years secondary (at 4 years)
5 (4.5%)
0
0
Fem-fem graft infection
4 (3.6%)
2 (1.8%)
5 (4.5%) endograft thrombosis leading to fem-fem thrombosis
Lipsitz et al. [31]
1 (0.9%) 3 (2.6%)
7.6%
8.5%
1
16 (14.2%)
2 (1.8%)
15 (13.3%) reduction; in flow, requiring reintervention
Yusuf et al. [61]
Pseudoaneurysm
Seroma
1 (2%)
Groin haematoma
Femoro-femoral graft complications
Endograft infection
1 (2%)
3 (6)
Rehring et al. [49] Clouse et al. [15]; Moore et al. [40]
Buttock claudication
Migration
Endograft Kinking/stenosis
Table 5.7.1 (continued)
96% at 12 months; 94% at 48 months
2
3
2
1
2
2
Yilmaz et al. [61]
5.7.9 Local Wound Complications, Graft Infection and Morbidity 393
6.1.6 Therapy
• Occasionally, satisfactory outcomes have been reported from repair of exclusively the inferior mesenteric artery usually in specific circumstances [49].
Surgical Reconstruction of the Splanchnic Arteries • Surgical reconstruction of the splanchnic arteries is a relatively safe procedure associated with a low morbidity and mortality between 2% and 5% but mortality can be as high as 15% depending on the extent of the pathology and the patient’s operative risk. • The mortality is increased with redo operations and when splanchnic repair is combined with aortic reconstruction [41]. • Specific complications are related to clamping of the splanchnic circulation: (1) ischaemia and reperfusion, which is not rare, and (2) bowel infarction, which is a rare but often fatal complication.
• All authors report satisfactory patency. However, patency objectively determined by angiography and/or Duplex ultrasonography and calculated by the life table method is rarely reported. McMillan et al. [34] presented their results as such and reported patency between 89% and 93% at 36 months and 89% at 72 months [34]. Kihara et al. [25] reported a 73% patency rate at 24 months and found superior results in females as opposed to males and superior patency rates in prosthetic by-pass grafts as opposed to autologous material [25].
Treatment of Coeliac Artery Compression Syndrome • The surgical treatment of coeliac artery compression syndrome consists of decompression of the coeliac artery at the diaphragm by careful division of fibres and fibrous and nerve tissue.
Fig. 6.1.2a Exposure of the aorta, coeliac artery, superior mesenteric artery and left renal artery and vein
405
394
5.7 Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair
stent and in various dimensions. In the Department of Surgery and Vascular Surgery, Aristotle University of Thessaloniki, Greece, we have accumulated great experience with the “Endofit” self-expanding device (Endomed, Phoenix, Ariz., USA), which is constructed from a nitinol frame and PTFE fabric, with a proximal suprarenal bare stent and a conical configuration. From 2002 to 2004 we treated 39 high-risk patients (ASA III+) with AAA (n=33) or AAA and common iliac aneurysm (n=6), who were submitted to EVAR using an AUI endograft and femoro-femoral crossover by-pass. Median follow-up was 14 months. Most patients were male (n=36, n=3 female patients), ranging in age from 63 to 84 (median 74 years), with a median aortic aneurysm diameter of 6.7 cm (5–11 cm). In all of these patients Endofit (Endomed, Phoenix, Ariz., USA) self-expanding aortouniiliac stent grafts with a proximal bare stent were deployed. An 8-mm PTFE graft with rings was always used for the femoro-femoral crossover by-pass. The types
of these grafts were: GORE ringed Goretex® stretch vascular graft (W.L. Gore, Flagstaff, Ariz., USA) in 6 cases, Seal ePTFE ringed Vascutek (Vascutek, Scotland) in 22 cases and Impra ePTFE ringed vascular graft (Bard Peripheral Vascular, Tempe, Ariz., USA) in 11 cases. The contralateral iliac axis was obstructed with an endoluminal occluder. Patient selection and measurements were based on preoperative spiral iv contrast CT angiography with 3D reconstruction. Follow-up included simple abdominal radiograph before release and abdominal contrast CT in postoperative months 1, 6 and 12. All patients gave informed consent. The method was feasible in all patients (100% technical success). Anaesthesia was 90% regional (n=35) and 10% (n=4) general. Surgically dissected femoral artery was the access vessel in all cases. The median operative time was 124 min (92–243 min) and the median fluoroscopy time was 13 min (9–38 min). The median amount of contrast media used was 155 ml (100–280 ml) and the
Table 5.7.2 Complications and treatment from 39 AUI endografts with adjacent femoro-femoral crossover by-pass. (AMI Acute myocardial infarction) Complications
Frequency
Comments
Treatment
Endoleak/type
3 (7.7%)
Two type II from internal iliac
Surveillance
One type I proximal
Proximal cuff
Migration
0
Fem-fem by-pass graft thrombosis/endograft thrombosis
1 (2.5%)
From endograft angulation and stenosis (low inflow)
Thrombectomy of the graft and angioplasty of the endograft
Deployment failure
0
Conversion
0
Rupture
0
Tunnel haematoma
2 (5.1%)
Conservative
Superficial infection - lymphorrhoea
2 (5.1%)
Conservative
Graft infection
0
Complications of access vessels
2 (5.1%)
Limited plaque dissection
Surgical patch angioplasty
Cardiac
2 (5.1%)
AMI (4th and 9th month)
Conservative
Pulmonary
2 (5.1%)
Pneumonia
Conservative
General complications
Stroke
0
Fever
5 (12.8%)
Renal
0
Death
0
Conservative
References
median blood loss was 350 ml (180–670 ml). The median preoperative serum creatinine level was 1.15 mg/dl while the median postoperative serum creatinine level was 1.22 mg/dl. Length of hospital stay ranged from 4 to 11 days (median 6 days) and the length of intensive care unit stay ranged 12–72 h (median 20 h). The ipsilateral internal iliac artery was intentionally occluded in six cases (15%) in order to accomplish safe distal attachment and sealing, only in the cases where a common iliac aneurysm co-existed. Perioperative mortality was zero. Moreover during follow-up all patients were alive. Complications are listed in Table 5.7.2. More specifically, endoleak occurred in three cases (7.7%). One of them was a proximal type I endoleak, which was identified at the first month and was treated with the deployment of a proximal cuff. The rest were type II endoleaks, which are under surveillance, without aneurysm sack enlargement. Thrombosis of the femorofemoral graft occurred in one case during the immediate postoperative period, due to insufficient in-flow caused by a residual stenosis of the endograft (primary patency 97.5%). The deficit was treated at once with thrombectomy of the PTFE graft and balloon dilatation of the endograft (secondary patency 100%). None of the aneurysms ruptured, or converted to open procedure during follow-up. In two cases, tunnel haematoma occurred and was treated conventionally (5.1%). Superficial infection – lymphorrhoea – was identified in other two cases (5.1%) and remitted after appropriate medical treatment. Graft migration, serious infection, paraplegia, distal embolization or any other serious complication was not observed.
5.7.10 Conclusion AUI endografting with endoluminal occlusion of the contralateral iliac artery and adjunctive femoro-femoral crossover by-pass is feasible, efficacious and has proven high mid-term patency rates. Because it utilizes extraanatomic by-pass (with potential surgical complications) and because long-term results are not yet confirmed, it should be applied in high-risk patients and only in those where a bifurcated endoprosthesis is contraindicated due to anatomical restrictions. References 1. Arko FR et al (2004) How many patients with infrarenal aneurysms are candidates for endovascular repair. The Northern California experience. J Endovasc Ther 11:33–40
2. Armon MP, Yusuf SW, Latief K, Whitaker SC, Gregson RH, Wenham PW et al (1997) Anatomical suitability of abdominal aortic aneurysms for endovascular repair. Br J Surg 84:178–180 3. Balm R, Stokking R, Kaatee R, Blankensteijn JD, Eikelboom BC, van Leeuwen MS (1997) Computed tomographic angiographic imaging of abdominal aortic aneurysms: implications for transfemoral endovascular aneurysm management. J Vasc Surg 26:231–237 4. Bernhard VM, Mitchell RS, Matsumura JS et al (2002) Ruptured abdominal aortic aneurysm after endovascular repair. 35:1155–1162 5. Brewster DC (2002) Do current results of endovascular abdominal aortic aneurysm repair justify more widespread use? Surgery 131:363–367 6. Brewster DC, Cronenwett JL, Hallett JW et al (2003) Guidelines for treatment of AAA. J Vasc Surg 37:1106–1117 7. Brief DK, Brener BJ (1987) Extra-anatomic bypasses: femorofemoral crossover grafts. In: Wilson SE, Veith FJ, Hobson RW, William RA (eds) Vascular surgery principals and practice. McGraw-Hill, New York, pp 415–418 8. Cardon JM, Cardon A, Joueux A, Vidal V, Noblet D (1996) Endovascular repair of iliac artery aneurysm with endoprosystem I: a multicentric French study. J Cardiovasc Surg 37:45–50 9. Carpenter JP et al (2001) Impact of exclusion criteria on patient selection for EVAR. J Vasc Surg 34:1050–1055 10. Carpenter JP, Neschis DG, Fairman RM et al (2001) Failure of endovascular abdominal aortic aneurysm graft limbs. J Vasc Surg 33:296–302 11. Carpenter JP, Baum RA, Barker CF et al (2002) Durability of benefits of endovascular versus conventional AAA repair. J Vasc Surg 35:222–228 12. Carroccio A, Faries PL, Morrissey NJ et al (2002) Predicting iliac limb occlusions after bifurcated aortic stent grafting: anatomic and device-related causes. J Vasc Surg 36:679–684 13. Chuter TA et al (1999) Aortouniiliac endovascular grafting combined with femorofemoral by-pass: an acceptable compromise or a preferred solution? Semin Vasc Surg 12:176–181 14. Chuter TA et al (2000) Endovascular aneurysm repair in high risk patients. J Vasc Surg 31:122–133 15. Clouse WD, Brewster DC, Marone LK et al (2003) Durability of aortouniiliac endografting with femorofemoral crossover: 4-year experience in the EVT/Guidant trials. J Vasc Surg 37:1142–1149 16. Criado E, Burnhum SJ, Tinsley EA et al (1993) Femorofemoral bypass grafts: analysis of patency and factors influencing long term outcome. J Vasc Surg 18:495–505
395
396
5.7 Aortouniiliac Endoprosthesis and Femoro-femoral Crossover for AAA Repair
17. Dattilo JB, Brewster DC, Fan C-M et al (2002) Clinical failures of endovascular abdominal aortic endograft repair: incidence, causes and management. J Vasc Surg 35:1137–1144 18. Dick LS, Brief DK, Alpert J et al (1980) 12- year experience with femorofemoral crossover grafts. Arch Surg 115:1359–1165 19. Eugene J, Goldstone J, Moore WS (1977) Fifteen year experience with subcutaneous bypass grafts for lower extremity ischemia. Ann Surg 186:177–183 20. Farber MA, Hollier LH, Eubanks R et al (1990) Femorofemoral bypass: a profile of graft failure. South Med J 83:1437–1443 21. Faries PL et al (2002) A multicenter experience with the Talent endovascular graft for the treatment of AAA. J Vasc Surg 35:1123–1128 22. Flaningan DP, Pratt DG, Goodreau JJ et al (1978) Aortofemoral or femorofemoral revascularization? A prospective evaluation of the papaverine test. Arch Surg 113:1257–1162 23. Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson SG; EVAR trial participants (2004) Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomised controlled trial. Lancet 364:843–848 24. Harris P, Vallabhaneni SR, Desgranges P et al (2000) For the EUROSTAR Collaborators. Incidence and risk factors of late rapture and death after endovascular repair of infrarenal aortic aneurysm: the EUROSTAR experience. J Vasc Surg 32:739–749 25. Hinchliffe RJ et al (2003) Durability of femorofemoral bypass grafting after AUI endovascular aneurysm repair. J Vasc Surg 38:498–503 26. Holzenbein TJ, Kretschmer G, Thurner S et al (2001) Midterm durability of abdominal aortic endograft repair: a word of caution. J Vasc Surg 33:S46–S54 27. Komori K, Okadome K, Funahashi S et al (1993) Correlation of long-term results of extra-anatomic bypass and flow wave-form analysis. Eur J Vasc Surg 7:479–482 28. Lamerton AJ et al (1985) The femorofemoral graft: hemodynamic improvement and patency rate. Arch Surg 120:1274–1278 29. Lederle FA (2004) Abdominal aortic aneurysm – open versus endovascular repair. N Engl J Med 351:1677–1679 30. Lee AW, Carter JW, Upchurch G et al (2004) Perioperative outcomes after open and endovascular repair of intact AAA in the USA during 2001. J Vasc Surg 39:491–496
31. Lipsitz EC, Ohki T, Veith FJ et al (2003) Patency rates of femorofemoral bypass associated with endovascular aneurysm repair surpass those performed for occlusive disease. J Endovasc Ther 10:1061–106532. Maini BS, Mannick JA (1978) Effect of arterial reconstruction on limb salvage: a ten-year appraisal. Arch Surg 113:1297–1304 33. Marin ML, Veith FJ, Cynamon J (1995) Initial experience with transluminally placed endovascular grafts for the treatment of complex vascular lesions. Ann Surg 22:449–469 34. May J, White G, Waugh R et al (1994) Treatment of complex aortic aneurysms by a combination of endoluminal and extraluminal aortofemoral grafts. J Vasc Surg 19:924–933 35. McCready RA, Paizolero PC, Gilmore JC et al (1983) Isolated iliac artery aneurysm. Surgery 93:688–693 36. Michel C, Laffy PY, Leblanc G, Angel CY, Riuou JY (1996) Traitement percutane d’ anevrismes iliaques par endoprothese couvert. J Radiol 77:433–436 37. Mingoli A, Sapienza P, Feldhaus RJ et al (2001) Femorofemoral bypass grafts: factors influencing long term patency rate and outcome. Surgery 129:451–458 38. Mofid R, Otal P, Boyer L, Ravel A, Garcier JM, Rousseau H (2003) Common iliac aneurysms with short or absent proximal necks: endoluminal repair with a covered endoprosthesis. Eur J Vasc Endovasc Surg 26:334–336 39. Moore WS, Kashyap VS, Vescera CL et al (1999) Abdominal aortic aneurysm: a 6-year comparison of endovascular versus transabdominal repair. Ann Surg 230:298–308 40. Moore WS et al (2000) AUI endograft for complex aortoiliac aneurysms compared with tube bifurcated endografts: results of the EVT trials. J Vasc Surg 33 [Suppl]:S11–S20 41. Mosley JG, Marston A (1983) Long term results of 66 femorofemoral bypass grafts: 9-year follow up. Br J Surg 70:631–634 42. Ohki T, Veith F, Sanchez L et al (1999) Endovascular graft repair of ruptured aortoiliac aneurysms. J Am Coll Surg 189:102–112 43. Ohki T, Veith FJ, Shaw P et al (2001) Increasing incidence of midterm and longterm complications after endovascular graft repair of AAA: a note of caution based on a 9-year experience. Ann Surg 234:323–335 44. Parodi JC (1995) Endovascular repair of abdominal aortic aneurysms and other arterial lesions. J Vasc Surg 21:549–557 45. Parodi JC, Palmaz JC, Barone HD (1991) Transfemoral intraluminal graft implantation for AAA. Ann Vasc Surg 5:491–499 46. Piotrowski JJ et al (1988) Aortobifemoral by pass: the operation of choice for unilateral iliac occlusion? J Vasc Surg 8:211–218
References
47. Plecha F et al (1984) Femorofemoral by pass grafts: ten-year experience. J Vasc Surg 1:555–561 48. Prager M, Polterauer P, Bohmig HJ et al (2001) Collagen versus gelatin-coated Dacron versus stretch polytetrafluoroethylene in abdominal aortic bifurcation graft surgery: results of a seven-year prospective, randomized multicenter trial. Surgery 130:408–414 49. Rehring TF, Brewster DC, Cambria RP et al (2000) Utility and reliability of endovascular Aortouniiliac with femorofemoral crossover graft for aortoiliac aneurysmal disease. J Vasc Surg 31:1135–1141 50. Richardson JW, Greenfield LJ (1988) Natural history and management of iliac aneurysms. J Vasc Surg 8:165–171 51. Rutherford RB, Krupski WC (2004) Current status of open versus endovascular stent-graft repair of abdominal aortic aneurysm. J Vasc Surg 39:1129–1139 52. Self SB, Rchardson JD, Klamer DW et al (1991) Utility of femorofemoral bypass. Comparison of results with indications for operations. Am Surg 57:602–606 53. Sneider JR, Besso SR, Walsh DB et al (1994) Femorofemoral versus aortobifemoral bypass: outcome and hemodynamic results. J Vasc Surg 19:43–57 54. Stanley BM, Semmens JB, Qun Mai BM et al (2001) Evaluation of patient selection guidelines for endoluminal AAA repair with the Zenith stent-graft: the Australian experience. J Endovasc Ther 8:457–464
55. Stelter W, Umscheid T, Zeigler P (1997) Three year experience with modular stent-graft devices for endovascular AAA treatment. J Endovasc Surg 4:362–369 56. Thompson MM et al (1997) AUI endovascular grafting: difficult solutions to difficult aneurysms. J Endovasc Surg 4:174–181 57. Tomson-Fawcett M, Moon M, Hands L et al (1998) The significance of donor leg distal runoff in femorofemoral bypass grafting. Aust NZ J Surg 68:493–497 58. Treiman GS et al (1999) An assessment of the current applicability of the EVT endovascular graft for treatment of patients with infrarenal AAA. J Vasc Surg 30:68–75 59. Walker SR et al (1998) Early complications of femorofemoral crossover bypass grafts after AUI endovascular repair of abdominal aortic aneurysms. J Vasc Surg 28:647–650 60. Yilmaz PK et al (2003) Is cross femoral bypass grafting a disadvantage of AUI endovascular aortic aneurysm repair? J Vasc Surg 38:753–757 61. Yusuf SW et al (1997) Early results of endovascular aortic aneurysm surgery with AUI graft, contralateral iliac occlusion and femorofemoral bypass. J Vasc Surg 25:162–172 62. Zarins CK, White RA, Fogarty TJ et al (2000) Aneurysm rupture after endovascular repair using AneuRX stent graft. J Vasc Surg 31:960–970 63. Zarins CK, White RA, Moll FL et al (2001) The AneuRX stent graft: 4-year results and worldwide experience 2000. J Vasc Surg 33:S135–S145
397
Visceral Arteries
401
6.1 Occlusive Disease of the Coeliac and Superior Mesenteric Arteries J. Hajo van Bockel, Robert H. Geelkerken
6.1.1 Definition • Splanchnic vascular diseases encompass a spectrum of acute and chronic occlusive and aneurysmal disorders affecting the vessels of the abdominal entrails. • Of these relatively uncommon disorders, splanchnic ischaemia occurs most frequently. • Chronic splanchnic disease is characterized by symptomless but significant stenosis in the coeliac artery, the superior mesenteric artery and/or the inferior mesenteric artery [45]. • It is important to distinguish chronic splanchnic disease from chronic splanchnic ischaemia or syndrome, which is the combination of splanchnic disease and symptoms of ischaemia. • In this respect, there is a close analogy between chronic splanchnic disease and renovascular disease. • A complete overview has been published recently [54].
6.1.2 Epidemiology • A recent angiographic study revealed a 40%, 29% and 25% incidence of asymptomatic stenosis of one splanchnic artery in a population with abdominal aortic aneurysms, aorta-iliac obstructive disease and lower extremity ischaemic disease respectively. • In 3.4% of the patients more than one splanchnic artery appeared to be involved [53]. • In another angiographic study of 980 patients, 82 patients (8%) were found to have 50% stenosis of at least one splanchnic artery, in 3.9% of the patients one splanchnic artery was occluded. Fifteen patients had significant three-vessel disease [52]. • Summarizing the available data, we conclude that in populations with manifestations of atherosclerotic
diseases the incidence of chronic splanchnic disease ranges between 8% and 70% [3, 7, 11, 23, 43, 47, 52, 53]. Of these patients, 0.5–15% had a greater than 50% narrowing of more than one splanchnic artery. • In spite of the relatively high prevalence of splanchnic disease, the incidence of chronic splanchnic ischaemia appears to be low [31].
6.1.3 Aetiology • Stenosis or occlusion of the splanchnic arteries can be caused by a variety of diseases, such as: atherosclerosis, fibrodysplasia, compression at the diaphragm and rare causes, e.g. vasculitis, Takayashu’s disease, etc. • Atherosclerosis is responsible for occlusions in probably more than 95% of cases. These lesions, like those of other visceral vessels affected by atherosclerosis (e.g. renal arteries), are mostly located in the origin (ostial lesions) and are caused by progressive atherosclerosis of the anterior wall of the aorta. This also explains why isolated stenosis or occlusion of the ostium of one of the visceral vessels by atherosclerosis is relatively rare. • Isolated occlusive disease of the coeliac trunk may be caused by the compression of this vessel by the arcuate ligament of the diaphragm, so-called coeliac axis compression syndrome or median arcuate ligament syndrome [12]. • The existence of this syndrome is controversial since it is commonly accepted that at least two of the three major splanchnic vessels must be involved before symptoms will occur [7]. • Finally, chronic splanchnic disease may rarely be caused by other disease, such as fibrodysplasia [37, 58], vasculitis and radiation and autoimmune arteritis. • A review of systemic disease affecting the mesenteric circulation has been published by Harris et al. [22].
402
6.1 Occlusive Disease of the Coeliac and Superior Mesenteric Arteries
6.1.4 Symptoms • The classical syndrome of chronic splanchnic ischaemia is characterized by: • upper abdominal pain that is usually provoked by eating • an epigastric bruit • loss of weight and haemodynamically significant stenosis of two or more of the splanchnic arteries [51]. • This classical triad does not always appear in patients with chronic splanchnic ischaemia [17]. • Only half of our patients exhibited all three classical symptoms, but after arterial repair relief of abdominal pain was achieved in all cases. This corroborates the observations of others, namely that weight loss and epigastric bruit do not occur in all patients with chronic splanchnic ischaemia [4, 6, 21, 24, 29, 40, 45, 46]. • It has been proposed that a vascular steal phenomenon is involved in chronic ischaemia. • Poole et al. [39] used a dog model. By tonometric assessment of the splanchnic blood flow, the haemodynamic changes produced by a meal in dogs with a fixed decreased splanchnic blood flow (50% stenosis of both the coeliac artery and the superior mesenteric artery) ischaemia was evaluated. It appeared that the intestinal intramural pH decreased significantly when blood flow was decreased to 50% after food intake. The haemodynamic explanation of the decrease was explained as a steal from the intestinal to the gastric circulation stimulated by food placed in the stomach. Such a steal could explain pain resulting from gastric ischaemia experienced by patients with chronic mesenteric ischaemia [39].
• Usually the classical triad of upper abdominal pain provoked by eating, weight loss and an epigastric bruit is incomplete or absent [1]. • Currently there is still no single test or combination of tests that can confirm or reject the diagnosis of chronic splanchnic ischaemia. • The diagnosis can only be made retrospectively if symptoms are relieved after a successful repair of the occlusive disease. • Meanwhile, a probable diagnosis is made preoperatively on the basis of a clinical suspicion after exclusion of more common causes of abdominal pain, combined with positive test results on Duplex ultrasound, angiography, magnetic resonance or tonometry, alone or in combination.
Duplex Ultrasound • Nine studies from five different institutions have compared splanchnic Duplex ultrasound results with multiplane angiography [18]. • Only two of these were performed in a prospective blinded setting [30, 36] and only two other studies dealt exclusively with patients suspected of chronic splanchnic ischaemia [38, 59]. • Commonly accepted criteria for diagnosing a haemodynamically significant stenosis in the coeliac artery are a peak systolic velocity (PSV) of more than 200 cm/s and an end-diastolic velocity of more than 55 cm/s. • For the superior mesenteric artery, these thresholds are a peak systolic velocity of more than 275–300 cm/s and an end-diastolic velocity of 45 cm/s. • In experienced hands a successful Duplex visualization of the coeliac and superior mesenteric arteries can be obtained in 80–95%, and in these cases ultrasound is a reliable screening test of chronic splanchnic disease.
6.1.5 Diagnosis Angiography 6.1.5.1 Recommended European Standard Diagnostic Steps of Investigation History/Physical Examination • The diagnosis of chronic splanchnic ischaemia is clinically difficult.
• Angiography is typically performed after more common disorders causing pain after a meal, such as ulcer disease, gallbladder stones, pancreatitis, etc., have been excluded. • A positive Duplex ultrasound is nowadays a prerequisite for performing angiography.
6.1.6 Therapy
• MRA, including physiological evaluation of flow, should be performed preferably before angiography. • The advantage of performing MRA first is that multiple projections can easily be made, which may help to select the optimal projection angle during angiography. • Since the mesenteric vessels originate anteriorly from the aorta, ostial lesions can be easily missed if just an AP film is taken; therefore, angiography in at least two projections (AP and lateral) is required. • Rapid filming is necessary to visualize the origins of the coeliac artery and the superior mesenteric artery. • Late filming is required to evaluate the retrograde flow, delayed proximal visualization and collateral pathways between the coeliac artery, the superior mesenteric artery and the inferior mesenteric artery. • An injection in the distal aorta may be required to identify collaterals between the branches of the internal iliac artery and the inferior mesenteric artery. • Additional films during deep inhalation and expiration may be required to evaluate compression of the coeliac artery if coeliac artery compression syndrome is anticipated [44]. • A selective angiogram of the superior mesenteric and occasionally the inferior mesenteric artery may visualize collaterals feeding the branches of the coeliac artery [13].
Magnetic Resonance Angiography (MRA) • Just like digital angiography, MRA can depict the morphological appearance of the mesenteric vessels but may also provide functional information on splanchnic blood flow. Flow volumes in both the superior mesenteric artery and superior mesenteric vein have been measured with MRI. Previously, we have shown that portal venous flow measurements are accurate and can be performed with low intra- and inter-subject variability [28].
6.1.5.2 Additional Useful Diagnostic Procedures Tonometry • The mucosa of the intestine is at immediate risk upon insufficient perfusion, which results in anaerobic metabolism [9, 56].
• A tonometer can be used to measure the PCO2 of the stomach, small intestine or sigmoid indirectly [26]. • The principle of tonometry was first published in 1965 [10]. • To this end a tonometry catheter is inserted into the stomach or the intestine. • Currently, tonometry has been advocated as a diagnostic test in patients with chronic splanchnic ischaemia [2, 14, 39]. • In a recent review Kolkman et al. [26] concluded that gastrointestinal tonometry of the luminal-to-blood PCO2 gradient can be used to assess the adequacy of mucosal perfusion provided that, if applied to an empty stomach, acid buffering and carbon dioxide generation are avoided. • Appropriate use may broaden the clinical applicability of gastrointestinal luminal tonometry as a monitoring tool in a variety of conditions [26].
6.1.6 Therapy • Unfortunately, information on the natural history of splanchnic occlusive disease and ischaemia is scarce. • Based on the natural history of chronic splanchnic disease Connolly et al. [5] advocated prophylactic reconstruction to prevent acute ischaemia and bowel infarction [5]. This statement was supported by their later report of 25 patients with acute intestinal ischaemia resulting from atherosclerotic occlusions requiring surgical exploration. These patients had symptoms that were inconspicuous but diagnostically significant, including progressive loss of body weight and symptoms mimicking peptic ulcer disease or cholecystitis. Delay and oversight in the clinical diagnosis resulted in 80% mortality [27]. • Recently, Thomas et al. [52] evaluated 980 consecutive aortograms with anteroposterior and lateral projections to identify patients who had significant chronic splanchnic disease but no symptoms of chronic splanchnic ischaemia. Fifteen patients had significant three-vessel disease and, after 1–6 years, 86% had splanchnic ischaemia, other vague abdominal symptoms, or had died. It was concluded that those with significant three-vessel chronic splanchnic disease should be considered for prophylactic arterial reconstruction [52]. In a comment it was argued that the incidence of acute and usually fatal bowel ischaemia
403
404
6.1 Occlusive Disease of the Coeliac and Superior Mesenteric Arteries
was only 6%, which is approximately the operative mortality rate of elective reconstruction, and that, therefore, the case for prophylactic repair was still not conclusive [19].
6.1.6.1 Surgery Surgical Techniques • A variety of surgical techniques have been advocated to repair the mesenteric arteries including: • reimplantation • transarterial and transaortic endarterectomy and • antegrade and retrograde aortovisceral by-pass using vein or arterial autograft by-passes and • prosthetic by-pass.
• The early success rates ranged between 91% and 96% while late success rates ranged between 80% and 90% [8, 17, 20, 25, 29, 33, 35, 40, 45, 46, 57]. • Each of the various series is too small to draw any conclusions with respect to the superiority of one technique over another. • The choice of technique is usually based on the preference and experience of the surgeon. • However, the majority of centres with greater experience believe that antegrade revascularization (Fig. 6.1.1) or transaortic endarterectomy (Fig. 6.1.2a,b) of both the coeliac artery and the superior mesenteric artery offers the best long-term results. • The best long-term results seem to have been reported from surgical repair of more than one artery. • Repair of only one of the occluded mesenteric arteries may relieve symptoms of chronic splanchnic ischaemia and satisfactory results have been reported [4, 18].
Fig. 6.1.1 Antegrade by-pass, obtained from endarterectomized superficial femoral artery, from the aorta to the coeliac artery and superior mesenteric artery
406
6.1 Occlusive Disease of the Coeliac and Superior Mesenteric Arteries
Fig. 6.1.2b Aorta has now been opened by a longitudinal incision showing the obstructed coeliac artery and superior mesenteric artery which will be treated by endarterectomy
• If a stenosis of the coeliac artery is still present after release, a reconstruction should be considered. • Some authors report satisfactory results of surgical treatment of this syndrome [42] but others have reported unsatisfactory results [16].
6.1.6.2 Angioplasty • An alternative to surgical reconstruction may be angioplasty with or without the use of a stent. • Favourable results have been reported with early success rates between 79% and 80%. • It appears that surgical reconstruction is still superior to angioplasty [32, 48]. However, the number of patients treated is still small and long-term results are not available yet.
• The combination of angioplasty with the placement of a stent seems to have a better result than angioplasty alone. • Sheeran et al. [50] reported on the treatment of 12 patients. Initial technical success was achieved in 11 of the 12 patients (92%). There was one post-procedural death (<30 days) due to bowel ischaemia and infarction, despite a technically successful procedure. Primary patency and up to 18 months was 74% but subsequent interventions were required to obtain a secondary patency of 83% at 3 years [50]. • Favourable results have also been reported in 27 patients with chronic splanchnic syndrome treated with coeliac and or superior mesenteric artery stenting. The primary clinical success was 67%, secondary clinical success was 81%, primary patency was 81% and the secondary patency was 100% after a mean follow-up of 19 months [55].
6.1.6 Therapy
Fig. 6.1.3 Algorithm for diagnosis and treatment of occlusive disease of the coeliac and superior mesenteric artery
407
408
6.1 Occlusive Disease of the Coeliac and Superior Mesenteric Arteries
6.1.7 Conclusion In conclusion, angioplasty seems a realistic alternative for treatment of chronic splanchnic ischaemia if surgical reconstruction is not feasible or associated with a high surgical risk. The procedure is not completely without risk and it seems that angioplasty in combination with a stent is superior to angioplasty alone. An algorithm for diagnosis and treatment of occlusive disease of the coeliac and superior mesenteric artery is provided (Fig 6.1.3.). References 1. Babu SC, Shah PM (1993) Celiac territory ischemic syndrome in visceral artery occlusion. Am J Surg 166:227–230 2. Boley SJ, Brandt LJ, Veith FJ, Kosches D, Sales C (1991) A new provocative test for chronic mesenteric ischemia [see comments]. Am J Gastroenterol 86:888–891 3. Bron KM, Redman HC (1969) Splanchnic artery stenosis and occlusion. Incidence; arteriographic and clinical manifestations. Radiology 92:323–328 4. Christensen MG, Lorentzen JE, Schroeder TV (1994) Revascularisation of atherosclerotic mesenteric arteries: experience in 90 consecutive patients [see comments]. Eur J Vasc Surg 8:297–302 5. Connolly JE, Kwaan JH (1979) Prophylactic revascularization of the gut. Ann Surg 190:514–522 6. Crawford ES, Morris GC, Myhre HO, Roehm JOF (1977) Celiac axis, superior mesenteric artery, and inferior mesenteric artery occlusion: surgical considerations. Surgery 82:856–866 7. Croft RJ, Menon GP, Marston A (1981) Does “intestinal angina” exist? A critical study of obstructed visceral arteries. Br J Surg 68:316–318 8. Cunningham CG, Reilly LM, Rapp JH, Schneider PA, Stoney RJ (1991) Chronic visceral ischemia. Three decades of progress. Ann Surg 214:276–287 9. Dantzker DR (1993) The gastrointestinal tract. The canary of the body? [editorial; comment]. J Am Med Assoc 270:1247–1248 10. Dawson AM, Trenchard D, Guz A (1965) Small bowel tonometry: assessment of small gut mucosal oxygen tension in dog and man. Nature 206:943–944 11. Derrick JR, Pollard JC, Moore RM (1959) The pattern of arteriosclerosis narrowing of the celiac and superior mesenteric arteries. Ann Surg 149:684–689 12. Dunbar JD, Molnar W, Beman FF, Marable SA (1965) Compression of the celiac trunk and abdominal angina. Am J Roentgenol 95:731–744
13. Evans WE, Hayes J (1991) Celiac compression syndrome. In: Ernst CB, Stanley JC (eds) Current therapy in vascular surgery. Decker, Philadelphia, pp 747–750 14. Fiddian-Green RG, Stanley JC, Nostrant T, Phillips D (1989) Chronic gastric ischemia. A cause of abdominal pain or bleeding identified from the presence of gastric mucosal acidosis. J Cardiovasc Surg (Torino) 30:852–859 15. Geelkerken RH, Van Bockel JH (1999) Duplex ultrasound examination of splanchnic vessels in the assessment of splanchnic ischaemic symptoms [editorial]. Eur J Vasc Endovasc Surg 18:371–374 16. Geelkerken RH, Van Bockel JH, De Roos WK, Hermans J (1990) Coeliac artery compression syndrome: the effect of decompression. Br J Surg 77:807–809 17. Geelkerken RH, Van Bockel JH, De Roos WK, Hermans J, Terpstra JL (1991) Chronic mesenteric vascular syndrome. Results of reconstructive surgery. Arch Surg 126:1101–1106 18. Gentile AT, Moneta GL, Taylor LM Jr, Park TC, McConnell DB, Porter JM (1994) Isolated bypass to the superior mesenteric artery for intestinal ischemia. Arch Surg 129:926–931 19. Geroulakos G (1998) Regarding “The clinical course of asymptomatic mesenteric arterial stenosis” [letter; comment]. J Vasc Surg 28:1122 20. Geroulakos G, Tober JC, Anderson L, Smead WL (1999) Antegrade visceral revascularisation via a thoracoabdominal approach for chronic mesenteric ischemia. Eur J Vasc Endovasc Surg 17:56–59 21. Hallett JW Jr., James ME, Ahlquist DA, Larson MV, McAfee MK, Cherry KJ Jr (1990) Recent trends in the diagnosis and management of chronic intestinal ischemia. Ann Vasc Surg 4:126–132 22. Harris MT, Lewis BS (1992) Systemic diseases affecting the mesenteric circulation. Surg Clin North Am 72:245–259 23. Jarvinen O, Laurikka J, Sisto T, Salenius JP, Tarkka MR (1995) Atherosclerosis of the visceral arteries. Vasa 24:9–14 24. Johnston KW, Lindsay TF, Walker PM, Kalman PG (1995) Mesenteric arterial bypass grafts: early and late results and suggested surgical approach for chronic and acute mesenteric ischemia. Surgery 118:1–7 25. Kihara TK, Blebea J, Anderson KM, Friedman D, Atnip RG (1999) Risk factors and outcomes following revascularization for chronic mesenteric ischemia. Ann Vasc Surg 13:37–44 26. Kolkman JJ, Otte JA, Groeneveld AB (2000) Gastrointestinal luminal PCO2 tonometry: an update on physiology, methodology and clinical applications. Br J Anaesth 84:74–86 27. Kwaan JH, Connolly JE (1983) Prevention of intestinal infarction resulting from mesenteric arterial occlusive disease. Surg Gynecol Obstet 157:321–324
References
28. Lycklama a Nijeholt GJ, Burggraaf K, Wasser MN, Schultze Kool LJ, Schoemaker RC, Cohen AF et al (1997) Variability of splanchnic blood flow measurements using MR velocity mapping under fasting and post-prandial conditions – comparison with echo-Doppler [see comments]. J Hepatol 26:298–304 29. MacFarlane SD, Beebe HG (1989) Progress in chronic mesenteric arterial ischemia. J Cardiovasc Surg 30:178–184 30. Mallek R, Mostbeck GH, Walter RM, Stumpflen A, Helbich T, Tscholakoff D (1993) Duplex Doppler sonography of celiac trunk and superior mesenteric artery: comparison with intra-arterial angiography. J Ultrasound Med 12:337–342 31. Marston A, Clarke JM, Garcia GJ, Miller AL (1985) Intestinal function and intestinal blood supply: a 20 year surgical study. Gut 26:656–666 32. Maspes F, Mazzetti dP, Gandini R, Innocenzi L, Lupattelli L, Barzi F et al (1998) Percutaneous transluminal angioplasty in the treatment of chronic mesenteric ischemia: results and 3 years of follow-up in 23 patients. Abdom Imaging 23:358–363 33. Mateo RB, O’Hara PJ, Hertzer NR, Mascha EJ, Beven EG, Krajewski LP (1999) Elective surgical treatment of symptomatic chronic mesenteric occlusive disease: early results and late outcomes. J Vasc Surg 29:821–831 34. McMillan WD, McCarthy WJ, Bresticker MR, Pearce WH, Schneider JR, Golan JF et al (1995) Mesenteric artery bypass: objective patency determination. J Vasc Surg 21:729–740 35. Moawad J, McKinsey JF, Wyble CW, Bassiouny HS, Schwartz LB, Gewertz BL (1997) Current results of surgical therapy for chronic mesenteric ischemia. Arch Surg 132:613–618 36. Moneta GL, Lee RW, Yeager RA, Taylor LM Jr., Porter JM (1993) Mesenteric duplex scanning: a blinded prospective study. J Vasc Surg 17:79–84 37. Palubinskas AJ, Ripley HR (1964) Fibromuscular hyperplasia in extra-renal arteries. Radiology 82:454 38. Perko MJ, Just S, Schroeder TV (1997) Importance of diastolic velocities in the detection of celiac and mesenteric artery disease by duplex ultrasound. J Vasc Surg 26:288–293 39. Poole JW, Sammartano RJ, Boley SJ (1987) Hemodynamic basis of the pain of chronic mesenteric ischemia. Am J Surg 153:171–176 40. Rapp JH, Reilly LM, Qvarfordt PG, Goldstone J, Ehrenfeld WK, Stoney RJ (1986) Durability of endarterectomy and antegrade grafts in the treatment of chronic visceral ischemia. J Vasc Surg 3:799–806 41. Reilly LM, Ammar AD, Stoney RJ, Ehrenfeld WK (1985) Late results following operative repair for celiac artery compression syndrome. J Vasc Surg 2:79–91
42. Reilly LM, Ramos TK, Murray SP, Cheng SW, Stoney RJ (1994) Optimal exposure of the proximal abdominal aorta: a critical appraisal of transabdominal medial visceral rotation [see comments]. J Vasc Surg 19:375–389 43. Reiner L, Jiminez FA, Rodriquez FL (1963) Atherosclerosis in the mesenteric circulation: observations and correlations with aortic and coronary atherosclerosis. Am Heart J 66:209 44. Reuter SR (1971) Accentuation of celiac compression by the median arcuate ligament of the diaphragm during deep expiration. Radiology 98:561–564 45. Rheudasil JM, Stewart MT, Schellack JV, Smith RB, III, Salam AA, Perdue GD (1988) Surgical treatment of chronic mesenteric arterial insufficiency. J Vasc Surg 8:495–500 46. Rogers DM, Thompson JE, Garrett WV, Talkington CM, Patman RD (1982) Mesenteric vascular problems. A 26-year experience. Ann Surg 195:554–565 47. Roobottom CA, Dubbins PA (1993) Significant disease of the celiac and superior mesenteric arteries in asymptomatic patients: predictive value of Doppler sonography. Am J Roentgenol 161:985–988 48. Rose SC, Quigley TM, Raker EJ (1995) Revascularization for chronic mesenteric ischemia: comparison of operative arterial bypass grafting and percutaneous transluminal angioplasty. J Vasc Interv Radiol 6:339–349 49. Schneider DB, Nelken NA, Messina LM, Ehrenfeld WK (1999) Isolated inferior mesenteric artery revascularization for chronic visceral ischemia. J Vasc Surg 30:51–58 50. Sheeran SR, Murphy TP, Khwaja A, Sussman SK, Hallisey MJ (1999) Stent placement for treatment of mesenteric artery stenoses or occlusions. J Vasc Interv Radiol 10:861–867 51. Stanton PE Jr., Hollier PA, Seidel TW, Rosenthal D, Clark M, Lamis PA (1986) Chronic intestinal ischemia: diagnosis and therapy. J Vasc Surg 4:338–344 52. Thomas JH, Blake K, Pierce GE, Hermreck AS, Seigel E (1998) The clinical course of asymptomatic mesenteric arterial stenosis [see comments]. J Vasc Surg 27:840–844 53. Valentine RJ, Martin JD, Myers SI, Rossi MB, Clagett GP (1991) Asymptomatic celiac and superior mesenteric artery stenoses are more prevalent among patients with unsuspected renal artery stenoses. J Vasc Surg 14:195–199 54. van Bockel JH, Geelkerken RH, Wasser MN (2001) Chronic splanchnic ischemia. Best Practice Res Clin Gastroenterol 15:99–119 55. van Wanroij JL, van Petersen AS, Huisman AB, Mensink PB, Gerrits DG, Kolkman JJ et al (2004) Endovascular treatment of chronic splanchnic syndrome. Eur J Vasc Endovasc Surg 28:193–200
409
410
6.1 Occlusive Disease of the Coeliac and Superior Mesenteric Arteries
56. Wilmore DW, Smith RJ, O‘Dwyer ST, Jacobs DO, Ziegler TR, Wang XD (1988) The gut: a central organ after surgical stress. Surgery 104:917–923 57. Wolf YG, Verstandig A, Sasson T, Eidelman L, Anner H, Berlatzky Y (1998) Mesenteric bypass for chronic mesenteric ischemia. Cardiovasc Surg 6:34–41
58. Wylie EJ, Binkley FM, Palubinskas AJ (1966) Extrarenal fibromuscular hyperplasia. Am J Surg 112:149–155 59. Zwolak RM, Fillinger MF, Walsh DB, LaBombard FE, Musson A, Darling CE et al (1998) Mesenteric and celiac duplex scanning: a validation study. J Vasc Surg 27:1078–1087
411
6.2 Visceral Artery Aneurysms J. Hajo van Bockel, Robert H. Geelkerken
6.2.1 Introduction Aneurysms of the renal and intestinal arteries are relatively rare. In 1970, Stanley et al. [17] and Deterling [6] published a review of the compiled clinical experience of the prevalence, diagnosis and treatment of 1500 aneurysms of the intestinal arteries as published in the literature [17]. Since then, in an additional 50 articles, “case reports” have often been published [9]. Recently, an overview of demographic data concerning the prevalence, diagnosis and treatment has been presented [16].
6.2.2 Epidemiology • The exact prevalence of renal aneurysms is unknown but probably low. • In a study on 8500 patients subjected to angiography for nonrenal disease, the prevalence was 0.9% [18]. • Swedish investigators estimated the prevalence from an autopsy study to be about 0.7–0.9% [19]. • The prevalence of aneurysms of the visceral arteries as reported in the literature varies. • Due to an increase in the quantity and quality of abdominal imaging by computer tomography (CT) and magnetic resonance (MR) techniques, these aneurysms are now more often detected as an accidental finding than in the past. • As a result more insight has developed with regard to the prevalence, natural history and complications. • Aneurysms can be present in all visceral arteries, in particular: the coeliac artery with its branches, the hepatic and splenic artery and its branches and more distal branches (the gastroduodenal and pancreatoduodenal arteries).
• The prevalence of aneurysms in the splenic artery, one of the more commonly observed aneurysms, has been estimated between 0.1 and 100/1000 patients [3]. • Aneurysms of the coeliac artery and superior mesenteric arteries are less frequent with an estimated prevalence of 0.13/1000 [10]. • Of aneurysms of the superior mesenteric artery and its branches, there are no data on prevalence but such aneurysms seem to be extremely rare.
6.2.3 Aetiology Aneurysms may be caused by varies diseases. The most frequent causes are: • Atherosclerosis • Fibrodysplasia • Medial degeneration • Trauma • Connective tissue diseases such as polyarthritis nodosa or Ehlers–Danlos syndrome • Infection.
Splenic Artery Aneurysms • In addition, splenic artery aneurysms may be associated with portal hypertension and splenomegaly. • They are also relatively frequent in fertile women for which a hormonal contribution has been postulated. In women, and particularly multiparous women, splenic artery aneurysms are seen four times more than in men [4]. • Associations with infectious disease such as syphilis, tuberculosis and bacterial infections were reported in the past but never since the introduction of antibiotic therapy.
412
6.2 Visceral Artery Aneurysms
6.2.4 Symptoms • Renal and visceral aneurysms are usually without symptoms and are often an incidental finding on ultrasound or, in particular, CT or MR. • In addition, they are too small for identification by physical examination.
Ischaemia and Distal Embolization • Ischaemia of visceral organs due to thrombosis of an aneurysm seems to be extremely rare. • Distal embolization can be deduced from the angiogram if renal infarcts are present [11].
Rupture 6.2.5 Complications • Two types of complications can be anticipated: ischaemia due to thrombosis or distal embolization and rupture.
• Rupture with bleeding is a rare but often catastrophic complication. • The symptoms are usually abdominal pain and shock. • If rupture occurs in the peritoneal cavity, shock is deep and the time for diagnostic tests is not available, then emergency laparotomy is performed, at which time the diagnosis is made often with high mortality.
Fig. 6.2.1a Asymptomatic aneurysm of the hepatic artery. The various branches [common hepatic artery, left (LHA) and right hepatic artery (RHA), gastroduodenal artery] are secured with vessel loops
6.2.7 Therapy
• If contained rupture occurs within the mesenterium or gastroduodenal ligament, the severity of shock is often moderate, allowing for time to perform diagnostic tests. • As a result, a diagnosis is made which allows for selection of optimal therapy, with either endovascular or open surgical techniques. • A review showed that aneurysms of the hepatic artery were associated in half of the patients with pain and/or gastrointestinal bleeding. • Lesions were diagnosed in only 65% when the patient presented with a rupture and the resulting mortality rate was 17%. • Aneurysms of the splenic artery associated with a rupture had an even higher mortality rate of 36%. • Aneurysms of the intestinal arteries may also present with gastrointestinal bleeding caused by rupture in the gastrointestinal tract.
6.2.6 Diagnosis Currently, an incidental finding of a visceral aneurysm can be evaluated by CT and, for precise localization of efferent and afferent artery(ies), digital subtraction angiography.
6.2.7 Therapy 6.2.7.1 Surgery • Open operation and ligation, with or without vascular surgical reconstruction, is still the gold standard of therapy (Fig. 6.2.1a,b).
Fig. 6.2.1b The same aneurysm now opened, please note the amount of thrombus
413
414
6.2 Visceral Artery Aneurysms
• The choice of intervention depends on the situation (elective or emergency intervention), the aetiology (fibrodysplasia, connective tissue disease, infection, etc.) and the artery (coeliac, splenic, renal, or a distal branch). • Various alternatives have been presented [21].
Emergency Intervention • In an emergency situation, the patient is in shock and the operative field is disorderly with a haematoma in the mesenterium. • This makes identification of the bleeding and the exact localization of the aneurysm very difficult, which may result in additional arterial and venous trauma.
Elective Repair • During elective repair, the operation is planned on the basis of CT and angiographic information. • Aneurysms of the renal artery and its branches can be repaired by either in situ or ex vivo techniques [20]. • Aneurysms of the coeliac or hepatic artery are usually reconstructed by interposition grafts, whereas aneurysms of the splenic artery are often ligated without splenectomy. • Occasionally it can be very difficult during open operation to identify a relatively small aneurysm in a branch of the visceral arteries.
6.2.7.2 Endovascular Therapy • Currently, endovascular therapy is in many cases an optimal alternative to open repair [1, 2, 7, 12, 14]. • Options are embolization with coils and/or glue or, in the case of larger arteries, a covered stent [13]. • After coiling, follow-up is required because recanalization occurs in 10–20% of aneurysms [15]. • An advantage of endovascular therapy over open repair is the identification of small arteries of visceral branches that may be treated very effectively. • A disadvantage is that it can be very difficult to exclude the aneurysm completely because of the presence of multiple small feeding arteries.
6.2.8 Prognosis • The natural history of the lesions is unknown but the course of renal aneurysms is usually benign and rupture rarely occurs [19]. • It stands to reason that the risk of rupture is associated with the pathology of the lesion and its dimensions. • It has been reported that fibrodysplastic aneurysms may expand rapidly [5]. • Arbitrarily, “small” aneurysms are defined as those with a diameter less than 1.5–2.0 cm. “Large” aneurysms are defined as those over 2.0–2.5 cm in diameter. • A review suggested that rupture might occur in 13% of cases and was fatal in 27% of patients [8]. • Again the risk of rupture appears to be increased during pregnancy. • Most probably, many small visceral aneurysms exist, are never detected and never produce any symptoms. It follows that watchful waiting and a conservative approach is indicated for small aneurysms. • However, large aneurysms may have a significant risk of rupture and the advice of Stanley et al. [17] still holds for these lesions, namely “the established morbidity and mortality attributed to all aneurysms of the splanchnic arteries justify prompt surgical treatment once their presence is known” [17]. • With regard to the results of surgical or endovascular treatment, published series are small and most information is obtained from reviews [9, 16]. • Mortality of open operation after emergency repair is still high. • Endovascular intervention may be a better alternative if the condition of the patient allows additional diagnostic tests. • Results after elective open reconstruction are very satisfactory with low morbidity and mortality. • If therapy consists mainly of exclusion of the aneurysm by thrombosis, endovascular intervention appears to be an attractive alternative with less morbidity. • Recurrent bleeding has been reported because of failure to occlude all feeding collaterals to the aneurysm.
References
References 1. Baggio E, Migliara B, Lipari G, Landoni L (2004) Treatment of six hepatic artery aneurysms. Ann Vasc Surg 18:93–99 2. Baker KS, Tisnado J, Cho SR, Beachley MC (1987) Splanchnic artery aneurysms and pseudoaneurysms: transcatheter embolization. Radiology 163:135–139 3. Busutill RW, Brin J (1980) The diagnosis and management of visceral artery aneurysms. Surgery 88:619–624 4. de Vries JE, Schattenkerk ME, Malt RA (1982) Complications of splenic artery aneurysm other than intraperitoneal rupture. Surgery 91:200–204 5. den Butter G, Van Bockel JH, Aarts JC (1988) Arterial fibrodysplasia: rapid progression complicated by rupture of a visceral aneurysm into the gastrointestinal tract. J Vasc Surg 7:449–453 6. Deterling RA (1970) Aneurysms of the visceral arteries. J Cardiovasc Surg (Torino) 24:309–322 7. Gabelmann A, Gorich J, Merkle EM (2002) Endovascular treatment of visceral artery aneurysms. J Endovasc Ther 9:38–47 8. Geelkerken RH, Van Bockel JH, De Roos WK, Hermans J (1990) Surgical treatment of intestinal artery aneurysms. Eur J Vasc Surg 4:563–567 9. Geelkerken RH, Van Bockel JH (1995) Mesenteric vascular disease: a review of diagnostic methods and therapies. Cardiovasc Surg 3:247–260 10. Gelabert HA, Busutill RW (1991) Celiac, hepatic and splenic artery aneurysms. In: Ernst CB, Stanley JC (eds) Current therapy in vascular surgery. Decker, Philadelphia, pp 733–740 11. Hupp T, Allenberg JR, Post K, Roeren T, Meier M, Clorius JH (1992) Renal artery aneurysm: surgical indications and results. Eur J Vasc Surg 6:477–486
12. Kasirajan K, O’Hara PJ, Gray BH, Hertzer NR, Clair DG, Greenberg RK et al (2001) Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 33:63–71 13. Larson RA, Solomon J, Carpenter JP (2002) Stent graft repair of visceral artery aneurysms. J Vasc Surg 36:1260–1263 14. Rokke O, Sondenaa K, Amundsen SR, Bjerke Larssen T, Jensen D (1997) Successful management of eleven splanchnic artery aneurysms. Eur J Surg 163:411–417 15. Salam TA, Lumsden AB, Martin LG, Smith RB, III (1992) Nonoperative management of visceral aneurysms and pseudoaneurysms. Am J Surg 164:215–219 16. Shanley CJ, Shah NL, Messina LM (1996) Common splanchnic artery aneurysms: splenic, hepatic, and celiac. Ann Vasc Surg 10:315–322 17. Stanley JC, Thompson NW, Fry JW (1970) Splanchnic artery aneurysms. Arch Surg 101:689–697 18. Stanley JC, Rhodes EL, Gewertz BL, Chang CY, Walter JF, Fry WJ (1975) Renal artery aneurysms. Significance of macroaneurysms exclusive of dissections and fibrodysplastic mural dilations. Arch Surg 110:1327–1333 19. Tham G, Ekelund L, Herrlin K, Lindstedt EL, Olin T, Bergentz SE (1983) Renal artery aneurysms. Natural history and prognosis. Ann Surg 197:348–352 20. van Bockel JH, Terpstra JL (1996) Aortorenal bypass and renal artery aneurysmectomy. In: Novick A, Scoble J, Hamilton G (eds) Renal vascular disease. Saunders, Philadelphia, pp 439–454 21. Zimmerman-Klima PM, Wixon CL, Bogey WM Jr., Lalikos JF, Powell CS (2000) Considerations in the management of aneurysms of the superior mesenteric artery. Ann Vasc Surg 14:410–414
415
417
6.3 Acute Ischaemia of the Visceral Arteries David Bergqvist, Stefan Acosta, Martin Björck
6.3.1 Acute Intestinal Ischaemia • 6.3.1.1 Basics Acute intestinal or mesenteric ischaemia may have several causes: • Nonocclusive ischaemia (NOMI) • Occlusive ischaemia: • Arterial embolism • Arterial thrombosis • Venous thrombosis • After aortoiliac surgery.
•
•
• NOMI will not be further discussed. Under fasting, basal conditions approximately 20–25% of the cardiac output is distributed to the splanchnic arteries; coeliac artery, superior mesenteric artery (SMA) and inferior mesenteric artery (IMA). The coeliac artery supplies the stomach, spleen, part of the liver and pancreas, and the proximal part of the duodenum. The SMA supplies the distal part of the duodenum, the small bowel and the large bowel up to the mid transverse colon. The IMA is a small artery supplying the distal part of the colon and proximal part of the rectum. Under basal conditions the coeliac artery receives 800 ml blood per minute, the SMA 500 ml/min and the IMA 20–50 ml/min [16]. The collateral network between these three arteries is exceedingly rich, as are collaterals from intercostal arteries and from the internal iliac arteries.
• •
•
8.6/100,000 person years based on a population with an autopsy rate of 87%. The incidence increased exponentially with age, equally in men and women, to 217/100,000 person years in the age group of 85 years and above [2]. Thrombosis occurs at areas of severe atherosclerotic narrowing. Many patients may have pre-existing symptoms of chronic mesenteric ischaemia such as postprandial abdominal pain (abdominal angina), food fear, diarrhoea and weight loss. Most patients are atherosclerotic with a history of coronary, cerebrovascular or peripheral arterial insufficiency. Atheroma at the origin of the visceral arteries may have developed over many years, resulting in collateral circulation. Dehydration, low cardiac output and thrombophilia are contributing factors to thrombosis. Mesenteric emboli usually originate from the heart, and are predominantly due to atrial fibrillation or acute myocardial infarction. Aortoarterial embolism is infrequent. Iatrogenic embolization has been reported after various catheterizations. A number of these patients have a history of prior or synchronous arterial embolism [3]. Emboli tend to lodge at anatomical narrowings, typically a few centimetres distal to the origin of the SMA, sparing the proximal jejunal branches.
6.3.2.2 Symptoms 6.3.2 Acute Thrombotic or Embolic Arterial Occlusion 6.3.2.1 Epidemiology/Aetiology • The estimated overall incidence in the population of Malmö, Sweden, between 1970 and 1982 was
• Diagnosis must be considered when there is severe abdominal pain with initially minimal abdominal signs (pain out of proportion) in an elderly patient. • Factors such as a history of generalized atherosclerosis and pre-existing symptoms of chronic mesenteric ischaemia are more commonly associated with thrombotic occlusion.
418
6.3 Acute Ischaemia of the Visceral Arteries
• Pain out of proportion to the abdominal status, accompanied by rapid and often forceful bowel evacuation, and a source of embolus/previous history of embolism is labelled the “clinical triad” of early acute embolic occlusion. • Initially the bowel responds to the ischaemic attack with contraction. Abdominal tenderness and spasm may be lacking early on. These symptoms sometimes fade, leaving the patient apparently improved or even asymptomatic until necrosis of the bowel develops.
6.3.2.3 Complications • With progression to transmural bowel necrosis, peristalsis ceases and signs of generalized peritonitis will occur.
• Contrast-enhanced computed tomography (CT) angiography is neither specific [23] nor sensitive [15]. If, however, a multi-slice technique is performed with three-dimensional reconstructed images of the SMA, the diagnostic accuracy on proximal occlusion may improve. • Selective angiography is a specific, but invasive, diagnostic method. Lateral projections are important for visualizing the outflow from the aorta, the most common location for atherosclerotic stenosis or occlusion. • Duplex ultrasonography can be useful in detecting proximal occlusion, particularly if performed early before paralytic ileus develops. Duplex is very operator dependent and a more distal occlusion, typical of embolic disease, cannot be expected to be recognized.
Laparotomy
6.3.2.4 Diagnosis Recommended European Standard Diagnostic Steps of Investigation Physical Examination
• Initially minimal abdominal signs despite severe abdominal pain.
Laboratory Tests
• A normal D-dimer at presentation most likely excludes the diagnosis [1]. • Plasma lactate concentration becomes elevated late in the disease, when gangrene has developed, and has little value in the early recognition [17]. • An elevated white cell blood count is a common early finding, but is highly unspecific. • Early metabolic alkalosis is due to profuse vomiting, but later when gangrene develops, metabolic acidosis is more likely. • Unfortunately, as yet there is no specific laboratory marker for intestinal ischaemic injury.
Imaging Techniques
• Plain radiography has both low specificity and sensitivity. Gas in the bowel wall is pathognomonic late in the disease process when the bowel has become gangrenous.
• Explorative laparotomy, to establish the diagnosis and estimate the extent of intestinal ischaemia, remains the gold standard. • The intestines often show signs of extensive, patchy cyanotic and reddish-black discoloration. • When an embolus is fractured and localized to the periphery, multiple short segments of ischaemia may occur. • Rarely, the intestines appear entirely normal when laparotomy is performed very early after an acute occlusion of the SMA. Prompt recognition and timely intestinal revascularization is crucial for avoiding extensive bowel resections in order to reduce mortality and to avoid short bowel syndrome. The degree of intestinal ischaemia caused by the occluding thrombus/embolus cannot be predicted. In the case of rapidly developing extensive intestinal ischaemia, only vigorous action can rescue the patient from death. Only laparotomy can estimate the extent of intestinal infarction, but patients with a limited bowel infarction can sometimes be saved late in the course by a bowel resection. Hence, patients suspected of having acute occlusion should not be refused therapy merely based on time limits.
6.3.3 Mesenteric Venous Thrombosis
6.3.2.5 Treatment Conservative Therapy
• A third alternative is to staple off the infarcted intestine and to leave the reconstruction until a second-look laparotomy. This alternative has become the preferred option in our department.
Recommended European Standard Therapeutic Steps
• It is important to remember that there are often massive fluid losses in patients with acute mesenteric ischaemia, primarily plasma loss resulting in haemoconcentration. • Acidosis, hyperpotassemia and temporary kidney failure are also common and should be treated accordingly.
Additional Useful Therapeutic Options
• There are some case reports of successful local thrombolysis without laparotomy [18]. • Thrombolysis may have the potential to be more complete than an embolectomy. • The need for a subsequent laparotomy to assess intestinal viability after local thrombolysis is unclear, but conservative treatment has been reported to be successful in the absence of peritoneal signs or persistent pain. • Other case reports, however, have described fatal bleeding from the ischaemic intestine after successful thrombolysis.
Surgery Recommended European Standard Surgical Procedures Bowel Resection
It is questionable whether an elderly patient with full wall intestinal infarction from near the ligamentum Treitz to the mid-transverse colon can be saved by a bowel resection and have a meaningful life. Humane palliation is what is needed in this case. The issue of anastomosis or diverting stomas following bowel resection is controversial: • Bowel resection with an end-to-end anastomosis at primary operation can be performed in patients with a short infarcted segment with a clear margin of viable bowel. • In contrast, bowel resection, followed by double stomata, may be considered a better treatment option in patients with extensive ischaemia or necrosis with an unclear demarcation zone, since the exteriorized bowel ends can easily be inspected.
Revascularization of the SMA
• Timely intestinal revascularization is a prerequisite for survival in most patients since most have proximal thromboembolic occlusions with extensive intestinal infarction [3]. • Abdominal surgeons need to collaborate with vascular surgeons. • In the case of embolism a Fogarty embolectomy is proper and simple. • A central stenosis may need a by-pass, often a retrograde aortomesenteric graft, or reimplantation of the SMA in the aorta just below the pancreas. • Revascularization attempts should be used liberally but the full wall necrotic bowel should be resected to avoid reperfusion of irreversibly infarcted intestines, which may lead to “splanchnic shock”, where patients may progress rapidly to death from cardiac arrest or multiorgan failure. Second-Look Laparotomy
• Second-look laparotomy is recommended in cases after revascularization procedures, regardless of the condition of the patient, at 18–36 h after primary surgery. • Segments of intestinal ischaemia may show recovered intestinal viability or a clearer demarcation of infarcted segments at second-look. • It also aims at reducing unnecessary bowel resections at primary exploration and at detecting insufficient bowel anastomoses.
6.3.3 Mesenteric Venous Thrombosis 6.3.3.1 Epidemiology/Aetiology • The overall incidence of mesenteric venous thrombosis with transmural intestinal infarction was estimated to be 1.8/100,000 person years in a population-based study in Malmö, Sweden, between 1970 and 1982 [4]. • More than 80% of patients with mesenteric venous thrombosis have an underlying condition.
419
420
6.3 Acute Ischaemia of the Visceral Arteries
• The predominant factor is thrombophilia (such as protein S or C or antithrombin deficiency, and factor V Leiden mutation) seen in around 40%. • Being overweight seems to be a risk factor [4], and mesenteric vein thrombosis is also seen in patients with nephrotic syndrome, polycythaemia, malignancies and those taking oral contraceptives. • Synchronous venous thromboembolism in the systemic circulation occurs frequently, especially pulmonary embolism [4].
6.3.3.2 Symptoms • Usually, venous thrombosis starts distally, with proximal propagation, and the degree of ischaemia depends on its extent and whether there is an occlusion and collateral flow. • The clinical development is similar to the arterial one but much slower and diffuse abdominal pain can be present for days or weeks.
6.3.3.3 Diagnosis • Abdominal CT with contrast is the most sensitive test, once the condition is suspected [12]. • Mesenteric arteriography with venous phase imaging is also diagnostic in most cases.
6.3.3.4 Therapy
6.3.4 Intestinal Ischaemia after Aortoiliac Surgery 6.3.4.1 Epidemiology/Aetiology • When searched for using routine sigmoidoscopy, the incidence of left colon ischaemia is around 7% after elective surgery and 35% after surgery for ruptured AAA [5, 8, 20]. • Most of these patients suffer superficial ischaemic injury, the clinical relevance of which is controversial. • When incidences of clinically detectable bowel ischaemia are compared, a decisive factor is the proportion of patients in preoperative shock due to a ruptured AAA in the population studied. Table 6.3.1 shows the incidences in the different patient categories according to data from the Swedish Vascular Registry (Swedvasc) [9]. • The incidence of intestinal ischaemia after endovascular therapy of abdominal aortic disease is insufficiently studied but fatal ischaemic intestinal complications have been reported [21]. The impression is that, if there is any difference, the incidence may decrease with endovascular therapy.
Preoperative Risk Factors • Preoperative shock due to rupture is the strongest risk factor [10, 19]. • Haemodynamically stable patients operated on for ruptured AAA do not have an increased risk.
Conservative Therapy • Anticoagulation with heparin and an oral vitamin K antagonist is used in operated as well as nonoperated cases. • Thrombolysis is also described but it is unclear whether this more aggressive treatment is superior to anticoagulation.
Surgery • When peritonitis has developed, laparotomy and bowel resection is necessary.
Table 6.3.1 Incidences of colonic ischaemia in the different categories of aortoiliac surgery No. with ischaemia
Incidence (%)
Patient category
No. of patients
All patients
2930
63
2.1
Elective surgery
2066
22
1.1
Emergency surgery
864
41
4.7
Ruptured AAA, all patients
563
33
5.9
Ruptured AAA, in shock
412
30
7.3
From [7, 9]
6.3.4 Intestinal Ischaemia after Aortoiliac Surgery
• Emergency surgery is an independent risk factor also, when excluding all patients in shock operated on for a ruptured AAA. • Renal insufficiency, defined as serum creatinine >150 μmol/l, is an independent risk factor, as is age. The risk increases by 5.5% per year [10].
• It should be recognized that the ischaemic insult is a combination of depth and duration. • Most patients who develop colonic gangrene do so in the postoperative period, often several days after the operation [8, 10, 11]. • An aggressive resuscitation of the colonic blood flow in the postoperative period can prevent the development of irreversible gangrene [11].
Intraoperative Risk Factors • In the past when the aetiology of this complication was discussed in the literature, the ligation of a patent IMA was considered a causative factor, a priori. Therefore, IMA was reimplanted selectively after IMA stump pressure measurements, with values below 40 mm Hg being an indication for reimplantation. • Some authors recommended routine reimplantation of the IMA, but this recommendation was not based on scientific evaluation [13]. • In contrast, based on prospective studies and retrospective case–control studies, occlusion of the IMA is a marker of more advanced disease and associated with an increased risk of this complication. • Ligation of an open IMA is not associated with an increased risk of postoperative intestinal ischaemia [8, 10, 20]. • Case–control studies and prospective clinical studies have shown that ligation of both internal iliac arteries is strongly associated with intestinal ischaemia [11, 14]. • There is an increased risk after aortobifemoral grafting as compared to the tube grafts, probably because of sacrifice of the internal iliac arteries [10]. • A blood loss exceeding 10 l is an independent risk factor for colonic ischaemia [10]. Based on multivariate analysis, operating time and cross-clamping are found to be independent risk factors [10].
Postoperative Risk Factors • Hypovolaemia and prolonged postoperative hypotension as well as intra-abdominal hypertension are associated with the complication. • In particular, after operation of a ruptured aortic aneurysm increased intra-abdominal pressure may result in a high central venous pressure despite hypovolaemia [11].
6.3.4.2 Symptoms • The cardinal symptoms and signs are early, bloody diarrhoea and peritonitis, but they are unreliable. • Sometimes the diarrhoea is not bloody and instead postoperative shock and fever could be the predominating symptoms. • The suspicion should be high when general signs such as fever, circulatory instability, oliguria or coagulopathy develop [9, 19].
6.3.4.3 Diagnosis • Sigmoid pHi measurements (Tonocap®) seem to be the best available method for continuous monitoring of the perfusion of the left colon. • A value of less than 6.9 for at least 4 h has a very high sensitivity and specificity. • The suspicion is verified with sigmoidoscopy [8, 11, 20].
6.3.4.4 Treatment • Once the complication has been diagnosed, treatment depends on the depth of the lesion, classified as follows: I Mucosal lesion II Mucosal and muscular lesion III Transmural gangrene. • In the immediate postoperative period, grades I and II are difficult to separate, the practical implication of grade II being that the patient may develop late stricture. • Treatment of the intestinal gangrene is straightforward; the gangrenous intestine must be removed without delay. In most cases the left colon is involved and the Hartmann procedure is preferred.
421
422
6.3 Acute Ischaemia of the Visceral Arteries
• If it can be verified by repeated sigmoidoscopy and pHi monitoring, or by laparotomy, that the lesion is not transmural there is no evidence that the patient benefits from bowel resection. • When a superficial lesion is identified, prophylactic measures to prevent the progression to a transmural lesion should be considered. • A combination of optimal haemodynamic treatment and of continuous sigmoid pHi monitoring to evaluate the effects of treatment is probably beneficial.
6.3.5 Acute Renal Ischaemia Acute nontraumatic ischaemic conditions in the kidney are usually caused by one of three disease processes: • Thrombosis in a healthy artery • Thrombosis in a stenotic artery • Embolism.
6.3.5.1 Thrombosis Thrombosis in a Healthy Artery • Thrombosis without previous alteration in the artery is extremely rare, as the renal artery blood flow is relatively very high, and thrombosis depends on a combination of factors as already indicated by Virchow’s triad: alteration in the vessel wall, in blood flow and in blood composition. • Thrombosis is primarily seen in thrombophilic conditions but is still rare. • Acute thrombosis of the main renal artery often results in kidney infarction.
Thrombosis in a Stenotic Artery • Thrombosis in a stenotic artery is usually seen in patients with advanced atherosclerotic disease (“chronic occlusion”). • The thrombotic process may lead to occlusion, which usually is asymptomatic because of the slow stenosing process, giving the time and opportunity to develop adequate collaterals (ureteral, capsular, adrenal, lumbar vessels).
• Often there is only a slight elevation in creatinine indicating that the occlusion has occurred [22]. • In patients with only one functioning kidney, however, there may be an acute onset of renal failure, sometimes with flash pulmonary oedema, because of rapid retention of fluid. In patients with an underlying stenosis, often atherosclerotic, the usual reconstructive options should be considered, provided the renal artery distal to the stenosis is healthy, and the kidney is not atrophied (length >8 cm). Thrombolysis, dilatation and stenting can sometimes be successful; otherwise the reconstructive solution is a by-pass, often aortorenal. Revascularization can be successful also in occlusions of long duration, weeks or even months.
6.3.5.2 Embolism • Arterial embolism has the same causes as embolism in other parts of the body, thus the dominating source is the heart (atrial fibrillation or myocardial infarction). • Embolism to the visceral arteries is often multiple, involving several organs [3]. • The symptomatology is difficult to interpret: sudden flank pain in a patient with an embolic source together with microscopic haematuria, often with nausea and vomiting. The picture is often wrongly diagnosed as a ureterolithiasis, which causes a diagnostic delay. The typical time course is treatment with a nonsteroidal anti-inflammatory drug (NSAID) without full effect, after which pyelography or CT is made, showing a silent, nonfunctioning kidney. • One problem with embolism generally, and not least with renal artery embolism, is that the embolus fractures at bifurcations, which means small emboli lodging in the distal arterial tree [6]. This makes embolectomy with a Fogarty catheter difficult because of the problem of reaching very distally from the main renal artery. • A more attractive option therefore is local intra-arterial thrombolysis offering the possibility of also cleaning the distal arterial tree. • This is also the method of choice in cases of acute thrombotic occlusion of an otherwise healthy artery. • The problem with both surgical and thrombolytic therapy, however, is to be in time to preserve kidney function.
References
• If this is not possible, the kidney will decrease in size, lose its excretory function but still produce renin resulting in renovascular hypertension. If this is the case nephrectomy is the treatment of choice. • The kidney salvage rate after renal artery embolectomy is low, in many series below 70%. References 1. Acosta S, Nilsson TK, Bjorck M (2004) D-dimer testing in patients with suspected acute thromboembolic occlusion of the superior mesenteric artery. Br J Surg 91:991–994 2. Acosta S, Ogren M, Sternby NH, Bergqvist D, Bjorck M (2004) Incidence of acute thrombo-embolic occlusion of the superior mesenteric artery – a population-based study. Eur J Vasc Endovasc Surg 27:145–150 3. Acosta S, ÖgrenM, Sternby N-H, Bergqvist D, Björck M (2005) Clinical implications for the management of acute thromboembolic occlusion of the superior mesenteric artery: autopsy findings in 213 patients. Ann Surg 241(3):516–522 4. Acosta S, Ögren M, Sternby N-H, Bergqvist D, Björck M (2005) Mesenteric venous thrombosis with transmural intestinal infarction – a population based study. J Vasc Surg 41(1):59–63 5. Bast TJ, van der Biezen JJ, Scherpenisse J, Eikelboom BC (1990) Ischaemic disease of the colon and rectum after surgery for abdominal aortic aneurysm: a prospective study of the incidence and risk factors. Eur J Vasc Surg 4:253–257 6. Bergentz S-E, Bergqvist D, Weibull H (1992) Renovascular emergencies. In: Greenhalgh R, Hollier L (eds) Emergency vascular surgery. Saunders, London 7. Björck M (1998) On intestinal ischaemia after aortoiliac surgery. Epidemiological, clinical and experimental studies. Acta Universitatis Upsaliensis 740 8. Bjorck M, Hedberg B (1994) Early detection of major complications after abdominal aortic surgery: predictive value of sigmoid colon and gastric intramucosal pH monitoring. Br J Surg 81:25–30 9. Bjorck M, Bergqvist D, Troëng T (1996) Incidence and clinical presentation of bowel ischaemia after aortoiliac surgery – 2930 operations from a population-based registry in Sweden. Eur J Vasc Endovasc Surg 12:139–144 10. Bjorck M, Troeng T, Bergqvist D (1997) Risk factors for intestinal ischaemia after aortoiliac surgery: a combined cohort and case-control study of 2824 operations. Eur J Vasc Endovasc Surg 13:531–539
11. Bjorck M, Lindberg F, Broman G, Bergqvist D (2000) pHi monitoring of the sigmoid colon after aortoiliac surgery. A five-year prospective study. Eur J Vasc Endovasc Surg 20:273–280 12. Brunaud L, Antunes L, Collinet-Adler S, Marchal F, Ayav A, Bresler L, Boissel P (2001) Acute mesenteric venous thrombosis: case for nonoperative management. J Vasc Surg 34:673–679 13. Ernst CB, Hagihara PF, Daugherty ME, Griffen WO Jr. (1978) Inferior mesenteric artery stump pressure: a reliable index for safe IMA ligation during abdominal aortic aneurysmectomy. Ann Surg 187:641–646 14. Johnston KW, Scobie TK (1988) Multicenter prospective study of nonruptured abdominal aortic aneurysms. I. Population and operative management. J Vasc Surg 7:69–81 15. Kirkpatrick ID, Kroeker MA, Greenberg HM (2003) Biphasic CT with mesenteric CT angiography in the evaluation of acute mesenteric ischaemia: initial experience. Radiology 229:91–98 16. Kolkman JJ, Mensink PB (2003) Non-occlusive mesenteric ischaemia: a common disorder in gastroenterology and intensive care. Best Pract Res Clin Gastroenterol 17:457–473 17. Lange H, Jackel R (1994) Usefulness of plasma lactate concentration in the diagnosis of acute abdominal disease. Eur J Surg 160:381–384 18. Mellander S, Hellberg R, Karlqvist PA, Svahn M (2001) Local fibrinolysis in acute thromboembolism of the superior mesenteric artery. Eur J Surg 167:308–311 19. Piotrowski JJ, Ripepi AJ, Yuhas JP, Alexander JJ, Brandt CP (1996) Colonic ischaemia: the Achilles heel of ruptured aortic aneurysm repair. Am Surg 62:557–561 20. Schiedler MG, Cutler BS, Fiddian-Green RG (1987) Sigmoid intramural pH for prediction of ischemic colitis during aortic surgery. A comparison with risk factors and inferior mesenteric artery stump pressures. Arch Surg 122:881–886 21. Thomas SM, Gaines PA, Beard JD (2001) Short-term (30day) outcome of endovascular treatment of abdominal aortic aneurism: results from the prospective Registry of Endovascular Treatment of Abdominal Aortic Aneurism (RETA). Eur J Vasc Endovasc Surg 21:57–64 22. Weibull H, Bergqvist D, Andersson I, Choi DL, Jonsson K, Bergentz SE (1990) Symptoms and signs of thrombotic occlusion of atherosclerotic renal artery stenosis. Eur J Vasc Surg 4:159–165 23. Wiesner W, Khurana B, Ji H, Ros PR (2003) CT of acute bowel ischaemia. Radiology 226:635–650
423
Lower Extremity Arteries
427
7.1 Lower Limb Arterial Recanalization Tomislav Šoša †, Vinko Vidjak
7.1.1 Introduction Lower limb arterial recanalization is a term that encompasses various therapeutic manoeuvres with the goal of re-opening or dilating occluded and stenotic arteries. This chapter deals primarily with the treatment of chronic infra-inguinal occlusive disease. Percutaneous transluminal angioplasty (PTA) and stents are, at present, accepted as effective treatment in a substantial portion of iliac artery lesions [52]. The role of endovascular repair in the femoro-popliteo-crural system is still the subject of debate [37, 55]. Percutaneous revascularization of femoro-popliteal arteries has shown high restenosis rates and stents should be confined to flow-limiting dissections or where there have been inadequate results from balloon angioplasty alone [27]. The clinical and cost-effective utilization of infra-inguinal instrumental recanalization (IR) relies upon weighing up the risks and benefits of the procedure against those of other treatment options in relation to the natural history of the patient’s underlying condition, whether that is intermittent claudication (IC) or critical limb ischaemia (CLI). It also relies, of course, on the durability of the endovascular procedure. The true magnitude and clinical consequences of IR’s early and late failure rate are difficult to gauge because of the lack of good studies. The vast majority of studies present only uncontrolled, observational evidence of efficacy [11, 66]. In any case, IR and surgical revascularization should be regarded as complementary, not competitive, treatment modalities.
7.1.2 Problems and Questions The following discussion will stick to the problems and questions that arise in the area of lower limb arterial recanalization. It is generally accepted that IC is not indicated for lower limb IR. Recent reports favour subintimal
angioplasty (SA) in patients with IC [24], but satisfactory results can be obtained in the hands of a highly skilled and experienced interventionalist, as well as under the conditions of conscientious surveillance, enabling the early treatment of any complication. Other reports support the fact that in a selected group of patients SA is feasible with a high technical success rate as a good alternative in patients who are poor candidates for by-pass surgery [18, 31, 75, 88]. It can be used for limb salvage [73]. The outback catheter for true lumen re-entry after subintimal guidewire passage offers an effective tool for complicated recanalization procedures [32]. CL ischaemia in patients unfit for surgery emerged as the only proper indication for IR of lower limb arteries. Unfortunately, in many publications on infra-inguinal IR, the study population consists of patients with different degrees of ischaemia, varying from IC to true CLI [12, 82]. Subcritical limb ischaemia (SCLI) is, however, included in the indication criteria [86], but with an uncertain number of patients. CLI is a major burden on vascular services, estimated at 1 patient in 2500 of the population on an annual basis. In Croatia, 45 CLI patients can be found per 100,000 of the population per year. The average burden on each vascular surgeon in the country is >130 lower limb revascularizations per year [72]. CLI poses a significant problem for the vascular services, with a mean mortality and amputation rate of 13.5% and 21.5% respectively [61]. In a retrospective series of patients, repeated procedures to maintain patency, the treating of wound complications, or the treating of recurrent or contralateral ischaemia is needed in 54% of cases. Large studies identified the risk factors associated with postoperative mortality in patients undergoing femoro-distal by-pass. Compared to patients who survived, patients who died at the time of surgery were older, were diabetic (30%), were 4 times more likely to have had a recent MI, were 2 times more likely to have had heart failure, were 4 times as likely to be on dialysis, had multisegmental lesions and were admitted as an emergency. For these reasons, consideration should be given to an endovascular technique. The endovascular
428
7.1 Lower Limb Arterial Recanalization
technique offers an alternative to patients unfit for surgery, and SA has been reported with promising results from an increasing number of centres [7, 47, 50 53, 61, 63, 69]. Hybrid procedures with intraoperative balloon superficial femoral artery (SFA) angioplasty and popliteal/distal by-pass graft can be performed in a selected group of patients [64]. At the present time, the problems named here can be classified as solved, unsolved or permanent.
7.1.2.1 Solved Problems • Endovascular therapy should be considered for patients unfit for surgery. • Localized atherosclerotic iliac stenosis and chronic occlusions combined with SFA occlusion should be treated by PTA and stenting before or together with femoro-popliteal by-pass, thanks to the durability of this procedure [12, 14, 65, 76, 78]. • Localized iliac stenosis alone should be treated with angioplasty (TASC consensus) [52]. • Balloon angioplasty does not require specialized equipment or materials and is a relatively inexpensive procedure [46]. • Failure after an attempted endovascular intervention rarely compromises a subsequent surgical by-pass option [25]. • Endovascular treatment, either simple or complex, offers an alternative for elderly and frail patients with CLI who lack a good surgical option [25, 29]. • Up to 37% of patients may be poor surgical candidates [45]. However, significantly more patients were alive and improved after surgery than after angioplasty at 1 month (82.3% vs. 77.7%) and at 1 year (49.6% vs. 44.3%) [89].
7.1.2.2 Unsolved Problems
• A superficial femoral artery (SFA) with a diameter at the occlusion site of ≤3.5 mm is not suitable for PTA, as the original arterial lumen cannot be reconstructed [43]. • It is wise to offer endovascular therapy to patients with a relatively short life expectancy [3], and it is advisable to offer endovascular therapy to patients without autologous vein for by-pass [9, 10]. • In cases with infrapopliteal disease, endovascular treatment could be the initial option while restenosis after PTA in this region still yields a 70–85% limb-salvage rate [19]. • SA offers a useful adjunct but only in experienced hands [24, 69]. It is still reserved for a selected group of patients [18, 31], and could be improved by intravascular ultrasonography- (IVUS-) guided luminal reentry [68], or by the retrograde approach [67, 88]. • True CLI is usually associated with two or more anatomical levels of arterial occlusion and here surgical by-pass is the most effective and durable treatment option [21]. • The BASIL (Bypass vs. Angioplasty in Severe Ischemia of the Leg) trial may be available in 2005/6 (in Birmingham). This study seeks to examine not only the clinical outcome in terms of amputation-free survival and health-related QOL, but also the cost-effective utilization of healthcare resources [3].
Lack of Evidence for the Effectiveness of Tibio-peroneal Angioplasty Few studies which compare above-knee and below-knee angioplasties have been performed. The mixed indications for tibio-peroneal angioplasty, including patients with high co-morbidity, stenotic and occlusive lesions and variable foot arch with one-, two- or three-vessel Table 7.1.1 Recently published 1-year limb-salvage rates after infrapopliteal percutaneous intraluminal angioplasty
Should Angioplasty be the First-line Treatment for CLI Patients?
Publication
• PTA offers primary endovascular therapy to the majority of patients with aortoiliac obstructions. • In the femoro-popliteal segment PTA is the first option in patients with significant co-morbidities and with lesions <3 cm in length [52].
Varty [79]
No. of limbs
One-year limb-salvage rate (%)
82
76
Wolfle [87]
84
82
Jämsen [37]
235
68
Peregrin [61]
375
72
7.1.2 Problems and Questions
run-off, lead to differences in outcome [60]. Follow-up is frequently lacking because the studies are done in frail and elderly patients. The procedure has low mortality and is performed under a local anaesthetic, but it should be borne in mind that only 17% of these patients can be considered for surgical reconstruction [4, 35]. However, recently published limb-salvage rates after infrapopliteal PTA show a 1-year limb-salvage rate of 68–82% compared with 54% in untreated patients (Table 7.1.1) [37, 61, 79, 87]. The number of patients followed-up dropped to 5.8% in 6 years [61]. Yet, in the case of infrapopliteal disease the endovascular approach is recommended as the first option because of its reduced invasiveness, which is more suitable for the predominantly multi-morbidity patient cohort [84] (Table 7.1.1).
Use of Stents Systematic stenting in the femoro-popliteal area for short SFA lesions is not justified. There are no data proving a benefit of routine stenting over PTA alone in the femoropopliteal arteries [80]. Yet, a recent meta-analysis shows that for more severe femoro-popliteal disease, the results of stent implantation seem a bit more favourable than those for PTA (3-year patency 63–66% vs. 61%) [58]. There are several papers which show a positive impact of stents on mid-term results [15, 28, 36, 51]. The overall evidence did not show that the efficacy of stents in the femoro-popliteal region is clearly superior to PTA alone. Using overlapping stents is reported to show early breaking of struts and, when avoidable, this should not be done [62].
TASC summarized the results of femoro-popliteal stenting as follows: in a comparison of 11 trials involving femoro-popliteal arterial stenting in 585 patients, the primary patency rate was 58% at 36 months. For PTA alone, patency rates were 51% at 36 months [56] (Table 7.1.2).
The Difference Between Stenosis and Occlusion, and Between Single and Multiple Stenosis A clear difference is observed between the primary success rate in limbs with SFA occlusion <5 cm and >5 cm with a 5-year patency rate of 12% vs. 32% respectively [49]. The best results were obtained in patients with single SFA stenosis (53% patency in 5 years). Patients with multiple stenoses had a 5-year patency of 42%. Analysis of our group demonstrated a 3-year patency rate of 74% in femoro-popliteal stenosis vs. 43% in patients with femoro-popliteal occlusions. For the small subgroup of patients with advanced limb ischaemia who have profound co-morbidity, the treatment should be limited to palliative care, including primary amputation [13].
The Role of Drug-eluting and Covered Stents in the Peripheral Arterial Recanalization Restenosis limits the efficacy of PTA and stenting. The highest rates of restenosis are in SFA. It is expected that drug-eluting stents will prove to be as valuable in peripheral applications as in coronary applications. We also expect drug-eluting stents to increase the durability of
Table 7.1.2 Overall patency rates after PTA and PTA/stent, University Hospital Merkur Zagreb, 2001–2003. No significant difference between stented and non-stented group Area/procedure
Technical success
6 months
12 months
24 months
Fem-pop n=53 PTA n=42
(40) 95.2%
(38) 90.4%
(36) 85.7%
(28) 66.6%
PTA/stent n=11
(11) 100%
(10) 90.9%
(10) 90.9%
(8) 72.7%
Overall patency
(51) 96.2%
(48) 90.9%
(46) 86.7%
(36) 67.9%
PTA n=39
(38) 97.4%
(36) 92.3%
(35) 89.7%
(35) 89.7%
PTA/stent n=20
(20) 100%
(19) 95%
(19) 95%
(18) 90.0%
Overall patency
(58) 98.3%
(55) 93.2%
(54) 91.5%
(53) 89.8%
Aorto-iliac n=59
429
430
7.1 Lower Limb Arterial Recanalization
peripheral stenting. However, the bulk of our knowledge of drug-eluting stents still comes from animal research and short-term controlled trials for coronary applications (MACE, ASPECT) [39, 59], and there are as yet no sufficient data to support the use of drug-eluting stents in the peripheral vessels. In the light of improving results with uncoated stents, currently it is very doubtful that drugeluting stents in SFA will ever be cost-effective [20, 62].
7.1.2.3 Permanent Problems The Vast Majority of Patients do not Have a Pattern of the Disease that Requires Angioplasty that would Remain Patent for Years The results in the CLI series are much worse than in the SCLI/IC series. Skin necrosis and ulceration may affect limbs with ankle systolic pressure >60 mmHg and with short occlusions, often because of trauma, sepsis or venous stasis. These limbs are unlikely to show progressive deterioration and angioplasty is frequently effective in such patients. This condition should be termed SCLI. Once healing has been achieved, occlusion after angioplasty may not precipitate relapse [21]. There are other less invasive modalities of treatment with promising results. Stents are winning the battle in the coronary area and vein could be harvested more for peripheral arterial surgery. Improving anaesthesiology and surgical skills, new anastomotic techniques, together with endoscopic vein harvesting for the in-situ by-passing offer safe procedures even to high-risk patients. In conclusion, angioplasty often is a useful adjunct for multilevel surgery.
12% immediate clinical failure rate [9–11, 48]. In other words, almost one of five patients submitted for angioplasty had an unsuccessful procedure.
Mid-term and Long-term Failures of Endovascular Repair of the Lower Limb Arteries are Still Unsatisfactory We need a thorough prospective analysis of the particular subgroups divided strictly on the basis of localization, type and stage of disease. Only then will we be able to decide the preferred therapeutic modality for patients with peripheral arterial obstructive disease (Figs. 7.1.1, 7.1.2).
7.1.2.4 Arising Questions Is the Flow-Dynamic Result More Important Than Quality of Life (QOL)? Peripheral arterial obstructive disease (PAD) decreases QOL of patients more than that of age-matched controls [42]. Flow-dynamic outcome does not determine QOL. The long-term goal of intervention is limb salvage rather than patency. Studies on the effect of endovascular treatment regarding the QOL in PAD patients showed substantial improvement from 1995 to 2003 [17, 41]. After the treatment, the greatest impact on QOL is cardiovascular co-morbidity [41]. QOL should be taken into account when considering invasive treatment in PAD patients and also when evaluating treatment.
Lack of Evidence
Is Failure After Angioplasty the Important Issue?
The vast majority of the studies of the durability of endovascular procedures present uncontrolled, observational level 3 evidence of efficacy [11].
Mid-term and long-term failure rates of endovascular repair of the lower limb arteries are still not satisfactory. We need a thorough, prospective analysis of the particular subgroups divided strictly on the basis of localization, type and stage of the disease. However, failure after angioplasty (restenosis and/or occlusion) occurs in a considerable number of patients. As stated before, these patients are categorized in the limb-salvage group with the QOL improvement, but also in the group with the clinical deterioration. In the latter group, immediate reintervention can provide secondary patency and limb salvage [24, 61].
Safety Although infra-inguinal endovascular procedures are safer than surgical by-pass regarding the in-hospital mortality, they are not risk free. Infra-inguinal endovascular procedures may have 6% major morbidity, a 7% technical failure rate and up to a
7.1.2 Problems and Questions
Fig. 7.1.1 Percutaneous transluminal angioplasty success according to the ankle/brachial blood pressure index (ABI) values in the aortoiliac and femoro-popliteal areas (University Hospital Merkur, Zagreb). Moderate, but not significantly better result in the femoro-popliteal stented group
Fig. 7.1.2 Angioplasty success in the aortoiliac and femoropopliteal areas depending of the number of patent calf arteries due to the ABI values before, and 6 months, 1 year and 2 years after the procedure. Significantly better follow-up in the group with two to three patent arteries
The Rising Role of Cutting Balloon Angioplasty?
with an acceptably low complication rate [77]. However, DA should not be used instead of balloon angioplasty because both techniques yielded similar results. Vibrational angioplasty showed positive preliminary results in the treatment of chronic femoropopliteal occlusions [54]. Ultrasonic angioplasty for the treatment of occluded peripheral arteries may be the next treatment modality if its efficacy can be proved in the future [38].
There are very limited data on the use of cutting balloons in the peripheral vascular system [57]. Cutting balloons were developed for use in the coronary circulation and on the basis of the available evidence cutting balloons may achieve success in lesions resistant to conventional angioplasty, such as in-stent stenosis [5]. There is no evidence that cutting balloons are better than conventional angioplasty for the treatment of nonresistant lesions. Recommended indications in the peripheral arterial system could be: treatment of lesions in native vessels resistant to conventional PTA, treatment of stenosis on vascular anastomosis and, of course, treatment of in-stent stenosis. Fresh reports show satisfactory results both in popliteal and infrapopliteal vessels in patients with symptomatic lower limb ischaemia [1, 23].
The Importance of the New Atherectomy Techniques? Despite the very high complication rate of the early atherectomies with rotational devices [16, 40, 83], a new paper demonstrates good results concluding that directional atherectomy (DA) is an acceptable and feasible technique for treating arterial lesions in the femoropopliteal artery
Excimer Laser Angioplasty The PELA trial (Peripheral Excimer Laser Angioplasty 1998–2002), established to evaluate the efficacy of laser angioplasty, randomized 251 patients with claudication and total occlusion to either laser plus PTA or PTA alone. This trial showed similar results with regard to crossing the lesion and procedural success, but in the laser group fewer patients required stent placement compared with those in the PTA-only group. There was a greater incidence of perforation in the laser group, but there was no difference in terms of procedural complications and their seriousness between the two groups [44]. Data from the recently completed Laser Angioplasty for CLI Phase 2 Trial (LACI) suggested that this is a viable treatment strategy for CLI patients who are otherwise not good can-
431
432
7.1 Lower Limb Arterial Recanalization
didates for by-pass surgery [29, 45, 85]. Without additional procedures, laser angioplasty does not appear to add any long-term benefit over balloon dilation despite the better initial recanalization rate [70, 74].
Radiologically Guided Endarterectomy (RSFAE) + Distal Stent This method, applied many years ago for iliac and femoral occlusive disease but substantially improved by construction of the MollRing Cutter (Vascular Architects, San Jose, Calif., USA) [34], combines classical orthograde femoral endarterectomy (or retrograde via the popliteal artery) with cutting the distal end of the plaque and placing the distal stent to prevent any further distal dissection. The stent tacks down the distal intimal flap, covering both the proximal endarterectomized surface and the distal part of the artery that is not endarterectomized [26, 71]. A high incidence of early stenosis has resulted in attempts to cover the treated segment with PTFE endograft (endolining) [2]. The acute, early and late graft occlusions and covering the collaterals led to the conclusion that endografting cannot be considered as an improved treatment modality. A new stent concept, aSpire, combines the advantages of covered and open stents. The double spiral configuration of the aSpire stent covered with the thin sleeve of PTFE preserves the collaterals and maintains the endarterectomized segment open. The early results of a European multicentre trial in patients with SFA occlusions treated with an aSpire stent after PTA or REA are promising [30].
Classic Endarterectomy Still Shows Comparable Results The series of 103 limbs with short femoro-popliteal occlusions, all in disabling claudicant patients, received either endarterectomy or angioplasty. Although the primary patency was significantly higher in the endarterectomy group (89% vs. 46% at 3 years), re-interventions resulted in similar tertiary patency at 3 years in both groups [12].
Reduction of Restenosis by Cryoplasty Using conventional transluminal percutaneous techniques, the cryoplasty balloon is positioned at the site of arterial narrowing. A small quantity of nitrous oxide is
delivered to inflate the balloon to 608 kPa (6 atm) with negligible cooling. Following a 10-s dilatation interval, the treatment cycle begins. During the treatment cycle, liquid nitrous oxide is delivered continuously into the balloon where it expands into gas, and the plaque is therefore cooled from –2°C to the final treatment temperature of –10°C. The melting of tissue ice resulting from the subsequent warming of the balloon to body temperature induces smooth muscle cell apoptosis and inhibits neointimal formation, probably by reducing collagen synthesis [6, 22]. The first clinical study was designed as a multicentre nonrandomized open registry with the involvement of 16 sites with 102 patients with high-degree stenosis or occlusion included. The study was completed in 2002. Dilating and cooling of the plaque seemed to be a valid method of achieving an acceptable long-term PTA result (13.7% re-stenosis at 9 months). The incidence of dissections was limited compared to that with PTA (7% vs. 43%), reducing the need for stents. Although the cryoplasty technology is promising, easy to use, apparently safe and well tolerated, the validity of cryoplasty for more complex SFA occlusions and for tibial lesions has yet to be proven.
What Could be the Endovascular Strategy for Limb Salvage in Patients with Below-knee Lesions as a Significant Cause of CLI? In the first place, we should achieve patient optimization with medical control of co-morbidities, and prove good inflow in the infragenicular region. CLI is the primary indication for treatment [61]. Haemodynamic assessment of the lesion after treatment is more important than static angiographic assessment. PTA, cutting balloon, SA, stenting and Excimer laser are methods of first choice in unisegmental below-knee disease. The choice of method depends on the personal experience of the highly skilled vascular therapist [8, 84]. The goal of the therapy should be limb salvage and relief of symptoms. Frequent surveillance of the results is recommended in order to avoid drawing the wrong conclusions.
7.1.3 Conclusions The results of lower limb recanalization are not equal to the results of surgery, but are continuously improving with time. Statistics are often applied incorrectly when
References
comparing surgery and angioplasty, especially regarding patient selection. The pressure from industry is high towards the “endovascular switch”. The indubitable first-line role of angioplasty is in the following groups of patients: • Patients with subcritical limb ischaemia, who usually have less extensive disease. They may be drawn back into the group of claudicant patients by a combination of aggressive best medical therapy (BMT) and limited angioplasty. • Those with venous ulcers and limited arterial disease, in order to relieve pain and permit compression therapy. • Those with neuroischaemic tissue loss: in diabetics where the primary problem is neuropathy but where the endovascular treatment of limited arterial disease may improve blood flow and accelerate healing. • In cases of infrapopliteal disease; due to the multiple co-morbidity and shorter life-expectancy of these patients, the less invasive endovascular option can be recommended as the first treatment option. At the present time, there is absolutely no credible evidence to suggest that, in patients with true CLI who are suitable for femoro-distal by-pass, angioplasty is the preferred option. Superficial femoral arteries with a diameter reduction to ≤3.5 mm are not suitable for percutaneous recanalization, as the original arterial lumen cannot be reconstructed. Angioplasty is a viable treatment strategy for patients with CLI who are otherwise not good candidates for by-pass surgery. However, further investigations are still needed. References 1. Ansel GM, Sample NS, Botti III CF et al (2004) Cutting balloon angioplasty of the popliteal and infrapopliteal vessels for symptomatic limb ischemia. Catheter Cardiovasc Interv 61(1):1–4 2. Bauermeister G (2001) Endovascular stent-grafting in the treatment of superficial femoral artery occlusive disease. J Endovasc Ther 8(3):315–320 3. Bell J, Papp I, Bradbury AW (2000) Bypass versus angioplasty for severe ischaemia of the leg: The BASIL trial. In: Greenhalgh RM, Powell JT, Mitchell AW (eds) Vascular and endovascular opportunities. Saunders, London, pp 485–494 4. Bell PRF (2003) There is no evidence for effectiveness of tibioperoneal angioplasty. Against the motion. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 315–320
5. Bendok BR, Roubin GS, Katzen BT et al (2003) Cutting balloon angioplasty to treat carotid in-stent restenosis: technical note. J Inv Cardiol 15:227–232 6. Biamino G, Scheinert S, Schmidt A et al (2004) Reduction of re-stenosis by cryoplasty. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, Massachusetts, pp 330–341 7. Boisiers M, Peeters P, Deloose K, Verbist J, Sprouse LR (2004) Endovascular below-the-knee strategies for limb salvage. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, London, pp 298–311 8. Boyer L, Therre T, Garcier JM et al (2000) Infrapopliteal percutaneous transluminal angioplasty for limb salvage. Acta Radiol 41(1):73–77 9. Bradbury A (2003) Angioplasty is the first-line treatment for critical limb ischaemia. Against the motion. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 295–307 10. Bradbury AW, Bell J, Lee AJ et al (2002) Bypass or angioplasty for severe limb ischaemia? A Delphi Consensus Study. Eur J Vasc Endovasc Surg 24:411–416 11. Burns P, Bradbury A(2002) Durability of infrainguinal balloon angioplasty: analysis of early and late failure. In: Branchereau A, Jacobs M (eds) Complications in vascular and endovascular surgery. Part II. Futura, Armonk, pp 295–301 12. Buth J, Yilmaz N, Cuypers P, Tielbeek A, Duijm L (2002) Mid-term and long-term failures of endovascular repair of the lower limb arteries. In: Branchereau A, Jacobs M (eds) Complication in vascular and endovascular surgery. Part II. Futura, Armonk, pp 311–318 13. Campbell WB, Verfaille P, Ridler BM, Thompson JF (2000) Non-operative treatment of advanced limb ischaemia: the decision for palliative care. Eur J Vasc Endovasc Surg 19:246–249 14. Carnevale FC, De Blas M, Merino S et al (2004) Percutaneous endovascular treatment of chronic iliac artery occlusion. Cardiovasc Interv Radiol 27(5):447–452 15. Cheng SW, Ting AC, Wong J (2001) Endovascular stenting of superficial femoral artery stenosis and occlusions: results and risk factor analysis. Cardiovasc Surg 9:133–140 16. Cull DL, Feinberg RL, Wheeler JR et al (1991) Experience with laser-assisted balloon angioplasty and a rotary angioplasty instrument: lessons learned. J Vasc Surg 14:332–339 17. Curie IC, Wilson YB, Baird RN et al (1995) Treatment of intermittent claudication: the impact on quality of life. Eur J Vasc Endovasc Surg 10:356–361 18. Desgranges P, Boufi M, Lapeyre M et al (2004) Subintimal angioplasty: feasible and durable. Eur J Vasc Endovasc Surg 28(2):138–141
433
434
7.1 Lower Limb Arterial Recanalization
19. Dorros, G, Aff MR, Dorros AM et al (2001) Tibioperoneal (outflow lesion) angioplasty can be used as primary treatment in 235 patients with critical limb ischaemia: five year follow-up. Circulation 104:2057–2062 20. Duda SH, Bosiers M, Pusich B et al (2002) Endovascular treatment of peripheral artery disease with expanded PTFEcovered nitinol stents: interim analysis from a prospective controlled study. Cardiovasc Interv Radiol 25:413–418 21. Duddy M, Mahmood A, Simms M (2003) Angioplasty is the first-line treatment for critical limb ischaemia. Against the motion. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 273–288 22. Durand E et al (2002) Time course of apoptosis and cell proliferation and their relationship to arterial remodelling and restenosis after angioplasty in an atherosclerotic rabbit model. J Am Coll Cardiol 39:1680–1685 23. Engelke C, Morgan RA, Belli AM (2002) Cutting balloon percutaneous transluminal angioplasty of lower limb arterial bypass grafts: feasibility. Radiology 223(1):106–114 24. Florenes T, Bay D, Sandbaek T, Jorgensen JJ, Slagsvold CE, Kroese AJ(2004) Subintimal angioplasty in the treatment of patients with intermittent claudication: long term results. Eur J Vasc Endovasc Surg 28:645–650 25. Franklin IJ, Rodway A (2003) Angioplasty is the first-line treatment for critical limb ischaemia. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 289–294 26. Galland RB, Whiteley MS, Gibson M et al (2000) Remote superficial femoral artery endarterectomy: medium-term results. Eur J Vasc Endovasc Surg 19:278–282 27. Garasic JM, Creager MA (2001) Percutaneous interventions for lower extremity peripheral atherosclerotic disease. Rev Cardiovasc Med 2(3):120–125 28. Gordon IL, Conroy RM, Arefi M et al (2001) Three-year outcome of endovascular treatment of superficial femoral artery occlusion. Arch Surg 136:221–228 29. Gray BH, Laird JR, Ansel GM, Shuck JW (2002) Complex endovascular treatment for critical limb ischemia in poor surgical candidates: a pilot study. J Endovasc Ther 9(5):599–604 30. Hagenaars T, Gussenhoven EJ, Athanassopoulos P et al (2001) Intravascular ultrasound evidence for stabilisation of compensatory enlargement of the femoropopliteal segment following endograft placement. J Endovasc Ther 8:308–314 31. Harthun NL, Cage DL, Spinosa DJ (2004) Subintimal recanalisation is safe and effective in treating critical limb ischemia in selected patients. Am Surg 70(6):479–482 32. Hausegger KA, Georgieva B, Portugaller H et al (2004) Cardiovasc Interv Radiol 27(1):26–30
33. Hayes PD, Bolia A (2004) Subintimal angioplasty in the superficial femoral artery. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, London, pp 258–268 34. Ho GH, Moll FL, Joosten PP et al (1995) The Mollring Cutter remote endarterectomy: preliminary experience with a new endovascular technique for treatment of occlusive superficial femoral artery disease. J Endovasc Surg 2:278–287 35. Ingle H, Nasin A, Bolia A et al (2002) Subintimal angioplasty of isolated infragenicular vessels in lower limb ischaemia. Long term results. J Vasc Surg 35:411–417 36. Jahnke T, Voshage G, Muller-Hulsbech S et al (2002) Endovascular placement of self-expanding nitinol stents for the treatment of femoropopliteal obstructive disease. J Vasc Interv Radiol 13:257–266 37. Jämsen T, Manninen H, Tulla H et al (2002) The final outcome of primary infrainguinal percutaneous transluminal angioplasty in 100 consecutive patients with chronic critical limb ischemia. J Vasc Interv Radiol 13(5):455–463 38. Jiang H, Feng B, Li CY et al (2003) Application of ultrasonic angioplasty in treating totally occluded peripheral arteries, a clinical study of 39 cases. Zhonghua Yi Xue Za Zhi 83(10):837–840 39. Katzen BT (2003) Drug-eluting stents will revolutionize stent outcome. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 335–342 40. Kim D, Gianturco LE, Porter DA et al (1992) Peripheral directional atherectomy; 4-year experience. Radiology 183:773–778 41. Klein WM, Buskens E, Mali WP et al (2003) Quality of life in patients with peripheral arterial disease after endovascular treatment: a randomized trial. In: Klein WM (ed) Peripheral arterial disease: diagnosis, treatment and prognosis. PhD Thesis, Department of Radiology, University Medical Centre, Utrecht, The Netherlands 42. Klein WM, Buskens E, Moll F (2004) Quality of life is more important than flow-dynamic results of iliac intervention. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, London, pp 275–281 43. Kroger K, Buss C, Goyen M et al (2002) Diameter of occluded superficial femoral arteries limits percutaneous recanalization: preliminary results. J Endovasc Ther 9(3):369–374 44. Laird JR (2002) Peripheral Excimer Laser Angioplasty (PELA) trial results. Presented at Late Breaking Clinical Trials. Transcatheter Cardiovascular Therapeutics (TCT) Annual Meeting, 24–28 September, Washington DC. Medscape 2002 45. Laird JR Jr., Reiser C, Biamino G, Zeller T (2004) Excimer laser angioplasty for the treatment of critical limb ischemia. J Cardiovasc Surg (Torino) 45(3):239–248
References
46. Laurila J, Brommels M, Standertskjold-Nerdenstam CG et al (2000) Cost-effectiveness of percutaneous transluminal angioplasty (PTA) versus vascular surgery in limb-threatening ischaemia. Int J Angiol 9:214–219 47. Laxdal E, Jenssen GL, Pedersen G, Aune S (2003) Subintimal angioplasty as a treatment of femoropopliteal artery occlusions. Eur J Vasc Endovasc Surg 25:578–582 48. Lofberg AM, Lorelius LE, Karacagil S et al (1996) The use of below-knee percutaneous transluminal angioplasty in arterial occlusive disease causing chronic critical limb ischaemia. Cardiovasc Interv Radiol 19:317–322 49. Lofberg AM, Karacagil S, Ljungman C et al (2001) Percutaneous intraluminal angioplasty of the femoropopliteal arteries in limbs with chronic critical limb ischemia. J Vasc Surg 34:114–121 50. London NJM, Srinivasan T, Sayers RD, Naylor AR, Hartshorne T, Ratcliff DA, Bell PRF, Bolia A (1994) Subintimal angioplasty of the femoropopliteal artery occlusions: the long-term results. Eur J Vasc Endovasc Surg 8:148–155 51. Lugmayr HF, Holzer H, Kastner M et al (2002) Treatment of complex arteriosclerotic lesions with nitinol stents in the superficial femoral and popliteal arteries: midterm followup. Radiology 222:37–43 52. Management of peripheral arterial disease (2000) TransAtlantic Inter-Society Consensus (TASC) Working Group. J Vasc Surg 31:S97–S113 53. McCarthy RJ, Neary W, Roobottom C, Tottle A, Ashley S (2000) Short-term results of femoropopliteal subintimal angioplasty. Br J Surg 87:1361–1365 54. Michalis LK, Tsetis DK, Katsamouris AN et al (2001) Vibrational angioplasty in treatment of chronic femoropopliteal arterial occlusions: preliminary experience. J Endovasc Ther 8(6):615–621 55. Molloy KJ, Nasim A, London NJ et al (2003) Percutaneous transluminal angioplasty in the treatment of critical limb ischaemia. J Endovasc Ther 10(2):298–303 56. Mongiardo A, Curcio A, Spaccarotella C et al (2004) Molecular mechanisms of restenosis after percutaneous peripheral angioplasty and approach to endovascular therapy. Curr Drug Targets Cardiovasc Haematol Disord 4(3):275–287 57. Morgan R (2004) Cutting balloon angioplasty. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, London, pp 290–297 58. Muradin GS, Bosch JL, Stijnen T, Hunink MG (2001) Balloon dilatation and stent implantation for treatment of femoropopliteal arterial disease: meta-analysis. Radiology 221:137–145
59. Park SJ, Shim WH, Ho DS et al (2001) The clinical effectiveness of paclitaxel-coated coronary stents for reduction of restenosis in the ASPECT trial [abstract]. Circulation 104 (Suppl II):II464 60. Paula K, Murphy M, Bradley MD, Baird RN (2003) There is no evidence for effectiveness of tibioperoneal angioplasty. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 309–314 61. Peregrin JH, Kožnar B (2004) Re-stenosis after infrapopliteal percutaneous transluminal angioplasty is not the point. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, London, pp 282–289 62. Reekers JA (2003) Arterial stents are not required for femoropopliteal angioplasty. Against the motion. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 330–333 63. Reekers JA, Kromhout JG, Jacobs MJHM (1994) Percutaneous intentional extraluminal recanalisation of the fermoropopliteal artery. Eur J Vasc Endovasc Surg 9:723–728 64. Ricco JB, Camiade C, Mangiacotti N (2002)Angioplastie transluminale associee a une revascularisation chirurgicale dans l’ischemie des membres inferieurs. In: Branchereau A, Jacobs M (eds) Ischemie critique des membres inferieurs. Futura, Armonk, pp 33–51 65. Rosset E, Poirier M, Aublet-Cuvellier B et al (2004) Combined aorto-iliac angioplasty and infra-inguinal revascularisation. In: Branchereau A, Jacobs M (eds) Hybrid vascular procedures. Futura, Massachusetts, pp 181–196 66. Rutherford RB, Baker JD, Ernst C, Johnston KW, Porter JM, Ahn S et al (1997) Recommended standards for reports dealing with lower extremity ischaemia: revised version. J Vasc Surg 26:517–538 67. Saha S, Gibson M, Magee TR et al (2001) Early results of retrograde transpopliteal angioplasty of iliofemoral lesions. Cardiovasc Interv Radiol 24(6):378–382 68. Saket RR, Razavi MK, Paddidar A et al (2004) Novel intravascular ultrasound-guided method to create transintimal arterial communications: initial experience in peripheral occlusive disease and aortic dissection. J Endovasc Ther 11(3):274–280 69. Salas C, Bolia A (2003) Angioplasty is the first-line treatment in critical limb ischaemia. For the motion. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 263–272 70. Scheinert D, Laird JR Jr, Schroder M et al (2001) Excimer laser-assisted recanalization of long, chronic superficial femoral artery occlusions. J Endovasc Ther 8(2):156–166
435
436
7.1 Lower Limb Arterial Recanalization
71. Smeets L, Ho G, Moll F (2004) Radiological guided endarterectomy with stenting for femoropopliteal reconstruction. In: Branchereau A, Jacobs M (eds) Hybrid vascular procedures. Futura, Massachusetts, pp 197–208 72. Šoša T (2001) Arterial surgery facing the 3rd millennium. Acta Med Croatica 55:103–106 73. Spinosa DJ, Leung DA, Matsumoto AH et al (2004) Percutaneous intentional extraluminal recanalization in patients with chronic critical limb ischemia. Radiology 232(2):499–507 74. Steinkamp HJ, Wisgott C, Rademaker J et al (2002) Short (1–10 cm) superficial femoral artery occlusions: results of treatment with excimer laser angioplasty. Cardivasc Intervent Radiol 25(5):388–396 75. Tartari S, Zattoni L, Rolma G, Sacco A (2004) Subintimal angioplasty of infrapopliteal artery occlusions in treatment of critical limb ischaemia. Short-term results. Radiol Med (Torino) 108(3):265–274 76. Thalhammer A, Balzer J, Jacobi V, Vogl T (2003) Stents in the iliac arteries: a minimally invasive method. Hämostaseologie 23(2):67–70 77. Tielbeek AV, Vroegindeweij D, Buth J, Landmann GH (1996) Comparison of balloon angioplasty and Simpson atherectomy for lesions in the femoropopliteal artery: angiographic and clinical results of a prospective randomized trial. J Vasc Interv Radiol 7:837–844 78. Uher P, Nyman U, Lindh M et al (2002) Long-term results of stenting for chronic iliac artery occlusion. J Endovasc Ther 9(1):67–75 79. Varty K, Nydahl S, Nasim A et al (1998) Results of surgery and angioplasty for the treatment of chronic severe lower limb ischaemia. Eur J Vasc Endovasc Surg 11:159–163
80. Vorwerk D (2003) Arterial stents are not required for femoropopliteal angioplasty. In: Greenhalgh RM (ed) Vascular and endovascular controversies. BIBA, London, pp 323–329 81. Vorwerk D (2004) New atherectomy techniques. In: Greenhalgh RM (ed) Vascular and endovascular challenges. BIBA, London, pp 269–274 82. Vraux H, Hammer F, Verhelst R et al (2000) Subintimal angioplasty of tibial vessel occlusions in the treatment of critical limb ischaemia: mid-term results. Eur J Vasc Endovasc Surg 20:441–446 83. Vroegindeweij D, Tielbeek AV, Buth J et al (1995) Directional atherectomy versus balloon angioplasty in segmental femoropopliteal artery disease: two-year follow-up with color-flow duplex scanning. J Vasc Surg 21:255–269 84. Wagner HJ, Alfke H (2004) Interventional therapy of peripheral arterial disease-potential limitations. Herz 29(1):57–67 85. Wissgott C, Sheinert D, Rademaker J et al (2004) Treatment of long superficial femoral artery occlusions with excimer laser angioplasty: long-term results after 48 months. Acta Radiol 45(1):23–29 86. Wolfe JH, Wyatt MG (1997)Critical and subcritical ischaemia. Eur J Vasc Endovasc Surg 13:578–582 87. Wolfle KD, Bruijnen H, Reeps C et al (2000) Tibioperoneal arterial lesions and critical foot ischaemia: successful management by use of short vein grafts and percutaneous transluminal angioplasty. Vasa 29:207–214 88. Yilmaz S, Sindel T, Luleci E (2002) Bilateral transpopliteal approach for treatment of complex SFA and iliac occlusions. Eur Radiol 12(4):911–914 89. Zdanowski Z, Troeng T, Norgren L (1998) Outcome and influence of age after infrainguinal revascularisation in critical limb ischaemia. The Swedish Vascular Registry. Eur J Vasc Endovasc Surg 16:137–141
437
7.2 Femorodistal By-pass Surgery Sotiris e. Georgopoulos, elias a. Bastounis
7.2.1 Introduction Disorders of the vascular system are the leading causes of death and disability in the western world. One of the most debilitating forms of vascular disease is peripheral arterial occlusive disease when it is manifested as critical limb ischaemia. Patients with limbs threatened by distal tibioperoneal occlusive disease present an ongoing challenge to the vascular surgeon. Since the first experimental venous by-pass graft by the Nobelist Alexis Carrel in 1906 [18] and the first femoropopliteal by-pass in a patient by Jean Kunlin in 1948 [48], infra-inguinal by-pass has become increasingly applied with markedly improved efficacy and safety. Despite the pioneering reports by Auer and Hershey [7] in the 1970s, distal by-passes were infrequently performed until two decades ago, when accumulated experience, the upgrading to fine surgical instrumentation and advances in arterial imaging made infrapopliteal by-passes widely acceptable. In recent years more aggressive attitudes in limb-salvage procedures have been adopted, related mostly to interventions on arteries distal to the popliteal artery. In any consideration of distal by-passes, one cannot escape the fact that these operations are required in patients with severe generalized atherosclerosis and, specifically, in patients whose disease involves not only the tibial and peroneal arteries but often the aorta as well as the iliac arteries and femoropopliteal system.
7.2.2 General Considerations Considerable attention has been given to improving the long-term results of peripheral grafting, mainly emphasizing proper patient selection and refinement of surgi-
cal technique. Several factors, such as patient characteristics, smoking, graft placement, surgical experience and adjunctive medications, have been investigated as to whether they affect the results of femorodistal by-passes [17, 24, 43, 52, 67, 74, 75]. Although certain diseases, such as renal failure and diabetes, have implications for peri-operative morbidity and long-term survival, none has any predictive value for graft patency [39, 45, 61, 94]. The only reliable predictors of graft patency are derived from the anatomical and haemodynamic aspects of the reconstruction itself, such as the quality and origin of the conduit and its outflow bed. There are, however, some critical issues that are decisive for the successful outcome of femorodistal reconstructions. The first is the arteriographic technique, with which all patent, named arteries in the leg and foot should be visualized. Only with accurate imaging of the extent of occlusive and stenotic disease can revascularization of distal arteries be planned appropriately. Of even greater importance is the fact that the limb-salvage surgeon should have appropriate training, experience and a meticulous and fine technique. Surgical manipulations (occlusion, arteriotomy and suturing) must be performed with diligence, since many patients have extensive atheromatous involvement or heavy calcification in the patent segment of the artery available for anastomosis. Moreover, the skilled surgeon should be familiar with all surgical options that are available. Finally, it has to be made clear that disadvantaged outflow arteries such as those connecting incomplete plantar arches, those consisting of isolated or blind segments, and those with considerable disease or heavy calcification can sometimes serve as effective sites for by-pass implantation. This high operability is further increased by the use of appropriate measures preoperatively, intraoperatively and postoperatively to accomplish with reasonable safety the sometimes long operation designed to save a limb. From this point of view, careful preoperative cardiac evaluation with a resting ECG and
438
7.2 Femorodistal By-pass Surgery
a transthoracic echocardiography is crucial since cardiac disease is the main source of morbidity and mortality in these operations. Last but not least, vein mapping, using ultrasound imaging, is considered to be an essential step in the completion of the preoperative evaluation of patients. Identification of usable autologous grafts facilitates operative plans and prevents unnecessary exploration, which has the potential to cause wound complications [77].
7.2.3 Operative Indications As by-passes to either the tibial arteries or the peroneal artery are generally complex, difficult operations with a significant incidence of early and late failure and considerable of operative morbidity and mortality, these operations should never be performed for intermittent claudication. All by-passes to arteries distal to the popliteal artery should be performed to save a critically ischaemic limb. Occasionally, however, patients with advanced ischaemia and limited ischaemic rest pain, small patches of gangrene, or ischaemic ulceration may improve through conservative management [9, 85]. In cases in which the lesions are limited and the outcome is uncertain, a trial period of hospitalization with conservative treatment may be warranted before undertaking a difficult distal by-pass. These cases are rare. Generally, these manifestations, if severe or extensive, will cause limb loss if the circulation is not restored by arterial reconstruction. Extensive gangrene in the foot, particularly gangrene of the heel, has long been regarded as a contraindication to performing a limb-salvage arterial by-pass. Increasingly, over the years, it has been shown that functional remnants of foot can be obtained even when extensive necrosis and gangrene involve the bones and soft tissues of the forefoot or heel. A healed foot remnant, which can sometimes only be obtained with a split-thickness skin graft, will allow some of these aged, debilitated patients to ambulate far better than a below-knee amputation. On the other hand limb-threatening ischaemia typically occurs in elderly patients with multiple, severe, coexisting medical conditions. There is appropriate concern regarding the advisability of revascularization surgery, especially because patients undergoing these major procedures often require multiple transfusions, prolonged hospitalization, intensive care and, frequently, subsequent procedures to achieve foot healing. Unfortunately, a decision not to perform revascularization in the setting of limb-threatening
ischaemia makes amputation virtually inevitable. Amputation is in itself a surgical procedure whose risks and length of hospitalization are at least equivalent to those of revascularization and with a far less desirable outcome from the patient’s point of view. Although there has never been a randomized study comparing revascularization with amputation for limb-threatening ischaemia, it has been demonstrated that operative mortality, hospital stay and long-term survival were all superior in the revascularization group [27, 62, 72]. Based on these studies, most vascular surgeons recognize few contraindications to revascularization for limb-threatening ischaemia. Only chronically institutionalized, neurologically impaired, permanently nonambulatory patients with severe organic mental syndrome or gangrene and infection of the midportion of the foot are absolute contraindications to attempts at limb salvage. In these cases there is no advantage to revascularization over amputation.
7.2.4 Technical Considerations 7.2.4.1 Proximal Anastomotic Site Traditionally, the common femoral artery has been the in-flow site of choice for infrapopliteal by-pass. The location of in-flow site has no impact on femorodistal by-pass patency provided that the chosen segment is relatively healthy and there is no proximal haemodynamically significant stenosis [84, 92]. Yet, patients requiring distal by-passes frequently present stenotic or occlusive lesions involving the distal aorta or the iliac arteries or both. In this setting percutaneous transluminal angioplasty offers an attractive solution since it should be performed in combination with the distal revascularization procedure [33]. It should be noted that frequently proximal repair will be enough to obviate the need for a more difficult distal procedure, which must be required if the iliac gradient were not large and would probably be required if the patient had ischaemic tissue loss in the foot. Since the early 1980s, the superficial femoral, deep femoral, popliteal and tibial arteries have all been used as in-flow sources when these vessels were relatively disease-free or when the amount of autologous vein available was limited [6, 57, 76, 95]. The strategy of utilizing more distal in-flow sources is particularly applicable to inframalleolar by-passes, in which very long vein segments would be required to reach the dorsalis pedis or other pedal arteries from the usual more proximal in-flow sites.
7.2.4 Technical Considerations
Since short by-passes have equal patency rate to long distal by-passes [55] and the progression of atherosclerotic disease in proximal arterial segments is slow enough to compromise blood flow in the graft in the majority of patients [88], they are a valuable alternative to conventional by-passes.
7.2.4.2 Graft Material There are many options in distal arterial grafting depending on the graft type and graft configuration. When available, the autogenous greater saphenous vein is the best arterial substitute for femorodistal revascularization. However, the vein may be too small in calibre, thrombosed, markedly varicose, or may have been removed surgically in the past. Also, its usable length may be too short for the scheduled operation. In this case, other autologous conduits such as the short saphenous, the cephalic and the basilic veins may be used, individually or in combination with a limited length of long saphenous vein. It is common for the vein to be assessed visually at the time of operation, but it is possible to assess the usefulness of the long saphenous vein before surgery by colour Duplex ultrasound scanning. Since veins contain valves, the grafts must be reversed or the valves must be rendered incompetent if nonreversed by valvulotome or left in situ.
Reversed Vein Graft (Fig. 7.2.1) The use of the greater saphenous vein (GSV) in a reversed configuration is the most preferred method in infrapopliteal by-passes. The vein is dissected from the saphenofemoral junction and exposed through separate, short incisions along its course leaving skin bridges between each incision. Recently, endoscopic saphenous vein harvest has allowed vein preparation through minimal incisions [41, 42, 44]. Sufficient vein length is exposed to reach the distal outflow vessel. The dissection must be made very carefully to avoid avulsion of the vein. Once the proximal and distal vessels are exposed, the GSV is gently removed from its bed by ligating its side branches and gently dilating the vein with a normal saline solution containing heparin. It is generally agreed that for use as a reversed by-pass graft, the vein must have a minimum diameter of 4 mm. The vein is checked for leaks and then if it is satisfactory, it is reversed to deactivate the valves, and anastomosed in an end-to-side fashion to the arteries.
Fig. 7.2.1 Reversed saphenous vein femoroperoneal by-pass
Two large prospective multicentre randomized trials have demonstrated the superiority of venous grafts over prosthetics in infrapopliteal vessels (level I evidence). Veith et al. [86] studied 360 infrapopliteal by-passes and found the 5-year primary patency rate for autogenous veins to be 49% compared with a 12% patency rate for PTFE. Similarly, investigators in 18 Veterans Affairs Medical Centers demonstrated a 73% patency rate for vein grafts versus 30% for a prosthetic one at 2 years [87]. Based on these differences, the use of vein grafts as the first-choice conduit for femorodistal reconstructions was well established.
439
440
7.2 Femorodistal By-pass Surgery
In Situ Vein Graft The in situ GSV by-pass technique differs in that the saphenous vein is left in its own bed rather than being removed and its orientation reversed. Although in situ GSV by-pass was originally introduced in the 1960s, this operation has enjoyed renewed popularity since the late 1980s, possibly because better instruments for disrupting venous valves have become available [23, 38, 50]. When using the vein in situ it is best to make the proximal anastomosis first and to declamp and allow the vein to fill with blood down to the first valve. A valve cutter (valvulotome) is then introduced from the distal end of the vein up to the femoral anastomosis. Withdrawing the valvulotome disrupts the valves and allows the blood to fill the graft as each set of valves is broken. Eventually the cutter is withdrawn followed by a spurt of pulsatile blood. The graft is then clamped and the lower anastomosis completed. The vein tributaries must all be recognized and tied off to prevent the development of significant arteriovenous fistulae which compromise the graft blood flow distally, cause generalized oedema and contribute to graft failure. The tributaries may be recognized by a variety of techniques, from exposing the whole length of the vein for visual inspection to methods using Doppler ultrasonography, angiography, or angioscopy. The advantage of the in situ technique, including maintenance of the venous blood supply, is the accomplishment of size matching between the graft and the arteries at the proximal and distal anastomosis. It is therefore possible to achieve good results with a vein diameter of 3 mm or even less. Such grafts may be successful not only when anastomosed to the popliteal and proximal crural vessels, but also when the distal anastomosis is fashioned at ankle level. Although excellent results have been achieved with in situ technique [78], their properties have never been proven to offer a clear advantage in terms of venous graft patency. Several prospective randomized studies have compared saphenous vein infrapopliteal grafts performed by the reversal or in situ technique, showing no differences (level II evidence) [58, 89, 91].
small-sized veins with good results. The technique was described early in the 1970s but was popularized after the 1980s [13, 22, 83]. There is only level III and level IV evidence that this technique offers results that equal those of alternatives [11, 15, 68, 80, 83], although some reports have shown a slightly inferior patency rate in comparison with in situ and reversed vein grafts [70].
Alternative Graft Option If there is a lack of available or suitable GSV, which ranges considerably in the literature from 15% to 45% [20, 81], a search should be made for another vein source, such as the contralateral saphenous, the short saphenous, the superficial arm veins and the superficial femoral vein. These grafts could be used as single grafts or after the construction of a vein-to-vein composite graft [20, 32, 36, 37]. When the length of the vein graft is inadequate, composite PTFE–vein grafts may be a valuable alternative [12] (Fig. 7.2.2). Using these grafts, the site of compliance mismatch between the arterial and the prosthetic interface is moved to the prosthetic graft – vein segment anastomosis – where the luminal cross-sectional area is larger to alleviate potential restenosis [28]. When an autologous grafting cannot be accomplished, human umbilical vein (HUV) [93], cryopreserved allografts [3, 90] or PTFE grafts with adjunctive procedures (cuff , patch or AV fistula) [31] may be used. Recently, a randomized trial has shown similar results between totally prosthetic, precuffed PTFE grafts and vein cuff/PTFE grafts [65]. Alternative grafts are generally superior to prosthetics, although there is a substantial variation among series (level III and IV evidence) [3, 12, 28, 31, 32, 37, 90, 93]. In any case, the use of a synthetic graft in femorodistal
Νonreversed Vein Graft The nonreversed vein graft theoretically combines the advantages of in situ and reversed autologous reconstruction, minimizing size mismatch at proximal and distal anastomoses, and increasing the possibility of using
Fig. 7.2.2 Composite vein–PTFE femoroposteriortibial by-pass
7.2.4 Technical Considerations
reconstructions is justified only after a meticulous search for a venous graft and if it is supplemented with a venous cuff, patch or AV fistula [53].
Choice of the Best Conduit There is general agreement that the graft of choice for femorodistal reconstructions is the ipsilateral GSV (either reversed or in situ). If this is not available, many options have been offered and in the case of a lack of powerful evidence favouring one of them, quite different strategies have been developed in various centres. In the authors’ experience, the need to consider an alternative conduit occurs in approximately 20% of primary operations and in 50% of reoperations. However, an all-autologous reconstruction should be advocated: we, and others as well [21], suggest contralateral GSV as the first-choice alternative, and when this is absent, arm veins or a composite PTFE–vein graft should be considered. If there is no venous segment available, a 6-mm PTFE reconstruction with a Miller cuff is performed. With this policy in mind, the vast majority of our cases are treated using single-segment or spliced venous grafts and the remainder (nearly 15%) with composite grafts. Only a few cases are amenable to cuffed PTFE reconstruction.
7.2.4.3 Distal Anastomotic Site (Fig. 7.2.3) The distal anastomotic site has no impact on the results of femorodistal reconstructions. As a rule, a tibial artery is used if its lumen runs into the foot without obstruction, though by-passes to disadvantaged outflow segments may be performed successfully. Generally, the peroneal artery is used only if it communicates with foot arteries. Although the ability of peroneal revascularization to perfuse the foot sufficiently has been criticized, many studies have demonstrated equivalent patencies of peroneal and other tibial or pedal by-pass grafts [16, 30, 63, 71, 79, 84]. The major determinant of by-pass patency is the status of the run-off bed. The integrity of the plantar arch is a reliable prognostic indicator of the primary patency rate of the grafts [64]. However, neither the absence of a plantar arch nor vascular calcification is considered a contraindication to a reconstruction. By-pass to the distal ankle and foot arteries (Fig. 7.2.4), the so-called para- or inframalleolar by-pass, has gained acceptance in recent years [5, 8]. Although many surgeons still hesitate to perform such by-passes, these are often
Fig. 7.2.3 Postoperative arteriography of a femoroperoneal bypass
the only alternative to limb amputation, with equivalent results to more proximal reconstructions [69].
Exposures The tibioperoneal trunk, the origin of the anterior tibial and proximal two-thirds of the posterior tibial and pe-
441
442
7.2 Femorodistal By-pass Surgery
Fig. 7.2.4 Postoperative arteriography of a paramalleolar bypass
roneal arteries is usually approached through a medial incision below the knee. The distal anterior tibial artery can be approached anterolaterally. The distal third of the peroneal artery is best accessed by removing a segment of overlying fibula. In cases of medial scarring, infection or both, all three leg arteries can be reached through a lateral approach with fibula resection [49]: the proximal anterior tibial artery can be reached posteromedially with division of the interosseous membrane; the distal branches of the posterior tibial artery (i.e. the medial and lateral plantar arteries) can be reached in the sole of the foot; and the terminal branches of the dorsalis pedis artery (lateral tarsal artery and deep plantar arch) can be reached through a dorsal incision.
7.2.5 Special Considerations There are three groups of patients who are traditionally confronted with scepticism by surgeons: diabetics, patients with end-stage renal disease (ESRD) and patients with heavily calcified distal vessels. Many studies have reported higher operative mortality and lower long-term survival in diabetics than in nondiabetic patients [63, 84] although diabetes mellitus does not affect graft function [2, 46, 96]. ESRD is associated with an increased rate of amputations due to healing problems and decreased survival expectancy. Most series show that by-pass grafting in these patients is associated with wellaccepted patency rates, though patient survival rates and limb-salvage rates are lower as anticipated [47, 51]. The combination of the two entities is the most fearful setting for the vascular surgeon; however, the limb-salvage rate in patients with ESRD and diabetes mellitus justifies an aggressive policy of revascularization, despite decreased survival of this population [35]. Severe calcification of the outflow artery during lower-extremity distal revascularization is considered a poor prognostic factor for bypass graft patency. These vessels present two difficulties: occlusion of the vessel and passing sutures. In order to avoid these obstacles, we use soft intraluminal occluders and perform the anastomosis carefully and gently. With a meticulous technique one can achieve much the same results to those obtained in uncalcified outflow arteries [10, 56].
7.2.7 Results
7.2.6 Graft Surveillance Several studies have shown that careful long-term follow-up of autogenous vein grafts using objective vascular laboratory techniques, especially Duplex scanning, can reliably detect stenotic lesions, permitting correction before the occurrence of recurrent symptoms and graft thrombosis [25, 54]. The ability of graft surveillance programmes to improve the overall results of both reversed and in situ autogenous grafting has been well established. In a prospective randomized study, Lundell et al. [54] demonstrated that the primary assisted patency of grafts in the surveillance category was 25% higher at 3 years compared with grafts followed clinically. However, this approach has not yet been shown to improve the results of prosthetic grafting.
7.2.7 Results Limb salvage, primary and secondary graft patency and limb-salvage rates are the most useful tools for objectively assessing the efficacy of femorodistal reconstructions. To depict the whole picture of operational benefit however, the amputation-free survival period and quality of life have to be known since the functional outcome has much greater importance than the technical success. On
interpreting the results of femorocrural procedures, one should bear in mind that there is a wide range of these indices among studies due to the inhomogeneity of material.
7.2.7.1 Survival Peri-operative mortality after femorodistal by-pass surgery ranges from 0% to 18%, but in recent large series it is below 3% (Table 7.2.1) [4, 14, 19, 21, 24, 34, 35, 60, 69]. These figures mainly reflect the diversity in distribution of risk factors (i.e. diabetes, ESRD, reoperations, heart disease, older age ) in the studied population. For the same reasons, survival varies greatly among series (Table 7.2.1), although a survival expectancy of approximately 60% at 5 years might be a reasonable estimation. In general, a reduced survival rate after revascularization procedures in patients with older age, diabetes, ESRD and ischaemic heart disease would be anticipated [4, 35].
7.2.7.2 Graft Patency and Limb Salvage Primary patency, secondary patency and the limb-salvage rate of saphenous vein femorodistal reconstructions are superior to those of any other treatment modality. An expected 5-year primary patency, secondary patency
Table 7.2.1 Peri-operative mortality of femorodistal by-pass surgery in selected series Author
Year of publication
Population
Schmiedt [76] Mainz, Germany
2002
Pomposelli [69] Harvard, USA
2003
1032
0.9
48.6 (5 years) 28.3 (10 years)
Oderich [60] Mayo Clinic, USA
2005
77
1.3
81 (1 year) 57 (3 years)
124 diabetics
Mortality (%) 1.4
Survival (%) –
Chew [21] Boston, USA
2002
203
1
–
Belkin [14] Boston USA
1995
300 reoperations
0.3
–
Feinglass [34] Chicago, USA
2001
4288
2.1
Ballotta [10] Padova, Italy
2004
441
0
Cavillon [19] Paris, France
1998
162
7.8
Wolfle [96] Düsseldorf, Germany
2003
211
–
63 (5 years)
66 (5 years) 95 (1 year)/nondiabetics 78 (1 year)/diabetics
443
444
7.2 Femorodistal By-pass Surgery
and limb-salvage rate near 60–70%, 70–80% and 75–85% seems to be realistic (Table 7.2.2). The interpretation of results when an alternative conduit must be used is more complex. The lack of level I or II data prevent valid conclusions regarding which is the best option. Table 7.2.3 shows the results of a modern series but the choice is mainly a matter of preference and familiarity.
A very useful index for complete evaluation of the long-term outcome of distal revascularization procedures at the population level is major amputation-free survival rate. Feinglass et al. [34], in a prospective study with 4288 patients who underwent various femorotibial procedures, demonstrated amputation-free survival probability rates at 1, 3, and 7.5 years of 74%, 56%, and 29%, respectively.
Table 7.2.2 Five-year patency and limb-salvage rates in saphenous vein femorodistal reconstructions (selected series) Author
year
n
Shah [78]
1995
1023
76
Donaldson [29]
1991
191
63
71
Schmiedt [76]
2002
140
63.6
69.2
Pomposelli [69]
2003
56.8
–
Chew [21]
2002
226
61
Belkin [14]
1995
300 (redo)
Bastounis [12]
1999
213
1032 (pedal)
Primary patency (%)
Primary assisted patency (%) –
Secondary patency (%)
Limb-salvage rate (%)
81
95
78
85
70
82
62.7
78.2
–
73
81
51.5
–
68.5
77.8
70
–
75
80
Table 7.2.3 Five-year patency and limb-salvage rates in femorodistal reconstructions with other than greater saphenous vein (GSV) graft (selected series). (HUV Human umbilical vein) Author
Year
n (graft type)
Londrey [53]
1993
128 (arm/lesser saphenous vein)
Holzenbein [40]
1993
100 (arm/lesser saphe- 70.6 (1 year) nous vein)
–
76.9 (1 year)
Chang [20]
1995
356 (vein–vein composite)
68 (1 year) 38 (single) 35 (sequential)
–
82 (1 year) 58 52
77 (2 years)
–
Goyal [37]
2002
21 (lesser saphenous)
Primary patency –
Primary assisted patency –
Secondary patency (%) 52
95 (2 years)
Limb-salvage rate (%) 69 88.2 (1 year)
53 65 100 (2 years)
Pappas [66]
1998
185 (vein cuff + PTFE)
62 (2 years)
–
–
76 (2 years)
Oderich [60]
2005
40 precuffed PTFE 40 vein cuff +PTFE
57 (3 years) 54 (3 years)
–
–
70 (3 years) 81 (3 years)
Bastounis [12]
1999
–
–
Rebane [73]
1997
Dardik [26]
1995
–
–
45
Taylor [82]
1992
54
–
–
60 (composite PTFE+vein)
59.7
67 allografts
21.3
167 HUV 83 PTFE+vein patch
– 29.2
–
References
7.2.7.3 Quality of Life The quality of life of patients after femorodistal procedures remains an underestimated component of longterm results. Technical success does not guarantee patient welfare: only 68% of patients maintain their preoperative ability of independent life and only 14% are free of remaining symptoms or complications or do not require reoperation [1, 59]. Preoperative ambulation and patient mental status have a great impact on postoperative functional outcome: it is clear that under some circumstances leg preservation at all costs makes no sense. References 1. Abou Zamzan AM, Lee RW, Moneta GL et al (1997) Functional outcome after infrainguinal bypass for limb salvage. J Vasc Surg 25:287–297 2. Akbari CM, Pomposelli FB, Gibbons GW, Campell DR, Pulling MC, Mydlarz D, LoGerfo FW (2000) Lower extremity revascularization in diabetics: late observations. Arch Surg 135:452–456 3. Albers M, Romiti M, Pereira CA, Antonini M, Wulkan M (2004) Metaanalysis of allograft bypass grafting to infrapopliteal arteries. Eur J Vasc Endovasc Surg 28:462–472 4. Al-Omran M, Tu JV, Johnston KW, Mamdani MM, Kucey DS (2003) Outcome of revascularization procedures for peripheral arterial occlusive disease in Ontario between 1991 and 1998: a population-based study. J Vasc Surg 38:279–288 5. Andros G (1995) Bypass graft to the ankle and foot. Surg Clin North Am 75:715–729 6. Ascer E, Veith FJ, Gupta SK, White SA, Bakal CW, Wengerter K, Sprayregen S (1988) Short vein grafts: a superior option for arterial reconstructions to poor or compromised outflow tracts? J Vasc Surg 7:370–378 7. Auer AI, Hershey FB (1973) Bypass vein grafts to distal tibial or dorsalis pedis arteries. Mo Med 70:93–100 8. Aulivola B, FB Pomposelli (2004) Dorsalis pedis, tarsal and plantar arteries bypass. J Cardiovasc Surg 45:203–212 9. Bailey CM, Saha S, Magee TR, Galland RB (2003) A 1 year prospective study of management and outcome of patients presenting with critical lower limb ischaemia. Eur J Vasc Endovasc Surg 25:131–134 10. Ballotta E, Renon L, Toffano M, Piccoli A, Da Giau G (2004) Patency and limb salvage rates after distal revascularization to unclampable calcified outflow arteries. J Vasc Surg 39:539–546 11. Banz M, Stierli P, Aeberhard P (1995) Infrainguinal arterial reconstruction with non-reversed autologous vein after angioscopy guided valvulotomy ex situ. Eur J Vasc Endovasc Surg 10:211–214
12. Bastounis E, Georgopoulos S, Maltezos C, Alexiou D, Chiotopoulos D, Bramis J (1999) PTFE-vein composite grafts for critical limb ischaemia: a valuable alternative to all-autogenous infrageniculate reconstructions. Eur J Vasc Endovasc Surg 18:127–132 13. Beard JD, Wyatt M, Scott DJ, Baird RN, Horrocks M (1989) The non-reversed vein femoro-distal bypass graft: a modification of the standard in situ technique. Eur J Vasc Surg 3:55–60 14. Belkin M, Conte MS, Donaldson MC, Mannick JA, Whittemore AD (1995) Preferred strategies for secondary infrainguinal bypass: lessons learned from 300 consecutive reoperations. J Vasc Surg 21:282–293 15. Belkin M, Knox J, Donaldson MC, Mannick JA, Whittemore AD (1996) Infrainguinal arterial reconstruction with nonreversed greater saphenous vein. J Vasc Surg 24:957–962 16. Bergamini TM, George SM, Massey HT et al (1994) Pedal or peroneal bypass: which is better when both are patent? J Vasc Surg 20:347–356 17. Blankenstein JD, Gertler JP, Brewster DC et al (1995) Intraoperative determinants of infrainguinal bypass patency a prospective study. Eur J Vasc Endovasc Surg 9:375–382 18. Carrel A, Gutherie C (1906) Uniterminal and biterminal venous transplantations. Surg Gynecol Obstet 266–286 19. Cavillon A, Melliere D, Allaire E, Blancas AE, Berrahal D, Desgranges P, Becquemin JP (1998) Are femoro-infrapopliteal bypasses worthwhile for limb salvage? J Cardiovasc Surg (Torino) 39:267–272 20. Chang BB, Darling RC, Bock DEM, Shah DM, Leather RP (1995) The use of spliced vein bypasses for infrainguinal arterial reconstructions. J Vasc Surg 21:403–412 21. Chew DK, Owens CD, Belkin M, Donaldson MC, Whittemore AD, Mannick JA, Conte MS (2002) Bypass in the absence of ipsilateral greater saphenous vein: safety and superiority of the contralateral greater saphenous vein. J Vasc Surg 35:1085–1092 22. Connolly JE, Stemmer EA (1970) The nonreversed saphenous vein bypass for femoral-popliteal occlusive disease. Surgery 68:602–609 23. Connolly JE, Kwaan JH (1982) In situ saphenous vein bypass. Arch Surg 117:1551–1557 24. Dalsing MC, White JV, Yao JS, Podrazik R, Flinn WR, Bergan JJ (1985) Infrapopliteal bypass for established gangrene of the forefoot or toes. J Vasc Surg 2:669–677 25. Dalsing MC, Cikrit DF, Lalka SG, Sawchuk AP, Schulz C (1995) Femorodistal vein grafts: the utility of graft surveillance criteria. J Vasc Surg 21:127–134 26. Dardik H (1995) The second decade of experience with the umbilical vein graft for lower-limb revascularization. Cardiovasc Surg 3:265–269
445
446
7.2 Femorodistal By-pass Surgery
27. De Frang RD, Taylor LM Jr, Porter JM (1991) Basic data related to amputations. Ann Vasc Surg 5:202–207 28. DeMasi RJ, Snyder SO (1995) The current status of prosthetic-vein composite grafts for lower extremity revascularization. Surg Clin North Am 75:741–752 29. Donaldson MC, Mannick JA, Whittemore A (1991) Femorodistal bypass with in situ greater saphenous vein. Long term results using Mills valvulotome Ann Surg 213:457–465 30. Elliott BM, Robinson JG, Brothers TE, Cross MA (1993) Limitations of peroneal artery bypass grafting for limb salvage. J Vasc Surg 18:881–888 31. Eugster T, Stierli P, Fischer G, Gurke L (2001) Long-term results of infrainguinal reconstruction with spliced veins are equal to results with non-spliced veins. Eur J Vasc Endovasc Surg 22:152–156 32. Faries PL, Lo Gerfo FW, Arora S et al (2000) A comparative study of alternative conduits for lower extremity revascularisation: all autogenous conduit versus prosthetic grafts. J Vasc Surg 32:1080–1090 33. Faries PL, Brophy D, LoGerfo FW, Akbari CM, Campbell DR, Spence LD, Hook SC, Pomposelli FB Jr. (2001) Combined iliac angioplasty and infrainguinal revascularization surgery are effective in diabetic patients with multilevel arterial disease. Ann Vasc Surg 15:67–72 34. Feinglass J, Pearce WH, Martin GJ, Gibbs J, Cowper D, Sorensen M, Khuri S, Daley J, Henderson WG (2001) Postoperative and amputation-free survival outcomes after femorodistal bypass grafting surgery: findings from the Department of Veterans Affairs National Surgical Quality Improvement Program. J Vasc Surg 34:283–290 35. Georgopoulos S, Filis K, Vourliotakis G, Bakoyannis C, Papapetrou A, Klonaris C, Papalambros E, Bastounis E (2005) Lower extremity bypass procedures in diabetic patients with end-stage renal disease: is it worthwhile? Nephron Clin Pract 99:c37–c41 36. Gibbons CP, Osman HY, Shiralkar S (2003) The use of alternative sources of autologous vein for infrainguinal bypass. Eur J Vasc Endovasc Surg 25:93–94 37. Goyal A, Shah PM, Babu SC, Mateo RB (2002) Poplitealcrural bypass through the posterior approach with lesser saphenous vein for limb salvage. J Vasc Surg 36:708–712 38. Hall KV, Rostad H. David M (1978) Hume memorial lecture. In situ vein bypass in the treatment of femoropopliteal atherosclerotic disease: a ten year study. Am J Surg 136:158–161 39. Holtzman J, Caldwell M, Walvatne C, Kane R (1999) Longterm functional status and quality of life after lower extremity revascularization. J Vasc Surg 29:395–402
40. Holzenbein TJ, Pomposelli FB, Miller A et al (1996) Results of policy with arm veins used as the first alternative to an unavailable ipsilateral greater saphenous vein for infrainguinal bypass. J Vasc Surg 23:130–140 41. Illig KA, Rhodes JM, Sternbach Y, Shortell CK, Davies MG, Green RM (2001) Reduction in wound morbidity rates following endoscopic saphenous vein harvest. Ann Vasc Surg 15:104–109 42. Illig KA, Rhodes JM, Sternbach Y, Green RM (2003) Financial impact of endoscopic vein harvest for infrainguinal bypass. J Vasc Surg 37:323–330 43. Jamsen T, Tulla H, Manninen H, Raisanen H, Lahtinen S, Aittola V, Jaakkola P (2001) Results of infrainguinal bypass surgery: an analysis of 263 consecutive operations. Ann Chir Gynaecol 90:92–99 44. Jordan WD Jr., Alcocer F, Voellinger DC, Wirthlin DJ (2001) The durability of endoscopic saphenous vein grafts: a 5-year observational study. J Vasc Surg 34:434–439 45. Kalman PG, Johnston KW (1997) Predictors of long-term patient survival after in situ vein leg bypass. J Vasc Surg 25:899–904 46. Karacagil S, Almgren B, Bowald S, Bergvist D (1995) Comparative analysis of patency, limb salvage and survival in diabetic and non-diabetic patients undergoing infrainguinal bypass surgery. Diabet Med 12:537–541 47. Kimura H, Miyata T, Sato O, Furuya T, Iyori K, Shigematsu H (2003) Infrainguinal arterial reconstruction for limb salvage in patients with end-stage renal disease. Eur J Vasc Endovasc Surg 25:29–34 48. Kunlin J (1949) Le traitement de l’artèrite oblitèrante par la greffe veineuse. Arch Mal Coeur 42:371–372 49. Lazarides MK, Tzilalis VD, Georgiadis GS, Georgopoulos SE, Arvanitis DP (2003) Femoral-anterior tibial reconstructions using cuffed PTFE grafts: routing alternatives. Vasa 32:22–25 50. Leather RP, Shan DM, Karmody AM (1981) Infrapopliteal arterial bypass for limb salvage: increased patency and utilization of the saphenous vein used “in situ”. Surgery 90:1000–1008 51. Leers SA, Reifsnyder T, Delmonte R, Caron M (1998) Realistic expectations for pedal bypass grafts in patients with end-stage renal disease. J Vasc Surg 28:976–980 52. Ljungman C, Ulus AT, Almgren B, Bergstrom R, Hellberg A, Bergqvist D, Karacagil S (2000) A multivariate analysis of factors affecting patency of femoropopliteal and femorodistal bypass grafting. Vasa 29:215–220
References
53. Londrey GL, Bosher LP, Brown PW, Stoneburger FG Jr., Pancoast JW, Davies RK (1994) Infrainguinal reconstruction with arm vein, lesser saphenous vein, and remnants of greater saphenous vein: a report of 257 cases. J Vasc Surg 20:451–457 54. Lundell A, Lindblad B, Bergqvist D, Hansen F (1995) Femoropopliteal-crural graft patency is improved by an intensive surveillance program : a prospective randomized study. J Vasc Surg 21:26–34 55. Lyon RT, Veith FJ, Marshan BU et al (1994) Eleven year experience with tibiotibial bypass: an unusual but effective solution to distal tibial artery occlusive disease and limited autologous vein. J Vasc Surg 20:61–69 56. Misare BD, Pomposelli FB Jr., Gibbons GW, Campbell DR, Freeman DV, LoGerfo FW (1996) Infrapopliteal bypasses to severely calcified, unclampable outflow arteries: two-year results. J Vasc Surg 24:6–15 57. Monux Ducaju G, Serrano Hernando FJ, Sanchez Hervas L (2001) Popliteo-distal and tibio-tibial bypasses: a viable alternative for the revascularisation of the critically ischaemic limb. J Cardiovasc Surg (Torino) 42:651–656 58. Moody AP, Edwards PR, Harris PL (1992) In situ versus reversed femoropopliteal vein grafts: long-term follow-up of a prospective, randomized trial. Br J Surg 79:750–752 59. Nicoloff AD, Taylor LM, McLafferty RB et al (1998) Patient recovery after infrainguinal bypass grafting for limb salvage J Vasc Surg 27:256–266 60. Oderich GS, Panneton JM, Yagubyan M, Bower TC, Hofer J, Noel AA, Sullivan T, Kalra M, Cherry KJ Jr., Gloviczki P (2005) Comparison of precuffed and vein-cuffed expanded polytetrafluoroethylene grafts for infragenicular arterial reconstructions: a case-matched study. Ann Vasc Surg 19(1):49–55 61. Olojugba DH, McCarthy MJ, Reid A, Varty K, Naylor AR, Bell PR, London NJM (1999) Infrainguinal revascularisation in the era of vein-graft surveillance – do clinical factors influence long-term outcome? Eur J Vasc Endovasc Surg 17:121–128 62. Ouriel K, Fiore WM, Geary JE (1988) Limb-threatening ischemia in the medically compromised patient: amputation or revascularization? Surgery 104:667–672 63. Panayiotopoulos YP, Tyrrell MR, Owen SE et al (1997) Outcome and cost analysis after femorocrural and femoropedal grafting for critical limb ischemia. Br J Surg 84:207–212 64. Panayiotopoulos YP, Edmondson RA, Reidy RF et al (1998) A scoring system to predict the outcome of long femorodistal arterial bypass graft to single calf or pedal vessels. Eur J Vasc Endovasc Surg 15:380–386
65. Panneton JM, Hollier LH, Hofer JM (2004) Multicenter randomized prospective trial comparing a pre-cuffed polytetrafluoroethylene graft to a vein cuffed polytetrafluoroethylene graft for infragenicular arterial bypass. Ann Vasc Surg 18:199–206 66. Pappas PJ, Hobson RW 2nd, Meyers MG, Jamil Z, Lee BC, Silva MB Jr., Goldberg MC, Padberg FT Jr. (1998) Patency of infrainguinal polytetrafluoroethylene bypass grafts with distal interposition vein cuffs. Cardiovasc Surg 6:19–26 67. Parsons RE, Suggs WD, Veith FJ et al (1996) PTFE bypasses to infrapopliteal arteries without cuffs or patches: a better option than amputation in patients without autologous vein. J Vasc Surg 23:347–356 68. Pomposelli FB Jr., Jepsen SJ, Gibbons GW, Campbell DR, Freeman DV, Gaughan BM, Miller A, LoGerfo FW (1991) A flexible approach to infrapopliteal vein grafts in patients with diabetes mellitus. Arch Surg 126:724–727 69. Pomposelli FB, Kansal N, Hamdan AD, Belfield A, Sheahan M, Campbell DR, Skillman JJ, Logerfo FW (2003) A decade of experience with dorsalis pedis artery bypass: analysis of outcome in more than 1000 cases. J Vasc Surg 37:307–315 70. Quinones-Baldrich WJ, Colburn MD, Ahn SS, Gelabert HA, Moore WS (1993) Very distal bypass for salvage of the severely ischemic extremity. Am J Surg 166:117–123 71. Raftery KB, Belkin M, Mackey WC, O’Donnell TF (1994) Are peroneal artery bypass grafts hemodynamically inferior to other tibial artery bypass grafts? J Vasc Surg 19:964–969 72. Raviola CA, Nichter LS, Baker JD, Busuttil RW, Machleder HI, Moore WS (1988) Cost of treating advanced leg ischemia: bypass graft vs. primary amputation. Arch Surg 123:495–496 73. Rebane E, Tikko H, Tunder E, Lepner U, Helberg A, Pulges A, Vaasna T, Suba S, Lieberg J, Tamm V, Ellervee T, Vasar O (1997) Venous allografts for infrainguinal vascular bypass. Cardiovasc Surg 5:21–25 74. Rutherford RB, Jones DN, Bergentz SE, Bergqvist D, Comerota AJ, Dardik H, Flinn WH, Fry WJ, McIntyre K, Moore WS et al (1988) Factors affecting the patency of infrainguinal bypass. J Vasc Surg 8:236–246 75. Sayers RD, Thompson MM, London NJ, Varty K, Naylor AR, Budd JS, Ratliff DA, Bell PR (1993) Selection of patients with critical limb ischaemia for femorodistal vein bypass. Eur J Vasc Surg 7:291–297 76. Schmiedt W, Neufang A, Dorweiler B, Espinola-Klein C, Reinstadler J, Kraus O, Herber S, Gerhards A, Oelert H (2003) [Short distal origin vein graft in diabetic foot syndrome.] Zentralbl Chir 128:720–725
447
448
7.2 Femorodistal By-pass Surgery
77. Seeger JM, Schmidt JH, Flynn TC (1987) Preoperative saphenous and cephalic vein mapping as an adjunct to reconstructive arterial surgery. Ann Surg 205:733–739 78. Shah DM, Darling RC 3rd, Chang BB, Fitzgerald KM, Paty PS, Leather RP (1995) Long-term results of in situ saphenous vein bypass. Analysis of 2058 cases. Ann Surg 222:438–446 79. Shortell CK, Ouriel K, DeWeese JA, Green RM (1992) Peroneal artery bypass: a multifactorial analysis. Ann Vasc Surg 16:15–19 80. Sottiurai VS (1993) Nonreversed translocated vein bypass. Semin Vasc Surg Sep 6:180–184 81. Taylor LM, Edwards JM, Porter JM (1990) Present status of reversed vein bypass grafting: five year results of a modern series. J Vasc Surg 1:193–206 82. Taylor RS, Loh A, McFarland RJ et al (1992) Improved technique for PTFE bypass grafting: long term results using anastomotic vein patches. Br J Surg 79:348–354 83. Thompson RW, Mannick JA, Whittemore AD (1987) Arterial reconstruction at diverse sites using nonreversed autogenous vein. An application of venous valvulotomy. Ann Surg 205:747–751 84. Tordoir JHM, van der Plas JPL, Jacobs MJHM, Kitslaar PJHM (1993) Factors determining the outcome of crural and pedal revascularization for critical limb ischaemia. Eur J Vasc Surg 7:82–86 85. Varty K, Nydahl S, Butterworth P, Errington M, Bolia A, Bell PR, London NJ (1996) Changes in the management of critical limb ischaemia Br J Surg 83:953–956 86. Veith FJ, Gupta SK, Ascer E, White-Flores S, Samson RH, Scher LA, Towne JB, Bernhard VM, Bonier P, Flinn WR (1986) Six-year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions. J Vasc Surg 3:104–114
87. Veterans Administration Cooperative Study Group (1988) Comparative evaluation of prosthetic, reversed, and in situ vein bypass grafts in distal popliteal and tibial-peroneal revascularization. Arch Surg 123:434–438 88. Walsh DB, Gilbertson JJ, Zwolak RM et al (1991) The natural history of superficial femoral artery stenosis. J Vasc Surg 14:299–304 89. Watelet J, Cheysson E, Poels D, Menard JF, Papion H, Saour N, Testart J (1987) In situ versus reversed saphenous vein for femoropopliteal bypass: a prospective randomized study of 100 cases. Ann Vasc Surg 1:441–452 90. Webb T (1995) Operative adjuncts for distal revascularization. Surg Clin North Am 75:753–759 91. Wengerter KR, Veith FJ, Gupta SK, Goldsmith J, Farrell E, Harris PL, Moore D, Shanik G (1991) Prospective randomized multicenter comparison of in situ and reversed vein infrapopliteal bypasses. J Vasc Surg 13:189–199 92. Wengerter KR, Yang PM, Veith FJ et al (1992) A twelve year experience with the popliteal-to-distal artery bypass: the significance and management of proximal disease. J Vasc Surg 15:143–151 93. Wengerter K, Dardik H (1999) Biological vascular grafts. Semin Vasc Surg 12:46–51 94. Whittemore AD, Donaldson MC, Mannick JA (1993) Infrainguinal reconstruction for patients with chronic renal insufficiency. J Vasc Surg 17:32–41 95. Wolfle KD, Bruijnen H, Reeps C, Reutemann S, Wack C, Campbell P, Loeprecht H, Hauser H, Bohndorf (2000) Tibioperoneal arterial lesions and critical foot ischaemia: successful management by the use of short vein grafts and percutaneous transluminal angioplasty. Vasa 29:207–214 96. Wolfle KD, Bruinjen H, Loeprecht H et al (2003) Graft patency and clinical outcome of femorodistal arterial reconstruction in diabetic and non-diabetic patients: results of a multicentered comparative analysis. Eur J Vasc Endovasc Surg 25:229–234
449
7.3 Acute Ischaemia of the Lower Extremities Christos D. Liapis, John D. Kakisis
7.3.1 Synonyms • Acute leg/limb/lower extremity ischaemia • Acute peripheral arterial occlusion.
• arterial embolism • thrombosis of an atherosclerotic artery or a vascular graft • arterial trauma.
7.3.4.1 Embolism 7.3.2 Definition • Acute ischaemia of the lower extremities is a condition of acutely decreased blood flow to the leg, due to a blocked artery, which leads to ischaemic tissue damage.
7.3.3 Epidemiology • Acute ischaemia of the lower extremities is one of the most common emergencies in vascular surgery. • However, it is a rather unusual condition for the general population, with an overall incidence of 1/5,000 to 1/14,000 per year, depending mainly on the age distribution of the community population. • It is most common among elderly people, with 65% of cases occurring at the age of 70 or older. • Its annual incidence increases from 0.9 per 105 at the age of <40 years to 180–250 per 105 at the age of >80 years. • As regards the male-to-female ratio, it seems that both sexes are about equally affected.
7.3.4 Aetiology The major causes of acute arterial occlusion of the extremities are:
• Embolism is by far the most common cause of acute arm ischaemia, accounting for 74–100% of cases. • In the lower extremities, controversy exists regarding the ratio between arterial embolism and thrombosis, with different studies giving numbers ranging from 4:1 to 1:9. • The heart is invariably the most common origin of peripheral arterial emboli, and is responsible for 58–93% of cases. However, the pattern of the underlying heart disease has changed recently as the incidence of rheumatic valvular disease has decreased significantly.
Cardiac Sources of Emboli Nowadays, the most common sources of arterial emboli of cardiac origin are: • atrial fibrillation due to atherosclerotic heart disease, accounting for 32–75% of cases, followed by • myocardial infarction with mural thrombi formation, which is responsible for 21–32% of peripheral emboli. Less common cardiac sources of emboli are: • idiopathic dilated cardiomyopathy • prosthetic valves • rheumatic mitral valve disease • intracavitary cardiac tumours (mainly myxomas) • paradoxical embolization through an intracardiac defect, usually a patent foramen ovale • fungal or bacterial endocarditis.
450
7.3 Acute Ischaemia of the Lower Extremities
Noncardiac Sources • Noncardiac sources of emboli are being identified with increasing frequency, at the expense of undetermined causes, the frequency of which has steadily decreased due to improvements in diagnostic methods. Noncardiac sources of emboli are nowadays found in 5–12% of patients, while in 9–12% the source of the emboli remains unknown. • Aneurysms are the most common noncardiac source of peripheral embolism, accounting for about 5% of distal emboli. • Ulcerated atherosclerotic plaques follow in order of frequency, carrying the risk of distal embolism from white thrombi adherent on their surface. Such emboli are usually sizeable, capable of obstructing major peripheral arteries. • A distinct variant of peripheral embolization due to an atherosclerotic plaque is atheroembolism, in which a portion of the plaque breaks off and undergoes embolization to peripheral arteries. Such emboli may evolve in three clinical forms: 1. The asymptomatic form, not diagnosed during the subject’s lifetime and only recognized in autopsy studies. 2. A benign form such as blue toe syndrome or cutaneous livedo, with a spontaneous mild prognosis. 3. A diffuse multisystemic form with a very poor prognosis.
Cryptogenic Emboli • Despite complete diagnostic work-up, including complex investigations, the precise source of the emboli cannot be identified in 5–12% of cases. Such emboli are called cryptogenic and represent either the limited sensitivity of current diagnostic modalities or, in some cases, confusion with local thrombosis in situ.
Site of Emboli • As regards the site of arterial obstruction, lower extremity vessels are involved about five to six times as frequently as those of the upper extremity. • Emboli usually lodge at the points of arterial bifurcation, where the vessel diameter decreases abruptly.
• In cases of concurrent occlusive disease, emboli can also lodge at the points of significant arterial stenoses. • The exact locations of embolic obstructions are depicted in Table 7.3.1.
7.3.4.2 Thrombosis Thrombosis of an atherosclerotic artery or a vascular graft is another major cause of acute arterial occlusion of the extremities. As Virchow suggested in 1856, thrombus formation is the result of an interaction between an injured surface, stasis and the hypercoagulability of blood: • Arterial thrombosis most often develops at the points of severe stenosis. Since the course of atherosclerotic disease is chronic, a collateral network will have already developed and the clinical picture will be milder compared with arterial embolism. However, a thrombus can be formed in the absence of significant preexisting stenosis, particularly when the surface of the plaque is ulcerated or after an intraplaque haemorrhage resulting in sudden arterial occlusion. • Low-flow conditions, such as congestive heart failure, hypovolaemia, hypotension of any cause or decreased blood flow due to a more proximal stenosis. • Hypercoagulable states, such as myeloproliferative disorders, hyperviscosity syndromes and coagulation disorders, may contribute to thrombosis of the diseased artery. Other causes of arterial thrombosis include: • Arterial aneurysms, with the risk of thrombosis being higher the more peripherally the aneurysm is located. • Arterial by-pass graft thrombosis, which frequently induces acute limb-threatening ischaemia, as the graft has usually allowed collateral vessels to regress. Early graft failure, within the first postoperative month, is usually due to a technically suboptimal result, inappropriate indication or a transient episode of hypotension. Late graft failure, after 1 month, is secondary to intimal hyperplasia at the anastomotic sites or to progression of atherosclerotic disease. • Aortic dissection. • Fibromuscular dysplasia, occasionally involving the iliac arteries. • Cystic adventitial disease, usually affecting the popliteal artery and rarely the femoral.
7.3.5 Symptoms
Table 7.3.1 Location of embolic obstruction Artery
%
Femoral
37–49
Iliac
20–27
Popliteal
12–16
Upper extremity:
15–18
Brachial
60
Axillary
25
Radial
8
Subclavian
7
Tibial
4–6
Aortic saddle
3–6
• Thromboangiitis obliterans, involving medium-sized muscular arteries. • Various arteritides, such as Takayasu’s aortitis and giant cell arteritis. • Compartment syndrome. • Thoracic outlet syndrome. • Popliteal entrapment syndrome. • Ergotism.
7.3.5 Symptoms • The classic manifestations of acute arterial occlusion of the extremities are: pain, paresthesia, paralysis, pallor and pulselessness (the 5 Ps).
7.3.5.1 Pain • Pain is the most common symptom of acute arterial occlusion. • The pain is constant, exacerbated by movement of the extremity and it is characteristically severe, though in diabetic and elderly patients it may not be pronounced. • The pain involves the muscles below the level of obstruction and is worse at the most distal part of the extremity.
7.3.5.2 Paraesthesia • With the progression of the ischaemic process, paraesthesia develops, reflecting peripheral nerve ischaemia and, hence, dictating the need for urgent intervention. • Paraesthesia begins as a feeling of numbness and gradually progresses to loss of sensation to light touch.
7.3.4.3 Trauma • Arterial injuries, either blunt or penetrating, are common causes of acute limb ischaemia. • Intimal disruption of an adjacent artery, intimal flap, or spasm due to a large expanding haematoma are possible mechanisms by which a blunt injury may cause arterial obstruction. • Arterial obstruction may also ensue from blunt injuries with associated bone fractures and dislocations. • Penetrating trauma causing vascular injury is even more common, accounting for up to two-thirds of vascular injuries. Gunshot and stab wounds account for most of these. • With the widespread use of percutaneous transluminal interventional techniques (either diagnostic or therapeutic), the incidence of iatrogenic arterial injury is steadily increasing. Intimal flaps, dissection and thrombosis are responsible for the ensuing ischaemia.
7.3.5.3 Paralysis • Paralysis ensues from ischaemia both of nerves and muscles. • Loss of motor function, presenting with failure of toe and ankle dorsiflexion, is an ominous sign indicating potential irreversibility. • As ischaemia progresses, muscle paralysis proceeds to rigor, a sign of muscle death. • Prompt revascularization may restore limb viability but motor function will be permanently impaired. • In addition, metabolic manifestations of revascularization may be profound and sometimes lethal. In such cases, early amputation may be preferable to revascularization.
451
452
7.3 Acute Ischaemia of the Lower Extremities
7.3.5.4 Pallor
7.3.6 Complications
• Immediately after the acute arterial occlusion, the skin of the extremity becomes pale due to complete emptying and vessel spasm of the arterial circulation below the level of the obstruction. • Poor capillary filling and collapsed superficial veins are additional findings of inspection. • Some hours later, the vessel spasm is replaced by secondary vasodilatation and blotchy mottled areas of cyanosis develop, representing areas of local stasis. • Failure of the blue blotches to blanch by digital pressure is a sign of capillary bed thrombosis, indicating irreversible ischaemia. • Blistering of the skin and dry gangrene develop subsequently.
7.3.5.5 Pulselessness • Sudden loss of a previously palpable pulse is pathognomonic for acute arterial occlusion. • Of course, the prior pulse status of the extremity is unlikely to be known, but, in most cases, it can be suggested by the pulse status of the opposite extremity. • Palpation will also disclose coldness of the extremity about one joint distal to the level of obstruction. In this context, the point of occlusion can be assumed by the level of colour and temperature demarcation and the site of pulse disappearance. Based on the severity of ischaemia, acute limb ischaemia can be classified into three categories, as proposed by SVS/ISCVS (Table 7.3.2) [5].
If left untreated, acute limb ischaemia will lead to: • gangrene and • systemic acidosis.
7.3.7 Diagnosis 7.3.7.1 Recommended European Standard Diagnostic Steps of Investigation • Inspection, revealing pallor or cyanosis. Signs of chronic limb ischaemia (trophic skin changes) should also be sought in both extremities. • Palpation, revealing coldness, pulselessness and loss of sensation. In cases of embolization, palpation may also disclose arrhythmia (atrial fibrillation). • Doppler examination, revealing absence of flow in the extremity. • Duplex ultrasonography can localize the point of arterial occlusion and identify patent proximal or distal vessels. It can also disclose the presence of an abdominal, femoral or popliteal aneurysm and rule out the diagnosis of phlegmasia cerulea dolens. • Arteriography can help in the differential diagnosis between thrombosis and embolism. The typical angiographic characteristics of an embolic obstruction are an abrupt occlusion of an otherwise normal artery, with a reversed meniscus and absence of collateral circulation (Fig. 7.3.1). In contrast, a tapering occlusion of a diffusely atherosclerotic artery with a rich net-
Table 7.3.2 Classification of limb ischaemia based on severity of ischaemia Category
Description/prognosis
Findings Sensory loss
Muscle weakness
Not immediately threatened
None
None
a. Marginally
Salvageable if promptly treated
Minimal (toes) or none
None
b. Immediately
Salvageable with immediate revascularization
More than toes, associated with rest pain
Mild, moderate
Major tissue loss or permanent nerve damage inevitable
Profound, anaesthetic
Profound, paralysis (rigor)
I. Viable II. Threatened
III. Irreversible
7.3.8 Treatment
7.3.7.2 Additional Useful Diagnostic Procedures • Echocardiography should be performed in patients with distal embolization with no obvious source.
7.3.8 Treatment 7.3.8.1 Conservative Treatment Recommended European Standard Therapeutic Steps
Fig. 7.3.1 Arteriogram revealing embolus in the popliteal artery, with the characteristic abrupt occlusion, reversed meniscus sign and absence of collateral circulation
work of collateral vessels denotes thrombosis. The site of occlusion is also indicative of its aetiology. Obstruction of the middle or distal portion of the superficial femoral artery is typical of thrombosis, while emboli usually lodge at arterial bifurcations. Arteriography is especially helpful in cases of thrombosis, since these patients will most probably need a by-pass procedure. Such a procedure will be designed on the basis of information provided by arteriography, regarding the exact site and extent of obstruction, potential proximal in-flow sources and patent run-off vessels.
• All patients presenting with acute arterial occlusion of the extremities should receive initially 5000–10,000 units of heparin intravenously, regardless of the exact cause of the occlusion. The goal is to prevent proximal and distal propagation of the thrombus, as well as deep venous thrombosis, until further action is taken. • The next step is to differentiate between embolism and thrombosis, since these two clinical entities require a different therapeutic approach. • Sudden onset of limb ischaemia in a patient without history of intermittent claudication and palpable pulses at the opposite extremity is more likely to be due to embolism. The presence of an identifiable source of emboli, such as atrial fibrillation, further supports the diagnosis. Such a patient should be submitted to embolectomy as soon as possible, without any delay for extensive preoperative examination, except for an evaluation and initial management of any underlying heart disease. • In contrast, a patient with a history of intermittent claudication, with physical signs of chronic limb ischaemia and no palpable pulses at the opposite extremity, is more likely affected by arterial thrombosis. Such a patient should undergo further evaluation in the direction of subsequent treatment planning.
7.3.8.2 Surgery Recommended European Standard Surgical Procedures ArterialEmbolus
• The treatment of choice in most patients with arterial embolism is prompt surgical embolectomy.
453
454
7.3 Acute Ischaemia of the Lower Extremities
• Before 1963, surgical embolectomy usually involved multiple arteriotomies under general anaesthesia and removal of the clot directly by milking out, or by the use of suction catheters, corkscrew wires and specially designed forceps. • The introduction of the Fogarty balloon catheter in 1963 greatly simplified the procedure, enabling complete removal of the thrombus through a single arteriotomy performed under local anaesthesia, remote to the site of obstruction. • In the upper extremity, a mid-brachial or an antecubital fossa incision is made to expose the brachial artery, while in the lower extremity, a vertical incision is made to explore the common femoral artery. • A transverse arteriotomy is performed to prevent narrowing when the arteriotomy is repaired, while a longitudinal arteriotomy is performed when endarterectomy is thought likely. • The balloon catheter is passed until two successive passes yield no further clots. • Establishment of forceful pulsatile in-flow is a good indicator of the completeness of proximal embolectomy, while the restoration of backflow is not a reliable indicator of successful removal of all distal thrombus. Intraoperative completion arteriography is therefore mandatory. • If residual thrombi are found, repeated embolectomy, more distal exploration or intraoperative thrombolysis can be performed. • Intraoperative angioscopy is a useful adjunct to embolectomy, allowing direct visualization of the arterial lumen. It permits accurate detection and retrieval of residual clot, manipulation of the balloon catheter to selected vessels, and removal of intimal flaps. It may also prevent surgical exploration of the distal popliteal and tibial arteries and decrease the requirement for repeated arteriograms. • Percutaneous aspiration embolectomy has also been reported as an alternative to surgical balloon embolectomy [1]. It is a simple technique with reduced invasiveness, combines a diagnostic and a therapeutic procedure, enables treatment of tibial and pedal vessels and can be combined with all other angioplastic methods. It can be useful, especially in high-risk patients for whom surgery is too risky.
Acute Arterial Thrombosis
• Contrary to embolism, arterial thrombosis is unlikely to be effectively treated by balloon catheter thrombectomy alone. • The therapeutic approach should always include treatment of the underlying cause of thrombosis. • Therefore, a preoperative angiography is desirable, to disclose the responsible lesion and suggest the appropriate intervention. • Thrombosis of a short segment with a satisfactory proximal and distal lumen can be treated by thromboendarterectomy with or without patch closure. • Conversely, thrombosis of a long segment or significant proximal or distal disease would be best treated with by-pass grafting.
By-passGraft Thrombosis
• By-pass graft thrombectomy is a relatively simple procedure, similar to balloon catheter embolectomy. Exploration of the graft at its distal anastomosis is advisable, because it allows identification of the most common cause of graft failure, which is intimal hyperplasia at the distal anastomosis and the first 1 or 2 cm of the native artery distally to the anastomosis. • If such a lesion is found, it can be treated by patch angioplasty including the distal part of the graft. • If restoration of patency cannot be achieved in this way, construction of an entirely new by-pass graft is preferable, particularly with the use of autologous vein. • Unlike prosthetic grafts, the results of autologous vein graft thrombectomies are disappointing. Exploration of a thrombosed vein graft will most probably disclose a fibrotic thickened graft, which cannot be repaired. For all that, if balloon thrombectomy is attempted, poor compliance of the graft will result in significant intimal injury.
Complications Complications of revascularization of an acutely ischaemic extremity can be divided into those related to the surgical intervention, those secondary to limb reperfusion and those secondary to the primary cause of the event, including recurrent embolization and rethrombosis.
7.3.8 Treatment
Recurrence
• The incidence of recurrent embolization ranges from 6% to 45%, emphasizing the need for long-term, adequate anticoagulation. • It should be noted that recurrent emboli could lodge at any artery of the human body, including cerebral and visceral arteries, with devastating consequences. • Rethrombosis is due to either intimal injury during balloon embolectomy or incomplete removal of the thromboembolic material. • Prompt reoperation is required, with repeat thromboembolectomy, endarterectomy, patch angioplasty and by-pass procedures being included in the therapeutic armamentarium.
ComplicationsRelated to the Surgical Intervention
• • • • •
Intimal dissection Arterial perforation Balloon fragment embolization Arteriovenous fistula Delayed manifestations, such as intimal hyperplasia caused by injury of the vessel wall during aggressive embolectomy.
ReperfusionSyndrome
• This includes both local (compartment syndrome) and systemic manifestations (acidosis, hyperkalaemia, renal, hepatointestinal and pulmonary failures, arrhythmia and cardiac arrest). • Initial tissue damage during the ischaemic phase is continued by the reintroduction of oxygenated blood. Oxygen-derived free radicals peroxidate the lipid component of cell membranes, leading to enhanced capillary permeability. • Large amounts of lactic acid, gathered during anaerobic metabolism in the phase of ischaemia, enter the circulation leading to a sudden decrease in pH and an increase in serum potassium. • Acidosis and hyperkalaemia can lead to cardiac arrhythmias, while acute renal tubular necrosis occurs from the precipitation of myoglobulin released from ischaemic muscle in an acidic environment. • Treatment of reperfusion syndrome includes correction of acidosis by sodium bicarbonate, correction of hyperkalaemia by glucose and insulin, ion-exchange resins, brisk diuresis and, in some cases, haemodialysis, and prevention of acute tubular necrosis by brisk
diuresis and alkalinization of the urine. Mannitol is quite useful, acting both as an osmotic agent to induce diuresis as well as a scavenger of deleterious oxygen free radicals. • Finally, management of the adult respiratory distress syndrome requires respiratory support and avoidance of early extubation. Compartment syndrome is a local manifestation of reperfusion injury, characterized by high pressure within a closed fascial space reducing capillary blood perfusion below a level necessary for tissue viability. The syndrome presents with pain, exacerbated by passive stretch, paresis of the muscles in the compartment, hypoaesthesia in the distribution of the nerves running through the compartment and tension and swelling of the fascial boundaries of the compartment. Prompt fasciotomy is required if permanent disability is to be prevented.
7.3.8.3 Thrombolytic Therapy • Catheter-directed thrombolysis can be used as part of a treatment strategy designed to eliminate the acute thrombotic or embolic material and restore perfusion. • Thrombolytic therapy may be conclusive. The meaning is that thrombolytic therapy may be the one and only therapy, evading the need of surgery, or it may convert an emergency operation for a poorly prepared, critically ill patient to an elective one. • It might decrease the magnitude of the subsequent vascular reconstruction, open branch vessels that are inaccessible to surgical thrombectomy and by-pass, or lower the level of amputation in patients without other options. • Gradual, low-pressure reperfusion is also believed to be advantageous in preference to sudden, high-pressure reperfusion. • Furthermore, by elimination of the thrombus, the underlying lesion is disclosed and is subsequently corrected by open or endovascular technique [8]. • Thrombolytic drugs in clinical use for leg arterial occlusion are streptokinase (SK), urokinase (UK) and recombinant human tissue plasminogen activator (rtPA, alteplase). Several new thrombolytic agents are under clinical development, including recombinant human UK, recombinant glycosylated pro-UK and recombinant staphylokinase.
455
456
7.3 Acute Ischaemia of the Lower Extremities
Table 7.3.3 Complications of intra-arterial fibrinolytic therapy
Proper selection of the appropriate patients is critical for successful therapy. In general, patients with a short duration and proximal location of occlusion, with patent distal vessels, as determined by Doppler signals and arteriography, are good candidates for lytic therapy, provided that no contraindication to therapy exists.
Contraindications Contraindications to intra-arterial fibrinolytic therapy are absolute or relative:
Drug-associated complica- Technique associated tions complications Haemorrhage
Pericatheter thrombosis
Due to lysis of haemostatic fibrin
Catheter-induced thrombosis
Due to the induced coagulopathy
Toxic complications of contrast
Distal emboli
Pseudoaneurysm of puncture site
Allergic reaction
Arteriogram complication
Pyretic reaction
Absolute Contraindications
Serum sickness
• • • •
Transgraft extravasation
Intolerable ischaemia Active internal bleeding Cerebrovascular accident within 3 months Intracranial pathology.
Relative Contraindications
• • • • • • • • • • •
Recent major surgery or trauma Minor gastrointestinal bleeding Severe hypertension Valvular heart disease Atrial fibrillation Endocarditis Coagulation disorders Pregnancy Minor surgery Severe liver disease Axillofemoral graft or knitted Dacron graft
Contraindications for Streptokinase Therapy
• Known allergy • Recent streptococcal infection • Previous therapy within 6 months.
Complications • The most common and most feared complication of thrombolytic therapy is bleeding. • The risk of major bleeding (requiring cessation of therapy and/or blood transfusions) ranges from 3% to 17% when appropriate precautions are taken.
• Intracerebral bleeding, the most dreaded of all haemorrhagic events, occurs in 1–2% of patients. • Other complications of thrombolysis are depicted in Table 7.3.3.
Outcome • A number of prospective randomized studies have tried to compare thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischaemia. • Ouriel and associates [3] showed that intra-arterial thrombolysis was associated with a reduction in the incidence of in-hospital cardiopulmonary complications and a corresponding increase in patient survival rates (84% versus 58% at 12 months, p=0.01). • The STILE trial [6] revealed that patients with acute ischaemia (0–14 days) who were treated with thrombolysis had improved amputation-free survival and shorter hospital stays. However, for patients with chronic ischaemia (>14 days) surgical revascularization was more effective and safer than thrombolysis. • Comerota and colleagues [2] found that acutely ischaemic patients (0–14 days) randomized to lysis demonstrated a trend towards a lower rate of major amputation at 30 days (p=0.074) and a significantly lower rate at 1 year (p=0.026) compared with surgical patients, while those with >14 days of ischaemia showed
References
no difference in limb salvage but higher ongoing/recurrent ischaemia in lytic patients (p<0.001). • Another prospective randomized trial, by Weaver et al. [7], showed that surgical revascularization for lower extremity native artery occlusions is more effective and durable than thrombolysis. Thrombolysis used initially provided a reduction in the surgical procedure for the majority of patients; however, the longterm outcome was inferior, particularly for patients with femoropopliteal occlusion, diabetes, or critical ischaemia. • Finally, the TOPAS study [4] revealed that recombinant urokinase therapy is associated with limb-salvage and patient-survival rates similar to those achieved with surgery, concurrent with a reduced requirement for complex surgery after thrombolytic intervention.
7.3.9 Differential Diagnosis The principal differential diagnosis is between embolism and thrombosis. Other clinical entities that should be differentiated are: • low-flow conditions • phlegmasia cerulea dolens • neurologic disorders presenting with limb numbness.
7.3.10 Prognosis • Despite considerable improvements in treatment modalities, acute arterial occlusion of the extremities is still associated with a high amputation rate of 5–76% and an equally high mortality rate of 5.2–55%, according to studies published during the past decade. • Several attempts have been made in order to identify parameters predictive of clinical outcome.
• Undoubtedly, the key to successful therapy is always a prompt diagnosis, including identification of the cause of the occlusion, followed by selection of the appropriate management. References 1. Canova CR, Schneider E, Fischer L, Leu AJ, Hoffmann U (2001) Long-term results of percutaneous thrombo-embolectomy in patients with infrainguinal embolic occlusions. Int Angiol 20:66–73 2. Comerota AJ, Weaver FA, Hosking JD, Froehlich J, Folander H, Sussman B, Rosenfield K (1996) Results of a prospective, randomized trial of surgery versus thrombolysis for occluded lower extremity bypass grafts. Am J Surg 172:105–112 3. Ouriel K, Shortell CK, DeWeese JA, Green RM, Francis CW, Azodo MV, Gutierrez OH, Manzione JV, Cox C, Marder VJ (1994) A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischaemia. J Vasc Surg 19:1021–1030 4. Ouriel K, Veith FJ, Sasahara AA (1996) Thrombolysis or peripheral arterial surgery: phase I results. TOPAS Investigators. J Vasc Surg 23:64–75 5. Rutherford RB et al (1997) Recommended standards for reports dealing with lower extremity ischaemia: revised version. J Vasc Surg 26:517–538 6. The STILE investigators (1994) Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischaemia of the lower extremity. Ann Surg 220:251–268 7. Weaver FA et al (1996) Surgical revascularization versus thrombolysis for nonembolic lower extremity native artery occlusions: results of a prospective randomized trial. The STILE Investigators. Surgery versus Thrombolysis for Ischaemia of the Lower Extremity. J Vasc Surg 24:513–523 8. Working Party on Thrombolysis in the Management of Limb Ischaemia (2003) Thrombolysis in the management of lower limb peripheral arterial occlusion – a consensus document. J Vasc Interv Radiol 14:S337–S349
457
459
7.4 Lower Extremity Aneurysms S. Riera, M. Cairols
7.4.1 Basic Concepts • An artery is considered to be aneurismal when it presents a dilatation above 50% as compared to the proximal diameter of the artery itself. • The following locations can be clearly differentiated according to their anatomy. The list below is made in order of decreasing importance: • Popliteal artery aneurysm
Algorithm 7.4.1 Therapeutic algorithm for popliteal aneurysms
• Common femoral artery aneurysms and its bifurcation • Superficial femoral artery aneurysms • Distal arterial branches aneurysms.
7.4.2 Popliteal Aneurysms (PA) • See Algorithm 1.
460
7.4 Lower Extremity Aneurysms
7.4.2.1 Definition • A PA is defined as those popliteal arteries that are more than 1.5–2 times the diameter of the proximal native artery, regardless of the individual differences in its diameter. • By and large, all popliteal arteries with a diameter above 2 cm are considered as being aneurysmal [8].
Prolonged compression can give rise to thrombosis and subacute ischaemia. • Rupture of a popliteal aneurysm is exceptional and only affects 1% of all patients.
7.4.2.5 Diagnosis Recommended European Standard Diagnostic Steps of Investigation
7.4.2.2 Epidemiology/Aetiology • Despite the fact that PA are an infrequent condition, they are the most common of all peripheral artery aneurysms, and account for about 70% of all lower limb aneurysms. • They are predominant in males in more than 90% of cases, and are often diagnosed in patients who are in their 60s or 70s. • Between 45% and 68% of the cases are bilateral. • They are associated with an aortic aneurysm in 30– 60% of these cases [3, 4, 31]. • Atherosclerosis is the most common aetiology, followed by infection and popliteal entrapment syndrome.
7.4.2.3 Symptoms • Approximately 30% of all PA are asymptomatic at the time of diagnosis. • When they are symptomatic, the clinical syndrome may be ischaemia or symptoms secondary to compression of the neighbouring structures.
7.4.2.4 Complications • Over 60% of all cases of ischaemia are of acute onset due to thrombosis of the aneurysmal sac. In such cases emergency treatment is required due to the high risk of amputation. Short-distance claudication and/or rest pain are typical in cases of chronic ischaemia. • In 5–10% of patients, symptoms take the form of blue toe syndrome, caused by distal mural thrombus embolization. • In cases of extrinsic compression (<10%), the clinical features may mimic a venous pseudothrombosis and/ or neurological condition affecting the sciatic nerve.
• A physical examination can help in reaching patients in whom a PA is suspected, such as the presence of a pulsating mass in the popliteal fossa. Feeling a spaceoccupying mass (whether it is pulsatile or not) in the popliteal region and symptoms of acute ischaemia of the limb, blue toe syndrome, a clinical picture of extrinsic compression, etc. will help lead to diagnosis. • Doppler ultrasound will confirm the diagnosis and enable measurement of the size of the aneurysm. It will also provide data on patency and the presence of mural thrombus (Figs. 7.4.1, 7.4.2). At the same time, it allows exploration of the contralateral popliteal artery and the aorta. Doppler ultrasound is the ideal test for screening, as it is easy to use, comfortable for the patient and has a high degree of cost-effectiveness. • Both magnetic resonance imaging (MRI) and computerized tomography (CT scan) are very accurate methods for accurately determining its location, size and patency. They define the thickness of the mural thrombus filling the aneurysmal sac. Nevertheless, their use must be restricted where surgery may be an indication. • Angiography is useful in planning the surgical treatment for extremities affected by symptoms of ischaemia; in fact, it is the best test for an accurate evaluation of the distal run-off as well as for choosing the best arterial segment for performing the distal anastomoses. In addition, in patients with acute ischaemia secondary to thrombosis, it also allows locoregional fibrinolytic therapy to be performed in order to improve distal run-off. However, angiography is not a good technique for diagnosing a PA as it only identifies the arterial lumen.
7.4.2 Popliteal Aneurysms (PA)
• For this reason prophylactic surgical repair is frequently recommended, especially when considering the high rate of amputation in cases when thrombosis of the aneurysm occurs. • In general terms, intervention is recommended in asymptomatic aneurysms larger than 2 cm in diameter with mural thrombus and anatomical distortion. • In the remaining cases, conservative treatment is advised and surgery is only recommended when symptoms appear or if enlargement of the diameter takes place.
Symptomatic Aneurysms Fig. 7.4.1 Doppler ultrasound imaging of a popliteal aneurysm. The artery is shown in red and the vein in blue. In this transverse cut the low density surrounding the vessels shows the aneurysm
In all cases they are eligible for surgical repair. Nevertheless, the following should be differentiated: • Patients with acute ischaemia. Preoperative locoregional fibrinolytic therapy and later revascularization is recommended. If preoperative fibrinolytic therapy cannot be performed, urgent revascularization with peroperative fibrinolysis of the distal branches is indicated [14, 17]. • Patients with chronic ischaemia and aneurysmal thrombosis. Conservative treatment seems to be the best option for intermittent claudication and revascularization is only considered if there is a worsening of symptoms. Revascularization must be carried out in all those patients with rest pain and/or trophic lesions. • Patients with PA producing distal embolization, extrinsic compression and rupture. The aneurysm must be excluded and revascularization performed.
Recommended European Standard Surgical Procedures Fig. 7.4.2 The same case in a longitudinal image. Observe the thickness of the mural thrombus
7.4.2.6 Treatment Asymptomatic Aneurysms • Their treatment is controversial. • In patients with asymptomatic PA left to their natural evolution, the literature reports an incidence of PA becoming symptomatic, and therefore worsening the outcome, in between 18% and 31% of cases [14].
• The first therapeutic option is open surgery with exclusion of the aneurysm and revascularization of the extremity by means of a by-pass, preferable made of autologous material. • However, if an adequately long saphenous vein is not available, the second recommended material is PTFE, although its medium-term patency rate, as known, is less satisfactory.
461
462
7.4 Lower Extremity Aneurysms
Additional Useful Surgical Procedures
7.4.3.1 Definition
• Endovascular reconstruction is restricted to a few particular cases, particularly for high-risk surgical patients. • It is also indicated when a skin incision may produce complications, such as healing in critical leg ischaemia. • Endovascular therapy has short- and medium-term results far below those achieved with open surgery (75% patency at 30 months in above-knee by-passes in contrast to only 27% when the procedure has to be carried out below the knee) [16, 22].
• Similarly to the PA, a femoral artery is considered to be aneurysmal when it is more than 1.5–2 times the size of the distal external iliac artery. • The mean diameter of the common femoral artery is 9.7 mm in males and 8.2 mm for females [30]. • This diameter increases with age, initially during the stages of growing, but also in adulthood. • Other parameters that influence the diameter of the common femoral artery are the gender and the individual body surface area. • A femoral artery is generally accepted as being aneurysmal when it is >2.5 cm in diameter.
7.4.2.7 Prognosis 7.4.3.2 Epidemiology/Aetiology • Asymptomatic aneurysms. Revascularization by means of an autologous by-pass graft offers an immediate patency rate close to 100% and above 80% at 5 years, while the rate of limb preservation is greater than 90%. Even though it is performed in elderly patients, morbidity and mortality are very low (<5%) [14, 17]. • Symptomatic aneurysms. In cases of acute ischaemia in which revascularization is attempted without prior fibrinolysis, the amputation rate is around 30% at 30 days. In patients who have been submitted to fibrinolysis prior to revascularization, the amputation rate at 30 days drops to 10–15% [2, 9, 12, 17]. In cases of chronic ischaemia, the patency resulting from the bypass and the rate of limb preservation is comparable to that obtained in below-knee by-passes, as distal runoff is often acceptable. • In patients with a clinical syndrome secondary to extrinsic compression, outcomes are comparable to those obtained in asymptomatic individuals since the distal segment remains undamaged.
7.4.3 Aneurysms of the Common Femoral Artery • See Algorithm 2.
• The common femoral artery is, after the popliteal, the most frequent location for the formation of peripheral aneurysms with a ratio of 1:10 with respect to the aorta. • In 50% of cases, a femoral aneurysm is accompanied by an aortic aneurysm and in 30% it occurs together with a popliteal aneurysm [11, 30]. • In terms of its topography, in 44% of cases they are limited to the common femoral, in 56% they encompass the bifurcation and in less than 1% they affect only the deep femoral artery. According to their aetiology they can be classified as: • True aneurysms, of atherosclerotic aetiology and involvement of all the layers of the vessel wall: they account for approximately 50% of all cases. • False aneurysms or pseudoaneurysms: they develop from a defect in the vessel wall or from a prior vascular anastomosis. These can in turn be divided into: • Iatrogenic: those are secondary to an invasive diagnostic test and/or therapeutic technique with an inguinal entry point. Their incidence rate has grown as the number of this type of technique has increased; besides this, recently, the majority of these patients are being treated medically with antiplatelet and/or anticoagulant drugs. • Noniatrogenic: secondary to accidental traumatic injuries.
7.4.3 Aneurysms of the Common Femoral Artery
Algorithm 7.4.2 Therapeutic algorithm of femoral aneurysms
• Anastomotic: those in which there was a dehiscence and/or rupture of a previous vascular anastomosis in the inguinal region. These account for 80% of anastomotic aneurysms in vascular surgery and complicate 1.5–3% of all femoral anastomoses. Predisposing factors include past history of surgical wound infection of a previous intervention, female gender and where there are antecedents of a previous pseudoaneurysm already repaired. • Mycotic aneurysms: due to colonization of a pre-existing atherosclerotic lesion at the femoral level as a consequence of bacteraemia or contaminated direct puncture in patients addicted to intravenous drugs.
Symptomatic Aneurysms • If they become symptomatic, the presenting symptoms are either ischaemia or due to compression of neighbouring structures. • The ischaemia can be of acute onset due to thrombosis or secondary to peripheral embolization. • Both entities are less frequent than those produced in patients with PA. • Compression of the neighbouring structures can affect the femoral nerve, the femoral vein or the inguinal lymphatic ganglia.
Iatrogenic Pseudoaneurysms 7.4.3.3 Symptoms • Most true femoral aneurysms are asymptomatic.
• Iatrogenic pseudoaneurysms always present a history of inguinal manipulation and course with a pulsatile mass at this level.
463
464
7.4 Lower Extremity Aneurysms
• Depending on their size and rate of growth, symptoms can take the form of pain, a feeling of tightness and skin lesions.
Doppler Ultrasound Imaging • This technique allows the diagnosis to be confirmed and provides us with information about its size, location and the existence of an endoluminal thrombus.
Noniatrogenic Traumatic Aneurysms • Non-iatrogenic traumatic pseudoaneurysms present a history of accidental traumatic injury and may be accompanied by other traumatic injuries in different territories.
Anastomotic Pseudoaneurysms • Anastomotic pseudoaneurysms are generally well tolerated, course as an inguinal pulsatile mass and constitute a late complication (normally more than 8 years) of previous arterial surgery involving the femoral artery.
Mycotic Aneurysms • In the case of infectious pseudoaneurysms, there are always symptoms of an accompanying bacteraemia with fever, general malaise and signs of local phlogosis in the inguinal region. • In individuals addicted to intravenous drugs, there is a history of repeated local punctures in the region. The rate of thrombosis for aneurysms > 5 cm in diameter is 17% in comparison to 5% for aneurysms < 5 cm. On the other hand, rupture is an infrequent complication. It is estimated that the rate of ruptures is only 1.6% in femoral aneurysms < 5 cm and 16% for those that are > 5 cm [7, 23, 24].
Arteriography, CT Scan and MRI • These are very useful diagnostic tests as they allow us to detect pseudoaneurysms in other anatomical locations and help us to plan their surgical repair. • Their value stems essentially from their capacity to identify the existence of coexisting distal occlusive lesions.
7.4.3.5 Treatment True Aneurysms • If they are asymptomatic, small (<3 cm) and without mural thrombi, conservative treatment with regular ultrasound controls is advised, as the rate of complications is low. • If they are over 3 cm in diameter and are accompanied by a mural thrombus, the chances of complications increase. • This type can be treated by surgical repair as a prophylactic measure, with exclusion of the aneurysm and replacement with a prosthetic graft [3, 23, 24, 32].
False Aneurysms or Pseudoaneurysms In these cases treatment will depend on the aetiology.
Iatrogenic
7.4.3.4 Diagnosis Physical Examination • Feeling a pulsatile mass in the inguinal region is characteristic of this condition. • The patient’s history will guide towards the aetiology.
• If they are small and asymptomatic, conservative treatment is recommended, since the rate of spontaneous resolution is high, above 70% [34]. • Should resolution not occur spontaneously, then selective compression of the aneurysmal neck is to be performed with ultrasound monitoring until thrombosis of the sac is achieved. • Until 1991 symptomatic or large-sized femoral aneurysms were eligible for surgical repair, but now ultrasound-scan-guided selective compression may give
7.4.3 Aneurysms of the Common Femoral Artery
Fig. 7.4.3 Intraoperative view of an open anastomotic pseudoaneurysm. Notice the anterior false wall and the prosthetic graft desinserted from the native artery
Fig. 7.4.4 The same case repaired by means of a PTFE graft
Mycotic Aneurysms
rise to resolution in 80% of cases, therefore this strategy is recommended as the first option [3, 5, 6, 10, 18]. • If this therapy is not effective or produces intense pain, ultrasound-guided selective injection of thrombin into the aneurysmal sac is recommended. • This technique enables thrombosis to be accomplished in almost 100% of cases despite concomitant treatment with antiplatelet and/or anticoagulant agents [20, 27, 28, 35]. • Should this technique fail or if the patient presents haemodynamic instability or a skin lesion, urgent surgical treatment is indicated.
• The specific treatment with antibiotics will be accompanied by excision of the affected area and revascularization of the extremity depending on its tolerance to the ischaemia.
Recommended European Standard Surgical Procedures The surgical technique will be closely related to their aetiology.
True Aneurysms Noniatrogenic Traumatic Injury
• In these cases surgical repair will always be indicated.
• Recommended treatment involves their exclusion with revascularization of the extremity with prosthetic graft, preferably PTFE.
Anastomotic Aneurysms
• If they are small (<2.5 cm) and asymptomatic, they are eligible for conservative treatment with periodic controls with ultrasound imaging; they are considered to be eligible for surgery (Figs. 7.4.3, 7.4.4) when changes in anatomy are detected or they produce symptoms. • Large-sized or symptomatic cases should be repaired surgically. • Infected anastomotic pseudoaneurysms are always eligible for surgical repair accompanied by specific treatment with antibiotics.
IatrogenicAneurysms
• Resolution should be achieved by means of ultrasound-guided selective compression of the neck and/ or thrombin injection as described previously. • Currently, the use of thrombin is frequently recommended as the first therapeutic option (high rate of resolution and a low complications). • In addition, it does not give rise to any discomfort for the patient and is very effective in individuals who are receiving medical treatment with antiplatelet and/or anticoagulant drugs [33].
465
466
7.4 Lower Extremity Aneurysms
• Surgical cases are those patients with haemodynamic instability, a large inguinal haematoma with skin involvement or those in whom resolution has not been otherwise achieved. • In those, an urgent surgical haemostasis and closure of the arterial leakage accompanied by drainage of the haematoma is indicated.
Noniatrogenic Traumatic Aneurysms
• These are always eligible for surgical repair with exclusion of the contused area and revascularization of the extremity by means of end-to-end by-pass graft. • In those cases autologous material is preferable to avoid infection of prosthetic material.
7.4.3.6 Prognosis True Aneurysms • Surgical repair of such, in asymptomatic individuals, has a patency rate close to 100% at 5 years. • In cases of acute ischaemia, prognosis depends more on the progression of the atherosclerotic disease than on the surgical repair itself, showing a late patency at 5 years above 80%.
Traumatic Aneurysms (Iatrogenic and Noniatrogenic) • This type of aneurysm has a very good prognosis, with patency close to 100%.
Anastomotic Aneurysms
• In those free from infection, surgical repair will consist of resection of the pseudoaneurysm with revascularization by means of an end-to-end prosthetic graft between the native artery and/or proximal prosthetic graft and the distal artery and/or patent femoral-popliteal-distal graft. • In those that are infected, surgical repair will involve excision of all the infected material, debridement of the area and an extra-anatomical revascularization of the extremity avoiding the infected inguinal region (through the obturator foramen, axillary or ilio-profunda femoris by-pass lateral to the sartorius). • In these cases, surgical repair will always be accompanied by specific treatment with antibiotics.
Mycotic Aneurysms
• Surgical treatment will consist of resection of the infected area with arterial ligature, as well as specific antibiotic treatment [1, 15]. • If the patient shows a good tolerance to ischaemia, in a later intervention an extra-anatomical revascularization should be performed. • If there is an ischaemic leg in danger of amputation an extra-anatomical by-pass must be carried out simultaneously, at the same time as surgery. • In this case, the use of autologous material is recommended, but if none is available we prefer to use cryopreserved arterial homograft to a prosthetic graft.
Anastomotic Aneurysms • In those that are free from infection, prognosis will be related to the progression of the underlying disease; these are cases of patients who have previously undergone surgery due to atherosclerotic disease. • Infected cases have a poor prognosis with a high rate of morbidity and mortality in the short and medium term (>50%).
Mycotic Aneurysms • As mentioned previously, these occur in patients with a previous bacteraemia and in poor condition, as well as in intravenous drug abusers with repeated septic punctures in the inguinal region. • Their prognosis is very ominous, with morbidity and mortality rates above 50%.
7.4.4 Aneurysms of the Superficial Femoral Artery 7.4.4.1 Definition • A superficial femoral artery will be considered to be aneurysmal when its diameter exceeds 2 times the diameter of the proximal superficial femoral artery.
7.4.4 Aneurysms of the Superficial Femoral Artery
7.4.4.2 Epidemiology/Aetiology • An isolated aneurysm of the superficial femoral artery (SFA) is a very uncommon condition. • For this reason its natural history and the frequency with which it is associated with other aneurysms remain unknown. • Thus, it is not known whether its natural history is similar to that of aortic aneurysms (high rate of rupture, low incidences of thrombosis and peripheral embolism), or whether it resembles a popliteal aneurysm with a high rate of thrombosis and distal embolization but a low rate of rupture. • It predominates in males (>80% of cases) and affects elderly patients (from their 70s onwards). • According to several different publications [19, 29], it is associated with an aortoiliac aneurysm in 40–69% of cases and an aneurysm of the common femoral or popliteal arteries in 54%. • In practically all cases the aetiology is atherosclerotic. • Other very rare causes include infections (syphilis, tuberculosis and others), inflammatory arteritis and diseases affecting the connective tissue (Ehlers–Danlos syndrome) [21, 29].
7.4.4.3 Symptoms • Approximately 30% of all aneurysms of the superficial femoral artery are asymptomatic and are usually found by chance during the course of a vascular examination. • A clinical picture of compression of neighbouring structures is rare in symptomatic cases. • In 30–35% of cases they may rupture, in 30% they have clinical symptoms of ischaemia of the extremity, and in the remaining cases they appear as a pulsatile mass in the inner side of the thigh with no symptoms [29]. • When symptomatic they usually course as chronic ischaemia and the degree of intensity depends on the associated distal and popliteal occlusive lesions.
7.4.4.4 Diagnosis • Many aneurysms of the SFA are very likely to remain undiagnosed particularly because of the high incidence of thrombosis in this artery.
• In fact, it is not possible to diagnose a thrombosed SFA aneurysm by an arteriogram, particularly in cases with complete occlusion of the SFA. • The diagnosis follows the same sequence as explained in other anatomical locations.
7.4.4.5 Treatment Surgical treatment is recommended in all cases.
Asymptomatic Aneurysms • Given the low morbidity and mortality rates of the intervention, exclusion of the aneurysm and aboveknee revascularization are recommended, by means of a (Dacron or PTFE) prosthetic by-pass.
Symptomatic Aneurysms • With clinical symptoms of rupture. Exclusion and haemostasis with revascularization by means of a prosthetic by-pass are recommended if there is no accompanying clinical picture of ischaemia. • With clinical symptoms of a pulsatile mass. Its exclusion and/or resection with prosthetic above-knee revascularization are recommended. • With symptoms of ischaemia due to thrombosis of the aneurysm whether or not it is accompanied by a distal embolization. Revascularization is performed by means of a by-pass using autologous material.
7.4.4.6 Prognosis • In asymptomatic aneurysms: the prognosis is excellent with high patency rates, and very low morbidity and mortality. • In symptomatic aneurysms: when there is rupture and a pulsatile mass in the thigh with no ischaemia in the extremity, prognosis is good. In cases of ischaemia requiring a femoro-popliteal by-pass graft, the prognosis is comparable to that obtained when performed for other arterial occlusions (patency 50–60% at 5 years with a limb-salvage rate of 70%).
467
468
7.4 Lower Extremity Aneurysms
7.4.5 Aneurysms of the Distal Branches 7.4.5.1 Epidemiology/Aetiology • Aneurysms of the distal arteries of the lower extremities are very rare and in most cases are secondary to traumatic injuries. • Approximately one-third of all cases are true atherosclerotic aneurysms and the other two-thirds are secondary to post-traumatic aetiologies [25]. • Extremely rare cases have been reported in other pathologies such as neurofibromatosis [36].
7.4.5.2 Clinical Symptoms • Most of them are asymptomatic and are diagnosed by chance during a vascular examination. • Occasionally they are diagnosed because of the appearance of a pulsatile mass somewhere along the course of an artery with no other accompanying symptoms.
7.4.5.3 Diagnosis • Physical examination can be relevant if a pulsatile mass is felt somewhere on the course of a distal artery. • Doppler ultrasound imaging may confirm the diagnosis and distinguish the affected artery. Usually it is the only test needed for performing surgery. • In cases with a doubtful diagnosis, arteriography is considered as the appropriate test to perform. Sometimes, an arteriogram can diagnose the pathology by chance during a study performed for some other reason.
7.4.5.4 Therapy • If they are small, a conservative attitude is recommended. • In cases of aneurysms >2 cm with good arterial compensation, exclusion and/or excision with proximal and distal ligation are preferred [25]. • If it affects a single distal branch, excision should be accompanied by revascularization by means of a graft using autologous material [13].
References 1. Arora S, Weber MA, Fox CJ, Neville R et al (2001) Common femoral artery ligation and local debridement: a safe treatment for infected femoral artery pseudoaneurysms. J Vasc Surg 33:990–993 2. Bowrey DJ, Osman H, Gibbons CP, Blackett RL (2003) Atherosclerotic popliteal aneurysms: management and outcome in forty-six patients. Eur J Vasc Endovasc Surg 25:79–81 3. Cairols M, Hernández E, Barjau E (2001) Management of peripheral arterial aneurysms. Up-date in vascular surgery. Foxwell and Davis, London, pp 99–109 4. Carpenter JP, Barker CF, Roberts B et al (1994) Popliteal artery aneurysms: current management and outcome. J Vasc Surg 19:65–73 5. Chua TP, Howling SJ, Wright C, Fox KM (1998) Ultrasound-guided compression of femoral pseudoaneurysm: an audit of practice. Int J Cardiol 63:245–250 6. Cox GS, Young JR, Gray BR, Grubb MW, Hertzer NR (1994) Ultrasound-guided compression repair of postcatheterization pseudoaneurysms: results of treatment in one hundred cases. J Vasc Surg 19:683–686 7. Cronenwett JL, Rutherford RB (2001) Femoral artery aneurysm. In: Decision making in vascular surgery. Saunders, New York, pp 136–145 8. Cronenwett Jl, Rutherford RB (2001) Popliteal artery aneurysm. In: Decision making in Vascular Surgery. Saunders, New York, pp 146–149 9. Dawson I, Sie RB, van Bochel JH (1997) Atherosclerotic popliteal aneurysm. Br J Surg 84:293–299 10. Dean SM, Olin JW, Piedmonte M, Grubb M, Young JR (1996) Ultrasound-guided compression closure of postcatheterization pseudoaneurysms during current anticoagulation: a review of seventy-seven patients. J Vasc Surg 23:28–35 11. Diwan A, Sarkar R, Stanley JC et al (2000) Incidence of femoral and popliteal artery aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg 31:863–869 12. Dorigo W, Pulli R, Turini F et al (2002) Acute leg ischaemia from thrombosed popliteal artery aneurysms: role of preoperative thrombolysis. Eur J Vasc Endovasc Surg 23:251–254 13. Fernández-Alonso L, Agúndez Gómez I (2002) Bilateral true aneurysms of popliteal and posterior tibial arteries. Eur J Vasc Endovasc Surg Extra 3:75–77 14. Gallard RB, Magee TR (2002) Management of popliteal aneurysm. Br J Surg 89:1382–1385 15. Gan JP, Lieberman DP, Pollock JG (2000) Outcome after ligation of infected false femoral aneurysms in intravenous drug abusers. Eur J Vasc Endovasc Surg 19:158–161
References
16. Gerasimidis T, Sfyroeras G, Papazagiou K et al (2003) Endovascular treatment of popliteal artery aneurysms. Eur J Vasc Endovasc Surg 26:506–511 17. Gouny P, Bertrand P, Duedal V et al (2000) Limb salvage and popliteal aneurysms: advantages of preventive surgery. Eur J Vasc Endovasc Surg 19:496–500 18. Hertz SM, Brener BJ (1997) Ultrasound-guided pseudoaneurysm compression: efficacy after coronary stenting and angioplasty. J Vasc Surg 26:913–918 19. Jarrett F, Makaroun MS, Rhee RY, Bertges J (2002) Superficial femoral artery aneurysms: an unusual entity? J Vasc Surg 36:571–574 20. Kang SS, Labropoulos N, Mansour MA, Michelini M et al (2000) Expanded indications for ultrasound-guided thrombin injection of pseudoaneurysms. J Vasc Surg 31:289–298 21. Kim DI, Huh SH, Lee BB, Ahn GH (2002) Tuberculous pseudoaneurysm of the superficial femoral artery: a case report and literature review. Eur J Vasc Endovasc Surg Extra 4:73–75 22. Kovenbach R, Pinter L (2003) Stent graft exclusion of asymptomatic popliteal artery aneurysms. Medium term results. Eur J Vasc Endovasc Surg 6:29–31 23. Laurian C, Paraskevas N, Elleuch N (2004) Anéurismes artériels des membres inferieurs. EMC – Cardiologie Angéologie 1:271–280 24. Levi N, Schroeder TV (1999) True and anastomotic femoral artery aneurysms: is the risk of rupture and thrombosis related to the size of the aneurysms? Eur J Vasc Endovasc Surg 18:111–113 25. McKee TI, Fisher JB (2000) Dorsalis pedis artery aneurysm: case report and literature review. J Vasc Surg 31:589–591 26. Möning SP, Walter M, Sorgatz S, Erasmi H (1996) True infrapopliteal artery aneurysms: report of two cases and literature review. J Vasc Surg 24:276–278
27. Norwood MGA, Lloyd GM, Moore S, Patel N et al (2004) The changing face of femoral artery false aneurysms. Eur J Vasc Endovasc Surg 27:385–388 28. Olsen DM, Rodriguez JA, Vranic M, Ramaiah V et al (2002) A prospective study of ultrasound scan-guided thrombin injection of femoral pseudoaneurysm: a trend toward minimal medication. J Vasc Surg 36:779–782 29. Rigdon EE, Monajjem N (1992) Aneurysms of the superficial femoral artery: a report of two cases and review of the literature. J Vasc Surg 16:790–793 30. Sandgren T, Sonesson B, Ahlgren AR, Länne T (1999) The diameter of the common femoral artery in healthy humans: influence of sex, age and body size. J Vasc Surg 29:503–510 31. Schellaek J, Smith RB, Perdue GD (1987) Nonoperative management of selected popliteal aneurysms. Arch Surg 122:372–375 32. Takagi H, Mizuno Y, Matsutomo M, Matsuno Y et al (2004) Aneurysm of the femoral artery occupationally exposed to a vibratory tool for more than 10 years. J Vasc Surg 39:1125–1127 33. Taylor BS, Rhee RY, Muluk S, Trachtenberg J et al (1999) Thrombin injection versus compression of femoral artery pseudoaneurysms. J Vasc Surg 30:1052–1059 34. Toursarkissian B, Allen BT, Petrinec D, Thompson RW et al (1997) Spontaneous closure of selected iatrogenic pseudoaneurysms and arteriovenous fistulae. J Vasc Surg 25:803–809 35. Vermeulen EGJ, Umans U, Rijbroek A, Rauwerda JA (2000) Percutaneous duplex-guided thrombin injection for treatment of iatrogenic femoral artery pseudoaneurysms. Eur J Vasc Endovasc Surg 20:302–304 36. Young LP, Stanley A, Menzoian JO (2001) An anterior tibial artery aneurysm in a patient with neurofibromatosis. J Vasc Surg 33:1114–1117
469
471
7.5 Buerger’s Disease of the Lower Extremities Fabrizio Benedetti-Valentini, Regina Stumpo, Ombretta Martinelli, Bruno Gossetti
7.5.1 Synonym • Thromboangiitis obliterans (TAO).
7.5.2 Definition • Thromboangiitis obliterans or Buerger’s disease has its own particular pathological features. • It is an inflammatory disease affecting both arteries and veins (angiitis), and it is an obstructive disease (obliterans) regularly complicated by thrombosis (thrombo). • Small peripheral vessels are mainly, if not exclusively, involved both in the lower and the upper limbs; coronaries, cerebral and visceral vessels are only seldom involved.
7.5.3 Epidemiology • TAO certainly originated with the use of tobacco, but it was only in 1908 that Leo Buerger [2] described its pathology, distinguished this form from atherosclerosis and gave it its name. • Although the pathogenetic mechanism is unclear TAO is always associated with smoking, particularly cigarette smoking, and also with chewing or snuff. • The earlier smoking begins, the larger the number of cigarettes smoked and the worse their quality, the higher the risk of developing TAO, resulting in disease progression, ulcers and amputations. • Even two to three cigarettes a day suffice for progression of the disease and worsening of the clinical condition and, for unclear reasons, marijuana smoking also contributes.
• TAO onset is usually well below 40 years of age; it may be observed above that age and sometimes in the fifties, but it usually occurs much earlier. • Men are more frequently affected than women, 3:1–5:1 in different experiences and countries. • The number of women sufferers seems to be on the increase [11] and the reason for this may be the larger number of women smokers. • TAO does not spare any race but at present its prevalence is higher in the Middle East, the Indian peninsula, the Far East and North Africa [8, 11]. • In Western Europe and North America it is relatively rare, but in some European countries it is increasing, probably due to immigration. • Generally speaking its prevalence may vary: 0.5–5.6% in Western Europe, 45–63% in India and 16–66% in Korea and Japan. • We cannot exclude that some variations may be due to the use of different diagnostic criteria.
7.5.4 Aetiology Only a small number of young, heavy smokers develop TAO, therefore some other factors are likely to be involved in its pathogenesis. Lots of research has been devoted to this problem and many observations made, but a lack of reliable evidence remains. Summarizing, there is: • An immunological mechanism, mainly an increased concentration of antiendothelial cell antibody [5] and increased cell sensitivity to collagen type I and III [14]. • A hypercoagulable state, such as an enhanced platelet response to serotonin [13]. • A vasomotor mechanism, such as impaired endothelium-dependent vasorelaxation in peripheral vasculature [10].
472
7.5 Buerger’s Disease of the Lower Extremities
• A genetic component, for example variations in human leukocyte antigen haplotypes were found in different populations [11]. TAO is an inflammatory, noninfectious disease very different from any other vasculitis. Distinctive histopathological features of the first or acute phase of TAO are (Fig. 7.5.1): • segmental distribution with interposed normal appearing areas • endothelial asymmetrical proliferation • preservation of the normal structure of the vessel and particularly of the inner lamina elastica • infiltration of all three layers of the wall • highly inflammatory thrombus with giant cells and micro abscesses and the presence of eosinophils in moderate number • extension of the disease to surrounding tissues (neuritis). An intermediate phase follows, in which: • fibrosis of the vessel wall and surrounding tissues as well as organization of the thrombus begins • cellularity is decreased, but distinctive features are still recognizable.
7.5.5 Symptoms • The identikit of a patient with TAO is young, a heavy smoker, has severe rest pain and ulcers of the toes (Fig. 7.5.2), cyanosis and cold sensitivity of the fingers, is nondiabetic, has a presenting history of actual superficial phlebitis and has normal or negative inflammatory/immunological markers. • Typically the lower extremities are the first and more severely affected, but the upper extremities and mainly the fingers are also involved in most cases. • Rather frequently, rest pain of the toes or forefoot or even ulcers appear prior to intermittent claudication and following one or more bursts of migrating phlebitis [1, 18]. • The pain is severe and resistant to analgesic medications. • The patient may also complain of sensitivity disturbances and/or cold sensitivity with or without clear Raynaud’s phenomenon or erythema or cyanosis [12].
The end or chronic phase shows: • advanced fibrosis of vessels and surrounding tissues • organization of the thrombus; the diagnostic peculiarities are no longer present.
Fig. 7.5.1 Thromboangiitis obliterans (TAO) in acute phase. Note preservation of inner lamina elastica, infiltration of all layers of the wall and highly inflammatory thrombus
Fig. 7.5.2 Early ulcers of the toes with rest pain but no calf claudication
7.5.6 Diagnosis
• Sometimes brief intermissions of symptoms are reported, particularly in the hot season or during periods of abstinence from smoking.
7.5.6 Diagnosis 7.5.6.1 Recommended European Standard Diagnostic Steps of Investigation Inspection • Will disclose digital cyanosis, ulceration or gangrene.
Palpation • Femoral pulses are present and normal with no bruits; popliteal pulses can be palpated in some cases and even pedal pulses can be found in a few patients in the early phase of the disease and very distal lesions. • In such cases the ankle/branchial index can be normal; however, in most patients there is a crucial drop of pressure in the distal arteries.
Blood Laboratory Investigations • Normal or negative for immunological or infectious disorders.
Duplex Scanning • Very contributory; it identifies the distal arterial lesions typical of TAO and rules out the presence of proximal disease. • It helps also to exclude aneurysms (aortic, femoral and popliteal), ulcerated plaques, popliteal entrapment, etc. • Venous disease can also be seen or confirmed.
Angiography • Excellent images can then be obtained by magnetic resonance angiography, which, with the use of some recent and refined techniques, depicts clearly the distal lesions, providing some clues for diagnosis.
Fig. 7.5.3 MR angiography shows multiple arterial lesions below the knee with segmentary occlusions and corkscrew-like collateral circulation
• Conventional arteriography is no longer mandatory at present since the disease can be identified otherwise and the appropriate treatment be established anyway. • Both MR angiography and conventional arteriography can present findings that are diagnostic in an adequate clinical setting (Figs. 7.5.3–7.5.6).
473
474
7.5 Buerger’s Disease of the Lower Extremities
Fig. 7.5.4 Conventional arteriography of the lower limbs shows normal appearing main trunks and occlusive distal disease particularly of the crural and pedal vessels
7.5.6 Diagnosis
Fig. 7.5.5 Arteriography of an upper limb in a patient with TAO shows segmentary occlusions in the vessels in the forearm and hand
• Small- to medium-calibre arterial disease in the lower and sometimes in the upper limb with normal proximal arteries and noninvolved segments is very suggestive. • Dilatation of tiny collateral vessels around the occluded arteries, some of them belonging to the vasa vasorum, give the picture called the corkscrew [4]. • When none or few distal vessels can be seen, the appearance is known as a “winter tree” which is also peculiar, but not frequently seen [1]. • Grossly ulcerated and embolizing lesions can also be excluded.
Other • Additional information can be obtained by plethysmography, capillaroscopy and TcpO2/TcpCO2 measurements, but ultimate diagnosis can only be made after exhaustive differential studies.
Fig. 7.5.6 Conventional arteriography of a lower limb showing the “winter tree” appearance with patent main trunk and no side branches
475
476
7.5 Buerger’s Disease of the Lower Extremities
7.5.7 Treatment 7.5.7.1 Conservative Treatment Recommended European Standard Therapeutic Steps • Abstinence from tobacco. Tobacco is poison for patients with TAO: they must stop smoking once and for all. Passive smoking has not been proven as harmful, but it certainly does not help and therefore should be avoided. Measuring nicotine or cotinine in the urine can check abstinence from tobacco in any form. Stubborn smokers (even smoking two to three cigarettes per day keeps the disease active) are much more likely to face amputations than those who quit smoking. If large ischaemic ulcers are not present when the patient stops smoking, then with adequate treatment they will very likely be spared amputations [1, 11, 12]. • Avoidance of exposure to low temperatures. • Local care, ulcer dressing as needed. • Analgesics. Pain increases vasospasm, accelerating and worsening ischaemia, and bounds the patient to keep his or her legs constantly downwards with consequent oedema and danger of infection. In resistant cases epidural anaesthesia may be needed for some days. • Prostanoids and particularly iloprost should be used as a vasoactive medication [3]. There is reliable evidence that daily intravenous infusion every 6 h of this prostaglandin analogue is highly effective at reducing or abolishing rest pain and at healing ulcers [7]. Oral preparation is not as effective as was previously suggested. • Calcium channel blockers are useful when a clear vasospastic condition is present; steroids may also be used to contain inflammation. Other drugs or methods may be applied, although their effectiveness has never been demonstrated, since they are beneficial episodically. Noninvasive management should always be tried first [6, 18].
7.5.7.2 Surgery Recommended European Standard Surgical Procedures • Endovascular techniques may have some role as an adjunct to basal treatment. Regional or selective thrombolysis was used with occasional success and recently percutaneous transluminal angioplasty (PTA) and stenting of the peroneal and tibial arteries have given some early benefit. • Lumbar sympathectomy has long been known to provide pain control and to help ulcer healing, mainly if carried out during the early acute phase of the disease (Table 7.5.1). In our experience sympathectomy has been crucial in many cases in avoiding amputation and recuperating a viable limb. Thoracic sympathectomy through thoracoscopy, though theoretically useful, is of unproven value. • In some cases where a distal “workable” segment of an artery exists and there is a reasonable outflow, a distal by-pass can be done using autogenous saphenous vein according to various techniques as needed. In this field, experiences vary very much with geographical location: in Western Europe and North America favourable cases for arterial repair are encountered rather rarely, whereas in Turkey [16] and Japan [15, 17] distal by-pass grafts have been carried out in a significant percentage of patients classified as TAO with an acceptable success rate. Sayin at al. [16] extensively applied lumbar sympathectomy in patients with TAO, but were also able to carry out by-pass repair in a significant number of cases. Long-term patency was reasonable and the limb-salvage rate rather high; a period of by-pass function, although brief, seems to contribute to avoiding amputation. Shionoya [17] was also able to treat with by-pass grafts: 17.4% of his patients with TAO and in his series had a major amputation rate as low as 2.7%; 51% of his patients were treated Table 7.5.1 Surgical management of thromboangiitis obliterans: type and results Sympathec- By-pass Amputation (%) tomy (%) (%) Minor Major Olin et al. [12]
26
–
Shionoya [17]
51
17.4
Sayin et al. [16]
85
7.4
26
18 –
3
2.7 1.85
References
by lumbar sympathectomy. Sasajima at al. [15] treated 61 patients with TAO by autogenous saphenous vein by-pass, below the knee in the vast majority; they were able to obtain good primary and secondary patency rates with a large difference between those who continued to smoke and those who stopped smoking. Further experience is obviously needed.
Additional Useful Surgical Procedures • Omental transplantation was used in a similar way as in the past for left ventricle revascularization: the results remain uncertain. • Spinal cord stimulation can be of some help in selected patients to provide relief from pain and help ulcer healing.
7.5.7.3 Differential Diagnosis A variety of conditions should be ruled out, including: • Autoimmune diseases • Scleroderma/CREST syndrome • Lupus erythematosus • Other connective tissue diseases • Infectious vasculitis • Antiphospholipid antibody syndrome • Takayasu’s arteritis • Vasospastic disorders • Early atherosclerosis • Embolism • Diabetes • Chronic reflex sympathetic dystrophy • Occupational neurovascular disorders. Appropriate investigations should be applied accordingly [9, 12].
7.5.7.4 Prognosis • Each of the suggested drugs and techniques can be useful in the management of TAO but none of them really works if the patient doesn’t stop smoking or using tobacco in any form. • Patients have the same life expectancy as the normal population of the same age, but frequently face even multiple amputations [1].
References 1. Benedetti-Valentini F, Gossetti B (1993) Buerger’s disease (thromboangiitis obliterans). In: Benedetti-Valentini F, Bertini D, D’Addato M, Marcialis A (eds) Surgical vascular diseases. Masson, Paris, pp 92–95 2. Buerger L (1908) Thromboangiitis obliterans: a study of the vascular lesions leading to presenile spontaneous gangrene. Am J Med Sci 136:567–580 3. De Gaetano G, Bertelé V, Cerletti C (1990) Mechanism of action and clinical use of prostanoids. In: Dormandy JA, Stock G (eds) Critical leg ischaemia: its pathophysiology and management. Springer, Berlin Heidelberg New York, pp XXXVII–XLI, pp 117–137 4. Diehm C, Allenberg JR, Nimura-Eckezt K, Veith FJ (2000) Color atlas of vascular diseases. Springer, Berlin Heidelberg New York, pp 204–213 5. Eichhorn J, Sima D, Lindschau C, Turowski A, Schmidt H, Schneider W, Heller H, Luft FC (1998) Antiendothelial cell antibodies in thromboangiitis obliterans. Am J Med Sci 315:17–23 6. European Consensus Document on Critical Limb Ischemia (1990) In: Dormandy JA, Stock G (eds) Critical leg ischemia: its pathophysiology and management. Springer, Berlin Heidelberg new York, pp XXXVI–XLI 7. Fiessinger JN, Schafer M (1990) Trial of iloprost versus aspirin treatment for critical limb ischaemia of thromboangiitis obliterans. The TAO Study. Lancet 335:555–557 8. Hill GL, Moeliono J, Tumewu F, Brataamadja D, Tohardi A (1973) The Buerger syndrome in Java: a description of the clinical syndrome and some aspects of its aetiology. Br J Surg 60:606–613 9. Kemler MA, Barendse GAM, van Kleef M (2000) Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med 343:618–624 10. Makita S, Nakamura M, Murakami H, Komoda K, Kawazoe K, Hiramori K (1996) Impaired endothelium-dependent vasorelaxation in peripheral vasculature of patients with thromboangiitis obliterans (Buerger’s disease). Circulation 94 [Suppl II]:II211–II215 11. Olin JW (2000) Thromboangiitis obliterans (Buerger’s disease) In: Rutherford RB (ed) Vascular surgery. Saunders, Philadelphia, pp 350–364 12. Olin JW, Young JR, Graor RA, Rushaupt WF, Bartholomew JR (1990) The changing clinical spectrum of thromboangiitis obliterans (Buerger’s disease). Circulation 82 [Suppl IV]:3–8 13. Pietraszek MH, Chaudhury NA, Koyano K, Sakaguchi S, Kamiya T, Urano T, Takada Y, Takada A (1990) Enhanced platelet response to serotonin in Buerger’s disease. Thromb Res 60:241–146
477
478
7.5 Buerger’s Disease of the Lower Extremities
14. Roncon de Albuquerque R, Delgado L, Correia P, Torrinha JF, Serrao D, Braga A (1989) Circulating immune complexes in Buerger’s disease. J Cardiovasc Surg 30:821–825 15. Sasajima T, Kibo Y, Inaba M, Goh K, Aruma N (1997) Role of infrainguinal bypass in Buerger’s disease: an eighteenyear experience. Eur J Vasc Endovasc Surg 13:186–192
16. Sayin A, Bokzurt AK, Tuzun H, Vural FS, Erdog G, Ozer D (1993) Surgical treatment of Buerger’s disease: experience with 216 patients. Cardiovasc Surg 1:377–380 17. Shionoya S (1993) Buerger’s disease: diagnosis and management. Cardiovasc Surg 1:207–214 18. TASC (Trans-Atlantic Inter-Society Consensus) (2000) Management of peripheral arterial disease (PAD). Eur J Vasc Endovasc Surg 19 [Suppl A]:S52, S160
479
7.6 Popliteal Artery Entrapment and Popliteal Adventitial Cystic Disease Jon Largiadèr and Bernhard Nachbur
7.6.1 Definition • Carter and Eban [1] were the first to report bilateral abnormality of the popliteal artery and gastrocnemius muscles, in 1962. • The term popliteal entrapment was then coined in 1965 by Love and Whelan [6], the same year that Hamming and Vink [3] published their clinical report of popliteal artery obstruction at an early age. • Popliteal artery entrapment is characterized by extrinsic compression of the popliteal artery, while in adventitial cystic disease the artery is compressed by a cyst located in the adventitia of the artery.
• In type I, the artery is displaced medially around the normally arising medial head of the gastrocnemius. • In type II the popliteal artery runs a normal course but is compressed by the medial head of the gastrocnemius muscle, which has a more lateral insertion. • In type III, entrapment of the popliteal artery is due to a lateral accessory slip of the medial head of the gastrocnemius muscle. • In type IV the popliteal artery is entrapped by the popliteus muscle or a fibrous band.
7.6.3 Symptoms 7.6.2 Epidemiology/Aetiology • Popliteal arterial entrapment and adventitial cystic disease account for 2–5% of all popliteal artery occlusions. • Popliteal entrapment is roughly 10 times more common than adventitial cystic disease. • The aetiology of adventitial cystic disease is not yet fully clarified. • The occasional presence of a stalk or tubular connection with the knee joint, the similarity of the mesenchymal lining of the cyst to synovial endothelium and the presence of hyaluronic acid within the cyst suggest a relationship between cyst and joint [5]. • Entrapment syndrome is caused by either an anatomical variation of the course of the popliteal artery or a more lateral insertion of the medial head of the gastrocnemius. • Four types of popliteal artery entrapment have been recognized [4] (Fig. 7.6.1):
• Popliteal entrapment is much more common than generally assumed and it affects mainly young males, often top athletes. • Intermittent claudication is the first symptom and as intimal pathology increases the popliteal artery can occlude and in doing so give rise to peripheral embolization. Intermittent pain on walking can then progress to continuous pain at rest. • Occasionally poststenotic aneurysm formation can be observed and this may also be the cause of peripheral embolization. • In adventitial cystic disease, intermittent claudication is likewise the typical first symptom. • Symptomatology is dependent upon and closely related to the intracystic pressure. • It is possible that the cystic contents drain into the joint thereby easing pressure within the cyst.
480
7.6 Popliteal Artery Entrapment and Popliteal Adventitial Cystic Disease
Fig. 7.6.1 Classification of popliteal entrapment according to Insua [4]
7.6.4 Diagnosis 7.6.4.1 Recommended European Standard Diagnostic Steps of Investigation
• As myointimal changes caused by repetitive trauma increase, the popliteal artery will occlude and this can lead to continuous pain at rest and even gangrene. • Additionally, with or without poststenotic aneurysm formation, peripheral embolization can change the clinical situation dramatically.
Imaging In principle, the same technical equipment and methods are applied for the diagnosis of adventitial cystic disease and popliteal entrapment syndrome as are commonly used for atherosclerotic occlusive disease: • Doppler sonographic ankle systolic pressure measurement • Duplex sonography • Digital subtraction angiography (DSA) • Computed tomography • Magnetic resonance imaging (MRI).
History • Important hints of adventitial cystic disease and popliteal entrapment can be drawn from the patient’s history. • In both diseases the first symptoms are those of intermittent claudication: pain arising in the calf and the foot after a certain walking distance.
Stress Tests • For the diagnosis of the popliteal entrapment syndrome, stress tests are of considerable importance. • By active extension or passive dorsiflexion of the foot, the pedal pulses can be suppressed. • The disappearance of peripheral arterial pulsation can be documented either by ankle systolic pressure measurement or by oscillographic pulse wave recording. • A deviation of the popliteal artery, such as in type I entrapment, can be identified by DSA well before important angiomorphological changes have occurred and point the way to a correct diagnosis (Fig. 7.6.2). • With the advent of complete segmental occlusion of the popliteal artery, accompanied by peripheral embolism, the differentiation between primary and secondary atherosclerotic disease becomes difficult if suggestive symptoms in the patient’s history cannot be traced.
7.6.5 Treatment
• With early surgical repair, irreversible secondary manifestations such as the formation of an aneurysm or peripheral embolism can be avoided. • Therefore, the success of surgical therapy of adventitial cystic disease and popliteal entrapment is dependent upon securing diagnostic clarification from the start in order to avoid secondary complications. • Because popliteal entrapment may be bilateral [1] it is important to examine the contralateral limb accordingly as well.
7.6.5.1 Recommended European Standard Surgical Procedures Popliteal Entrapment Syndrome Fig. 7.6.2a,b Popliteal entrapment. a Distinct deviation of the artery medially with constriction in the knee joint. b Situation during stress testing with total occlusion in muscular entrapment
The Scimitar Sign • The telltale sign of adventitial cystic disease is the hourglass or crescent-shaped partial or subtotal occlusion of the popliteal artery seen in DSA, the so-called scimitar sign. • With CT and especially DSA, the morphological relationship between cyst, knee joint and artery can be evaluated and the exact location of the adventitial cyst can be determined.
7.6.5 Treatment • Noninvasive methods such as percutaneous guided aspiration [2] or a stent implantation cannot prevent recurrence and are therefore unsuitable for definitive treatment of adventitial cystic disease. • The correct therapy of both adventitial cystic disease and entrapment syndrome is surgical, even before initial changes within the arterial wall have become evident. • One way or another, the pathological changes in the vascular wall get worse and give rise to irreversible secondary atherosclerotic occlusion.
• In order to offer optimal therapy the vascular surgeon must be capable of mastering a wide range of surgical options. • In the surgical management of popliteal entrapment syndrome the stepwise approach to the fossa poplitea has proven to be worthwhile. • By applying this method, complete access to the popliteal artery can be gained from where it exits the adductor canal down to the popliteal bifurcation. • This approach allows for all therapeutic options in early disease stages.
Entrapment Syndrome • In early entrapment syndrome (Insua types I and II), orthotopic repositioning of the popliteal artery should be envisaged (Figs. 7.6.2–7.6.6). • To this avail the popliteal artery must be transected at the distal end of entrapment, then dissected out behind the medial head of the gastrocnemius muscle, replaced in the orthotopic position and reattached endto-end to the distal stump of the popliteal artery with interrupted sutures.
Secondary Atherosclerotic Manifestations • In the presence of secondary atherosclerotic manifestations, it might be possible to perform endarterectomy with removal of an appositional thrombus or an eversion procedure with re-anastomosis end-to-end.
481
482
7.6 Popliteal Artery Entrapment and Popliteal Adventitial Cystic Disease
Fig. 7.6.3 Intraoperative situation with deviation of the artery behind the medial head of the gastrocnemius with vein and nerve running an orthotopic course
Fig. 7.6.4 Transverse arteriotomy distal to occlusion. Mobilization and releasing of artery behind the muscle and orthotopic advancement
Fig. 7.6.5 Endarterectomy specimen removed by eversion
Fig. 7.6.6 Orthotopic re-anastomosis of the endarterectomized artery
• With this technique the muscle insertion of the medial head of the gastrocnemius need not be transected. • This has the advantage that a released muscle will not slip into the already tight fossa poplitea and cause a purely muscular entrapment; thereby, the proper functioning of the gastrocnemius muscle is not interfered with. • In entrapment types III and IV the popliteal artery runs an orthotopic course but is impinged upon by musculofibrous bands that need to be transected and resected. • When secondary complications are manifest and the popliteal artery is either occluded or aneurysmal, re-
section of the diseased arterial segment and replacement by interposition of autologous vein is the treatment of choice.
Femoro-distal Vein By-pass • If traumatic disease has progressed to such an extent that the length of the arterial occlusion necessitates the distal anastomosis be to a crural artery, then it is preferable to perform a conventional femoro-distal vein by-pass.
7.6.6 Special Remarks
• In this case the medial approach to both the superficial femoral artery above the knee and the infrapopliteal crural arteries below the knee is used.
Treatment of Adventitial Cystic Disease • Treatment of adventitial cystic disease demands careful dissection to allow for identification and transection of the tubular stalk close to the joint. • The cyst must be completely eradicated in order to avoid recurrence (Figs. 7.6.7–7.6.10). • As a result, the remaining vascular wall may become so thin as to rupture, for which reason it might be recommended to resect the arterial segment and replace it with autologous vein. • It has, however, recently been shown that the danger of rupture is not real [7].
7.6.6 Special Remarks • It is most important to be aware of the fact that intermittent claudication is the first sign of popliteal entrapment and usually affects young patients. For this reason a high index of suspicion is of the essence. In our personal experience the youngest patient was 7 years old and presented with poststenotic dilatation and peripheral embolism. • Intermittent claudication in the patient’s history must always evoke the suspicion of popliteal artery entrapment or adventitial cystic disease. Moreover, popliteal entrapment often occurs bilaterally. However, symptomatology in the contralateral limb is usually discreet. In the personal experience of the authors, about 30% of all entrapments are bilateral. • In the early stages of disease and before segmental arterial occlusion has occurred, stress testing is most meaningful for the detection of entrapment. In rare cases entrapment is purely muscular, or in other words the popliteal artery runs an orthotopic course and the gastrocnemius muscular insertion is normal. In such cases some authors recommend operative revision and arteriolysis. In our personal experience, this method has proven unsatisfactory and the symptoms remained after the operation. However, it should be noted that this form of entrapment only occurs in top athletes.
Fig. 7.6.7 Cystic adventitia degeneration. Left: preoperative condition with crescent-shaped constriction of the lumen. Right: postoperative condition after removal of cystic change
• For diagnostic purposes both Duplex sonography with and without stress testing and MRI angiography have proven their value. By applying these two methods both adventitial cystic disease and the abnormal popliteal arterial course with entrapment can be detected. In future, MRI angiography with three-dimensional imaging will become the method of choice for visualization of adventitial cystic disease and popliteal artery entrapment. • In view of the fact that disease progression is relentless, surgical therapy at an early stage becomes important. Secondary complications – myointimal apposition, segmental occlusion, aneurysm formation and peripheral embolism – can thereby be prevented. • Under the given circumstances, long-term prognosis is good for popliteal entrapment as well as for adventitial cystic disease, provided that complete eradication
483
484
7.6 Popliteal Artery Entrapment and Popliteal Adventitial Cystic Disease
Fig. 7.6.8 Intraoperative finding with the presence of a stalk (arrow) connecting the cyst to the knee joint
Fig. 7.6.9 Condition after removal of cyst stalk kept open by pincers
References 1
2
3 4 5
Fig. 7.6.10 View during dissection of the artery from the cystic entrapment. The proximal part has been released with the cystic material distal still in situ. Observe the ideal layer
of the cyst has been carried out. A 5-year symptomfree rate of over 80% can be obtained.
6 7
Carter AE, Eban R (1962) A case of bilateral development abnormality of the popliteal arteries and the gastrocnemius muscles. Br J Surg 51:518 Do DD, Braunschweig M, Baumgartner I, Furrer M, Mahler F (1997) Adventitial cystic disease of the popliteal artery; percutaneous guided aspiration. Radiology 2303:743–746 Hamming JJ, Vink M (1965) Obstruction of the popliteal artery at early age. J Cardiovasc Surg 6:516 Insua JA, Young JR Humphries AW (1970) Popliteal artery entrapment syndrome. Arch Surg 101:771 Largiadèr J, Leu HJ (1984) Sogenannte zystische AdventitiaDegeneration der Arteria Poplitea mit Stielverbindung zum Knieglelenk. VASA Bd 13:267–371 Love JW, Whelan TJ (1965) Popliteal artery entrapment syndrome. Am J Surg 109:620 Stierli P, Mauch J, Koella C, Huber A, Eugster T, Gürke L (2005) Circumferential removal of the adventitia for cystic degeneration of the popliteal artery (short note). Br J Surg 92(1):56–57
485
7.7 Vascular Trauma of the Lower Limb Bernhard Nachbur
Whilst many problems affecting the vascular system may be managed by vascular surgical procedures or alternatively by minimally invasive catheter-directed interventions, the treatment of vascular injury and definitive care thereof are unquestionably the unchallenged fiefdom and responsibility of the well-trained vascular surgeon, whose clinical and diagnostic acumen, expediency and operative skill are in demand. • It is important to recognize vascular injury because of the danger of limb-threatening ischaemia if arteries are involved. • Venous injury is also of significance at anatomical sites where venous flow passes through a bottleneck, such as the popliteal or the external iliac vein. • Disturbance or disruption of venous return can give rise to venous hypertension, compartment syndrome and necrosis of striated muscle and nerve tissue. The vascular surgical techniques for the treatment of vascular trauma have been repeatedly described in the literature and are most authoritatively and comprehensively dealt with by Barros D’Sa [1]. Hafez, Woolgar and Robbs report the outcome of the surgical management of lower limb arterial injury (LLAI) in a busy metropolitan vascular unit in 550 patients with 641 arterial injuries [5]. Their results represent state-of-the-art standard, with a limbsalvage rate of 84% and survival at 98.5%. Failed arterial reconstruction (occluded graft) carried by far the greatest risk of limb amputation, followed by combined aboveand below-knee vascular injury and tense compartment. Stab wounds are the least likely to lead to amputation; high-velocity firearm injuries the most likely to do so.
7.7.1 The Problem The problem is not solely a question of how to treat vascular trauma, the essential principles of which remain un-
changed, but also how to recognize and avoid missing a vascular injury when the clinical picture is not obvious or dominated by profuse external bleeding and decreasing blood pressure. • Vascular trauma can be concealed, unexpected and occur in association with fractures or orthopaedic operations that are apt to distract attention from an underlying lurking vascular problem. • If missed during primary care, however, the result of ischaemia of the lower limb can have disastrous medico-legal consequences and – with the growing assertiveness of health consumers and their demands in malpractice suits – can become devastating for both the patient and the responsible physician. Time is therefore of the essence. • The tolerance of muscle and nerve tissue of the lower limbs to ischaemia is limited to very few hours, following which reconstruction (restoration) of arterial vascular patency may be technically successful, but, if too late, will be followed by: • ischaemia-reperfusion injury [2] • muscle necrosis with contracture • compartment syndrome • complex regional pain syndrome [11] • disabling efferent neuralgia [12] • or even major amputation. • Ischaemia tolerance depends upon the duration and the degree of ischaemia and on how well a supportive collateral circulation can be established within the short time following vascular injury. Ischaemia may therefore vary from complete to partial and is not always a yes or no situation. For example, a fracture of the femur shaft may, due to the proximity of bone and vessel, occlude the superficial femoral artery (Fig. 7.7.1), which is usually a consequence of intimal fracture, intimal dissection and ensuing intravascular thrombosis (Figs. 7.7.2, 7.7.3). In otherwise healthy and young individuals such an event catches a vascular system by surprise because the vasculature is unpre-
486
7.7 Vascular Trauma of the Lower Limb
pared; collateral flow via the deep femoral artery is not sufficiently developed as it is for instance in patients with chronic occlusive arterial disease, and the symptoms of ischaemia might be missed. Persistent pain in the toes and numbness may easily be overlooked and are frequently misinterpreted as temporary neurological deficits attending the underlying bone fracture. It is not uncommon for unsuspecting physicians to overlook a looming threat that can be associated with blunt injury.
7.7.1.1 Encountering Vascular Injury The present-day surgeon may encounter vascular injury of the lower limb when they are a resident, a registrar or an intern practising general surgery and traumatology in a community hospital, as an orthopaedic surgeon in specialized practice, or as a physician going to war serving in noncombatant roles. Vascular injury will present differently in the various activities, but awareness of possible ischaemia is necessary whenever and wherever.
7.7.1.2 How Can Ischaemia of the Lower Limb be Detected or Ruled Out Reliably? In a prospective study on healthy individuals without degenerative arterial disease having incurred knee dislocation, it has been clearly shown that the ankle/brachial index (ABI) is a rapid, reliable, noninvasive screening tool for diagnosing or ruling out vascular injury of the lower limb [7]. The index is a quotient easily derived from
Fig. 7.7.1 Fracture of the femur shaft causing thrombotic occlusion of the superficial femoral artery
Fig. 7.7.2 Thrombotic occlusion of the right common iliac artery after traumatic compression of the abdomen by a steamroller. A slight dilatation and a discreet darkish hue are telling
Fig. 7.7.3 The same artery as in Fig. 7.7.2. A dissected intimal flap is clearly visible within fresh thrombus above and below. This situation requires careful intimectomy with distal tack sutures to avoid further dissection
7.7.1 The Problem
487
488
7.7 Vascular Trauma of the Lower Limb
the blood pressure at the ankle and the systemic pressure measured at the arm and can be performed in a matter of 1–2 min [6]. In this study patients with an ABI of 0.90 or higher did not have arterial injury, whilst in all patients with an ABI of less than 0.90 there was arterial injury. The sensitivity, specificity and positive predictive value of an ABI lower than 0.90 was 100%. Duplex evaluation or angiography with modern digital subtraction methods is therefore indicated only in those patients with an ABI of less than 0.90. This is valid for all arterial injuries of the lower limb. This rule is, of course, not without restrictions, i.e. elderly patients in need of orthopaedic surgery may have pre-existing chronic occlusive arterial disease associated with an ABI of less than 0.90. It is therefore essential to have measured the ABI both before and after orthopaedic surgery, for comparison. It is most important to realize that it is not enough to search for a Doppler signal at the ankle or the foot and then to be reassured by an acoustic signal alone without having measured the ABI!
7.7.2 Mechanisms of Injury 7.7.2.1 Sharp Injury In sharp injuries the vascular lesions are caused by direct penetration and give rise to vascular perforation, transection or dissection. The consequence is haemorrhage with the danger of exsanguination, hypotension and haemodynamic shock, the treatment of which is standard. Fortunately a transected artery is apt to bleed less than a perforated or partially torn artery. Haemostasis in the case of a transected artery may be effected as follows: the contractile tension of the lamina elastica interna shortens the artery, which constricts as the transected inner layers approach each other and then roll in, thereby occluding the vessel. Open warfare, civil war, terrorism and natural disasters all result in the assignment of doctors, especially surgeons, to scenes of extreme violence to which they were not exposed to previously in civilian life [4]. In war, management of vascular injury is primarily aimed at saving life and the chances of performing vascular reconstruction for limb salvage are minor (less than 2% during the civil war in Afghanistan). • Missile wounds caused by bullets from assault rifles, blast injuries inflicted by land mines, suicide bombs
•
•
•
•
•
and the carnage caused by improvised explosive devices (IED) are the distinguishing marks of modern warfare and terrorist suicide attacks. In the case of explosive wounds, reconstructive arterial surgery is rarely possible owing to the magnitude of vital structure injury, and major lower limb (guillotine) amputation is therefore usually unavoidable. In many cases, such as in the Afghan civil war, war-wounded present with limbs that have already been torn away by explosive devices. In principle, bleeding wounds are controlled by packing if the wounded person is to be transported to a centre with a higher level of surgical capacities. War wounds are infected and therefore the use of synthetic material, be it for internal fixation of bone or arterial reconstruction, is strictly contraindicated (ICRC [3]). Stab wounds affect the upper limb far more often than the lower limb, where the self-inflicted butcher’s injury is best known. This mechanism involves the external iliac artery or the common femoral artery and bleeding can be torrential or even fatal if immediate and direct digital compression all the way to the operating theatre is not carried out effectively! Bleeding can easily be controlled and the clean-cut artery reconstructed by using the lateral retroperitoneal approach. Although clean, the cut segment of artery should be resected whereupon an end-to-end anastomosis may be envisaged.
7.7.2.2 Blunt injury Blunt injury is indirect and causes: • contusion • compression • constriction or strain, by overextension and overstretching of arteries.
Trauma of the Thigh The mechanisms of blunt, nonpenetrating injuries are among the most treacherous because the hidden pathology might not be obvious at first sight. • Conspicuous signs of vascular injury such as a rapidly waxing haematoma or external haemorrhage are missing.
7.7.2 Mechanisms of Injury
• Fractures of the femur shaft, for instance, are not infrequently associated with collateral damage to the adjacent superficial femoral artery, as illustrated in Fig. 7.7.1. Sometimes the orthopaedic surgeon or the traumatologist has performed internal fixation and stabilization of a fracture, totally unaware of an accompanying arterial injury as depicted in Fig. 7.7.4 (a fracture of the femur shaft stabilized with a plate, Fig. 7.7.5). Whether the result is contusion or overstretching, the consequences are much the same. Whilst the elastic external layers of the artery can adapt to the indirect forces of trauma, there is a fracture of the intima which rolls into the lumen. Subsequently thrombosis occurs and the vascular lumen occludes. Figure 7.7.2 shows the appearance of the contused artery with the slight vascular dilatation and the discreet and telling dark hue resulting from the subintimal haematoma. Following longitudinal incision of the artery, thrombus occludes the artery both above and beyond the dissected intimal flap, as clearly visible in Fig. 7.7.3. This mechanism is typical of most forms of indirect injury of arteries and is not associated with any signs of haemorrhage. The classical signs of ischaemia (pain, paraesthesia, anaesthesia, disturbance of motor function) are present and can be observed, as long as they are looked for and not misinterpreted. In these situations measuring the ABI can be most helpful and reassuring.
Trauma of the Knee Trauma of the knee joint holds a special place for two main reasons: • The potentially serious threat to limb salvage in the case of arterial injury. • The policy formulated around the use of intraluminal shunts [1], which has shown the way for exemplary close co-operation between vascular and orthopaedic surgeons. Simple or complex fractures around the knee joint and knee dislocation are sometimes associated with injury to the popliteal artery. Here the proximity of bone and artery is especially close (Fig. 7.7.5) and the pressure exerted by the haematoma attending bone fractures can critically hamper the development of collateral circulation. If occlusion of the popliteal artery is missed or not managed
Fig. 7.7.4 This segmental occlusion of the superficial femoral and popliteal artery remained unsuspected during stabilization of a fractured femur shaft with a steel plate
489
490
7.7 Vascular Trauma of the Lower Limb
Fig. 7.7.5 Schematic illustration of the mechanisms of vascular injury caused by posterior knee dislocation and rupture of the posterior cruciate ligament (left panel) and supracondylar fracture (right panel)
in time the amputation rate will be very high. A high index of suspicion is therefore in demand and – as stated repeatedly – measurement of the ABI is invaluable [7]. Interestingly, it has been shown [9] that in knee dislocations it is rupture of the posterior cruciate ligament only that is associated with popliteal artery injury, not rupture of the anterior cruciate ligament.
7.7.2.3 Iatrogenic Hip Surgery • Orthopaedic surgery of the hip joint is especially prone to causing vascular injury involving the external iliac, the common, deep and superficial femoral arter-
ies as well as the lateral and medial circumflex femoral arteries. • The injury can manifest itself by an unexpected sudden gush of blood and is especially disturbing when, for instance, the tip of a long-pointed Hohmann retractor (which hooks into the pelvis above the anterior lip of the acetabulum) is dug into the external iliac artery. This calls for immediate management and control of haemorrhage with restoration of vascular patency. • Potentially far more dangerous are arterial injuries that remain concealed and missed if limb perfusion is not checked at the end of the orthopaedic intervention. Measurement of the ABI is an invaluable method for ascertaining freedom from arterial injury, as stated earlier, and the first step is to be suspicious, especially
7.7.2 Mechanisms of Injury
in the elderly patient with probable atherosclerotic arterial disease. Other mechanisms of vascular trauma occurring during hip surgery that should be borne in mind include: • Intimal tear at the femoral bifurcation with subsequent thrombotic occlusion (Fig. 7.7.6) is a not uncommon hidden cause of limb ischaemia. It is most likely that this happens by overextension in patients with pre-existing atherosclerotic arterial disease during the manoeuvre necessary to dislocate the head of the femur (adduction and maximal external rotation). • Injury of major arteries during replacement of total hip prosthesis. For example, the external iliac artery can be ripped open by adherent bone cement the moment the acetabulum is extracted (Fig. 7.7.7). Similar vascular injuries can occur, caused by the cutting edges of bone or the sharp instruments necessary for the operation or simply by a screw reaching too far (Fig. 7.7.8). • Arterial thrombosis may be initiated by the polymerization heat of bone cement (110°C) as shown in Fig. 7.7.9 (total occlusion of the external iliac artery).
False Aneurysms Due to Catheter Interventions Two-thirds of iatrogenic vascular injury of the lower limbs are false aneurysms or large haematomas caused by diagnostic and therapeutic procedures using the common femoral artery as the port of entry (angiography, percutaneous transluminal angioplasty, positioning of intravascular stents, etc.) and these may have medico-legal implications. The treatment of these false aneurysms is usually readily achieved by digital compression if noticed early.
Knee Surgery Since the advent of arthroscopic interventions, vascular injuries occurring during surgery on the knee have decreased in number, but not in seriousness. The vascular surgeon can be called for accidental injury of the popliteal artery caused by the blade of a cutting instrument during meniscectomy or a Kirschner’s wire used for reconstruction of a torn cruciate ligament. The surgeon’s vision may suddenly become blurred by onrushing blood if the artery is accidentally cut. In the case of an artery that has been perforated but not transected, thrombotic occlusion
Fig. 7.7.6 Dissecting intimal fracture with thrombotic occlusion at the bifurcation of the common femoral artery and ensuing embolic occlusion of the superficial femoral artery. Pain in the foot was misinterpreted for 4 days at which time the patient was referred for vascular surgery. Arterial patency was successfully restored, but tissue death was irrevocable and the patient subsequently underwent below-knee amputation
491
492
7.7 Vascular Trauma of the Lower Limb
Fig. 7.7.7 Difficult replacement of a hip prosthesis. The external iliac artery was ripped open by adherent bone cement when extraction of the acetabulum was tried. A large periarticular haematoma is outlined
of the popliteal artery might occur, causing unremitting pain in the foot (which again is often misinterpreted and missed within the critical time limits).
7.7.3 Consequences of Arterial Injury of the Lower Limb
Fig. 7.7.8 Arterial thrombosis with occlusion of the external iliac artery which was most likely thought to have been caused by the polymerization heat of bone cement which had inadvertently entered the pelvic floor
7.7.3 Consequences of Arterial Injury of the Lower Limb 7.7.3.1 Compartment Syndrome • If restoration of reperfusion is delayed or venous return from the periphery impaired, hypertension within the muscle compartments due to oedema may ensue, with the danger of impending necrosis of both striated muscle and nerve tissue. • Tension within the compartments can be relieved by full-length fasciotomy of all four compartments, which should be performed if there is any concern. It is possible to measure the intra-compartmental pressure (Fig. 7.7.10), which should be lower than 15–20 mmHg. It has been demonstrated in a follow-up study that radical fasciotomy does not impair the calf pump [10]. Secondary closure of fascia is therefore not obligatory.
Fig. 7.7.9 A screw has perforated the external iliac artery and caused thrombotic occlusion
493
494
7.7 Vascular Trauma of the Lower Limb
Fig. 7.7.10 Measuring the intra-compartmental pressure, which should not exceed 15–20 mm Hg
7.7.3.2 False Aneurysms and Arterio-Venous Fistulas Less invasive vascular injuries might come to light by presenting weeks or months later with a false aneurysm (Fig. 7.7.11). The groin and the popliteal fossa are typical sites for false aneurysms. These can grow and burst and must therefore be resected without compromising vascular patency. Because of the anatomical situation of the artery and vein running side by side, it is readily comprehensible that minor vascular injury can give rise to an arterio-venous fistula, a direct communication between artery and vein which can become clinically relevant due to a steal effect of the shunt, as suspected in the case of Fig. 7.7.12. Also, all arterio-venous shunts may imply cardiac overload and this can become clinically relevant.
7.7.4 The Management of Vascular Trauma (With Special Reference to the Knee Joint) Simple or complex fractures near the knee joint and knee dislocation are often associated with injury to the popliteal artery. Here the proximity of bone and artery is especially close (Fig. 7.7.5) and the pressure of the haematoma attending bone fractures of the knee is critical to the development of any collateral circulation. If occlusion of the popliteal artery is missed or not managed in time the amputation rate will be very high. A high index of suspicion is therefore in demand and measurement of the ABI – as stated before – is invaluable [7]. Interestingly, it has been shown [9] that in knee dislocations it is rupture of the posterior cruciate ligament only that is associated with popliteal artery injury, not rupture of the anterior cruciate ligament.
7.7.4 The Management of Vascular Trauma (With Special Reference to the Knee Joint)
Fig. 7.7.11 False aneurysm of the popliteal artery, a late sequence of arterial injury
The practice of interdisciplinary management for vascular injury is highlighted in the treatment of knee trauma. In these cases there is a pressing urgency to secure adequate circulation to and from the leg without having this delicate form of vascular surgical repair compromised by the forceful dynamics necessary for reducing and stabilizing a concomitant fracture (external fixation Fig. 7.7.13). Indecisiveness about the order of sequence can be overcome if artery and (if necessary in order to avoid venous hypertension and compartment syndrome) vein are bridged by intraluminal shunts (Fig. 7.7.14) right from the beginning.
Fig. 7.7.12 Arterio-venous fistula between superficial femoral artery and vein, a late consequence of limb trauma
495
496
7.7 Vascular Trauma of the Lower Limb
Fig. 7.7.13 External fixation for stabilization of a supracondylar fracture in a patient operated on for injury of the popliteal artery and vein. Fasciotomy has been performed for prevention of compartment syndrome
Fig. 7.7.14 The principle of intraluminal shunting to ensure adequate limb perfusion during orthopaedic repair
This allows the orthopaedic surgeon to perform an unhurried reduction of the fracture followed by external or internal fixation as the case may be. Thereafter the vascular surgeon can carry on with careful debridement where necessary, resect the contused vasculature and interpose vein grafts (Fig. 7.7.15). Thus, successful repair of popliteal arterial and venous injury relies on: • Uncompromising resection of all parts of the damaged vessel, which will need to be bridged by a segment of autologous saphenous vein. • Avoiding the temptation to perform an end-to-end anastomosis between two potentially damaged ends with the attendant risk of undue tension and hourglass narrowing. If venous return is severely compromised this can cause venous hypertension and trigger the development of compartment syndrome.
References
Fig. 7.7.15 Interposition saphenous vein graft for management of lacerated artery and vein
7.7.5 Bulleted Summary • Management of vascular injury of the lower limb is fundamentally different in war compared to civilian life. • In war as well as in the course of terrorist attacks, explosions cause enormous injury to vital structures and life-saving procedures such as resuscitation, shock management and control of haemorrhage take precedence over selective repair of vascular injury. Very often guillotine limb amputation is the only solution. • In civilian medical practice a hidden cause of limb ischaemia must be suspected at all times. Vascular injury and arterial occlusion may occur in association with bone fractures and during orthopaedic interventions. A high index of suspicion and the need to react quickly are of the essence. • The policy of an interdisciplinary approach to the management of combined bone and vascular injury
with the use of intraluminal shunts in both injured arteries and veins is the most important step towards improved outcome. Reduction and stabilization of fractures can be carried with less haste while adequate limb perfusion is secured. • The most reliable screening method of detecting as well as ruling out vascular injury and critical ischaemia is to measure the ankle/brachial index both prior to and immediately following the orthopaedic intervention. References 1. Aires AB, Barros D’Sa (1997) Vascular injuries of the limb. In: Chant ADB, Barros D’Sa AAB (eds) Emergency vascular practice. Arnold, London 2. Chan RK, Austen WG Jr., Ibrahim S, Ding GY, Verna N, Hechtman, Moore FD Jr. (2004) Reperfusion injury to skeletal muscle affects primarily type I muscle fibers. J Surg Res 122:54–60 3. Coupland, Robin M (1993) War wounds of limb. Butterworth-Heinemann, Oxford
497
498
7.7 Vascular Trauma of the Lower Limb
4. Gawande A (2004) Casualties of war – military care for the wounded from Iraq and Afghanistan. N Engl J Med 351:2471–2475 5. Hafez HM, Woolgar J, Robbs JV (2001) Lower extremity arterial injury: results of 550 cases and review of risk associated with limb loss. J Vasc Surg 33:1212–1219 6. Holland T (2002) Utilizing ankle brachial index in clinical practice. Ostomy Wound Management 48:38–40, 48–49 7. Mills WJ, Barel DP, McNair P (2004) The value of the anklebrachial index for diagnosing arterial trauma after knee dislocation: a prospective study. J Trauma 56:1261–1265 8. Nachbur B, Meyer R.P, Verkkala K, Zürcher R (1979) The mechanisms of severe arterial injury in surgery of the hip joint. Clin Orthop Rel Res 141:122–133
9. Pedrotti M, Ris HB, Stirnemann P (1990) Ischemia in acute knee joint instability. Chirurg 61:792–796 10. Ris HB, Gfeller C, Mahler F, Nachbur B (1991) Comparative evaluation of three ambulatory plethysmographic devices regards accuracy and handling in daily practice. Eur J Vasc Surg 5:159–164 11. Singh B, Moodley J, Shaik AS, Robbs JV (2003) Sympathectomy for complex regional pain syndrome. J Vasc Surg 37:508–511 12. Wasner G, Schattscheider J, Heckmann K, Maier C, Baron R (2001) Vascular abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms and diagnostic value. Brain 124:387–399
Diabetic Foot
501
8.1 Diabetic Foot Nicholas Katsilambros, Konstantinos Makrilakis, Nicholas Tentolouris, Panagiotis Tsapogas
8.1.1 Definition • According to the World Health Organization and to the International Working Group on the Diabetic Foot [32], diabetic foot is defined as the foot of diabetic patients with ulceration, infection and/or destruction of the deep tissues, associated with neurological abnormalities and various degrees of peripheral vascular disease in the lower limb.
8.1.2 Epidemiology • Diabetes mellitus ranks as a leading cause of blindness, chronic kidney failure, cardiovascular disease and chronic foot ulceration, often culminating in lower limb amputation [68].
• •
•
•
8.1.2.1 Foot Ulcers • The prevalence of foot ulcers in patients with diabetes in developed countries is approximately 4–10% [10]. • The annual incidence of foot ulcers in the general diabetes population is 2.2–5.9%. The prevalence is lower (1.7–3.3%) in younger patients with either type 1 or type 2 diabetes and higher (5–10%) in older individuals with mainly type 2 diabetes [68]. • Ulceration is much more common among patients with predisposing risk factors such as neuropathy (annual incidence 5–7%), irrespective of age and type of diabetes. • It is estimated that about 5% of patients with diabetes have a history of foot ulcers, whereas 15% of individuals with diabetes are bound to experience this complication during their lifetime [69]. • It must be taken into account that most of the data on the epidemiology of foot problems in diabetes come
•
•
from cross-sectional, hospital-based studies. This probably creates a bias in the estimation of the true prevalence of foot problems in diabetes. A selection of epidemiological data on diabetic foot problems is shown in Table 8.1.1. Risk factors for foot ulceration may vary considerably among patients from different ethnic groups. Foot ulcers are commoner in Caucasian subjects than in Asian patients of the Indian subcontinent [15]. This may be related to physical factors (limited joint mobility and foot pressures) and to better foot care in certain religious groups such as Muslims. In contrast, the risk for ulceration is higher in Blacks [71], Hispanic Americans and native Americans than in white Americans [44]. A comparative multicentre study performed in Germany, Tanzania and India showed that although peripheral neuropathy was very common among diabetic patients with foot lesions in the above countries (prevalence of 79%, 84% and 80%, respectively), peripheral vascular disease was very common in Germany (48%), and much less common in the other two centres (14% in Tanzania and 13% in India) [56]. Genetic differences and different dietary as well as smoking habits may account for the difference in the prevalence of peripheral vascular disease among various nations. However, there is no evidence that the risk is associated with any geographic differences. Veves et al. [84] showed that the risk factors of foot ulceration were common in different centres within Europe.
8.1.2.2 Amputation • The most serious sequela of the foot problems in diabetes is amputation. • Approximately 40–70% of all nontraumatic amputations on the lower limb are performed on patients with diabetes.
502
8.1 Diabetic Foot
Table 8.1.1 Epidemiological data on the diabetic foot Reference
Country
Populationor clinic-based
Prevalence (%) Foot ulcers
Incidence
Amputation Foot ulcers 4
Amputation
Neil et al. [59]
UK
Population
7
Borssen et al. [8]
Sweden
Population
0.75
McLeod et al. [52]
UK
Clinic
2.6
Moss et al. [57]
USA
Population
–
3.6
10.1ª
2.1ª
b
0.4b
–
–
–
–
–
–
2.1
–
–
Bouter et al. [12]
The Netherlands
Population
–
0.8
Siitonen et al. [77]
Finland
Population
–
–
–
0.5
Pendsey [64]
India
Clinic
3.6
–
–
–
Kumar et al. [42]
UK
Population
1.4
–
–
–
Humphrey et al. [31]
Nauru
Population
–
–
–
0.76
Abbott et al. [1]
UK
Population
1.7
1.3
2.2
–
Mueller et al. [58]
The Netherlands
Population
–
–
2.1
0.6
Lavery et al. [44]
USA
Population
–
–
6.8
0.6
7.6
–
–
–
Manes et al. [51]
c
Balkan region
Clinic
a Incidence over 4 years. b Include annual incidence of foot ulcers in patients hospitalized for this problem. c
Includes the countries Greece, Romania, Bulgaria, Serbia, Albania, and the former republic of Macedonia.
• The risk of amputation is 10–15 times higher in diabetic than in nondiabetic patients. • In the USA, more than 50,000 diabetes-related amputations are performed annually. • About 85% of all diabetes-related amputations are preceded by a foot ulcer [68]. • The most common cause of amputations in diabetic patients is ischaemia and infection: gangrene or nonhealing foot ulcer is the cause of amputations in 50– 70% and infection in 20–50% of patients with diabetes [80]. • In most cases, however, amputation had to be performed because of the combination of infection and ischaemia.
8.1.2.3 Social and Economic Costs • Chronic foot ulcers and/or amputations have devastating effects on the individual’s physical and psychosocial functioning and quality of life [85].
• One study [43] has shown that nearly 77% of individuals over 75 years of age undergoing amputation were unable to return to their own homes after surgery, and required additional financial support and social service. • The economic cost of ulcers and amputation is high. • A comparison of the costs associated with foot ulcers and amputations in different studies is difficult because they differ in terms of design, definitions, healthcare system and reimbursements. • Usually these studies consider only the cost for the healthcare system (direct cost). • The average in-patient costs for lower-limb complications in the USA in 1997 were: foot ulcers $16,580; toe/ transmetatarsal amputation $25,241; transtibial amputation $31,436; transfemoral amputation $32,214. • In addition to these costs, indirect costs due to loss of productivity and the individual patient’s costs should also be considered [5].
8.1.3 Aetiology
8.1.3 Aetiology There are two main types of ulcer: neuropathic and ischaemic. In patients with diabetes, pure ischaemic ulcers are less common and the vast majority of the ulcers are either pure neuropathic or mixed neuroischaemic.
Diabetic Neuropathy The diabetic neuropathies are a heterogeneous group of conditions that may be sub-classified into various polyneuropathies and mononeuropathies. The commonest forms of diabetic neuropathies are: • distal sensorimotor neuropathy (also called peripheral neuropathy) • autonomic neuropathy [39].
8.1.3.1 Pathogenesis of the Neuropathic Ulcer Neuropathic foot ulcers result from a combination of two or more contributory factors occurring together. • The neuropathic foot, for example, does not ulcerate spontaneously. It is the combination of loss of protective sensation and either extrinsic factors (e.g. walking barefoot, ill-fitting shoes, foreign bodies in the shoes) or intrinsic factors (peripheral vascular disease, foot deformities, callosities) causing minor or major trauma that ultimately result in ulceration. • Neuropathy is the most important contributory cause in the pathway to foot ulceration (Fig. 8.1.1).
Fig. 8.1.1 Neuropathic ulcer of the head of the first metatarsal
Distal Sensorimotor Neuropathy/Peripheral Neuropathy Epidemiology/Aetiology
• This affects about 30% of patients with both types of diabetes. • Its prevalence increases with both age and duration of diabetes [91]. • The onset of this type of neuropathy is gradual and insidious. Symptoms
• In the majority of affected individuals, it is asymptomatic; however, 15–25% have symptoms.
503
504
8.1 Diabetic Foot
• Typical symptoms include paraesthesia, hyperaesthesia, and sharp, stabbing, shooting and burning pain, all of which are exacerbated at rest and particularly at night. • Walking and/or exercise often relieve symptoms and this can be an important discriminator between neuropathic pain and the rest pain of critical limb ischaemia [91]. Investigations/Diagnosis
• Clinical examination usually reveals a sensory deficit in a glove and stocking distribution. • Signs of motor dysfunction are usually present, with wasting of the small muscles of the hands and feet and absent ankle reflexes. • The 10-g monofilament, used to test pressure perception, and the biothesiometer, used to test the vibration perception threshold, are also simple adjunctive tests used to investigate and identify those at risk for foot ulceration. • Inability to perceive the 10-g monofilament has been associated with a tenfold increased risk for foot ulceration [72]. • Vibration perception threshold >25 V has been associated with a fourfold increase in risk for ulceration in comparison with a group with a vibration perception threshold of 13 V over a 10-year period of follow-up [92]. • The diagnosis of peripheral neuropathy is made easily by assessment of large fibre function (e.g. loss of vibration perception using a 128-Hz tuning fork), small fibre function (e.g. hot-cold rod and/or pin-prick sensation) in the feet, together with assessment of ankle reflexes. • A composite score of these modalities, the modified neuropathy disability score, has been evaluated in prospective studies and it was found to discriminate the patients at risk for foot ulceration [1]. • A particularly dangerous situation is the “painfulpainless leg”. In this situation the patient has severe painful symptoms, but the examination reveals severe sensory loss; such patients are at great risk of painless injury to their feet [86]. • Diabetic neuropathy is the common denominator in 85% of diabetic foot ulcers. Two cross-sectional studies confirmed the frequency of neuropathy in patients presenting with new foot ulcers. In London [24], 87% of patients with ulcers had neuropathy (62% primarily neuropathic and 25% neuroischaemic ulcers), where-
as in Manchester [42] 85% of patients with ulcers had neuropathy (40% neuropathic ulcers, 45% neuroischaemic). • Other prospective studies have also established that the presence of neuropathy was associated with a several-fold increase in foot ulceration [1, 72, 92]. Treatment
• Optimal glycaemic control is important in the prevention of diabetic neuropathy. • A number of drugs (mainly antidepressants and anticonvulsants) can relieve symptoms of painful diabetic neuropathy. • At present, there are no drugs that have an effect on the natural history of neuropathy, which is one of gradual deterioration of nerve function [11].
Autonomic Neuropathy
• Peripheral autonomic neuropathy affecting the lower limbs leads to reduced sweating and dry skin, which is prone to crack and fissure. • In addition, the loss of sympathetic control of arteriovenous shunting results, in the absence of peripheral vascular disease, in increased blood flow and warm feet with distended dorsal foot veins [38]. • However, the highest-risk foot is the pulseless insensitive foot, because it indicates the presence of somatic and autonomic neuropathy together with peripheral vascular disease. • The interaction between the causative pathways to foot ulceration is summarized in Fig. 8.1.2.
Other Risk Factors • Callus formation is the result of both increased plantar pressure and dry skin. The presence of callus is associated with a 77-fold increase in foot ulceration risk in patients with neuropathy. Regular removal of callosities results in a significant reduction in foot pressure and in prevention of ulceration [59]. • The presence of foot deformities (claw toes, prominent metatarsal heads, hallux valgus, nail deformities) is associated with an increased risk of foot ulceration. • The presence of other microvascular complications, increased duration of diabetes, high plantar pressures, peripheral oedema, postural instability due to periph-
8.1.3 Aetiology
Fig. 8.1.2 Pathways to foot ulceration in diabetic patients. From Boulton AJM (2000) The pathway to ulceration: aetiopathogenesis. In: Boulton AJM, Connor H, Cavanagh PR (eds) The foot in diabetes, 3rd edn. Wiley, Chichester, p 21, with permission) [9]
eral neuropathy, living alone or in nursery care facilities, negative attitude to foot care and refusal to adopt preventive foot care actions have all been associated with increased risk for foot ulceration. • The most predictive factor, however, for foot ulceration is a previous history of ulceration or amputation. Indeed, in many diabetic foot clinics more than 50% of patients with new foot ulcers have a past history of similar problems [10].
•
• •
8.1.3.2 Pathogenesis of the Ischaemic Ulcer Epidemiology/Aetiology • Peripheral vascular disease (see below) alone is not usually able to lead to ulceration, if no other risk factors and a minor trauma combine. • An increased demand for blood supply beyond the circulatory capacity, as is the situation in injury and local infection, is usually the cause of an ulcer. Nevertheless,
•
rates of ischaemic vascular disease reported in patients with diabetes are higher than those in nondiabetic subjects, and occur at a younger age. The male:female ratio is 2:1 (while in nondiabetics it is 30:1) and multiple stenoses are found (while in nondiabetics a single or just a few occlusions are the norm). Collateral circulation may also be occluded. A long list of abnormalities that apply especially to diabetes accelerate atherogenicity. Increased nonenzymatic glycosylation of proteins leads to advanced glycation end-products (AGEs) in diabetes. AGE generation is paralleled by oxidative damage and lipid peroxidation within target tissues, with features of inflammation through the involvement of monocytes/ macrophages expressing receptors for glycated macromolecules [55]. In patients with poorly controlled diabetes, plasma levels of low-density (LDL), intermediate-density (IDL) and very low density (VLDL) lipoproteins are elevated, while in type 2 diabetes (and in poorly controlled type 1) HDL levels are low.
505
506
8.1 Diabetic Foot
• Qualitative lipid differences most likely augment the atherosclerotic process; small, dense LDL particles, which are found in enhanced rates in diabetic patients, being more atherogenic. • Diabetes causes accelerated LDL transport through the endothelium due to its increased permeability [33], and retention of LDL in the subendothelial space, because of increased collagen-linked AGEs, which may act as LDL traps. • Furthermore, AGE-LDL and oxidized LDL are chemoattractants for monocytes/macrophages, and may induce endothelial dysfunction through increased expression of vascular cell adhesion molecule-1 (VCAM-1) in endothelial cells [40], as well as the release of tumour necrosis factor-α (TNF-α), interleukin-1 and platelet derived growth factor (PDGF) from macrophages. • Eventually nearby connective tissue cells proliferate and become activated to produce extracellular matrix components. • Nitric oxide (NO), a free radical whose production by endothelial cells may be modulated by oxidized lipoproteins, is reported to have an ambivalent role in diabetic atherosclerosis, either protecting LDL from oxidation or stimulating the process. • Autoantibodies against oxidized LDL and AGE-LDL and immune complexes may also play a role in diabetic endothelial dysfunction. • Prostacyclin, a vasodilator produced by vascular endothelium, is decreased in the plasma of diabetic patients, and prostacyclin stimulating factor is also decreased in coronary smooth muscle cells of diabetic patients as compared to nondiabetics [76]. • Thromboxane A2 – a contractile agent synthesized both by the endothelium and platelets, which counteracts the vascular effects of NO – is found at higher
rates in patients with risk factors such as peripheral vascular disease and diabetes [21]. • The following characterize diabetes as a hypercoagulable disease: abnormalities of diabetic platelet function both in vivo and in vitro, the possible general activation of blood coagulation, elevated plasma levels of fibrinogen, a postulated increase in fibrin formation, decreased levels of activated protein C (a plasma anticoagulant), plus several other atherogenic conditions [16]. Thrombosis is the final event, which leads to vascular occlusion and ischaemic injury.
Peripheral Vascular Disease Epidemiology/Aetiology
• Peripheral arterial disease is almost 3 times more common in diabetic patients in comparison with age-, and sex-matched individuals. • It exhibits a diffuse pattern of distribution, and the lesions are more extensive, frequently bilateral, and tend to involve arteries below the knee level. • Peripheral ischaemia gives a component cause in the pathway to ulceration in almost 50% of cases [24, 42] while its presence is associated with prolonged healing time and increased risk for amputation.
Symptoms
• The ischaemic foot is red, dry, with thin skin and often neuropathic (Fig. 8.1.3). • It is therefore more susceptible to foot ulceration [38].
8.1.4 Complications: Neuro-Osteoarthropathy 8.1.4.1 Definition • Neuro-osteoarthropathy (Charcot arthropathy, Charcot osteoarthropathy, neuropathic osteoarthropathy) is one of the most serious complications of diabetic foot.
8.1.4.2 Epidemiology
Fig. 8.1.3 Ischaemic feet
• Its prevalence is between 1% and 7.5%; bilateral involvement has been reported to occur in 6–40% of patients in several series.
8.1.5 Diagnosis/Investigations
• The mean age of presentation is approximately 60 years, and the duration of diabetes in the majority of the patients is 15 years. • Men and women are affected equally.
• The coalescent stage is characterized by periosteal bone formation, stabilization of the affected joints and the fusion of bone fragments to adjacent bones. • The reconstructive stage is characterized by subchondral osteosclerosis, intra-articular and marginal osteophytes, and ossification of ligaments and cartilage [37].
8.1.4.3 Aetiology • Both peripheral somatic and autonomic neuropathy, together with adequate blood supply to the foot are prerequisites for the development of this complication [37]. • A minor trauma, often unrecognized by the patient, may initiate the process of joint and bone destruction. • Somatic neuropathy allows repeated insensate injury to go un-noticed, while autonomic neuropathy results in increased peripheral blood flow with arteriovenous shunting [74]. • Some cases have been reported after foot infection, surgery on the ipsilateral or contralateral foot, or restoration of blood supply to the leg.
8.1.4.4 Symptoms/Investigations/ Diagnosis/Treatment • Many patients experience pain or discomfort in the acute phase.
Examination • On examination, there are findings of inflammation (oedema, increased temperature and in some cases redness of the skin), together with findings of severe peripheral neuropathy and bounding peripheral pulses. • The presence of unilateral heat and swelling in a neuropathic diabetic patient with long-standing diabetes is a clue to the diagnosis, and such a lesion should be presumed to be acute neuro-osteoarthropathy until proven otherwise [37].
Imaging Radiological findings depend on the stage of the disease. • The acute stage (development stage) is characterized by soft tissue swelling, hydrarthrosis, subluxations, erosion of the cartilage and subchondral bone and bone fragmentation.
Treatment • The essence of treatment in the acute phase remains non-weight-bearing immobilization in a total contact cast or removable cast walker [10]. • Any delay in proper treatment has devastating sequelae, with the development of irreversible severe foot deformities. • Recent data suggest that the use of pamidronate, together with non-weight-bearing immobilization improve symptoms and normalize the skin temperature differential as well as the markers of increased bone turnover (bone-specific alkaline phosphatase and urine deoxypyridinoline) [35].
8.1.5 Diagnosis/Investigations 8.1.5.1 Clinical Examination • Foot deformities, a usual consequence of diabetic somatic neuropathy, predispose to ulceration. Hallux valgus, claw-, hammer-, mallet-, or curly-toes, toe overriding, triangular foot (hallux valgus and quintus varus), prominent metatarsal heads, pes planus (flat foot), pes cavus, bunion and bunionette formation are some of the deformities that should be noted by inspection [37, 38]. • Inspection of the patient’s gait can give information about abnormal proprioception, footdrop and claudication, all situations predisposing to foot ulceration. • Clinical examination of the foot includes verification of the perception of light touch (with the use of a cotton wisp); pain (with the use of a disposable pin); temperature (with the use of a cold and a warm metal rod); pressure (using a Semmes-Weinstein 5.07 monofilament which bends with the application of a 10-g force); vibration (using a tuning fork and a biothesiometer if available); and proprioception. • Two-point discrimination (using a pair of thin rods) is also used by some as a measure of nerve fibre density.
507
508
8.1 Diabetic Foot
• Deep tendon reflexes (Achilles’, patellar, brachioradialis, biceps and triceps) provide information on the condition of large motor nerves. • Neurotrophic ulcers usually appear after the development of a callus or thickening of the skin over pressure points on the plantar aspects of the foot, usually under the metatarsal heads, the hallux and on the heel. • Corns, fissures, dryness and onychomycoses are also important, because they may predispose to ulceration, and denote the care of the foot. A local haemorrhage (haemorrhagic callus) and a blister may develop, and eventually a skin crack. • A midfoot ulceration develops over the bony prominences of a Charcot’s foot. • Fractures or postoperative changes of the architecture of the foot may also expose the skin under a bony prominence, such as toe removal or Chopart’s disarticulation due to osteomyelitis. • Wound characteristics are critically important for treatment [41]. The location of the ulcer, as well as its length, width and depth (measured with a probe) should be documented at each visit, as should any bone or joint exposure (suggesting osteomyelitis), or sinus formation. The base of the ulcer may be pink (granulation tissue), yellow (fibrous) or black (necrotic), and a soft or firm eschar may be present. • Signs of infection may also be present. Usually increased discharge precedes purulence and malodour. The skin may be erythematous, warm and oedematous. Systemic sepsis may develop and the patient should be educated in order to recognize it early.
8.1.5.2 Circulation • The condition of lower limb circulation should be determined in all diabetic patients on an annual basis, in advance of any other assessment of foot/lower-limb problem, since good blood flow is a prerequisite for the prevention/therapy of foot lesions. • History and physical examination determine the level and severity of arterial narrowing with high accuracy.
Early Symptoms • Intermittent claudication is the earliest symptom. The distance (measured in blocks) at which claudication appears decreases with the severity of occlusion, the intensity and the duration of exercise. When arter-
ies are still patent, rest corrects oxygen demands and allows for the removal of metabolic products of muscle exercise, such as lactic acid, and pain disappears quickly. Weakness or cramping may be felt instead of pain, while the level of the discomfort is suggestive of the level of the occlusion. Aortoiliac narrowing causes thigh and buttock symptoms, or Leriche’s syndrome (in combination with impotence); and femoral or popliteal disease produces calf claudication. • All adults with diabetes should be asked whether they suffer from intermittent claudication and, if they do, they should be referred for specialist vascular assessment.
Later Symptoms • Pain at rest is the next stage, although in patients with diabetic neuropathy this symptom may be lacking, even when gangrene – the final stage of the disease – is present. • Before this, healing of minor wounds may not succeed, and persisting ischaemic ulcers develop. • Pain at rest of the distal forefoot emerges after 1 h of resting in the supine position and is caused by multilevel narrowing or total occlusion, when arterial pressure fails to force blood to the distal forefoot against gravity. It may be relieved by dangling the foot over the side of the bed, a short walk or sleeping in a sitting position, but it returns in the supine position. • Observation of the ischaemic foot may reveal skin atrophy or rubor, hair loss and nail thickening. • Colour may change with elevation and dependency, due to deranged autonomic autoregulation as a result of ischaemia. When dependent the foot may be ruborous due to dilated vessels, but when elevated to 45° above the examination table it blanches rapidly. • Capillary refill time is normal when return to baseline, after pressure applied to the skin in the supine position, is shorter than 5 s. • Venous refill time is determined by identifying a prominent vein in the foot in the supine position; after this the leg is elevated to 45° for 1 min; then the patient sits up and hangs their leg over the side of the bed. The time needed for the vein to refill after assuming the upright position is venous refill time and should be less than 20 s when normal. • Pulses of the femoral, popliteal, dorsalis pedis and posterior tibialis arteries should be palpated on an annual basis for all patients with diabetes and graded as nor-
8.1.6 Differential Diagnosis
mal, diminished or absent; auscultation of the femoral artery for a bruit should be performed. • Arterial narrowing of 50% usually produces a bruit, which disappears when stenosis is over 90%.
8.1.5.3 Paraclinical Evaluation Ankle/Brachial Blood Pressure Index (ABI) Noninvasive vascular testing includes calculation of the ankle/brachial index (ABI) with the use of a Doppler probe. • ABI should be measured in the following groups: (1) patients with type 1 diabetes over 35 years old, or who have had diabetes for over 20 years; (2) patients with type 2 diabetes at baseline; (3) all diabetic patients who mention leg pain of unknown origin, intermittent claudication, and whose lower-limb artery pulses are not felt, or who have a femoral bruit; (4) all diabetic patients with a foot ulcer [63]. • If ABI values are normal (between 1 and 1.2), ABI measurements should be repeated every 2–3 years. A patient with an ABI level between 0.5 and 0.89, which is indicative of occlusive arterial disease, needs intensive management of cardiovascular risk factors and measurement should be repeated within 3 months. • The patient should be referred for specialist vascular assessment at ABI values below 0.5. ABI values over 1.2 may result from medial calcification, a condition very common in diabetes. If this is the case, other tests of arterial condition are used.
8.1.5.4 Classification Systems • The Meggitt–Wagner classification (Table 8.1.2) has been widely accepted, and is the most utilized system. • The original system has four grades (0–3) based on the depth of the ulcer, and two more grades (4–5) describing ischaemia [54]. • A modification of the Wagner–Meggitt system is Depth–Ischemia classification, combining grades for both the depth of an ulcer (0–3) and ischaemia of the foot (A–D) [14]. • The University of Texas (UT) classification system for diabetic foot wounds (Table 8.1.3) is more descriptive and provides a guide for a more profound examination [90]; it includes reference to ulcer depth, arteriopathy and the presence or not of infection. Criteria missing from the UT system are now included in a new, recently validated [83], classification system (Table 8.1.4) under the name size (area, depth), sepsis, arteriopathy, denervation [S(AD) SAD]. • Classification systems apply to groups of patients, and do not influence treatment regimens, since other parameters, such as social factors, diabetes control and treatment compliance, render each individual with diabetes and a foot ulcer a unique patient deserving a personalized approach.
8.1.6 Differential Diagnosis • The differential diagnosis of the neurological and neuroischaemic diabetic ulcer is presented in Table 8.1.5 [82].
Other Investigations • Segmental pressures, toe pressures (measured by a pneumatic cuff), transcutaneous oximetry (normal values of transcutaneous oxygen pressure, TcPO2, are between 40 and 70 mmHg), segmental plethysmography and ultrasonography are discussed in detail in other chapters of this book (see Chapter 1.5, Noninvasive diagnosis of vascular disease, by P. Berg). • Modern noninvasive methods include helical or spiral computed tomography and magnetic resonance angiography. • Arteriography is the definitive (invasive) diagnostic test, and should be performed before any decision about an amputation is taken.
Table 8.1.2 Meggitt–Wagner classification of foot ulcers Grade 0
Pre- or post-ulcerative lesion completely epithelialized
Grade 1
Superficial, full thickness ulcer, limited to the dermis, not extending to the subcutis
Grade 2
Ulcer of the skin extending through the subcutis with exposed tendon or bone and without osteomyelitis or abscess formation
Grade 3
Deep ulcer with osteomyelitis or abscess formation
Grade 4
Localized gangrene of the toes or the forefoot
Grade 5
Foot with extensive gangrene
509
510
8.1 Diabetic Foot
Table 8.1.3 University of Texas classification system for diabetic foot wounds Grade Stage
0
1
2
3
A
Pre- or post-ulcerative lesion completely epithelialized
Wound penetrating to Superficial wound not involving tendon, capsule tendon or capsule or bone
Wound penetrating to bone or joint
B
With infection
With infection
With infection
With infection
C
With ischaemia
With ischaemia
With ischaemia
With ischaemia
D
With infection and ischaemia
With infection and ischaemia
With infection and ischaemia
With infection and ischaemia
Table 8.1.4 The S(AD) SAD classification Size Grade
Area
Depth
Sepsis
Arteriopathy
Denervation
0
Skin intact
Skin intact
None
Pedal pulses present
Pin pricks intact
1
<1 cm2
Superficial (skin and subcutaneous tissue)
Surface
Pedal pulses reduced or one missing
Pin pricks reduced
2
1–3 cm2
Tendon, periosteum, joint capsule
Cellulitis
Absence of both pedal pulses
Pin pricks absent
3
>3 cm2
Bone or joint space
Osteomyelitis
Gangrene
Charcot
Table 8.1.5 Differential diagnosis of the neurological and neuroischaemic diabetic ulcers Neuropathic ulcer
Neuroischaemic ulcer
Foot deformities present
Variable architecture
Painless
Painful
Normal pulses
Absent pulses
Located over bony prominences
Located on toes (often)
Callus present
No callus
Diabetic neuropathy indexes Variable findings positive Warm due to increased blood flow
Cold (if not infected)
Dilated veins
Collapsed veins
Red
Pale or cyanotic
8.1.7 Infections 8.1.7.1 Introduction • Diabetic patients have an increased propensity to develop a variety of infections, which are often more severe than in the general population. They include urinary tract infections, cholecystitis, external ear infections, fungal and skin and soft tissue infections. Foot infections are probably the commonest and most important of them, being responsible for more hospital days than any other complication of diabetes [66, 67]. • Diabetic foot infections pose a potentially serious acute medical problem, usually requiring immediate medical attention, appropriate diagnostic evaluations and various therapeutic modalities. At other times they constitute a long-term medical problem, with increased morbidity (due to recurrences, bone involve-
8.1.7 Infections
•
•
•
•
•
ment and the need for surgical resections or amputations) and even, though seldom, increased mortality, especially if not managed properly. Dealing with this problem requires an in-depth understanding of the pathophysiology of these infections and adequate systems for implementing proven effective measures. Despite the substantial morbidity and occasional mortality associated with foot infections in diabetes though, there are no widely accepted guidelines for assessing and treating these lesions. During the last two decades much has been learned about the epidemiology and the underlying causes of these infections, the methods to diagnose them, the usual causative microorganisms, the risk factors for adverse outcomes and the approaches to treatment. In the year 2003, the International Working Group on the Diabetic Foot issued a Consensus Document approving the guidelines developed by their Committee on diagnosing and treating infection [47], together with two more Consensus Documents called “Wound healing and treatments for people with diabetic foot ulcers” and “Diabetic foot ulcer classification system for research purposes”. An interactive CD-ROM has been developed containing the three documents, along with a picture gallery, that can be ordered at the IDF website (www.idf.org/bookshop). This section will review the pathophysiology, microbiology, clinical presentation, diagnosis, severity classification and treatment of diabetic foot infections.
8.1.7.2 Pathophysiology Risk Factors Foot cellulitis is more than nine times more frequent in diabetic compared to nondiabetic persons, and hospitalization for osteomyelitis of the foot is almost 12 times greater in diabetics [13]. There are several factors that place patients with diabetes at high risk for foot infections. These include: • Defects in host defences, secondary to hyperglycaemia. Among the host defences that are impaired in diabetes are functions of polymorphonuclear leucocytes (including abnormalities of migration, phagocytosis, intracellular killing and chemotaxis), correlated with poor glycaemic control [53]. Monocyte and comple-
•
• •
•
ment functions appear to be worsened by hyperglycaemia as well. Sensory neuropathy (causing a decreased appreciation of temperature and pain, thereby making injuries and blisters less noticeable). Motor neuropathy (causing anatomical foot deformities). Autonomic neuropathy (causing decreased sweat and sebaceous gland secretion, resulting in dry, cracked skin). Peripheral vascular disease (either macro- or microvascular, or both, causing a decrease of the blood supply needed to heal ulcers and infections).
The Development of Infection • Trauma in patients with one or more of the above risk factors is usually the precipitating event for the onset of a foot infection. After the tissues are injured, the above factors may act synergistically to prevent normal healing and promote infection. • Infection may initially begin superficially in an ulcer or crack of the skin but, depending on the microorganism(s) involved and the anatomical structure, it can spread to involve the deep tissues of the foot, including tendons and bones (osteomyelitis). • The structure of the various compartments of the foot, tendon sheaths and neurovascular bundles tend to favour the proximal spread of infection. • Normal foot anatomy consists of a medial compartment, extending from the calcaneus to the hallux and containing the intrinsic foot muscles. There is a central compartment that contains the intrinsic foot muscles from toes 2 to 4, and a lateral compartment that contains the intrinsic foot muscles of the 5th toe. These compartments are separated from each other by an inter-muscular septum. The nerve-vessel bundles located in these compartments can be compressed by oedema, caused by an infected ulcer of the plantar surface of the foot. This can lead to a so-called compartment syndrome, causing arterial thrombosis and tissue necrosis of the involved compartment or the digital arteries, even in the presence of intact arterial circulation of the foot [45]. • Necrotizing infections involving gas-forming organisms can cause gas gangrene and even septicaemia may develop.
511
512
8.1 Diabetic Foot
8.1.7.3 Microbiology • The surface of the body is coated with bacteria, present in a harmless association known as colonization. • The predominant bacteria of normal skin are Grampositive aerobes, particularly the low-virulence coagulase-negative staphylococci, α-haemolytic streptococci and the Corynebacteriae (diphtheroids). • Thus, because all open wounds are colonized by microflora, the mere presence of bacteria in a wound does not define infection. • Infection indicates actively multiplying microorganisms that have invaded tissues, leading to injury and a host response, typically manifested by symptoms or signs of inflammation. • Superficial infection is confined to soft tissues external to the fascia (skin and subcutaneous fat), while deep infection involves invasion of fascia, muscle, tendon, joint or bone. • Staphylococcus aureus is the most frequent and perhaps the most virulent pathogen in diabetic foot ulcers. β-haemolytic streptococci are also common and obligate anaerobes (Bacteroides, Peptostreptococcus species, etc) infect deep wounds with accompanying gangrene or ischaemia. • Previous antibiotic therapy tends to alter the colonizing flora of the skin and wounds, favouring organisms resistant to the agent administered. • Recent lesions tend to have monomicrobial infections [48], whereas chronic wounds tend to develop more complex infections, with aerobic Gram-negative rods (Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, etc.), anaerobes (Gram-positive and Gramnegative) and enterococci, in addition to the Grampositive aerobes [62]. • Fungi (Candida and Tinea species) are also found more frequently in diabetes, although their contribution to infection is questionable [81].
• Since, as mentioned earlier, the mere presence of bacteria does not necessarily define infection, an infection needs to be defined clinically [50]. • It is most typically manifested by signs and symptoms of inflammation, including induration, erythema, warmth, pain, tenderness or purulence. • The clinical manifestations vary, according to the extent and depth of bacterial invasion, and to some degree according to the pathogen(s). • The chronicity of the infection also plays a role: acute infections are usually associated with more prominent inflammatory findings, whereas chronic infections are usually not. • Patients with ischaemia or neuropathy may have less prominent (or even absent) symptoms of an infection, due to their loss of pain perception and/or reduced blood flow. • Clinical features of cellulitis are usually present as an early manifestation of a foot infection. • Cellulitis is a soft tissue infection marked by erythema, warmth and swelling over the involved area (Fig. 8.1.4). Later the infection may spread to deeper tissues and it may be possible to express pus from a sinus tract or from an ulcer. As infection spreads deeper, soft tissue fluctuance may be present. • Cutaneous bullae, soft tissue gas (with crepitus) or purple/black discoloration of the skin may occur in necrotizing infections (gangrene). • Osteomyelitis may result from contiguous spread of the infection to the underlying bone(s). The clinical features of osteomyelitis often do not differ from more superficial infections in the diabetic foot and that poses a great challenge for the diagnosis (Fig. 8.1.5). • Systemic signs and symptoms, such as fever, a high white blood cell (WBC) count and elevated eryth-
8.1.7.4 Clinical Presentation • Foot infections in diabetes often begin around the toe nail bed (paronychia), around cracks in the skin of the foot, or arise from neuropathic or ischaemic ulcers. • Infections are usually the consequence and not the cause of foot ulcerations. They can be divided into superficial (local), soft tissue and spreading (cellulitis) and osteomyelitis [34].
Fig. 8.1.4 Cellulitis of the dorsum of the foot
8.1.7 Infections
rocyte sedimentation rate (ESR) may or may not be present. In fact more than half of all patients, including those with serious infections, lack a fever, a high WBC count and an elevated ESR [2, 26].
8.1.7.5 Diagnosis • The first step in dealing with infection is to recognize its presence. • The clinician must identify the causative pathogen(s) and its/their antibacterial sensitivities, in order to select appropriate antibacterial therapy. • A foot infection should be suspected at the first sign of a local foot problem (e.g. pain, swelling, ulceration, sinus tract formation, crepitation), a systemic infection (e.g. fever, vomiting, rigors, tachycardia, confusion, malaise) or metabolic disturbance (e.g. severe hyperglycaemia, ketosis, azotemia) in a diabetic person. • Appropriate diagnostic and therapeutic modalities should be immediately implemented. A careful, thorough physical examination, with focus on the foot, should be performed. • Signs of cellulitis, ulcers, drainage, inflammation signs, evidence of crepitation, sinus tract formation, abscesses or skin breaks should be documented. • Ulcers should be measured and preferably photographed for future comparison. • Probing of skin breaks with a sterile metal probe to see if bone can be reached is very useful for diagnosis of possible osteomyelitis.
• Palpation of pedal pulses and measurement of the ABI by Doppler ultrasonography is helpful in evaluating the presence of peripheral vascular disease. • Evaluation of the neurological status, by examining sensation to light touch and pain, vibration perception and motor and autonomic function, are also extremely useful. • Cleansing and debridement of wounds, removal of any foreign material and eschars and culturing of the cleansed wound by curettage, aspiration or swab will help both diagnostically and therapeutically. • The correlation between microorganisms recovered from superficial ulcer swabs and those obtained from deeper tissue specimens is very poor [48]. • Superficial wound cultures, especially without prior cleansing or debriding of the wound, will contain the colonizing flora from where the infection originated, lowering the culture’s specificity. • Furthermore, the hostile environment of the air-filled cotton swab inhibits growth of anaerobes and fastidious organisms, lowering the sensitivity of the procedure. • A curettage or tissue scraping from the base of a debrided ulcer, with proper transfer of the specimen to the microbiology laboratory in a sterile container, provides more accurate results than a swab [75]. • Alternatively, obtaining an aspirate of any available purulent material provides reliable results. • Specimens should be promptly cultured for both aerobes and anaerobes. • Obtaining a plain radiograph of the foot is good clinical practice in nearly every situation in which an infected wound is suspected, given the frequently deceptive symptomatology of osteomyelitis. • Blood for a complete blood count, ESR and C-reactive protein (CRP) determination should also be sent. • The diagnosis of osteomyelitis is usually a challenge to the clinician.
Diagnosing Osteomyelitis
Fig. 8.1.5 Extensive cellulitis of the foot, creating the suspicion of the spread of the infection to deeper tissues and possible osteomyelitis
• Osteomyelitis is a common complication of diabetic foot ulceration [46] that can be difficult to diagnose and eradicate [6, 7]. • Bone infection generally results from contiguous spread of a deep soft tissue infection through the cortex (osteitis) to the bone marrow (osteomyelitis).
513
514
8.1 Diabetic Foot
• About 50–60% of serious foot infections and even about 20–30% of apparently mild-to-moderate infections are complicated by osteomyelitis. Its symptoms may not differ from soft tissue foot infections that are not complicated by bone involvement. But over time bone infection may progress, resulting in necrosis, secondary abscess formation and extension into soft tissues and adjacent foot compartments, or even cause serious systemic illness. Thus, the diagnosis should not be missed and many times is a great challenge. • Patients who have soft tissue infections for more than 2 weeks, especially if located over bony prominences, are at high risk for osteomyelitis. • Ulcers larger than 2×2 cm or >3 mm in depth are significantly more likely to overly infected bone [61]. Ulcers in which bone is exposed or in which a probe can be passed directly to bone are almost always associated with osteomyelitis [30]. A so-called sausage toe, a red swollen digit, frequently indicates osteomyelitis [65]. • A substantially elevated ESR (>70 mm/h), without any other obvious cause, also significantly increases the likelihood of osteomyelitis (sensitivity 28% and specificity 100%) [61]. • Plain radiographs should be ordered for most patients with a diabetic foot infection. • Abnormalities in plain films are not usually detected until 10–20 days after infection, when more than 50% of the bone has been resorbed. • Sensitivity and specificity are about 60%, with the characteristic changes including focal osteopenia, cortical erosions or periosteal reaction early, and sequestration of sclerotic bone late. • Many times bony abnormalities are difficult to distinguish from those of Charcot neuroarthropathy. • When there is doubt, a second film in a couple of weeks can be repeated, or another imaging modality used. • Technetium-99m bone scans reflect osteoblastic activity of the bone and can be positive 2 weeks before plain films. Their sensitivity is high (86%), but their specificity is relatively low (45%), because they will detect any condition that causes bone turnover, including Charcot arthropathy. • Indium-111 WBC scans reflect areas of leucocyte accumulation and have a high sensitivity (89%) and relatively good specificity (78%) for osteomyelitis. It may be difficult to differentiate from soft tissue infections though, and they are expensive and time-consuming.
• Magnetic resonance imaging (MRI) has the best sensitivity and specificity of all the imaging techniques used (99% and 83%, respectively) and is considered now the diagnostic procedure of choice [19]. • The definitive diagnosis can be done with a bone biopsy. Specimens can be obtained through an open (at the time of debridement or surgery) or percutaneous biopsy. • This will allow a histopathological diagnosis to be made, based upon necrosis and infiltration with leucocytes or chronic inflammatory cells, as well as cultures and antimicrobial susceptibilities to be determined. • Patients who are receiving antibiotic therapy may have a negative culture, but histopathology should help diagnose infection. • Bone biopsy is usually needed if the diagnosis remains in doubt after other diagnostic tests have been performed or if the aetiological agent cannot be determined because of confusing culture results or previous antibiotic treatment. However, it is not always possible or practical to obtain a bone biopsy in all diabetic patients with suspected osteomyelitis, since the incision made for the biopsy may not heal in patients with advanced ischaemia. In such patients, empiric therapy for the expected pathogens should be given (usually polymicrobial infections, with S. aureus the most common aetiological agent and streptococci, Enterobacteriaceae and anaerobes also commonly contributing).
8.1.7.6 Severity Classification • Classifying the severity of a foot infection requires defining the extent of the tissues involved, determining the adequacy of arterial perfusion and assessing systemic toxicity [3]. • Deep infections may have deceptively few superficial signs, and so debridement of callus and necrotic tissues is usually required to assess the depth of the wound and to determine the tissues involved. • The severity of the infection will help to determine the choice of antibiotics that will be used, the route of administration (per os or intravenous), the need for hospitalization and the potential necessity for and timing of surgery. A systematic approach is needed. • The classification scheme proposed by the International Consensus on Diagnosing and Treating the Diabetic Foot is presented in Table 8.1.6 [50].
8.1.7 Infections
Table 8.1.6 International Consensus on the Diabetic Foot: Infection Classification Scheme (from Lipsky [47] A report from the international consensus on diagnosing and treating the infected diabetic foot. Diabetes Metab Res Rev 20 [Suppl 1]:S68– S77, Wiley, with permission) Classification
Definition
Grade 1
No symptoms or signs of infection
Grade 2
Infection involving the skin and subcutaneous tissue only, with no involvement of deeper tissues and no systemic signs and symptoms. No other causes of an inflammatory response (e.g. gout, trauma, acute Charcot neuro-osteoarthropathy, fracture, thrombosis, venostasis). At least two of the following are present: Localized swelling or induration Erythema >0.5–2 cm around the ulcer Local tenderness or pain Local warmth Purulent discharge
Grade 3
Infection involving structures deeper than skin and subcutaneous tissues (e.g. abscesses, osteomyelitis, septic arthritis or necrotizing fasciitis) Erythema (cellulitis) extending >2 cm around an ulcer in addition to one of the following: oedema, tenderness, heat, purulent discharge No signs of a systemic inflammatory response as shown in the grade 4 infection
Grade 4
Any foot infection with signs of a systemic inflammatory response syndrome, manifested by two or more of the following: Temperature <36°C or >38°C Heart rate >90 beats/min Respiratory rate >20 breaths/min PaCO2 <32 mmHg White blood cell count >12,000 or <4000 cells/mm3 ≥10% immature (band) forms
•
•
•
•
•
•
•
•
8.1.7.7 Treatment • Clinical experience and commonly accepted practice suggest that successful treatment of foot infections in diabetes requires control of hyperglycaemia, local wound care, relief of pressure on the ulcer, evaluation
•
of the vascular supply and revascularization if needed, and appropriate antibiotic therapy. Antibiotic therapy should ideally be based on appropriate culture results. Surface bacterial cultures of the wound are often misleading and may not represent the organisms within the underlying tissues of the wound. While the gold standard is a tissue biopsy, this is an invasive approach and needs specialized microbiological processing. Therefore, simpler methods are usually practised. After cleansing and debridement of the wound, cultures of the deep portion of the ulcer base should be collected. Abscesses should be aspirated and the aspirate sent for both aerobic and anaerobic cultures. Exudates from draining sinuses should also be sent for cultures. Superficial foot infections can be treated with oral antimicrobial therapy, without hospitalization, provided appropriate follow-up (every 2–3 days initially) is arranged. Severe infections and the majority of patients with a moderate infection should be hospitalized, at least initially. Limb-threatening infections and osteomyelitis are more difficult to treat and surgical resection of affected bone is often required to achieve a cure. Parenteral therapy is usually required for these infections, as well as for severely sick people with comorbidities, the immunocompromised, or those who cannot tolerate oral therapy (e.g. due to excessive vomiting, etc). In addition, any patient who requires more complex wound care or multiple diagnostic studies or consultations should be hospitalized. Finally, patients who are unable to care for themselves and do not have adequate social support (e.g. to do dressing changes, practise off-loading of the infected foot, keep follow-up appointments, etc.) should also be hospitalized. Empirical therapy, covering the commonest pathogens (especially aerobic Gram-positive cocci), is given initially, awaiting culture results. Local prevalence of antibiotic resistance {especially to methicillin-resistant Staphylococcus aureus (MRSA), a common problem lately [79]}, any patient allergies, organ dysfunction (e.g. liver, kidney insufficiency, etc.), and cost and availability of various antimicrobial agents should be taken into consideration. Recent culture results and recent antibiotic administration should also be considered. For mild infections, narrow-spectrum agents are usually sufficient, whereas
515
516
8.1 Diabetic Foot
for more severe infections, broad-spectrum antibiotics are needed to cover the wide array of microorganisms usually involved. Topical antibiotic therapy is controversial, but may be adequate for mild infections. It also has the advantage of drawing the attention of both the patient and the physician to the wound, and the need for good wound care. • Antiseptics (e.g. povidone-iodine or chlorhexidine) are not recommended since they are too harsh on the host tissues. Topical antibiotics, such as silver sulfadiazine, neomycin, polymixin B, gentamicin and mupirocin have been used for soft tissue infections at other sites of the body, but there are no published data on their efficacy in diabetic foot infections. Once culture results and susceptibilities are known, they should be considered together with the clinical response of the patient to the empirical therapy given. If the patient is doing well and the infection is improving, no change in treatment is warranted, no matter what the culture results are (even if some or all of the isolated organisms show resistance to the agents used). If the patient is not responding adequately and the culture reveals pathogens resistant to the selected empirical therapy, then appropriate alternative or additional agents should be utilized. If the infection is worsening despite susceptibility of the isolated bacteria to the chosen regimen, the need for surgical intervention or the possibility that fastidious organisms were missed should be entertained. The choice of specific antibiotics is not straightforward. Antibiotic agents that have shown clinical effectiveness, alone or in combination, in published studies include the following [27, 29, 49]: • Cephalosporins (cephalexin orally, cefoxitin and ceftizoxime parenterally). • Penicillin/β-lactamase inhibitors (amoxicillin/clavulanate orally, ampicillin/sulbactam, piperacillin/tazobactam, ticarcillin/clavulanate parenterally). • Fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin orally and parenterally). • Other agents: clindamycin (orally and parenterally), imipenem/cilastatin (parenterally), linezolid (orally and parenterally). Overall the clinical and microbiological effectiveness of the various antibiotics in the various trials has been similar, with no one agent showing superiority over the others [20]. Therapy should therefore be individualized, taking into consideration the various other factors of the patient
and his or her disease mentioned above. Infection recurs in 20–30% of patients, especially in those with underlying osteomyelitis. The optimal duration of therapy is not definitely established either. Mild to moderate infections usually require 1–2 weeks of treatment, whereas for more serious infections, 2–4 weeks is usually needed. Longer duration may be needed for immunocompromised patients, and patients with osteomyelitis or ischaemic wounds. Peripheral vascular disease may limit antibiotic penetration to infected foot tissues. Even then though, antibiotics are necessary to prevent spread of infection. A revascularization procedure (by-pass of angioplasty) will be extremely helpful in delivering the antibiotics and host leucocytes to the infected area. Novel approaches have been tried for antibiotic delivery to ischaemic limbs; for example, retrograde intravenous perfusion under pressure [25], intraarterial (e.g. femoral) administration of antibiotics [23], or primary closure of debrided wounds with catheter instillation of antibiotics [17]. These techniques require further study. Osteomyelitis in particular poses a great therapeutic problem. • Although intravenous therapy is generally more effective than oral therapy, oral therapy can also be effective if the known or suspected pathogens are susceptible and the patient is likely to be compliant with the regimen. • Antimicrobial therapy is less likely to be effective if there are extensive bony abnormalities, unless a thorough debridement is performed. Patients with severe neuropathy and/or severe vascular insufficiency often respond better to measures to limit pressure-induced tissue damage or to increase blood flow to the foot (such as angioplasty) than to repetitive or prolonged courses of antibiotics. • The usual therapy for osteomyelitis is parenteral initially and prolonged (at least 4 weeks), although the optimal regimen and when to switch to oral therapy remain unclear. Doses at the highest recommended ranges, for at least 2 months (and usually 3–6 months), have generally been employed. If all of the infected bone is removed, a shorter course of antibiotics (e.g. around 2 weeks) may be sufficient. • For some patients, long-term suppressive therapy or intermittent short courses of treatment for recrudescent symptoms may be the most appropriate approach. Antibiotic impregnated beads may be useful, especially to fill wound dead space [73]. Also antibiot-
8.1.8 Treatment of the Diabetic Ulcer
ic-impregnated orthopaedic implants have been used successfully in a few small series [88]. • While it is difficult to know when osteomyelitis is cured, evidence for this includes a drop in an elevated ESR or CRP level, reconstitution of destroyed bone on plain radiograph or resolution of increased uptake on a radioisotope leucocyte scan [46]. • A short-term study comparing granulocyte colonystimulating factor (G-CSF) with placebo in 40 diabetic patients with foot infections demonstrated earlier eradication of pathogens (4 vs. 8 days), quicker resolution of cellulitis (7 vs. 12 days), shorter duration of intravenous antibiotic therapy (8 vs. 14 days) and a shorter hospital stay (10 vs. 18 days) in those receiving G-CSF [28]. These results were not confirmed in three consecutive studies however [22, 36, 89] but the combined results suggested that adding G-CSF was associated with fewer surgical procedures, including amputations [50]. • Systemic hyperbaric oxygen (HBO) has also been used in some studies, with improvement in wound healing and a reduced rate of amputations [87]. It is an expensive and burdensome procedure and needs further evaluation to define which patients will definitely benefit from its use. For the time being, both procedures (G-CSF and HBO) are used only as adjunctive measures for refractory, severe infections.
8.1.8 Treatment of the Diabetic Ulcer • Clinical evaluation will determine the extent and duration of the treatment of a diabetic ulcer. • Local and systemic factors play a role. The presence of neuropathy, ischaemia, infection or a combination of these is very crucial in deciding treatment options. Foot deformity and rigidity and previous ulcerations and amputations are significant risk factors for nonhealing. • A team approach is usually required. • Successful treatment requires control of hyperglycaemia, local wound care, pressure relief, evaluation of the vascular supply and revascularization if needed and appropriate antibiotic therapy, if needed. Continuous re-evaluation of these treatment modalities is mandatory, in order to assure adequate healing. • Local wound care is not a simple, straightforward matter. It requires cleansing, irrigation and debridement
of the ulcer and the surrounding tissues and application of a variety of available wound dressings. For nonhealing ulcers, newer biological techniques have been tried, such as human skin equivalents and growth factors. • There are several methods of wound debridement. Sharp surgical debridement of the hyperkeratotic rim and ulcer base, with removal of surface debris and necrotic material is considered the most selective and efficacious method. Other methods include those that are mechanical (with wet-to-dry gauze dressings, irrigation, pulsatile lavage or whirlpool), autolytic (with moist interactive dressings – hydrogels, alginates, transparent films and hydrocolloids) and enzymatic (collaginase, papain, urokinase, etc.), but these have frequent problems (cost, time, trauma to the wound, allergies, etc.) and their results are not as good as surgical debridement. Recently, biological debridement with sterile maggots has been tried in small series with some success [18], but data on efficacy are currently limited. • Dressings are used to cover the wound and insulate it from the environment. A moist wound environment provides the best local conditions for wound regeneration and repair and optimizes wound healing. An ideal dressing should be able to remove excess exudates and toxic components from the wound, maintain a high humidity at the wound/dressing interface, allow gaseous exchange, provide thermal insulation, afford protection from secondary infection, be free from particulate or toxic contaminants, allow removal without trauma at dressing changes, allow wound monitoring, be comfortable and easy to use and be small enough to allow usage of the patients’ footwear. It is evident that no single dressing meets all these diverse requirements. Available dressing materials are broadly classified into films, foams, hydrogels, hydrocolloids, alginates, hydrofibres and medicated dressings. • The use of various local growth factors has produced promising results for nonhealing ulcers and currently becaplermin (PDGF) is the only one approved for clinical use in diabetic foot ulcers [78]. Post-marketing experience has not been very encouraging though. Hyaluronic acid (a polysaccharide that stimulates fibroblasts and the formation of extracellular matrix) and inhibitors of matrix metalloproteinases are also under investigation. Stem cell and gene therapy (especially with the use of genes for vascular endothelial growth factor, VEGF) also show some promise, but are
517
518
8.1 Diabetic Foot
•
•
•
•
still in their infancy. Bioengineered skin products have been used as well to cover ulcers that are nonhealing. They survive for no longer than a few weeks and their principal benefit lies in their ability to stimulate tissue regeneration by the release of growth factors and cytokines. Bioengineered human dermis from neonatal foreskin is available as Dermagraft, while graftskin (Apligraf®) is a bioengineered composite graft. These products are expensive and require skilled handling for usage. Results of their efficacy are still not definite. Pressure relief of the wound is vitally important for achieving healing. Several devices can be used to relieve pressure on the ulcer (mechanical off-loading), including removable cast walkers, half-shoes and total contact casts. The latter appears to be the best for enhancing healing [4]. The disadvantages of the total contact cast include the need for expertise in applying it, inability to look at the wound on a daily basis, inconvenience in activities of daily living and expense. It is contraindicated for patients with infected wounds or osteomyelitis. The presence of ischaemia needs to be evaluated and corrected with appropriate revascularization procedures if needed (see Chapter 5.5, Aortoiliac occlusive disease, by D. Palombo, and Chapter 7.2, Femoro-distal by-pass surgery, by E. Bastounis) and the presence of infection needs to be appropriately addressed (see Section 8.1.7, Infections). Usually the treatment programme does not require hospitalization of the patient and most ulcers that heal do so within 4–6 weeks. Close monitoring is mandatory though and hospitalization for bed rest and intravenous antibiotic therapy are advisable if the ulcer does not improve. Extra-depth and extra-wide shoes with special inserts are often prescribed for prophylactic reasons once the ulcer has healed, but their efficacy in preventing an ulcer is questionable [70].
References 1. Abbott CA, Carrington AL, Ashe H, Bath S, Every LC, Griffiths J, Hann AW, Hussein A, Jackson N, Johnson KE, Ryder CH, Torkington R, Van Ross ER, Whalley AM, Widdows P, Williamson S, Boulton AJ, North-West Diabetes Foot Care Study (2002) The North-West Diabetic Foot Care Study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based patient cohort. Diabet Med 20:377–384
2. Armstrong DG, Perales TA, Murff RT et al (1996) Value of white blood cell count with differential in the acute diabetic foot infection. J Am Podiatr Med Assoc 86:224–227 3. Armstrong DG, Lavery LA, Harkless LB (1998) Validation of a diabetic wound classification system. The contribution of depth, infection and ischemia to risk of amputation. Diabetes Care 21:855–859 4. Armstrong DG, Nguyen HC, Lavery LA et al (2001) Offloading the diabetic foot wound: a randomized clinical trial. Diabetes Care 24:1019–1022 5. Assal JP, Mehnert H, Tritschler HS, Sidorenko A, Keen H (2002) “On your feet” workshop on the diabetic foot. J Diabet Comp 16:183–191 6. Bonham P (2001) A critical review of the literature. Part i: Diagnosing osteomyelitis in patients with diabetes and foot ulcers. J Wound Ostomy Continence Nurs 28:73–88 7. Bonham P (2001) A critical review of the literature. Part ii: Antibiotic treatment of osteomyelitis in patients with diabetes and foot ulcers. J Wound Ostomy Continence Nurs 28:141–149 8. Borssen B, Bergenheim T, Lithner F (1990) The epidemiology of foot lesions in diabetic patients aged 15–50. Diabet Med 7:438–444 9. Boulton AJM (2000) The pathway to ulceration: aetiopathogenesis. In: Boulton AJM, Connor H, Cavanagh PR (eds) The foot in diabetes, 3rd edn. Wiley, Chichester, p 21 10. Boulton AJM (2004) The diabetic foot: from art to science. The 18th Camillo Golgi lecture. Diabetologia 47:1343–1353 11. Boulton AJ, Malik RA (1998) Diabetic neuropathy. Med Clin North Am 82:909–929 12. Bouter KP, Storm AJ, Groot RRM, Uitslager R, Erkelens DW, Diepersloot RJA (1993) The diabetic foot in Dutch hospitals: epidemiological features and clinical outcomes. Eur J Med 2:215–218 13. Boyko EJ, Lipsky PA (1995) Infection and diabetes mellitus. In: Harris MI (ed) Diabetes in America, 2nd edn. NIH Publication No 95–1468. National Institutes of Health, Bethesda, pp 485–499 14. Brodsky J (1999) In: Coughlin MJ, Mann RA (eds) Surgery of the foot and ankle, 7th edn. Mosby, Philadelphia 15. Chaturvedi N, Abbott CA, Whalley A, Leggetter SY, Boulton AJM (2002) Risk of diabetes-related amputation in south Asians vs Europeans in the UK. Diabet Med 19:99–106 16. Colwell JA, Lyons TJ, Klein RL et al (2001) Atherosclerosis and thrombosis in diabetes mellitus: new aspects of pathogenesis. In: Bowker JH, Pfeifer MA (eds) Levin and O’Neil’s: the diabetic foot, 6th edn. Mosby, Philadelphia, pp 65–106 17. Connolly JE, Wrobel JS, Anderson RF (2000) Primary closure of infected diabetic foot wounds. A report of closed instillation in 30 cases. J Am Podiatr Med Assoc 90:175–182
References
18. Courtney M (1999) The use of larval therapy in wound management in the UK. J Wound Care 8:177–179 19. Craig JG, Amin MB, Wu K et al (1997) Osteomyelitis of the diabetic foot. MR imaging – pathological correlation. Radiology 203:849–855 20. Cunha BA (2000) Antibiotic selection for diabetic foot infections: a review J Foot Ankle Surg 39:253–257 21. Davi G, Gresele P, Violi F et al (1997) Diabetes mellitus, hypercholesterolemia, and hypertension but not vascular disease per se are associated with persistent platelet activation in vivo. Evidence from the study of peripheral arterial disease. Circulation 96:69–75 22. de Lalla F, Pellizzer G, Strazzabosco M et al (2001) Randomized prospective controlled trial of recombinant granulocyte colony-stimulating factor as adjunctive therapy for limbthreatening diabetic foot infection. Antimicrob Agents Chemother 45:1094–1098 23. Dorigo B, Cameli AM, Trapani M et al (1995) Efficacy of femoral intra-arterial administration of teicoplanin in grampositive diabetic foot infections. Angiology 46:1115–1122 24. Edmonds ME, Blundell MP, Morris ME, Thomas EM, Cotton LT, Watkins PJ (1986) Improved survival of the diabetic foot: the role of a specialized foot clinic. Q J Med 60:763–771 25. el-Sarkey Mel S (1997) Local intravenous therapy in chronic inflammatory and vascular disorders of the foot. Int Surg 82:175–181 26. Eneroth M, Apelqvist J, Stenstrom A (1997) Clinical characteristics and outcome in 223 diabetic patients with deep foot infections. Foot Ankle Int 18:716–722 27. Gentry LO, Rodriguez G (1990) Oral ciprofloxacin compared with parenteral antibiotics in the treatment of osteomyelitis. Antimicrob Agents Chemother 34:40–43 28. Gough A, Clapperton M, Rolando M et al (1997) Randomized placebo-controlled trial of granulocyte colony-stimulating factor in diabetic foot infection. Lancet 350:855–859 29. Grayson ML, Gibbons GW, Haberson GM et al (1994) Use of ampicillin/sulbactam vs. imipenem/cilastatin in treatment of limb-threatening foot infections in diabetic patients. Clin Infect Dis 18:683–693 30. Grayson ML, Gibbons GW, Balogh K et al (1995) Probing to bone in infected pedal ulcers. A clinical sign of underlying osteomyelitis in diabetic patients. J Am Med Assoc 273:721–723 31. Humphrey ARG, Thomas K, Dowse GK, Zimmet PZ (1996) Diabetes and non-traumatic lower extremity amputations. Incidence, risk factors and prevention: a 12 years follow-up study in Nauru. Diabetes Care 19:710–716
32. International Working Group on the Diabetic Foot (1999) In: International consensus on the diabetic foot. International Working Group on the Diabetic Foot, The Netherlands, pp 20–96 33. James RW, Pometta D (1991) The distribution profiles of very low and low density lipoproteins in poorly controlled male, type 2 (non-insulin-dependent) diabetic patients. Diabetologia 34:246–252 34. Jeffcoate WJ, Harding KG (2003) Diabetic foot ulcers. Lancet 361:1545–1551 35. Jude EB, Selby PL, Burgess J, Lilleystone P, Mawer EB, Page SR, Donohoe M, Foster AV, Edmonds ME, Boulton AJ (2001) Bisphosphonates in the treatment of Charcot neuroarthropathy: a double-blind randomised controlled trial. Diabetologia 44:2032–2037 36. Kastenbauer T, Hornlein B, Sokol G et al (2003) Evaluation of granulocyte colony-stimulating factor (filgrastim) in infected diabetic foot ulcers. Diabetologia 46:27–30 37. Katsilambros N, Tentolouris N, Tsapogas P, Dounis E (2003) Neuro-osteoarthropathy. The Charcot foot. In: Katsilambros N, Tentolouris N, Tsapogas P, Dounis E (eds) Atlas of the diabetic foot. John Wiley, Chichester, pp 185–212 38. Katsilambros N, Tentolouris N, Tsapogas P, Dounis E (2003) Anatomical risk factors for diabetic foot ulceration. Atlas of the diabetic foot. John Wiley, Chichester, pp 41–72 39. Kempler P (2002) Types, clinical presentation and diagnosis of somatic neuropathy. In: Kempler P (ed) Neuropathies. Springer, Berlin Heidelberg New York, pp 53–78 40. Khan BV, Parthasarathy SS, Alexander RW, Medford RM (1995) Modified LDL and its constituents augment cytokine-activated vascular cell adhesion molecule-1 gene expression in human vascular endothelial cells. J Clin Invest 95:1262–1270 41. Krasner DL, Sibbald RG (2001) Diabetic foot ulcer care: assessment and management. In: Bowker JH, Pfeifer MA (eds) Levin and O’Neal’s: the diabetic foot, 6th edn. Mosby, St. Louis, pp 283–300 42. Kumar S, Ashe HA, Parnell LN, Fernando DJS, Tsigos C, Young RJ, Boulton AJM (1994) The prevalence of foot ulceration and its correlates in type 2 diabetic patients: a population-based study. Diabet Med 11:480–484 43. Lavery LA, Van Houtum WH, Armstrong DG (1997) Institutionalization following diabetes-related lower extremity amputation. Am J Med 5:383–388 44. Lavery LA, Armstrong DG, Wunderlich RP, Tredwell J, Boulton AJM (2003) Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in Mexican Americans and non-Hispanic whites from a diabetes management cohort. Diabetes Care 26:1435–1438
519
520
8.1 Diabetic Foot
45. Lee BY, Guerra J, Civelek B (1995) Compartment syndrome in the diabetic foot. Adv Wound Care 8(6):36,38,41–42 46. Lipsky BA (1997) Osteomyelitis of the foot in diabetic patients. Clin Infect Dis 25:1318–1326 47. Lipsky BA (2004) A report from the international consensus on diagnosing and treating the infected diabetic foot. Diabetes Metab Res Rev 20 [Suppl 1]:S68–S77 48. Lipsky BA, Pecoraro RE, Larson SA et al (1990) Outpatient management of uncomplicated lower-extremity infections in diabetic patients. Arch Intern Med 150:790–797 49. Lipsky BA, Baker PD, Landon GC, Fernau R (1997) Antibiotic therapy for diabetic foot infections: comparison of two parenteral-to-oral regimens. Clin Infect Dis 24:643–648 50. Lipsky BA, Berendt AR, Embil J, de Lalla F (2004) Diagnosing and treating diabetic foot infections. Diabetes Metab Res Rev 20 [Suppl 1]:S56–S64 51. Manes C, Ionescu-Tirgoviste C, Koeva L, Koev D, Agaci F, Djordjevic P, Bogoev M (2003) High prevalence of foot ulceration in the Balkan region-a multicenter study from the BALKANDIAB network. Diabetologia 46 [Suppl 2]:A3 52. McLeod AF, Williams DRR, Sonksen PH, Boulton AJM (1991) Risk factors for foot ulcers in hospital clinic attenders. Diabetologia 34 [Suppl 2]:A39 53. McMahon MM, Bistrian BR (1995) Host defenses and susceptibility to infection in patients with diabetes mellitus. Infect Dis Clin North Am 9:1–10 54. Meggitt B (1976) Surgical management of the diabetic foot. Br J Hosp Med 16:227–232 55. Mene P, Festuccia F, Pugliese F (2003) Clinical potential of advanced glycation end-product inhibitors in diabetes mellitus. Am J Cardiovasc Drugs 3:315–320 56. Morbach S, Lutale JK, Viswanathan V, Mollenberg J, Ochs HR, Rajashekar S, Ramachandran A, Abbas ZG (2004) Regional differences in risk factors and clinical presentation of diabetic foot lesions. Diabet Med 21:91–95 57. Moss S, Klein R, Klein B (1992) The prevalence and incidence of lower extremity amputation in a diabetic population. Arch Intern Med 152:510–616 58. Mueller IS, de Grauw WJ, van Gerwen WH, Bartelink ML, van Den Hoogen HJ, Rutten GE (2002) Foot ulceration and lower limb amputation in type 2 diabetic patients in Dutch primary health care. Diabetes Care 25:570–574 59. Murray HJ, Young MJ, Boulton AJM (1996) The relationship between callus formation, high pressures and neuropathy in diabetic foot ulceration. Diabet Med 13:979–982 60. Neil HAW, Thompson AV, Thorogood M, Fowler GH, Mann IJ (1989) Diabetes in the elderly: the Oxford community study. Diabet Med 6:608–613
61. Newman LG, Waller J, Palestro CJ et al (1991) Unsuspected osteomyelitis in diabetic foot ulcers. J Am Med Assoc 266:1246–1251 62. O’Meara SM, Cullum NA, Majid M, Sheldon TA (2001) Systematic review of antimicrobial agents used for chronic wounds. Br J Surg 88:4–21 63. Orchard TJ, Strandness DE (1993) Assessment of peripheral vascular disease in diabetes. Diabetes Care 15:1199–1209 64. Pendsey S (1994) Epidemiological aspects of the diabetic foot. J Diabetes Dev Countries 2:37–38 65. Rajbhandari SM, Sutton M, Davies C et al (2000) “Sausage toe”: a reliable sign of underlying osteomyelitis. Diabet Med 17:74–77 66. Ramsey SD, Newton K, Blough D et al (1999) Incidence, outcomes and cost of foot ulcers in patients with diabetes. Diabetes Care 22:382–387 67. Reiber GE (1996) The epidemiology of diabetic foot problems. Diabet Med 13 [Suppl 1]:S6–S11 68. Reiber GE, Ledoux WR (2002) Epidemiology of diabetic foot ulcers and amputations: evidence for prevention. In: Williams B, Herman W, Kinmonth AL, Warehan NJ (eds) The evidence-base for diabetes care. John Wiley, Chichester, pp 641–665 69. Reiber GE, Boyko E, Smith DG (1995) Lower extremity ulcers and amputations in individuals with diabetes. In: Harris MI (ed) Diabetes in America, 2nd edn. National Institutes of Health Publication No. 95–1468. National Institutes of Health, Bethesda, pp 409–427 70. Reiber GE, Smith DG, Wallace C et al (2002) Effect of therapeutic footwear on foot reulceration in patients with diabetes: a randomized controlled trial. J Am Med Assoc 287:2552–2558 71. Resnick HE, Valsania P, Philips CL (1999) Diabetes mellitus and non-traumatic lower extremity amputation in black and white Americans: the national health and nutrition examination survey epidemiology follow-up study 1971-1992. Arch Intern Med 159:2470–2475 72. Rith-Najarian SJ, Stolusky T, Gohdes DM (1992) Identifying diabetic patients at high risk of lower-extremity amputation in a primary health care setting: a prospective evaluation of simple screening criteria. Diabetes Care 15:1386–138 73. Roeder B, Van Gills CC, Maling S (2000) Antibiotic beads in the treatment of diabetic pedal osteomyelitis. J Foot Ankle Surg 39:124–130 74. Sanders LJ (2004) The Charcot foot: historical perspectives 1827–2003. Diabetes Metab Res Rev 20 [Suppl 1]:S4–S8 75. Sapico FL, Witte JL, Canawati HL et al (1984) The infected foot of the diabetic patient: quantitative microbiology and analysis of clinical features. Rev Infect Dis 6 [Suppl 1]:171–176
References
76. Sekiguchi N, Umeda F, Masakado M et al (1997) Immunohistochemical study of prostacyclin-stimulating factor (PSF) in the diabetic and atherosclerotic human coronary artery. Diabetes 46:1627–1632 77. Siitonen OI, Niskanen LK, Laakso M, Siitonen JT, Pyorala K (1993) Lower extremity amputation in diabetic and nondiabetic patients: a population based study in Eastern Finland. Diabetes Care 16:16–20 78. Smiel JM, Wieman TJ, Steed DL et al (1999) Efficacy and safety of becaplermin (recombinant human platelet-derived growth factor-BB) in patients with nonhealing, lower extremity diabetic ulcers: a combined analysis of four randomized studies. Wound Repair Regen 7:335–346 79. Tentolouris N, Jude EB, Smirnof I et al (1999) Methicillinresistant Staphylococcus aureus: an increasing problem in a diabetic foot clinic. Diabet Med 16:767–771 80. Tentolouris N, Al-Sabbach S, Walker M, Boulton AJM, Jude EB (2004) Mortality in diabetic and nondiabetic patients after amputations performed from 1990 to 1995: a 5-year follow-up study. Diabetes Care 27:1598–1604 81. Thompson P (1998) The microbiology of wounds. J Wound Care 7:477–478 82. Trans-Atlantic Inter-Society Consensus (TASC) working group (2000) Clinical evaluation of critical limb ischemia. J Vasc Surg 31 [Suppl]:S186 83. Treece KA, Macgarlane RM, Pound N et al (2004) Validation of a system of foot ulcer classification in diabetes mellitus. Diabet Med 21:987–991
84. Veves A, Uccioli L, Manes C, Van Acker K, Komninou H, Philippides P, Katsilambros N, De Leeuw I, Manzinger G, Boulton AJ (1994) Comparison of risk factors for foot problems in diabetic patients attending teaching hospital outpatient clinics in four different European states. Diabet Med 11:709–713 85. Vileikyte L (2001) Diabetic foot ulcers: a quality of life issue. Diabetes Metab Res Rev 17:246–249 86. Ward JD (1982) The diabetic leg. Diabetologia 22:141–147 87. Wunderlich RP, Petrs EJG, Lavery L (2000) Systemic hyperbaric oxygen therapy. Lower-extremity wound healing and the diabetic foot. Diabetes Care 23:1551–1555 88. Yamashita Y, Uchida A, Yamakawa T et al (1998) Treatment of chronic osteomyelitis using calcium hydroxyapatite ceramic implants impregnated with antibiotics. Int Orthop (SICOT) 22:247–251 89. Yonem A, Cakir B, Guler S, Azal O O, Corakci A (2001) Effects of granulocyte-colony stimulating factor in the treatment of diabetic foot infection. Diabetes Obes Metab 3:332–327 90. Young MJ (2000) Classifications of ulcers and its relevance to management. In: Boulton AJM, Connor H, Cavanagh PR (eds) The foot in diabetes, 3rd edn. John Wiley, Chichester, pp 61–80 91. Young MJ, Jones GC (1997) Diabetic neuropathy: symptoms, signs and assessment. In: Boulton AJM (ed) Diabetic neuropathy. Marius, Carnforth, pp 41–62 92. Young MJ, Breddy JL, Veves A, Boulton AJM (1994) The prediction of diabetic foot ulceration using vibration perception thresholds: a prospective study. Diabetes Care 17:557–560
521
Amputations
525
9.1 Amputation of Extremities Vladimir Sefranek
9.1.1 Introduction 9.1.1.1 Scope of the Problem The main goal of all vascular surgeons in the field of arterial diseases or trauma in the extremities is arterial reconstruction in order to save vitality and function. However, despite substantial improvement of limb-salvage rates in patients with peripheral vascular disease, extremity amputation can be, in some cases, the only possible treatment for a limb severely affected by trauma, infection, tumour, or at the last stage of ischaemia [8]. Many vascular surgeons have traditionally viewed amputations in the treatment of an ischaemic patient as a failure to save the threatened extremity. Instead, amputation surgery should be considered as a very important part of the therapeutic armamentarium in the complex management of patients with limb-threatening disorders of the extremities. Extremity amputation can create enormous potential for the rehabilitation of many patients temporarily immobilized by vascular disease of their extremity. In the context of surgical and endovascular procedures, extremity amputation has very often been viewed as a somewhat inferior management tool. This attitude can create: • technical errors • problems in stump healing • a painful, functionally inappropriate stump (too long or too short) disabling mobilization • problems with rehabilitation • problems with proper prosthesis manufacturing. From the tactical point of view, incorrect timing of the management steps is often encountered, thus causing failure and further devastation. The majority of patients involved are diabetics with signs of diabetic foot. Many
surgeons indicate minor amputation for all cases of gangrene without taking any other steps into consideration. In my opinion it is imperative to follow these rules: • First, manage the infection • Then do the arterial reconstruction • Finally, carry out minor amputation. This is the so-called Vollmar IRA principle [16]. The ratio of number of arterial reconstructions to number of major leg amputations due to occlusive disease can give quite precise information about the level of vascular disease management in a particular region or institution. From the historical point of view, amputation is one of the oldest known surgical procedures. However, it was not until the mid sixteenth century that Ambroise Paré described the surgical techniques that are still in use today. Although often considered a destructive procedure, amputation, when appropriately performed, offers enormous potential for rehabilitation in most patients [4].
9.1.2 Incidence and Morbidity of Amputation In general, the mortality associated with amputation depends not so much on the procedure itself as on the presence or absence of risk factors, especially cardiorespiratory insufficiency and cerebrovascular disease. The amputation rate in the USA is approximately 30 per 100,000 people per year but is 15–20 times higher among diabetic patients, who have an incidence of amputation of 600 per 100,000 [2, 3, 5]. Overall, more than 50,000–60,000 major limb amputations are estimated to be performed each year in the USA [9]. In the United Kingdom, approximately 65,000 amputees are known to the Department of Health, with 6000 new patients being referred to limb-fitting centres annually [13, 18].
526
9.1 Amputation of Extremities
9.1.3 Classification and Indications Causes of extremity amputation in occlusive disease or trauma include severe devastation of the extremity tissues and infection that has seriously destroyed those tissues and at the same time is life-threatening for the patient because of sepsis and toxaemia. The timing of the procedure depends on the patient’s clinical situation. In cases of serious tissue damage with an associated infection and sepsis, amputation can be considered as life-saving surgery, qualified as emergency amputation. Patients with necroses and gangrene in extremities that have not been subjected to revascularization or those who have had more or less successful arterial revascularization and whose general condition is not threatening are indicated to an elective amputation (Table 9.1.1).
9.1.3.1 Emergency Amputation Emergency amputation in vascular patients due to occlusive disease or trauma has to be considered in cases of extensive tissue necroses, often with secondary infection causing wet gangrene or cellulitis presenting with massive putrid secretion, odour and general signs and symptoms of sepsis. An infection can also be the primary cause of tissue destruction, especially where there is impaired perfusion (e.g. patients with diabetes or immunodeficiency states). The basic therapy for all these patients is major emergency amputation with exact debridement. The term guillotine-like amputation is usually used; namely, a procedure without sutures of the stump or with only several stitches approaching the wound margins.
After overcoming the infection a secondary closure can be performed. Acute or critical chronic ischaemia of an extremity, or severe trauma with extensive tissue loss or damage may, in some cases almost instantly, cause irreversible changes in tissues, thus hindering successful arterial reconstruction. Moreover, in the cases mentioned above there is a serious risk of complicating ischaemic and reperfusion changes, threatening the patient’s life. In all these circumstances emergency major amputation is a life-saving procedure.
9.1.3.2 Elective Amputations Secondary Amputation Revascularization of the lower extremity remains the treatment of choice for most patients with significant arterial occlusive disease. Redo vascular reconstructive procedures are also beneficial for limb salvage and for preserving ambulation ability. Unfortunately, in many patients, the continued progression of atherosclerosis obliterates all major distal vessels, eliminating the possibility of further reconstruction. Vascular disease that is not reconstructable has become the most common indication for secondary amputation, accounting for nearly 60% of patients. Persistent infection, despite aggressive vascular reconstruction and appropriate treatment, is the second most common indication. The goals of secondary amputation are: • relief of ischaemic pain • complete removal of diseased, infected and necrotic tissue • achievement of complete healing • construction of a stump suitable for ambulation with prosthesis.
Table 9.1.1 Indications for leg amputation Occurrence (%) Complications of diabetes mellitus
60–80
Nondiabetic infection with ischaemia
15–25
Ischaemia without infection
5–10
Chronic osteomyelitis
3–5
Trauma
2–5
Miscellaneous
5–10
The antecedent reconstructions do not worsen the condition of the leg and do not predispose the patient to a higher level of amputation. Therefore, initial attempts at vascular reconstruction are indicated. Secondary amputation is indicated when vascular intervention is no longer possible or when the limb continues to deteriorate despite the presence of patent reconstruction [15]. In a dysvascular patient, an elective amputation of the extremity may be considered because of chronic progressive ischaemia with rest pain and/or
9.1.4 Determination of Amputation Level
gangrene or necroses after one or more unsuccessful arterial reconstructions. Another indication may be the inability to improve perfusion because of an inappropriate out-flow tract. Finally, patients with extreme destruction and/or necrosis of tissues causing extensive, profound or proximal damage (tarsal bones involved) are also candidates for elective amputation.
Primary Amputation Primary amputation is defined as amputation of the ischaemic lower extremity without an antecedent attempt at revascularization. Amputation is considered as a primary therapy only in selected cases. The complete absence of detectable distal vessels using modern imaging techniques (magnetic resonance angiography, Duplex ultrasonography and high-resolution digital angiography), especially in the setting of advanced distal ischaemia associated with a low ankle/brachial blood pressure index (ABI) (<0.30), suggests that vascular reconstruction is not possible and that major amputation is inevitable. Such patients are best served by primary amputation. Ulceration and necrosis of the weight-bearing surface of the foot and loss of the heel are frequent causes of primary amputation. Revascularization is useless for the preservation of ambulation in these cases. The use of
myocutaneous free flaps does not yield a positive effect in the majority of cases. Nonambulatory, bed-ridden elderly patients with severe occlusive disease associated with rest pain and tissue loss often with flexion contractures are not candidates for aggressive revascularization. They need only a stable, pain-free limb that can be used for positioning in bed or in a wheelchair and this is better enabled by primary amputation. Other reasons for needing primary major amputation include multi-infarct dementia, immobility after serious brain infarctions, etc. Finally, there are often physical as well as ethical contraindications to aggressive lower-extremity arterial reconstructions in patients with severe occlusive disease and terminal or near-terminal comorbid conditions. These patients require relief from pain and this calls for amputation [15] (Table 9.1.2).
9.1.4 Determination of Amputation Level The level of amputation is determined by a balance between the natural tendency to try to save as much as possible of the extremity and the surgeon’s need to be sure that the amputation will heal at the chosen level. The surgeon’s goal is to avoid an inappropriately high level of amputation and revision of an amputation to a
Table 9.1.2 Indications for primary leg amputation Absolute Psychosocial
Nonambulatory, immobile patient, without transfer capability, with limited cognitive ability, with ipsilateral limb contractures
Anatomical
No reconstructable arteries, uncontrolled pedal sepsis, progressive gangrene beyond midforefoot
Relative Anatomical
Large heel ulcer with no possibility of plastic cover using a free flap
Situational
Life expectation of the patient less than 1 year, excessive risk of a revascularization because of high level of comorbidity, patient has been evaluated by a surgeon skilled in distal bypass surgery and reconstruction excluded as an option, life-threatening sepsis or haemorrhage
Less important
No venous conduit available, no skilled vascular surgeon available
From Durham JR (2000) Lower extremity amputation levels. In: Rutherford RB (ed) Vascular surgery, 5th edn, Vol 2. Saunders, Philadelphia, p 2185, with permission
527
528
9.1 Amputation of Extremities
higher level. In practice, when clinical observation alone is used to choose the site of amputation, the resultant reamputation rate ranges from 15% to 40% [9, 15]. Clinical evaluation consists of detection of the most distal pulse level, skin viability, nutritional changes, physical signs of ischaemia and skin temperature. Although skin viability is the major factor influencing stump healing, clinical determination has little predictive value. Predicting the healing potential of forefoot amputation may be particularly difficult, even with noninvasive techniques [6, 9]. Many special investigative techniques and tests have been advocated for determination of the amputation level: • Transcutaneous PO2 measurement • Skin clearance of [133Xe] • Segmental Doppler blood pressures • Laser Doppler flowmetry • Segmental skin perfusion pressures • Skin temperature measurements (thermography) • Photoplethysmography and digital plethysmography The most reliable noninvasive techniques are transcutaneous PO2 and measurement of skin clearance of [133Xe], and less sensitive tools are segmental Doppler blood pressures and skin perfusion pressures.
The other techniques, namely laser Doppler flowmetry, segmental blood pressure, skin temperature measurement, photoplethysmography and digital plethysmography, do not have as high a predictive value as the techniques mentioned above.
9.1.5 Preoperative Management Preoperative care and peri-procedural management involve treatment of the affected limb and the general condition and stabilization of the patient. It is necessary to treat infection intravenously with antibiotics and incision, debridement and drainage of abscesses and inflammation. Pain should be controlled adequately using strong analgesics. The prevention of large joint contractures is essential for achieving eventual rehabilitation and ambulation. A meticulous assessment of the patient’s cardiorespiratory and renal systems is necessary. Even if urgent amputation is indicated, a period of 4–8 h for cardiac and metabolic stabilization is unavoidable. It is necessary to perform elective procedures with the patient’s condition optimized. Also, the patient should be informed about the possible outcome of the amputation. This, coupled with a sensitive approach and rehabilitation, should moderate the emotional trauma and depression.
9.1.4.1 Transcutaneous Oxygen Tension (PtCO₂) Measurement Transcutaneous oxygen tension (PtCO2) measurement should be taken with a skin sensor electrode heated to 45°C. It provides an accurate indication of the severity of ischaemia and predicts eventual healing success very well (blood oxygen contents depend on local blood flow). Successful healing has generally been reported if the local PtCO2 exceeds 40 mmHg and failure has always occurred at a PtCO2 of <20 mmHg [1, 7, 10, 15, 17].
9.1.4.2 Clearance of [¹³³Xe] It is possible to calculate local skin blood flow (at the proposed site of amputation) by the rate of clearance of an intracutaneous injected dose of [133Xe]. Borderline skin blood flow by this method has been reported to be 2.6 ml·100 g–1 ·min– 1 . Values above this border predict successful healing; values lower than 2.6 ml·100 g– 1 ·min– 1 predict healing only in 50% of cases [9, 11, 15].
9.1.6 Surgical Techniques of Amputation The most frequent types of extremity amputation are as follows: • Lower extremity • Minor amputations: toe amputation, ray amputation, transmetatarsal amputation, Syme’s amputation. • Major amputations: below-knee amputation, above-knee amputation (Fig. 9.1.1). • Upper extremity • Phalangectomy, ray amputation, amputation of the forearm, brachial amputation, arm disarticulation.
9.1.6.1 Toe Amputation • A circular skin incision is made near the base of the toe.
9.1.6 Surgical Techniques of Amputation
• The incision is brought through all tissue planes until the bone surface is scored circumferentially. • It is necessary to strip the periosteum cephalad for a short distance, and then the phalanx is divided distal to the metatarsophalangeal joint using a bone cutter. • After smoothing the edges of the bone, debridement of the wound, and excision of tendons and ligaments, it is necessary to decide on whether to close the skin or not (using interrupted monofilament sutures). This decision is made with regard to the presence or absence of infection and diabetes.
9.1.6.2 Ray Amputation Tissue necrosis or infection extending to the metatarsophalangeal crease is an indication for ray amputation. • A circular skin incision is made at the metatarsophalangeal crease. • The toe is amputated in the same way as described above. • It is necessary to remove the remaining phalangeal bone with the use of a rongeur. • Then the metatarsal head is freed from the attached tendons and ligaments and excised using a rongeur (Fig. 9.1.2). • The ligaments and tendons will then be excised as proximally as possible. • After irrigation, the wound may be closed using interrupted monofilament sutures in a vertical mattress technique. • Ray amputation of the great toe requires a modified skin incision, with the amputation of the metatarsal bone more proximally and a similar skin closure (Fig. 9.1.3).
Fig. 9.1.1 Possible levels for major amputations of the lower limb. (A Hip disarticulation, B–D above-knee amputation, B high-thigh, C mid-thigh, D low-thigh, E supracondylar amputation, F knee disarticulation, G below-knee amputation). From Malone JM (2004) Amputation in dysvascular patient. In: Hobson RW, Wilson SE, Veith FJ (eds) Vascular surgery. Principles and practice, 3rd edn. Dekker, New York, p 557, with permission, [9]
529
530
9.1 Amputation of Extremities
Fig. 9.1.2a,b Ray amputation. a Before amputation, b after amputation
9.1.6.3 Transmetatarsal Amputation Indication for transmetatarsal amputation includes the situation in which gangrene extends slightly beyond the metatarsophalangeal crease. In order to be able to create a reliable posterior flap the plantar skin must be viable. • A slightly semi-arched incision is made on the dorsum of the foot 5–10 mm distal to the midpoint of the metatarsal shafts (Fig. 9.1.4). The incision is gently curved 90° tightly beyond the medial and lateral aspects of the foot. • The incision is continued to the metatarsophalangeal crease and completed by extension across the plantar surface of the foot.
• The incision is carried down to the level of the metatarsal bones, dividing them slightly proximal to the skin incision using a bone cutter or oscillating saw. • The bone edges are smoothed and the tendons and ligaments are divided as proximally as possible. • It is necessary to trim the plantar flap sharply, preserving a thin layer of subcutaneous tissue. • After stopping the bleeding the plantar flap is rotated dorsally, and interrupted absorbable sutures are used to close the subcutaneous layer. • The skin is then closed with interrupted monofilament sutures applying the vertical mattress technique.
9.1.6 Surgical Techniques of Amputation
Fig. 9.1.3a,b Ray amputation of great toe. a Before amputation, b after amputation
9.1.6.4 Syme’s Amputation (Ankle Disarticulation) This type of amputation has been advocated recently because of its satisfactory rehabilitation potential [4]. • A dorsal incision is made anterior to the ankle crease starting at a point distal to the lateral malleolus. • The incision is then curved down and carried through the sole bilaterally to the calcaneus bone; the dorsal incision is brought down to the talus bone anterior to the ankle joint. • Both posterior and anterior tibial arteries are ligated as necessary. The tendons are divided, permitting extreme plantar flexion of the foot.
• After cutting both lateral and medial collateral ligaments the talus may be disarticulated. Then the calcaneus is isolated and excised. • The articular cartilage of the fibula and tibia are cut with a saw and smoothed with a bone file. • Haemostasis is achieved and the heel pad rotated upwards. • The fascia is sutured to the deep fascia over the tibia. • The skin is then closed using interrupted vertical mattress monofilament sutures, which can be left in place for several weeks.
531
532
9.1 Amputation of Extremities
9.1.6.5 Below-knee Amputation
Fig. 9.1.4a–c Transmetatarsal amputation. a Before amputation, b amputation line, c after amputation
Fig. 9.1.5 Below-knee amputation. Skin incision delineation
• Preservation of the knee joint is extremely important for motion and transfer, even in immobile patients. • Below-knee amputation is therefore advantageous compared with above-knee amputation. • There are many ways to perform a below-knee amputation and, in my opinion, it is preferable to use the method of the long posterior myocutaneous flap. • The ideal level of tibial bone transection must not be too distal. The optimal length of the tibial stump is as long as approximately 12 cm distal from the tibial tuberosity. • An anterior skin incision is made about 1 cm distal from this level and should be continued bilaterally to a point 1 cm posterior to the edges of both bones (Fig. 9.1.5). • Following this the incisions are angled and extended distally for a distance between one-third and one-half the circumference of the leg as measured at the level of the proximal incision. • Another possibility for ensuring the correct length of the dorsal flap is to place the apex of the flap into the border between the middle and distal third of the leg. • It is advisable to paint the dorsal flap before beginning the surgery. The right length of the dorsal flap is very important for the final success of the amputation. • The greater and lesser saphenous veins are divided between silk ties, and the sural nerve is transected as high as possible to avoid painful neuromas of the stump. • After dividing the anterior musculature it is necessary to identify the anterior neurovascular bundle and ligate these structures. The remaining muscles
9.1.6 Surgical Techniques of Amputation
• • •
•
•
are carefully divided from the bony attachments, the tibia is scored circumferentially and the periosteum is stripped cephalad. The tibia bone is divided 2 cm proximal to the skin incision with the use of a pneumatic or hand saw. The anterior edge of the tibia is then bevelled at a 45° angle and the surface is made smooth. The fibula is managed in the same manner but it is cut approximately 2 cm proximal to the level of tibia transection. The posterior tibial and peroneal neurovascular bundles are divided. The remaining muscles are then divided using a large amputation knife. It is advisable to remove the soleus muscle in order to thin the posterior flap. The wound is irrigated to remove all debris, haemostasis is achieved and after the placement of a suction drain the skin is closed with monofilament sutures, which are removed approximately 3 weeks after surgery (Fig. 9.1.6).
9.1.6.6 Above-knee Amputation This type of amputation is indicated in patients who are not candidates for below-knee amputation because of ischaemia, infection and irreversibly damaged tissues, or in those whose general condition precludes rehabilitation and mobility. The way to determine the amputation level is mentioned above. Maximal femur length must be preserved, because it will lessen the energy expenditure required for ambulation and improve the chances for successful rehabilitation of the patient. There are three ways to perform above-knee amputation depending on the leg condition, arterial perfusion and tissue damage (see also Fig. 9.1.1): supracondylar amputation, mid-thigh amputation, high femoral amputation. • A circumferential skin incision is made 2–3 cm distal to the site of division of the femur. • The greater saphenous vein is divided and the anterior and medial muscle groups are cut using electro cautery or a large amputation knife. • The superficial femoral artery and vein are suture ligated and the remaining musculature divided. • The sciatic nerve is identified posteriorly, dissected free and suture ligated after gentle traction and shortening. • The femur is then scored 2–3 cm proximal to the skin incision and the periosteum is stripped and transected.
Fig. 9.1.6a–c Below-knee amputation. a Initial phase, b musculocutaneous flaps, c suture line
• The edges of the bone are then smoothed with a bone rasp.
533
534
9.1 Amputation of Extremities
• Haemostasis is achieved, the wound is irrigated and after placement of a suction drain the skin is closed with monofilament sutures, which are removed approximately 3 weeks after surgery.
9.1.6.7 Amputation of the Upper Extremity Although vascular problems in the upper extremities are substantially less frequent than in the lower extremities, occasionally there may arise a situation when a minor or major amputation is unavoidable. Most frequently, causes are irreparable vascular injury, chronic vascular disease (critical ischaemia especially in cases of multisegmental occlusive disease) or tumours. Acute ischaemia (inveterate or recurrent embolization from cardiac sources or thoracic-outlet syndrome) can also lead to irreparable changes and amputation. The ultimate goal of amputation surgery is to restore the maximal functional level of activity for the patient as quickly as possible [14]. • Amputations of the upper extremity are most easily performed with the patient positioned supine and their arm placed on the hand table. Either regional or general anaesthesia is satisfactory for these procedures. • For determination of the level and technique we can apply the same rules as for leg amputations. • Incisions used for these amputations should similarly create two flaps (shown in Fig. 9.1.7). We can distinguish between digital amputation, ray amputation, wrist disarticulation, below-elbow and above-elbow amputation and shoulder disarticulation. Everything mentioned in this chapter regarding the perioperative management, rehabilitation and complications related to leg amputations also hold for upper-extremity amputations.
9.1.7 Postoperative Considerations and Rehabilitation The most commonly used postoperative amputation dressing is the soft stump wrap. Gauze pads are applied to the wound followed by the gauze wrap and an elastic bandage. The amputation stump should be elevated to reduce swelling. It is necessary to hinder the flexion contractures after below-knee amputation using this type of wrap.
Fig. 9.1.7a,b Upper-extremity amputations. a Amputation of the wrist, b possible levels for major amputations. From Seiler JG et al (1995) Upper extremity amputation. In: Ernst CB, Stanley JC (eds) Current therapy in vascular surgery, 3rd edn. Mosby, St. Louis, pp 681, 683, with permission, [14]
Amputation of an extremity is in itself a strong shock for every patient. Rehabilitation of a patient involves moderating his emotional trauma and depression as well as making an effort to enhance his maximal independence, mobility and ambulation.
References
Immediately after the patient is haemodynamically stabilized, it is necessary to start respiratory physiotherapy and intensive exercise of the extremities that are not involved. Prevention of contractures is very important in the early postoperative period because it enables ambulation exercise in the next period.
References 1
2 3
9.1.8 Complications The complications of amputation surgery may be divided into those that are specific to the operation and those that are due to severe cardiopulmonary disease and diabetes. Mortality rates following major amputation have been reported to be as high as 10% for below-knee and 40% for above-knee amputations [4, 9, 12]. The main cause of this enormous mortality is coronary artery disease and cerebrovascular disease, very often present in these polymorbid patients. The long-term survival prospects for diabetics are significantly worse than for nondiabetics. With recent improvements in patient preparation for surgery, anaesthetic techniques and intensive care, there should now be a mortality rate of less than 5% for below-knee and perhaps 10% for above-knee amputations [9]. The main complications of the procedure itself are infection and failure of stump healing due to ischaemia. Amputation level selection by objective tests can minimize postoperative healing failures. Small areas of wound breakdown will often heal with conservative management. Healing failure due to ischaemia with or without infection often requires revision. Haematomata formation can be prevented by meticulous intraoperative haemostasis and using suction drainage. Peri-operative antibiotic prophylaxis is appropriate for minimizing postoperative infection, which has been reported in 12–28% of major amputations. The most frequent late complication is phantom limb pain and disabling stump pain. Reported incidence of these complications is 5–30% [4]. These pain syndromes develop more commonly in patients following amputation for trauma or prolonged ischaemia and are difficult to treat. To avoid them it is advisable to start with aggressive rehabilitation from the early postoperative period. Failure to rehabilitate should also be regarded as a complication.
4
5
6
7
8
9
10
11
12
13 14
Ameli FM, Byrne P, Provan JL (1989) Selection of amputation level and prediction of healing using transcutaneous tissue oxygen tension (PtcO2). J Cardiovasc Surg (Torino) 30:220–224 Berardi RS, Keonin Y (1978) Amputations in peripheral vascular occlusive disease. Am J Surg 135:231–234 Bild DE, Selby JV, Sinnock P, Browner WS, Braveman P, Showstack JA (1989) Lower-extremity amputation in people with diabetes. Epidemiology and prevention. Diabetes Care 12:24–31 Dietzek AM, Scher LA (1994) Lower extremity amputation. In: Clifford M, Sales MD, Goldsmith J, Veith FJ (eds) Handbook of vascular surgery. Quality Medical, St. Louis Dietzek AM, Gupta SK, Kram HB, Wengerter KR, Veith FJ (1990) Limb loss with patent infra-inguinal bypasses. Eur J Vasc Surg 4:413–417 Goldsmith J, Sales CM, Veith FJ (1994) Surgical treatment of lower extremity ischaemia. In: Clifford M, Sales MD, Goldsmith J, Veith FJ (eds) Handbook of vascular surgery. Quality Medical, St. Louis Katsamouris A, Brewster DC, Megerman J, Cina C, Darling RC, Abbott WM (1984) Transcutaneous oxygen tension in selection of amputation level. Am J Surg 147:510–517 Krupski WC (2000) Overview of extremity amputation. In: Rutherford RB (ed) Vascular surgery, 5th edn, Vol 2. Saunders, Philadelphia, pp 2175–2180 Malone JM (2004) Amputation in dysvascular patient. In: Hobson RW, Wilson SE, Veith FJ (eds) Vascular surgery. Principles and practice, 3rd edn. Dekker, New York, pp 555–573 Malone JM, Anderson GG, Lalka SG, Hagaman RM, Henry R, McIntyre KE, Bernhard VM (1987) Prospective comparison of noninvasive techniques for amputation level selection. Am J Surg 154:179–184 Moore WS, Henry RE, Malone JM, Daly MJ, Patton D, Childers SJ (1981) Prospective use of xenon Xe 133 clearance for amputation level selection. Arch Surg 116:86–88 Otteman MG, Stahlgren LH (1965) Evaluation of factors which influence mortality and morbidity following major lower extremity amputation for atherosclerosis. Surg Gynecol Obstet 120:1217–1220 Sarin S, Sharmi S, Shields DA et al (1991) Selection of amputation level: a review. Eur J Vasc Surg 5:611 Seiler JG et al (1995) Upper extremity amputation. In: Ernst CB, Stanley JC (eds) Current therapy in vascular surgery, 3rd edn. Mosby, St. Louis, pp 680–685
535
536
9.1 Amputation of Extremities
15 TASC (2000) Management of peripheral arterial disease. Transatlantic inter-society consensus. Developed by TASC working group. Inter Angiol 19(1):[Suppl 1]1–310 16 Vollmar J (1982) Reconstructive surgery of arteries [in German]. Thieme, Stuttgart
17 Wyss CR, Robertson C, Love SJ, Harrington RM, Matsen FA 3rd (1987) Relationship between transcutaneous oxygen tension, ankle blood pressure, and clinical outcome of vascular surgery in diabetic and nondiabetic patients. Surgery 101:56–62 18 Yao JST (1988) Choice of amputation level. J Vasc Surg 8:544–545
Venous Diseases
539
10.1 Chronic Venous Insufficiency K. Balzer
10.1.1 Introduction • Nearly every second adult in Europe suffers from venous disorders. • In only 15% are they considered to be venous diseases threatening the patient. • The spectrum ranges from spider telangiectasia to chronic states and acute, potentially lethal, pulmonary embolism – generally described as chronic venous insufficiency (CVI). • In vascular surgery, varicosities of the greater saphenous vein in particular are important. • In principle, every varicose disorder leading to symptoms such as oedema and lower leg ulcer should be treated surgically [1, 4, 16, 21].
10.1.2 Functional Anatomy and Physiology of the Venous System 10.1.2.1 Superficial Veins • The greater and lesser saphenous veins belong to the superficial venous system [16, 18, 22, 25]. • They drain the area between the skin and muscle fascia, carrying blood to the deep venous system. • Before the greater saphenous vein enters the deep femoral vein numerous small tributaries join the system. • The saphenofemoral junction plays an essential part in the function of the venous system during deep venous thrombosis and in treatment of varicosities.
• Duplication of these veins exists in most patients. • They drain 90% of the blood in the legs [4, 5, 16, 25].
10.1.2.3 Perforating Veins • In the upper and lower leg perforating veins (venae perforantes or communicantes) link the superficial and deep venous systems in a step-like manner. • Important perforating veins are the Cockett’s (medial ankle), Boyd’s (proximal medial calf) and Dodd’s group (medial upper leg). • Upright body posture demands transportation of blood back to the heart against the force of gravity. To a certain degree, this is accomplished by the suction effect of the heart and the thoracoabdominal pump function of breathing. The tone of the venous system, arteriovenous coupling (transfer of the arterial pulse to a neighbouring vein) and relative venous blood volume (total body blood volume is usually split 80% venous and 20% arterial, with different proportions during exertion) also play an important role. However, the most important mechanism is the calf muscle pump which, in combination with competent venous valves, guarantees blood flow to the heart by muscle contraction. • Physiologically, valves of the deep, superficial and perforating veins open unidirectionally, preventing flow reversal in the venous system and thus protecting the legs from the effects of continuous hydrostatic pressure [10, 14, 16, 18].
10.1.3 Chronic Venous Insufficiency
10.1.2.2 Deep Veins
10.1.3.1 Definition
• Because the deep veins are located close to the arteries, they are called popliteal and femoral veins.
• Chronic venous insufficiency (CVI) describes the state of continuous venous hypertension of the lower limb
540
10.1 Chronic Venous Insufficiency
• The most common cause is varicose disease. • Varicose veins are dilated, tortuous and superficial veins occurring mainly in the lower limb area. Three types exist (Fig. 10.1.1): • dilated saphenous (stem) veins • reticular varices (dilated tributaries of saphenous veins) • dilated venules (telangiectasia).
10.1.3.2 Epidemiology/Aetiology
Fig. 10.1.1a–c Different types of varices. a Stem varicosis of greater saphenous vein. b Reticular varices in the area of the popliteal fossa, with pigmentation. c Telangiectasia
due to venous stasis, agenesia of valves, deep venous thrombosis (post-thrombotic syndrome) or progressive primary varicosis.
• Based on their pathogenesis, varicose veins are divided into primary varices, which are more common (95%), and secondary varices, which develop as collateral pathways and essentially as a result of deep venous thrombosis [14, 16, 25]. • More than 50% of patients with diagnosed postthrombotic syndrome have no knowledge of previous deep venous thrombosis, for it often remains clinically silent.
10.1.3 Chronic Venous Insufficiency
• Therefore, the pathogenetic centre of CVI is valve dysfunction with permanent venous hypertension of subcutaneous tissue and skin. • Subsequently, typical lesions form. • The disease develops in stages over the years with the following factors worsening its course as in a vicious circle: • Eczematoid changes of skin and subcutaneous tissue (more than 50% of patients) • Recurrent deep venous thrombosis (about 20% of patients) • Primary and secondary varicosis. • The prevalence of CVI is 15% of the general population. • Females are affected three times as much as men [1, 9, 16, 18, 22, 25]. • Based on insufficient perforating veins and valve incompetence of the deep venous system, blood does not flow unidirectionally to the heart, but moves between the deep and superficial venous systems in a pendular way (pendular blood, private circulation). • This leads to the so-called crash syndrome: inward and outward flowing blood collides in the perforating veins. Erythrocytes are thus damaged mechanically with subsequent deposit of haemosiderin in the skin (hyperpigmentation) [5, 6, 10, 14]. • Lower leg ulcerations and eczematoid dermatitis may develop. • Eventually, the chronic volume overload creates rigidity of the vein wall. • Venous tone can no longer be regulated.
right ventricular failure, renal dysfunction, local trauma) have to be excluded. • Swelling without simultaneous varicosity can be a sign of acute or chronic deep venous thrombosis. • On the other hand, acute thrombosis of the iliofemoral and calf veins is closely related to pulmonary embolism, which is often lethal. Therefore, if suspected, Duplex ultrasonography or ascending venography is needed. • This is true as well if other risk factors exist, such as an incidence of thrombosis in the family, coagulation disorder and immobility (e.g. long-distance flights or economy-class syndrome) [1, 14, 21].
Skin Lesions • Signs of CVI may be present in the form of hyper- or depigmentation of the skin, eczematoid dermatitis and ulcerations, most common at the medial side of the lower leg, resulting from progressive varicosity or deep venous thrombosis. • Long-term venous hypertension with secondary dysfunction of the deep venous system is mainly responsible for the severity of skin changes [9, 14, 16, 18, 25]. • The typical changes of the skin and veins can be subdivided into three stages, often overlapping: • Stage I has been referred to as corona phlebectatica paraplantaris (Figs. 10.1.2, 10.1.3) – the dilatation of venules at the side aspect of the foot as well as stasis oedema at the end of day, particularly in warm temperatures.
10.1.3.3 Symptoms • A typical early symptom of post-thrombotic syndrome and CVI is a tendency for the lower extremity to swell. • Leg ulcer is a leading sign of full extent of the disease [4].
Venous Stasis • In the case of primary varicosis, unilateral stasis-oedema, generally appearing at the end of the day, may occur prior to the development of varicose veins. • Aching heaviness is associated with it. • At the early stage of CVI, considering differential diagnostic aspects, other disorders causing oedema (e.g.
Fig. 10.1.2 Corona phlebectatica as an early symptom of chronic venous insufficiency (CVI)
541
542
10.1 Chronic Venous Insufficiency
Fig. 10.1.3a,b Dilated veins of the lower leg based on postthrombotic syndrome and CVI. a Corona phlebectatica, dilated veins and blow-out phenomenon of perforating veins. b Typical Pratt vein as a sign of pretibial venous stasis
• Stage II is characterized by stasis eczema. Based on the oedema, the skin tends to allergic reaction (eczematoid dermatosis) and hyper- or depigmentation up to the development of atrophie blanche [14, 16, 25]. • Florid and healed cutaneous ulceration represent stage III of CVI (Fig. 10.1.4).
Diffuse Leg Pain
Fig. 10.1.4a,b Swelling as a sign of CVI, healed ulceration. Pigmentation of the skin, atrophie blanche and central ulceration at the stage of progressive CVI
• Cramp-like pain may also be a manifestation of CVI, aggravated by prolonged standing and similar to a muscle ache.
• By elevating the legs, the pain can be decreased. • This is typical of CVI [1, 9, 14, 16, 18, 21].
10.1.3 Chronic Venous Insufficiency
Fig. 10.1.5a,b Classification of truncal varicosity as described by Hach. a Different stages – stage I: saphenofemoral incompetence; stage II: varicosity of greater saphenous vein between groin and upper calf; stage III: varicose veins from saphenofemoral junction to proximal lower extremity; stage IV: varicosity of entire great saphenous vein. b Distal termination of incompetence below knee (stage III)
10.1.3.4 Diagnosis Recommended European Standard Diagnostic Steps of Investigation External Haemorrhage • The most common location of spontaneous haemorrhage of varices is the medial aspect of the ankle. • External haemorrhage is a frequent indication for varicose vein treatment [16, 25].
• In all patients with varicosity, the extent of the damage to superficial and deep veins has to be determined. • Classification of truncal varicosis of the greater saphenous vein according to Hach depicts the different categories of valve dysfunction (Fig. 10.1.5) [9, 10]. • Today, traditional functional tests (Perthes’ test, Trendelenburg test) are seldom used. • In addition to thorough clinical examination, diagnostic modalities such as Doppler ultrasonography (Fig. 10.1.6b), Duplex scanning in particular (Figs. 10.1.6a,
543
544
10.1 Chronic Venous Insufficiency
Fig. 10.1.6a,b Ultrasonography for determination of competent and incompetent venous segments. a Duplex scanning with visible reflux into the greater saphenous vein during a Valsalva manoeuvre. b Determination of distal location of insufficiency with Doppler ultrasonography
10.1.7), and, in critical cases, ascending venography can be performed to assess venous dysfunction [5].
DuplexScanning
• Because of its reliability, use of Duplex scanning in combination with a functional haemodynamic measurement technique is accepted as the preoperative standard diagnostic procedure. • The technique permits anatomical examination as well as assessment of the haemodynamic status of the veins [1, 11, 21].
Ascending Venography
• If determination of the patency of venous drainage and differentiation between incompetent and healthy venous segments by Duplex scanning is not sufficient, ascending venography has to be performed.
• This invasive method may cause complications [9, 10, 21, 25].
Additional Useful Diagnostic Procedures • Phlebodynamometry. Peripheral phlebodynamometry is a highly sensitive method of assessing venous disorders. It enables statements to be made concerning prognosis – including those for legal and insurance purposes – and also the disease progression to be monitored. By using this technique, peripheral venous pressure in the unbandaged and bandaged limb is measured. An indication for surgery on incompetent epifascial veins is given when the measurement curve improves after tight dressing with elastic bandages [5, 14, 16, 18]. • Photoplethysmography. Nowadays the invasive method of phlebodynamometry has been virtually su-
10.1.3 Chronic Venous Insufficiency
perseded by photoplethysmography. Measurement of reflecting light documents the speed of venous refill in the foot [11].
10.1.3.5 Treatment Conservative Therapy of CVI
• The method gives better results than the conventional treatment of injection of highly concentrated saline solutions or aethoxysclerol, because under control of Duplex scanning the foam can be applied close to the saphenofemoral or saphenopopliteal junction. • This way obliteration of the greater and lesser saphenous veins and side branches is possible. • It should be pointed out that reflux into the stem veins may cause recurrent varicosity [8, 16, 18].
External Compression
• Indispensable in the therapy of chronic venous insufficiency is external compression of the limb. • Nonsurgical treatment is based on sufficient compression to prevent oedema and on acceleration of the venous blood flow by using compression stockings of strength type II. • After lower limb ulcerations have healed, type III stockings are necessary. • Compression is especially important in the periulcerous area, when ulcus cruris is present [22, 25].
Application of Drugs
• If risk factors for recurrent thrombosis exist, life-long anticoagulation therapy is indicated. • The application of agents influencing venous tone or reducing oedema (flavonoids, chestnut seed extracts) does not correct the underlying cause [1, 18, 21, 25].
Conservative Treatment of Varicose Veins Sclerotherapy
• If the greater and lesser saphenous veins are not affected by a varicose condition, conventional sclerotherapy can be performed. • Today, sclerotherapy with its modification by using foam may be an alternative to operative treatment.
Fig. 10.1.7a,b Examination of popliteal fossa in varicosis of the lesser saphenous vein. a Incompetent lesser saphenous vein with typical varicosis. b Corresponding clinical finding
545
546
10.1 Chronic Venous Insufficiency
Surgery • If removal of varicose veins is possible, healing of ulcerations is significantly accelerated. • This includes dissection of venae perforantes, nowadays primarily done endoscopically to avoid traumatizing the skin already affected by trophical lesions. • If CVI is based on isolated obliteration of the iliac vein, venous by-pass procedures may be indicated. • In incompetence of the deep venous system, the method of transposition of valves may be useful to prevent lower limb ulceration [1, 2, 11, 13, 21].
Surgical Treatment of Varicose Veins • Removal of varicose veins is one of the most common surgical procedures and can be performed in day-case surgery [1, 3, 6, 20, 21, 24–26]. • The intention is to completely remove veins with incompetent valves in order to prevent long-term damage such as leg ulceration. • Depending on the time of the surgery, secondary changes such as swelling, thrombophlebitis or ulceration may regress. • In general, skin pigmentation remains.
Indications
• There is differentiation between carriers of asymptomatic varices and patients actually suffering from varicose disease. • The first group has no subjective complaints except for occasional heaviness of the legs (relative indication for surgery). The other develops complications up to chronic venous insufficiency (absolute indication for surgical treatment). • In primary varicosity, surgical therapy is indicated for saphenous, perforating and branch vein varicosis [16, 18, 21]. • The decision on surgical treatment of secondary varicosities has to be made carefully! Sufficient blood flow from the lower extremities to the heart has to be ensured after surgery. Preoperative use of high-compression bandages over a period of several weeks simulates removal of varices. If the patients experience improvement of symptoms, surgical intervention is justified [16, 18, 25].
• Surgical treatment is indicated according to the severity and pathophysiological significance of the varicosity.
Contraindications
• Absolute contraindications are the incidence of peripheral arterial occlusive disease and angiodysplasia, particularly arteriovenous fistulas as in Parkes-Weber syndrome. • Systemic connective tissue disorders (e.g. Marfan’s syndrome), dysfunction of venous flow (e.g. postthrombotic syndrome, agenesia of valves) and progressive degenerative joint disease are relative contraindications [16].
Risks and Complications of Surgery
• Trauma of the femoral and popliteal artery and vein is a rare complication. • More commonly, lesions of lymphatic vessels occur. • The saphenous nerve in the calf area and sural nerve (medial ankle), which are close to the saphenous veins, can also be injured [3, 16, 18]. • Generally, resulting postoperative sensory dysfunction disappears, only occasionally appearing as permanent paraesthesia. • Infection is a rare but serious complication often based on haematomas, which are an ideal prerequisite for colonization of microorganisms. • In principle, surgeons should only perform techniques whose complications they are able to manage.
Preparation for Operation
• Different opinions exist about general thrombosis prophylaxis with heparin in varicose surgery. • Peri-operative application in high-risk patients reduces the incidence of deep venous thrombosis. • Patients under permanent anticoagulation therapy take heparin instead [21]. • Meticulous marking of the varicose veins with indelible ink precedes surgical procedure.
Surgical Techniques High Ligation and Stripping
• The high ligation and stripping procedure as described by Babcock may be performed in truncal varicosis of
10.1.3 Chronic Venous Insufficiency
• • •
•
the greater saphenous vein (saphenus = hidden) with or without perforating varices. The entire incompetent vein is extracted by intraluminal stripper from groin to ankle. Healthy segments of the saphenous vein are preserved [21, 25]. With regards to future arterial by-pass surgery, the saphenous veins play a major role as physiological vascular grafts. Analogously, this procedure is performed for varicosity of the lesser saphenous vein with incision at the lateral aspect of the ankle and the popliteal fossa. Prior to operation, identification of the exact termination of the lesser saphenous vein with the help of Duplex scanning is advisable. Active preparation of the sural nerve is necessary in order to protect it from injury [9].
Dissection of Perforating Veins
• By using the method of endoscopic dissection, an endoscope is inserted in the area of healthy skin (Fig. 10.1.8). • In this way, further damage to existing trophical lesions of the skin can be avoided. • Perforating veins are interrupted by clipping or coagulation under visual control. • If no pathological skin conditions exist, open preparation with ligation of the incompetent perforating vein (blow out phenomenon) can be done [11, 21].
Fig. 10.1.8a,b Endoscopical ligation of perforating veins. a Endoscope inserted subfascially. b Vena perforans, which will be interrupted
Removal of Local Varices
• Larger varicosites of the side branches are extirpated locally by stab avulsion through incisions, which may lead to scars. • When using a phlebextractor, a modified hook instrument, only small punctual incisions are required, which do not need to be sutured, thus optimizing cosmetic results [4, 8, 11, 21].
Postoperative Procedure • After applying the wound dressing, the leg has to be bandaged elastically with sufficient compression from the basal toe joints up to the groin. • In order to avoid pressure damage, the bandaged leg has to be observed during the day of surgery. • In some cases wound drainage is necessary, because the above-mentioned surgical techniques can cause extensive haematomas. • Certainly, haematomas should not be mistaken for haemorrhage demanding instant revision [16, 18].
Postoperative Results • Excellent cosmetic and functional results of 95% have been reported using a combination of surgical treatment and postoperative sclerotherapy [3, 20, 26].
547
548
10.1 Chronic Venous Insufficiency
Recurrent Varicosity • The appearance of recurrent varices based on incomplete removal of the greater saphenous vein is rare. • However, development of varicosities in the area of healthy side branches after a period of years is common. • In this case, once again therapeutic methods have to be taken into consideration and surgical intervention is carried out if indicated [1, 3, 6, 9, 11, 12, 20, 21, 25].
dynamique de l’insuffisance veineuse en ambulatoire)] and reconstructive techniques such as “banding” (external valvuloplasty). These methods are the subject of controversial discussion [11, 15, 17, 21].
Surgical Treatment of Venous Thrombosis • The operative therapy of deep venous thrombosis requires special indication. • However, in a number of cases it reduces the risk of developing post-thrombotic changes [16, 18].
Complications • Manifestations of injury to the femoral and popliteal artery or vein, deep venous thrombosis and pulmonary embolism are considered serious complications. • With meticulous surgery technique and proper perioperative management they rarely occur. • Lethality of varicose surgery is 0.02% [3]. • Minor complications include lesion of local sensory nerves in 8–10% (mainly the saphenous nerve, often reversible), lymphatic fistulas in the groin in 5% and impaired wound healing.
Alternative Treatment of Varicose Veins • Modern therapeutic methods compete with conventional stripping operations [e.g. endovenous ablation using radiofrequency or laser, transluminal phlebectomy (TriVex), CHIVA (cure conservatrice et hemo-
Rare Operations for CVI By-pass in Unilateral Occlusion of the Iliac Vein
• Today, the procedure described by Palma is the only operation which may be carried out in the case of severe post-thrombotic syndrome or unilateral occlusion of the common iliac vein (Fig. 10.1.9). • Criteria for indication are pressure measurements in the iliac vein that are three times higher during exercise than while resting. • A prerequisite is patency of the deep venous system of the lower and upper leg. • The by-pass consists of autologous vein or alloplastic material [4, 16, 18, 23]. • The technique of the Palma procedure is to transfer the greater saphenous vein of the healthy side through a suprapubic subcutaneous tunnel to the contralateral, occluded side. An end-to-side anastomosis with the
Fig. 10.1.9a,b a Post-thrombotic syndrome with CVI and decompensated venous stasis: extensive oedema, skin pigmentation and florid ulcer. b Radiograph of patient after by-pass operation according to Palma without significant improvement
References
femoral or iliac vein is performed. Simultaneously, distal to the anastomosis, a temporary arteriovenous fistula is made. It remains for 3–6 months, preventing recurrent thrombosis, particularly when the calibre of the vein is small [16].
• If the cause of CVI is post-thrombotic syndrome, an adequate form of therapy has to be chosen. In some cases surgical therapy is required. • It is difficult to treat CVI when severe damage of tissue or ulceration has already developed.
Reconstruction and Transposition of Valves
References
• Kistner [13] suggested direct reconstruction of insufficient deep veins to re-establish patency of the deep venous system. • As an alternative, transposition of healthy venous segments (mainly axillary vein) is described. • Transposition of leg veins from the side not affected by thrombosis is not considered favourable, because lesion to the healthy side might occur. • Likewise, by-pass procedures with normal epifascial veins as described by May [16] have not proven to be useful. • The operation consists of by-passing an occluded superficial femoral vein by using the greater saphenous vein. • Nature takes advantage of this physiological collateral pathway. Elevated pressure in the deep venous system leads to reversal of flow in the perforating veins.
1. Agus GB, Allegra C, Arpalla G et al (2001) Guidelines for the diagnosis and therapy of disease of the veins and lymphatic vessels. Int Angiol 20 [Suppl. 2] 2. Babcock WW (1907) A new operation for the extirpation of varicose veins of the leg. NY Med J 86:153–156 3. Balzer K (2001) Komplikationen bei Varizenoperationen. Zentralbl Chir 126:537–542 4. Balzer K (2004) Venenerkrankungen. In: Hirner A, Weise K (eds) Chirurgie Schnitt für Schnitt. Thieme, Stuttgart, pp 738–741 5. Balzer K, Bernert J, Carstensen G (1978) Die Beurteilung der venösen Hämodynamik als entscheidendes diagnostisches Kriterium vor venenchirurgischen Eingriffen. Chirurg 49:290–295 6. Bergan JJ, Yao JST (1991) Surgical procedures for varicose veins. In: Bergan JJ, Yao JST (eds) Venous disorders. Saunders, Philadelphia, pp 201–216 7. Carstensen G (1978) Rundgespräch: Chirurgie der Venen. Langenbecks Arch Chir 347:367 8. Fratila A, Rabe E (1993) The differentiated surgical treatment of primary varicosis. Semn Dermatol 12:102–116 9. Hach W (1988) Diagnostik und Operationsmethoden bei der primären Varikose. Langenbecks Arch Chir [Suppl. II] (Kongressber.) 145 10. Hach W, Hach-Wunderle V (1994) Die Rezirkulationskreise der primären Varikose. Springer, Berlin Heidelberg New York 11. Heidrich M, Balzer K (2004) Standardisierte Varizenchirurgie – Operationstechnik, Komplikationen, Ergebnisse. Gefaesschirurgie 9:276–283 12. Hobbs JT (1983) Operations for varicose veins. In: De Weese JA (ed) Rob and Smiths operative surgery. Butterworth, London 13. Kistner RL (1996) Definitive diagnosis and definitive treatment in chronic venous disease: a concept what time has come? J Vasc Surg 24(5):703–710 14. Leu HJ (1990) Chronisch-venöse Insuffizienz heute (eine Standortbestimmung). Vasa 19:195–202 15. Lurie F, Creton D, Eklof B et al (2003) Prospective randomized study of endovenous radiofrequency obliteration (closure procedure) versus ligation and stripping in a selected patient population (EVOLVeS Study). J Vasc Surg 38:207–214
Surgical Treatment of Leg Ulcers
• Prior to venous reconstruction, arterial lesions have to be treated if the arterial system is affected at the same time (combined ulcer) [14, 16, 21]. • After proper elimination of venous stasis, adequate additional treatment of the ulceration must follow. • Debridement of the ulcer with subsequent skin grafting leads to improved healing, provided that subcutaneous tissue and the muscle fascia show no extensive lesions (as in dermatoliposclerosis) caused by permanent venous hypertension. • If deep subdermal layers are already indurated and degenerated, generous excision and closure of the wound by applying skin graft is the method of choice. • Medial or lateral paratibial fasciotomy may reduce pressure in the different compartments and support the healing process [11].
10.1.3.6 Conclusion • CVI can be avoided if varicose veins are treated in time.
549
550
10.1 Chronic Venous Insufficiency
16. May R (1974) Chirurgie der Bein- und Beckenvenen. Thieme, Stuttgart 17. Min RJ, Khilnani N, Zimmet SE (2003) Endovenous laser treatment of saphenous vein reflux: long-term results. J Vasc Interv Radiol 14/8:991–996 18. Neugebauer J, Müller JHA (1982) Venenerkrankungen der Extremitäten. Volk and Gesundheit, Berlin 19. Neumann HAM (1999) Behandlung von Krampfadern mit Radiowellen. Phlebologie 28:49–51 20. Noppeney T, Noppeney J, Kurth I (2002) Results of standard varicose vein surgery. Zentralbl Chir 127:748–751 21. Noppeney T, Kluess HG, Gerlach H, Braunbork W, Ehresmann U et al (2004). Leitlinien zur Diagnostik und Therapie des Krampfaderleidens. Gefaesschirurgie 9:290–308
22. Ramelet AA, Monti M (eds) (1999) Phlebology. The guide, 4th edn. Elsevier, Paris 23. Ris H-B, Wittwer P, Tschudi J, Stirnemann H, Doran JE (1988) Langzeitresultate nach Varicenoperation. Chirurg 59:592–597 24. Salzmann G (2002) Peripheral venous diseases: the surgical approach. In: Lancer P, Topol EJ (eds) Panvascular medicine. Springer, Berlin Heidelberg New York, pp 1526–1538 25. Tibbs DJ (1992) Varicose veins and related disorders. Butterworth-Heinemann, Oxford 26. Wigger P (1998) Surgical therapy of primary varicose veins. Schweiz Med Wochenschr 128:1781–1788
551
10.2 Deep Venous Thrombosis Jukka P. Saarinen, Maarit A. Heikkinen, Juha-Pekka Salenius
10.2.1 Epidemiology/Aetiology • The following three factors, primarily postulated by Virchow, are most important in the pathophysiology of deep venous thrombosis (DVT) [10]: • Injury of vessel wall • Abnormalities of blood (coagulation disorders) • Abnormalities of blood flow (stasis). • There are multiple risk factors for DVT, but the independence and magnitude of each are unclear [10, 11, 12, 34]: • Increasing age • Cancer • Coagulation disorder • Smoking • Obesity • Oestrogen substitution • Surgery (hip or knee arthroplasty, cancer surgery in the abdominopelvic area, neurosurgery) • Trauma • Immobilization (air-related DVT) • Previous DVT. • Calf veins are the most common site of thrombus [20]. Acute DVT is more frequently left-sided, and this phenomenon can be noted more clearly in proximal DVTs. Acute DVT affects vein segments from calf to iliac level in 5% of cases (iliofemoral DVT). Postoperative DVT is restricted to calf veins in 80% [21]. Propagation into more proximal veins may occur in 5–15% [16]. • The annual incidence of DVT is 5 per 10,000 in the general population. The 5-year cumulative incidence of recurrent DVT is approximately 20%. Prevalence of DVT is 0.5% at age 50 years and 4.5% at age 75 years. The risk of DVT increases twofold during each 10-year increase in age [9, 11]. • Without prophylaxis, the incidence of postoperative DVT is 40–80% in patients undergoing large ortho-
paedic surgery. The corresponding numbers in general surgery are 20–40%. In vascular surgery, several Duplex or venography-based studies have shown that the rate of DVT is 18–32% after abdominal or lower limb reconstructions. Postoperative DVT has been noted in 12% of the legs after abdominal vascular surgery despite medical prophylaxis [10]. • Superficial thrombophlebitis may be associated with DVT. In legs with large-scale thrombophlebitis involving the saphenofemoral or saphenopopliteal junction, DVT may be present in as much as 40% of cases [10].
10.2.2 Symptoms • Typical symptoms are calf pain (pain at rest and also during walking), and oedema of the calf or the whole leg [10]. • Acute DVT may be asymptomatic, especially in postoperative patients, or the first sign may be pulmonary embolism [34].
10.2.3 Diagnosis 10.2.3.1 Clinical Signs • Typical signs are pain in calf palpation and pitting oedem [10]. • Cyanotic or pale colour may be seen in massive DVT occluding all collateral veins and finally arteries (phlegmasia cerulea dolens, phlegmasia cerulea alba). • Anamnestic risk factors should be mapped: existing cancer, significant immobilization (extremity paresis, use of a cast, bedrest), recent (< 1 month) surgery or trauma, existing coagulation disorder [4, 32].
552
10.2 Deep Venous Thrombosis
10.2.3.2 Laboratory Tests and Imaging • Degradation of fibrin can be measured by D-dimer. Fibrin levels are elevated in acute DVT, but some other conditions may elevate these levels too (e.g. cancer, inflammation) [2, 8]. • C-reactive protein may be elevated in acute DVT [2, 8]. • Duplex ultrasound imaging is accurate in detecting symptomatic DVT at the popliteal level proximally [7, 23]. • Ascending venography can be used as an alternative method, especially in postoperative patients. • Ultrasound has no contraindications whereas venography is an invasive method, and the use of contrast media may lead to allergic reactions. • Coagulation disorders should be screened in selected cases: idiopathic DVT, a family history of DVT or pulmonary embolism, and recurrent DVT. • Congenital and acquired disorders have to be evaluated: factor V Leiden, prothrombin, antithrombin deficiency, protein S and protein C deficiency, hyperhomocysteinaemia (congenital), antiphospholipid antibodies (acquired) [4]. • Genetic studies can be performed during anticoagulation, but most other measurements need to be done later. • The risk of underlying malignancy is significantly increased in patients with idiopathic DVT; therefore, additional studies may be considered in each case [4, 32].
10.2.3.3 Recommended European Standard • Symptom-based diagnosis of acute DVT is insufficient. • Normal D-dimer is accurate at excluding DVT in patients with a low or moderate clinical probability of DVT. No further studies (including ultrasound) are needed. • Duplex ultrasound imaging should be used together with D-dimer in patients with a high clinical probability of DVT. • Venography should be used in cases where the Duplex ultrasound imaging results are unclear.
10.2.4 Treatment 10.2.4.1 Conservative Treatment of DVT The Use of Anticoagulants • •
•
•
•
•
Low-molecularweight heparin (LMWH) can be used as a primary treatment of acute DVT. LMWHs are as efficient as intravenous unfractionated heparin, but they have several advantages (e.g. no need to observe coagulation parameters, subcutaneous injections and safety). Medical treatment should be started as quickly as possible, because this may reduce the rate of recurrence [13]. Warfarinsodium is given simultaneously with LMWH, but the doses need to be adjusted carefully in each case (3–10 mg per day), especially in elderly patients. The international normalized ratio (INR) should be adjusted to between 2.0 and 3.0 for 2 days before LMWH treatment is stopped. Outpatient treatment of acute DVT is an acceptable alternative in co-operative patients.
Compression Therapy • Compression therapy may reduce the incidence of post-thrombotic syndrome up to 50% in patients with DVT at the popliteal level or more proximally [5]. • A knee-length stocking is sufficient, and its efficacy is based on enhancement of calf muscle-pump function [27]. • Early ambulation with adequate compression treatment in proximal DVTs may reduce leg symptoms, and there is no increased risk of pulmonary embolism [22].
Duration of Treatment • The duration of anticoagulation should be more than 3 months in patients with idiopathic DVT [14]. • A 3-month treatment may be adequate in patients with nonidiopathic DVT. • Permanent anticoagulation can be considered in recurrent cases with sustained aetiological factors such as cancer or coagulation disorder [14, 24].
10.2.4 Treatment
• Compression therapy needs to be continued for up to 2 years, because post-thrombotic syndrome typically occurs within the first 2 years after acute DVT [5, 27]. • The main problems during anticoagulant treatment with warfarin are bleeding and not optimal INR levels. • The prevalence of bleeding is approximately 2%, and the risk increases markedly when the INR level is higher than 3.0. • A low INR level may raise the risk of recurrence, and even have an influence on the resolution of the thrombus.
Recommended European Standard • Subcutaneously administered LMWHs are first-line treatment of acute DVT. • Treatment with LMWHs should be started as quickly as possible. • Length of warfarin treatment needs to be more than 3 months in idiopathic cases, and the INR should be maintained between 2.0 and 3.0. • Compression treatment with below-knee stocking (30–40 mmHg pressure at the ankle) is indicated in the treatment of acute DVT. • Duration of compression treatment is 2 years. • The coagulation system has to be screened in selected patients
10.2.4.2 Invasive Treatment of DVT Indications for Invasive Treatment • Preservation of valvular function has been the main reason for treating acute DVT invasively [1]. • There is only moderate evidence as to how this preservation can be achieved. • Acute massive (supra-inguinal DVT) thrombosis may indicate invasive treatment in selected cases. • The symptomatic period should be less than 1 week. However, it is difficult to determine the duration of DVT [18]. • Patient’s life-expectancy should be long, because the main goal is to maintain the long-term function of venous valves. Therefore, having cancer and being old (>70 years) are relatively contraindications to these treatments (Fig. 10.2.1) [29].
• Invasive treatment should be considered in complicated DVT such as phlegmasia cerulea dolens, phlegmasia cerulea alba and venous gangrene. However, no randomized studies comparing conservative and invasive treatment or comparing different invasive treatments are available [15, 18, 25, 30]. • Data on treatment of complicated DVT are mainly based on case reports and uncontrolled series.
Thrombolysis • Thrombolysis can be done systemically or locally (catheter-directed) into the thrombus by using tissue plasminogen activator or urokinase or streptokinase [18]. • Catheter-directed lysis seems to have a better outcome compared to anticoagulant treatment or systemic lysis [15]. • Large randomized data are still not available. • In catheter-directed lysis, the catheter is placed intravenously inside the thrombus and slow infusion is given. Treatment is followed by repeated venograms, and the duration of treatment is typically 24–48 h [18]. • It is very important to detect underlying stenotic segments, typically in the left common iliac vein, and to treat them with balloon angioplasty and, if necessary, with stenting [18]. • Anticoagulation with LMWHs should be started before invasive treatment [1, 18, 30]. • The risk of significant bleeding varies between 6% and 11% in clinical series. • The incidence of pulmonary embolism in catheter-directed lysis is low, 0–1% [18, 30].
Thrombectomy • Thrombectomy, too, can be used in the removal of acute thrombus. However, its protective power to prevent post-thrombotic sequelae is also unclear. • Surgical thrombectomy should be done under general anaesthesia, and positive end expiratory pressure (20 mmHg) needs to be used to prevent pulmonary embolism. • Thrombectomy of a proximal thrombus can be achieved with a Fogarthy catheter. • Distally the thrombus can be removed mechanically with compression bandages or by hand compression.
553
554
10.2 Deep Venous Thrombosis
Fig. 10.2.1 Flowchart of invasive treatment of deep venous thrombosis (DVT)
10.2.4 Treatment
Fig. 10.2.2 Right iliac veins after surgical thrombectomy
Fig. 10.2.4 Right iliac veins after stenting
• If stenosis is detected, balloon angioplasty (Fig. 10.2.3) and stenting (Fig. 10.2.4) should be considered. • Several devices for mechanical endovascular thrombectomy are currently available. • Short-term studies have shown that they are effective in removing thrombus. • These methods combine the use of local lytic therapy and mechanical removal of the thrombus. No longterm results are so far available. • The duration of treatment is less than in catheter-directed lysis and the risk of bleeding may be reduced.
Recommended European Standard
Fig. 10.2.3 Right iliac veins after angioplasty
• Reconstruction of arteriovenous fistula can be combined with the procedure [25]. • Surgical thrombectomy should always be combined with peri- or an immediate post-operative venogram to image the proximal (iliac) veins (Fig. 10.2.2) [19, 25].
• Catheter-directed thrombolysis can be considered in massive (supra-inguinal) acute DVTs with relatively young and healthy patients. • Patients with poor outcome (cancer, old age) should be treated with anticoagulants. • Long-term symptoms (i.e. more than 1 week) should contraindicate invasive treatment. • Regardless of the method of invasive treatment, such as catheter-directed lysis, surgical thrombectomy and endovascular mechanical thrombectomy, the proximal outflow tract has to be imaged in all cases to reveal and treat the underlying pathology.
555
556
10.2 Deep Venous Thrombosis
• Treatment with LMWHs should be started before invasive treatment.
10.2.4.3 Prevention of DVT Postoperative DVT • Without prophylaxis the incidence of DVT is very high after hip or knee arthroplasty, hip fracture surgery and abdominopelvic cancer surgery. • The risk of postoperative thromboembolism is sustained for at least 1 month after surgery [10]. • In general, postoperative patients can be divided into three categories according to consensus statement: low risk, moderate risk and high risk [10]. • Medical prophylaxis is performed by using LMWHs, which can be started either preoperatively (12 h before the operation) or postoperatively (6–12 h after the operation) [10]. • Fondaparinux is a selective factor Xa inhibitor, and can be used for prophylaxis after knee or hip surgery (elective arthroplasty or hip fracture surgery). Fondaparinux is started 6 h postoperatively. There are strong data available on the superiority of fondaparinux over enoxaparin in preventing DVT in orthopaedic surgery [33]. • Ximelagatran is a direct thrombin inhibitor, which is more effective than dalteparin for prophylaxis of postoperative DVT. Ximelagatran can be given orally, whereas LMWHs and fondaparinux are administered subcutaneously. • Knee-length compression stockings and early ambulation after surgery should be used to prevent DVT, together with medical prophylaxis [10]. • The duration of prophylaxis should be 5–7 days in patients without high risk. • Prolonged prophylaxis is indicated in hip or knee arthroplasty, abdominopelvic cancer surgery and in patients with coagulation disorder. In these cases, treatment with LMWHs or fondaparinux is continued up to 4 weeks [3, 10, 33, 34].
Air-related DVT • The risk of DVT is increased during long-haul flights. • Air pressure changes, immobilization and dehydration may be the main risk factors.
• Randomized data have shown that the incidence of distal (calf) DVT is lower in patients wearing kneelength compression stockings during intercontinental flights. • In high-risk patients (e.g. coagulation disorder, previous DVT) prophylactic use of LMWHs should be considered.
Trauma and DVT • The incidence of DVT is strongly elevated in patients with severe trauma. • Medical prophylaxis should be used in all cases without contraindications. However, the risk of bleeding needs to be considered in each case [10, 34].
Recommended European Standard • Medical prophylaxis should be considered in surgical patients and only low-risk patients may be excluded. • Medical prophylaxis with LMWHs can be started preor postoperatively. • Fondaparinux should be considered in high-risk orthopaedic patients. • The duration of prophylaxis is 5–7 days, but prolonged prophylaxis is indicated in selected patients, including hip or knee surgery, abdominopelvic cancer surgery and large surgery in patients with coagulation disorder. • Compression stockings should be combined with medical prophylaxis. • Compression stockings can be recommended in intercontinental long-haul flights and prophylactic use of LMWHs in high-risk patients should be considered.
10.2.5 Differential Diagnosis Differential diagnosis of DVT includes: • Ruptured Baker’s cyst • Superficial thrombophlebitis • Acute arterial ischaemia • Cellulitis • Haemorrhage inside the limb • Acute arthritis • Torn calf muscles
References
• Pelvic or intra-abdominal tumours obstructing the veins.
10.2.6 Prognosis • Acute thrombosis may destroy venous valves in affected segments. • The rate of recanalization is high after acute DVT, but valvular reflux may remain. • Recanalization typically occurs during the first year after DVT. It may be delayed or fail at iliac veins [17]. • The 5-year incidence of post-thrombotic syndrome is about 30% in patients treated with anticoagulants [26]. • Prognosis after acute DVT is difficult to determine; even calf DVT may lead to late sequelae [17, 28]. • Subsequent events after the acute phase, such propagation and re-thrombosis, may have an impact on prognosis [26]. References 1. AbuRahma AF, Perkins SE, Wulu JT, Ng HK (2001) Iliofemoral deep vein thrombosis: conventional therapy versus lysis and percutaneous transilluminal angioplasty and stenting. Ann Surg 233:752–760 2. Akman MN, Cetin N, Bayramoglu M, Isiklar I, Kilinc S (2004) Value of the D-dimer test in diagnosing deep vein thrombosis in rehabilitation inpatients. Arch Phys Med Rehabil 85:1091–1094 3. Bergqvist D, Agnelli G, Cohen AT et al (2002) Duration of prophylaxis against venous thromboembolism with enoxaparin after surgery for cancer. N Engl J Med 346:975–980 4. Blattler W, Martinez I, Blattler IK (2004) Diagnosis of deep venous thrombosis and alternative diseases in symptomatic outpatients. Eur J Intern Med 15:305–311 5. Brandjes DPM, Buller HR, Heijboer H et al (1997) Randomized trial of effect of compression stockings in patients with symptomatic proximal-vein thrombosis. Lancet 349:759–762 6. Caprini JA, Arcelus JI, Reyna JJ et al (1999) Deep vein thrombosis outcome and the level of oral anticoagulation therapy. J Vasc Surg 30:805–812 7. Cogo A, Lensing AWA, Koopman MMW et al (1998) Compression ultrasonography for diagnostic management of patients with clinically suspected deep vein thrombosis: a prospective cohort study. BMJ 316:17–20
8. Fancher TL, White RH, Kravitz RL (2004) Combined use of rapid D-dimer testing and estimation of clinical probability in the diagnosis of deep vein thrombosis: systematic review. BMJ 329:821–823 9. Fowkes FJI, Price JF, Fowkes FGR (2003) Incidence of diagnosed deep venous thrombosis in the general population: systematic review. Eur J Vasc Endovasc Surg 25:1–5 10. Geerts WH, Heit JA, Clagett GP et al (2001) Prevention of venous thromboembolsim. Chest 199 [Suppl 1]:132S–175S 11. Hansson P-O, Welin L, Tibblin G, Eriksson H (1997) Deep vein thrombosis and pulmonary embolism in the general population. Arch Intern Med 157:1665–1670 12. Heit JA, Silverstein MD, Mohr DN et al (2000) Risk factors for deep vein thrombosis and pulmonary embolism. Arch Intern Med 160:809–815 13. Hull RD, Raskob GE, Brant RF, Pineo GF, Valentine KA (1997) Relation between the time to achieve the lower limit of the APTT therapeutic range and recurrent venous thromboembolism during heparin treatment for deep vein thrombosis. Arch Intern Med 157:2562–2568 14. Kearon C, Kent M, Hirsh J et al (1999) Comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med 340:901–907 15. Laiho MK, Oinonen A, Sugano N et al (2004) Preservation of venous valve function after catheter-directed and systemic thrombolysis for deep venous thrombosis. Eur J Vasc Endovasc Surg 28:391–396 16. Meissner MH, Caps MT, Bergelin RO, Manzo RA, Strandness DE Jr. (1995) Propagation, rethrombosis and new thrombus formation after acute deep venous thrombosis. J Vasc Surg 22:558–567 17. Meissner MH, Caps MT, Zierler BK et al (1998) Determinants of chronic venous disease after acute deep venous thrombosis. J Vasc Surg 28:826–833 18. Mewissen MW, Seabrook GR, Meissner MH, Cynamon J, Labropoulos N, Haughton SH (1999) Catheter-directed thrombolysis for lower extremity deep venous thrombosis: report of a national multicenter registry. Radiology 211:39–49 19. Murphy KD (2004) Mechanical thrombectomy for DVT. Tech Vasc Interv Radiol 7:79–85 20. Nicolaides AN, Kakkar VV, Field ES, Rennay JTG (1971) The origin of deep venous thrombosis: a venographic study. Br J Radiol 44:653–663 21. Ouriel K, Green RM, Greenberg RK, Clair DG (2000) The anatomy of deep venous thrombosis of the lower extremity. J Vasc Surg 31:895–900
557
558
10.2 Deep Venous Thrombosis
22. Partsch H, Blättler W (2000) Compression and walking versus bed rest in the treatment of proximal deep venous thrombosis with low molecular weight heparin. J Vasc Surg 32:861–869 23. Perrier A, Desmarais S, Miron M-J et al (1999) Non-invasive diagnosis of venous thromboembolism in outpatients. Lancet 353:190–195 24. Pinede L, Ninet J, Duhaut P et al (2001) Comparison of 3 and 6 months of oral anticoagulant therapy after a first episode of proximal deep vein thrombosis or pulmonary embolism and comparison of 6 and 12 weeks of therapy after isolated deep vein thrombosis. Circulation 103:2453–2460 25. Plate G, Eklöf B, Norgren L, Ohlin P, Dahlström JA (1997) Venous thrombectomy for iliofemoral vein thrombosis – 10-year results of a prospective randomized study. Eur J Vasc Endovasc Surg 14:367–374 26. Prandoni P, Lensing AWA, Cogo A et al (1996) The longterm clinical course of acute deep venous thrombosis. Ann Intern Med 125:1–7 27. Prandoni P, Lensing AWA, Prins MH et al (2004) Belowknee elastic compression stockings to prevent the postthrombotic syndrome. Ann Intern Med 141:249–256
28. Saarinen J, Domonyi K, Zeitlin R, Salenius J-P (2002) Postthrombotic syndrome after isolated calf deep venous thrombosis: the role of popliteal reflux. J Vasc Surg 36:959–964 29. Saarinen J, Anturaniemi M, Heikkinen M, Suominen V, Salenius J-P (2004) Clinical and anatomical findings of acute iliofemoral deep venous thrombosis. Phlebology 19:42–46 30. Schweizer J, Kirch W, Koch R et al (2000) Short- and longterm results after thrombolytic treatment of deep venous thrombosis. J Am Coll Cardiol 36:1336–1343 31. Scurr JH, Machin SJ, Bailey-King S et al (2001) Frequency and prevention of symptomless deep-vein thrombosis in longhaul flights. A randomized trial. Lancet 357:1485–1489 32. Tamariz LJ, Eng J, Segal JB et al (2004) Usefulness of clinical prediction rules for the diagnosis of venous thromboembolism: a systematic review. Am J Med 117:676–684 33. Turpie AG, Bauer KA, Eriksson BI, Lassen MR (2002) Fondaparinux versus enoxaparin for the prevention of venous thromboembolism in major orthopedic surgery. A meta-analysis of four randomized double-blind studies. Arch Intern Med 162:1833–1840 34. White RH, Zhou H, Romano PS (2003) Incidence of symptomatic venous thromboembolism after different elective or urgent surgical procedures. Thromb Haemost 90:446–455
Lymphatics
561
11.1 Lymphoedema Peter Lamont
11.1.1 Introduction The lymphatic system is a significant pathway for the drainage of fluid, large protein molecules and white blood cells from the interstitial spaces within capillary beds. Lymphatic capillaries lie in the dermis and subcutaneous fat, in the fascial planes between muscles and in perivascular tissues. Lymphatic vessels transport lymph from these areas through regional lymph nodes towards the thoracic duct. Lymph returns to the venous circulation via the termination of the thoracic duct at the left internal jugular vein close to its junction with the left subclavian vein. The system plays a major immunological role, with the regional lymph nodes processing antigens presented to them by white blood cells from the peripheries. Antigen-specific lymphocytes proliferate in the lymph nodes and are then released into the circulation via the main lymph ducts and also through small lymphovenous connections within the lymph nodes themselves. Impaired drainage of lymph from a limb, usually due to obstruction of the system, leads to the accumulation of fluid and protein in the subcutaneous tissues with eventual irreversible fibrosis and swelling, known as lymphoedema [8].
11.1.1.1 Capillary Microcirculation Fluid and protein fluxes in the capillary bed follow both hydrostatic and colloid osmotic pressure gradients. Since hydrostatic pressure outside the capillary is negligible, hydrostatic pressures tend to force fluid out of the capillary lumen into the tissues, whereas colloid osmotic pressures generated by intravascular proteins tend to draw fluid back into the vessel lumen. White cells pass through gaps in the capillary endothelium by an active process of diapedesis, drawn towards sites of inflammation by chemoattractant molecules. Fluid, proteins and white blood
cells are delivered to the tissues at the arterial end of the capillary bed, where the hydrostatic pressure at around 32 mmHg exceeds the colloid osmotic pressure. Fluid and proteins, particularly albumin, globulin and fibrinogen, pass through the capillary wall along the hydrostatic pressure gradient. The majority of the fluid returns to the capillary lumen at the venous end, where the intraluminal hydrostatic pressure has fallen to around 15 mmHg and is now overcome by the colloid osmotic pressure. The latter increases as fluid leaves the capillary at the arterial end, increasing the concentration of colloids within the vessel lumen and drawing fluid back into the capillary. Very little protein returns via the capillary, with up to 95% of it entering the lymphatics along with some fluid. The lymphatic endothelium is poorly organized with gaps between the cells and little basement membrane, so fluid and proteins enter via a combination of passive and active transport. Overall around 20 l of fluid and up to 200 g of protein pass through the capillary bed every day, with 2–4 l of fluid and the majority of the protein returning to the circulation via lymphatic pathways [3]. Once within the lymphatic vessels, there is very little leakage of fluid and protein back out. Lymph vessels contain both valves in the lumen and smooth muscle cells in their walls. Intrinsic contraction of the vessel walls pushes lymph proximally through the valves. Skeletal muscle contraction increases the extrinsic pressure on the lymph and also drives it through the valves, and negative pressure within the thorax encourages proximal flow. As lymph flow is relatively sluggish, it can be impeded by the effects of gravity and by any increase in central venous pressure which limits egress of lymph from the thoracic duct. The lymph nodes also act as filters of the lymph, increasing resistance to flow along the drainage pathway. An understanding of the capillary microcirculation is important when considering the differential diagnosis of lymphoedema, as limb swelling can result when any component of the system malfunctions or becomes diseased.
562
11.1 Lymphoedema
11.1.1.2 Capillary Circulation and Limb Oedema Conditions which affect the hydrostatic or colloid osmotic pressure gradients in the capillary beds may lead to accumulation of fluid (Table 11.1.1).
Venous Hypertension • Venous hypertension, whether superficial or deep, will increase the intraluminal hydrostatic pressure at the venous end of the capillary so that it resists the colloid osmotic pressure and reduces the force drawing fluid from the tissues into the capillaries. • Fluid then accumulates within the tissues causing oedema.
• As protein clearance by the lymphatics is not affected, the fluid is low in protein and fibrotic changes are slow to develop, so the oedema remains pitting and can be reversed by increasing the tissue’s hydrostatic pressure with externally applied compression gradients using graduated compression stockings. • Likewise the intraluminal hydrostatic pressure can be reduced by elevating an affected limb and reversing gravitational pressures, thus encouraging fluid to follow colloid osmotic pressure back into the capillary at the venous end. • Other causes of high venous pressure, such as extrinsic compression of iliac veins by a pelvic mass, deep venous thrombosis or heart failure, will have the same effect on the capillary circulation and lead to tissue oedema.
Low Intravascular Colloid Osmotic Pressure Table 11.1.1 Causes of limb oedema Venous
Superficial venous incompetence Deep vein insufficiency Deep vein thrombosis Deep vein occlusion Extrinsic venous compression
Circulatory
Excess intravenous fluid Heart failure Caval obstruction Aortocaval fistula
Hypoproteinaemia
Malnutrition Renal failure Liver failure
Capillary damage
Anaphylaxis Septicaemia
Dependency
Paralysis Orthopnoea Ischaemic rest pain Air travel
Lymphatic
Primary lymphoedema Secondary lymphoedema • infection • malignant infiltration • radiotherapy • block dissection
Hysteria Idiopathic
Dependency Constricting band
• Intravascular colloid osmotic pressure at the venous end of the capillary bed may fall in patients with low levels of plasma proteins due to malnutrition, liver failure or renal failure. • In such patients, although hydrostatic forces remain low, they become sufficient to impede the deficient colloid osmotic pressure and leave fluid within the tissues. • The capillary walls may become leaky through damage from anaphylactic reactions or septicaemia. • Dependency of a limb, particularly when it is immobile, impairs the mechanisms of venous and lymphatic drainage by increasing gravitational pressures and impairing extrinsic muscle pump activity, causing an increased intraluminal hydrostatic pressure and impairing fluid movement back into both capillaries and lymphatics. • Such patients may be wheelchair bound after a stroke or an amputation, they may be paraplegic or they may sit and sleep with their legs dependent because of orthopnoea or ischaemic rest pain.
Obstruction • Obstruction to the lymphatic system will impair fluid drainage from a limb in a mechanical way, as a result of either poor lymphatic development or damage to the lymphatic channels by infection, malignancy surgery or radiotherapy.
11.1.3 Aetiology/Epidemiology
• Some patients with hysteria may hold their limb in a dependent position with resistance to any movement or may apply constricting bands around a limb, causing either increased gravitational pressure or venous and lymphatic obstruction.
Idiopathic Oedema • There is also a group of patients who develop idiopathic oedema for whom no cause is found, although the swelling in such patients is usually mild.
11.1.2 Definition of Lymphoedema • Lymphoedema is an abnormal accumulation of protein rich fluid in the tissues. • The proteins raise the colloid osmotic pressure within the tissues and so more fluid is attracted. • Fibroblast proliferation occurs, causing the subcutaneous tissues to thicken and the oedema becomes nonpitting as a result.
11.1.3 Aetiology/Epidemiology • Lymphoedema may be either primary [10], due to intrinsic abnormalities of the lymph vessels, or secondary [2]. • Secondary lymphoedema is commoner and arises from pathological or iatrogenic damage to lymph nodes.
11.1.3.1 Primary Lymphoedema • Primary lymphoedema was initially classified as congenital when present at birth, praecox when it started in early life and tarda when the onset was after the age of 35 years. • Current definitions focus more on whether the lymphoedema arises from either obliteration or hyperplasia of the lymphatics. • Over 90% of patients have the obliterative version and of these a small number are born with developmental aplasia of lymphatics (Milroy disease, Fig. 11.1.1). • The genetic basis of congenital forms of primary lymphoedema is currently the subject of active re-
Fig. 11.1.1 A child with bilateral congenital lymphoedema (Milroy disease)
search [6]. The most common type of primary, familial lymphoedema is that first described by Meige (isolated pubertal-onset lymphoedema), but to date no locus has been reported. The gene for Milroy disease (congenital familial lymphoedema) has recently been mapped to chromosome 5q35.3 and probable causative mutations have been found in the VEGFR3 gene. • Lymphoedema-distichiasis syndrome is a rare, primary lymphoedema of pubertal onset, associated with distichiasis. Distichiasis is a congenital anomaly in which accessory eyelashes occur along the posterior border of the lid margins. Lymphoedema-distichiasis has been mapped to chromosome 16q24 with a high incidence of mutations in the FOXC2 gene [1, 5]. • Aside from these rare forms of congenital lymphoedema, obliterative lymphoedema may be broken down into three clinical sub-groups. • The first of these, distal obliteration, occurs when the lymphatic vessels of the thigh are hypoplastic, being narrow and reduced in number (Fig. 11.1.2a,b). The lymphoedema is often bilateral, below the knee and mild, occurs mainly in women with an onset in their teenage years and is not usually progressive provided the pelvic lymphatics are normal.
563
564
11.1 Lymphoedema
Fig. 11.1.2a,b a A lady in her 20s with mild lymphoedema in the left leg below the knee. b An isotope lymphangiogram of the patient in a, showing delayed lymphatic filling in the left thigh, although the groin and pelvic lymph nodes are not affected (distal obliteration)
• A more severe form of progressive lymphoedema occurs in the second sub-group, where there is pelvic obstruction. Lymph vessels and lymph nodes are small and few in the pelvis and groin (Fig. 11.1.3), although the lymph vessels below the groin may be numerous and dilated due to the proximal obstruction. This form occurs in around 20% of patients, with equal incidence in men and women. It is usually unilateral and involves the whole limb. These patients might be considered for lymphatic by-pass surgery to the lymphatics below the groin if they are unaffected, but over time the obstruction leads to thrombosis and obliteration of the thigh lymphatics and so early diagnosis and treatment are important. • The final sub-group of primary obliterative lymphoedema show a mixed picture between the above two categories, with proximal and distal oblitera-
Fig. 11.1.3 Isotope lymphangiogram showing no isotope in the left groin lymph nodes (pelvic obstruction)
11.1.3 Aetiology/Epidemiology
tion. The lymph vessels and lymph nodes are small and few both above and below the groin (Fig. 11.1.4) and lymphatic by-pass surgery is not indicated. • The remaining 10% of patients with primary lymphoedema have the hyperplastic type, which is sub-categorized into bilateral hyperplasia and megalymphatics. • Bilateral hyperplasia may occur due to obstruction at the level of the cisterna chyli or thoracic duct, causing distal dilatation of the lymphatics. Lymphatic vessels retain their valves and do not become varicose. • Patients with megalymphatics, on the other hand, have large, valveless and varicose lymphatic vessels, and chylous skin vesicles may occur. There are large numbers of inguinal and pelvic lymph nodes present on lymphography and the condition is often associated with angiomas on the lower limb or trunk or multiple diffuse arteriovenous fistulae.
11.1.3.2 Secondary Lymphoedema • Secondary lymphoedema occurs when some other pathological process acts to obstruct or destroy lymphatic vessels and lymph nodes. • In the Western world, malignancy is the commonest culprit, whereas in the tropical world, infection plays a much bigger role.
Malignancy • Metastatic cancer deposits in regional lymph nodes may obstruct the flow of lymph and present with lymphoedema (Fig. 11.1.5). • Common cancers doing this include prostate, cervix, testis or melanoma. • Primary lymph node tumours such as Hodgkin’s or non-Hodgkin’s lymphoma may also occasionally present in this way. • Surgery or radiation therapy for cancer in the regional lymph nodes may also induce lymphoedema. • Block dissection to excise involved lymph nodes destroys the normal lymphatic pathways. Although some regeneration of lymphatics occurs, the addition of external beam irradiation causes subcutaneous thickening and fibrosis which inhibits the regrowth of lymphatics. Hence significant arm lymphoedema after breast cancer surgery is much more likely after a com-
Fig. 11.1.4 Isotope lymphangiogram from a 38-year-old patient with left-sided lymphoedema extending into the thigh. There is no isotope take up in either the distal lymph vessels or the groin lymph nodes (proximal and distal obliteration)
bination of radical block dissection and radiotherapy than after surgery or radiotherapy alone.
565
566
11.1 Lymphoedema
ing around barefoot and suffering repeated minor injuries and soft tissue infections. • The recurrent infections induce fibrosis of the lymph nodes, with subsequent lymphatic obstruction.
11.1.4 Symptoms
Fig. 11.1.5 Isotope lymphangiogram showing enhanced uptake of isotope in enlarged left pelvic lymph nodes
Infection • Filariasis is the commonest secondary cause of lymphoedema and is endemic in many tropical areas, particularly in Indonesia, India and China. • The worm Wuchereria bancrofti enters the body in microfilarial form through insect bites. • The worm lodges in lymph nodes, where it matures and starts producing microfilariae which are released into the bloodstream and are thence transmitted back to biting insects, so completing the cycle of reproduction. • The adult worm induces fibrosis within the lymph node, obstructing lymph flow. Even if the parasite is destroyed, the lymph node changes are irreversible and the lymphoedema does not resolve. • Elephantiasis also occurs in many tropical areas where filariasis is not endemic, such as parts of East Africa. • Some of these patients may have tuberculosis, with caseation and destruction of lymph nodes. • Some may just have repeated episodes of infection and inflammation in the lymph nodes as a result of walk-
• Patients note a gradual onset of swelling, starting distally and gradually spreading proximally (Fig. 11.1.2a). • Lymphoedema is not confined solely to the limbs and some patients may present with genital swelling or with involvement of the intestine or pleura causing diarrhoea, chylous ascites or pleural effusions due to leakage of lymph. • In the lower limb, where the condition is most common, swelling above the knee is unusual. The swelling subsides at night initially, when the leg is elevated, but through a gradual process of subcutaneous fibrosis the swelling becomes more established and permanent with less pitting on finger pressure. • In severe cases, particularly those due to megalymphatics, cutaneous vesicles develop and discharge lymphatic fluid with surrounding excoriation and crusting (Fig. 11.1.6). • The skin may become coarse and pitted and the patients may become susceptible to repeated episodes of cellulitis, both from infection entering the limb through the damaged skin and from the loss of function of the regional lymphatics in defence against infection. • Rarely patients with longstanding swelling may develop lymphangiosarcoma in the affected limb, with purple red nodules on the skin.
11.1.5 Diagnosis 11.1.5.1 History and Examination • A careful medical history and examination will establish the likelihood of many of the conditions listed in Table 11.1.1. • The history should include enquiry about the age of onset and whether any family members are also affected. • Secondary causes might be suspected if there is a history of malignant disease or radiotherapy or if the pa-
11.1.5 Diagnosis
lower limb oedema, the abdomen and pelvis should be carefully palpated for masses, as well as being examined for ascites. • In older patients, the prostate or cervix should be examined for signs of malignancy. • The skin of the limb needs to be carefully inspected and the web-spaces between the digits inspected for evidence of fungal infection such as athletes’ foot. • A finding of nonpitting oedema, particularly if it appears chronic and has developed slowly over a prolonged period of time, raises the clinical suspicion of lymphoedema. Further investigation is needed if the diagnosis is uncertain, to rule out other treatable causes of limb oedema and to aid decision making in the few patients with lymphoedema where surgery is being considered.
11.1.5.2 Laboratory Tests • Measurement of serum prostate-specific antigen (PSA) may help to rule out prostate malignancy in male patients. • Liver function tests and creatinine can be used if there is suspicion of hypoproteinaemia, liver or renal failure.
11.1.5.3 Imaging
Fig. 11.1.6 Unilateral lymphoedema with skin vesicles and crusting. The patient suffered recurrent episodes of cellulitis in the left leg
tient has travelled to a tropical country, particularly where filaria is endemic. • The patient should be asked about complications, including recurrent cellulitis, discharging vesicles, diarrhoea and whether or not the swelling interferes with quality of life or walking, especially if the thighs are involved and rub together because of the swelling. • On examination, the extent of the swelling should be noted and circumference measurements made in relation to fixed bony points, to allow future comparisons. • Regional lymph nodes should be palpated for any enlargement or suspicious features and, in the case of
• Most venous abnormalities can be excluded by Duplex ultrasonography, which may reveal deep or superficial venous reflux and can demonstrate venous obstruction by a lack of flow in, and incompressibility of, a vein. • Ultrasound, CT or MR scans of the abdomen and pelvis may demonstrate extrinsic compression of the pelvic veins or enlargement of intra-abdominal lymph nodes. • Image-guided needle aspiration cytology of a mass or an enlarged lymph node is also possible with these modalities and is the method of choice for obtaining histological diagnosis (Fig. 11.1.7), as removal of a node may aggravate the oedema. • Contrast lymphography has nowadays been replaced by isotope lymphangiography [4] in the routine investigation of lymphatic drainage from the limb. • A gamma-emitting isotope such as rhenium is injected subcutaneously in both feet and a gamma camera is used to record the speed of uptake of the isotope into the groin and pelvic lymph nodes. Patients with
567
568
11.1 Lymphoedema
•
•
Fig. 11.1.7 CT-guided needle aspiration of left pelvic mass, which turned out to be metastatic prostate cancer replacing a lymph node. The mass is compressing the left external iliac vein, causing left leg swelling from a mixture of lymphatic and venous obstruction
•
• lymphoedema will show delayed or absent uptake of the isotope on the affected side (Fig. 11.1.4). • Where a patient is being considered for lymphatic bypass surgery, the more detailed images of lymphatic vessels obtained with contrast lymphography help with the careful case selection needed, but the technique requires skill and patience to undertake open cannulation of a lymphatic vessel on the dorsum of the foot.
•
•
11.1.6 Treatment • • Most patients with lymphoedema can be managed conservatively. • Reconstructive surgical options are very limited, with few patients being suitable and with uncertain results. • Limb reduction surgery is disfiguring and so is reserved only for the most severely affected patients.
11.1.6.1 Conservative Treatment • Most patients have modest, nonprogressive limb swelling which does not give rise to complications such as recurrent cellulitis but can cause concern about the cosmetic appearances. • The mainstay of treatment in such patients is a combination of elevation and compression stockings [11].
Patients should sleep with the limb elevated to assist fluid drainage overnight. Graduated compression stockings need to be applied before getting out of bed in the morning to try to maintain any reduction in swelling. The stockings need to apply a minimum of 30 mmHg pressure at the ankle. If the swelling is confined to the below-knee area then knee-length stockings are acceptable and are more likely to be complied with in men. More severe limb swelling may respond to a 2- to 6week course of complex decompressive therapy, which involves careful skin cleansing, nail care and the application of simple skin creams to avoid infection setting in through skin cracks. Specially trained practitioners massage the affected limb using the technique of manual lymphatic drainage and then apply multi-layer compression bandaging each day. Patients are encouraged to exercise gently each day and to lose weight. Any improvement is maintained after a course of treatment by the use of graduated compression stockings and the course may need to be repeated after 6–12 months. A variety of commercially available external compression devices are available, which the patient wears in bed at night. The devices use a pneumatic pump to alternately compress and relax a knee- or thigh-length boot around the leg. Patients use the devices in bed at night and apply compression stockings during the day. Sleep can be difficult with the pump working and there have been no convincing studies of benefit in lymphoedema. Other forms of lower-limb pitting oedema may respond better to these devices than the more fixed swelling of lymphoedema.
11.1.6.2 Surgery • Surgical options fall into two categories, namely operations designed to by-pass lymphatic flow around an obstructed part of the system or those designed to reduce the bulk of the limb. Because the former is not always successful and the latter causes a lot of scarring, such operations are reserved for those with recurrent cellulitis or lymphangitis or those in whom walking is impaired because of the heaviness or the bulk of the limb, which causes the thighs to rub together.
11.1.6 Treatment
Lymphatic By-pass • Attempts at lymphatic by-pass have been made by directly anastomosing bivalved lymph nodes to adjacent veins or by microanastomosis of dilated distal lymphatic vessels directly onto adjacent veins but the outcomes of these procedures have been poor. • An alternative approach is to use pedicles of skin, omentum or mesentery which originate proximal to the lymphatic obstruction and are anastomosed to lymph nodes distal to it. • Of these the mesenteric bridge has proved most successful, although it only helps around 50% of carefully selected patients [7]. • The procedure is reserved for patients with primary lymphoedema due to proximal obstruction, where the lymphatics above the pelvis and groin are normal and the lymphatics in the thigh are patent within reach of the mesenteric pedicle. • Only 20% of patients with primary lymphoedema have proximal obstruction of this nature and a proportion of them will have obliterated proximal thigh lymphatics, so the operation is only suitable for a few, carefully selected patients with lymphoedema. • The mesenteric by-pass is fashioned by resecting a 5cm segment of terminal ileum on its mesentery, opening it along its antimesenteric border and stripping off the mucosal surface to expose the submucosal lymphatics of the bowel. • The mesenteric pedicle is then tunnelled down to the groin and the stripped mucosal surface is sutured across the cut surface of bivalved lymph nodes below the obstruction. • Results are better in younger patients, especially if the limb swelling is not excessive.
• •
•
•
•
• •
•
•
• Limb Reduction • • In patients where walking is impaired because the thighs rub together and the leg is too heavy to lift or where the limb swelling is excessive and associated with recurrent cellulitis then a limb reduction operation may be considered. • Several variants are described but only two are in common use today, the Charles reduction and the Homans procedure [9]. • In patients where there is extensive skin damage in the limb below the knee, the Charles reduction replaces all of the skin and subcutaneous fat from the knee to
•
•
the ankle with split skin grafts to cover the deep fascia overlying the muscle and the tibial periosteum. The cosmetic result is poor, although there is good reduction in limb size. It is important to retain the patient’s skin over the knee itself, so that they avoid kneeling on the thin split skin graft. It is also more cosmetically acceptable if the skin and subcutaneous tissues at the top and bottom of the denuded area are tapered in towards the skin grafts by undermining the cut edges of skin and excising some of the bulky subcutaneous tissues underneath. The Charles operation in the calf can be combined with a Homans operation in the thigh, or the Homans can be used both above and below the knee if the skin is healthy. In the Homans operation, the medial side of the thigh or calf is incised vertically, with horizontal T-shaped incisions at the top and bottom of the vertical incision. Skin flaps are then lifted anteriorly and posteriorly with an underlying layer of subcutaneous fat. It is possible to raise the flaps across to the midline of the limb without damaging the blood supply to the flaps, although care should be taken to preserve any vessels entering the flaps at the limits of their dissection. The underlying thickened subcutaneous tissue is then excised down to the deep fascia and the skin flaps laid back down on the new fascial bed and sutured back together. This operation gives a better cosmetic result than the Charles reduction, although the edges of the flaps may undergo necrosis, eventually healing with more prominent scars. The lateral side of the limb can be tackled in a similar fashion after an interval to ensure full healing of the medial side. Where debulking of the medial aspect of the thigh is all that is needed, a simpler alternative to the Homans operation is that described by Sistrunk. A vertical wedge of skin and underlying subcutaneous tissue is excised down to muscle fascia and the skin wound is then closed primarily. This may be used to help taper the thigh down towards a Charles excision and skin grafting area of the calf to prevent a pantaloon effect or may be all that is needed where the patient has trouble walking because the thighs rub together. None of these procedures is problem free, with the risk of wound breakdown and excessive scarring.
569
570
11.1 Lymphoedema
• They should be viewed as a palliative procedure to achieve a functional result such as improved walking or reduced episodes of cellulitis and they are not indicated for cosmetic reasons alone. • Surgery should be avoided in patients with secondary lymphoedema due to metastatic disease, as there is often an element of venous obstruction on top of the lymphatic obstruction and the results are poor. References 1
2 3
4
Brice G, Mansour S, Bell R, Collin JRO, Child AH, Brady AF, Sarfarazi M, Burnand KG, Jeffery S, Mortimer P, Murday VA (2002) Analysis of the phenotypic abnormalities in lymphoedema-distichiasis syndrome in 74 patients with FOXC2 mutations or linkage to 16q24. J Med Genet 39:478–483 Browse NL, Stewart G (1985) Lymphoedema: pathophysiology and classification. J Cardiovasc Surg 26:91–106 Burnand K, McGuiness L (2000) Abnormalities of the lymphatic system. In: Morris PJ, Wood WC (eds) Oxford textbook of surgery. Oxford University Press, Oxford, pp 1063–1076 Burnand KG, McGuinness CL, Lagattolla NR, Browse NL, El-Aradi A, Nunan T (2002) Value of isotope lymphography in the diagnosis of lymphoedema of the leg. Br J Surg 89:74–78
5
Fang J, Dagenais SL, Erickson RP, Arlt MF, Glynn MW, Gorski JL, Seaver LH, Glover TW (2000) Mutations in FOXC2 (MFH-1), a forkhead family transcription factor, are responsible for the hereditary lymphedema-distichiasis syndrome. Am J Hum Genet 67:1382–1388 6 Ferrell RE, Levinson KL, Esman JH, Kimak MA, Lawrence EC, Barmada MM, Finegold DN (1998) Hereditary lymphedema: evidence for linkage and genetic heterogeneity. Hum Mol Genet 7:2073–2078 7 Hurst PA, Stewart G, Kinmonth JB, Browse NL (1985) Long term results of the enteromesenteric bridge operation in the treatment of primary lymphoedema. Br J Surg 72:272–274 8 Kinmonth JB (1972) The lymphatics. Disease, lymphography and surgery. Arnold, London 9 Kinmonth JB, Patrick JH, Chilvers AS (1975) Comments on operations for lower limb lymphoedema. Lymphology 8:56–61 10 Wolfe JHN (1984) The prognosis and possible cause of severe primary lymphoedema. Ann R Coll Surg Engl 66:251–257 11 Wolfe J (1989) The management of lymphoedema. In: Rutherford RB (ed) Vascular surgery. Saunders, Philadelphia, pp 1648–1677
Arteriovenous Malformations
573
12.1 Arteriovenous Malformations P.B. Dimakakos, T.E. Kotsis
12.1.1 Synonyms • Arteriovenous malformations • Vascular malformations • Arteriovenous fistulas • Angiodysplasias.
12.1.2 Definition 12.1.2.1 Terminology • Birth defects involving the vasculature of both the macro and microcirculation – in particular when various types of interconnections between arteries and veins occur – are generally named arteriovenous malformations. • Arteriovenous malformations are the most common vascular anomalies. • However, it is misleading to apply this term as a generic descriptive definition of all vascular defects, as not all malformations include clinically significant arteriovenous interconnections. • Another misleading term is arteriovenous fistulas. This term can be used for both acquired and congenital arteriovenous conditions, but is better used only for acquired defects. • Acquired defects are created by penetrating injuries, following diagnostic or therapeutic procedures, by tumours or atherosclerotic or aneurysmal disease. • Vascular malformations (VMs) is the appropriate inclusive term to use for all types of vascular malformations; by definition these are congenital and they encompass any combination of defects in blood vascular and lymph systems independent of the amount of blood shunted through arteriovenous communications.
• Angiodysplasia is a similar, appropriate compound term from the Greek words αγγείο meaning vessel and δυσπλασία meaning malformation with alterable potential.
12.1.3 Epidemiology • The estimated incidence of VMs is approximately 5.4% of all hospitalized patients; in our department the incidence was 1.06% over a 20-year period (256 cases in 25,000 examinations in the outpatient clinic). • VMs can exist anywhere in the body: they can be a mixed development between the right and left macroor microcirculation, a malformation with or without A–V communication involving the head or neck, or in specific thoracic, abdominal or retroperitoneal organs as well as in the extremities. • Occasionally, more than one malformation might exist, involving visceral, central or peripheral vessels. • The distribution of lesions is variable: in a multiple or in an isolated pattern in a specific area (e.g. central nervous system, pelvis), alternatively in individual organs such as the brain, spinal cord, liver, pancreas, lung, intestine, spleen or kidneys. • Those associated with the heart are not discussed here, as they are congenital cardiopathies and include atrial septal anomaly, persistence of the aortic trunk, inversion of the great vessels and open aortic duct.
12.1.3.1 Classification • Many investigators, namely Malan [7], Puglionisi, Szilagyi [9], Vollmar, Mulliken [8], Leu, Belov [2, 3], Loose [6], Schobinger, Papendieck, Lee, Gloviczki and others, have attempted to classify these lesions.
574
12.1 Arteriovenous Malformations
• Their important contribution has had one common aim: to offer a uniform and universal system to aid diagnosis, treatment and communication among specialists. • However, the criteria used for the classification were embryological, clinical, histopathological, haemodynamic and topographic, and so numerous classification systems have been reported. • Historically, many of the VMs were discovered following their association with other pathological states
Table 12.1.1 Modified ISSVA classification of vascular anomalies. (A/A-VS Arterial/arterio-venous shunt, C/V/L combined/ venous/lymphatic malformations)
Vascular Tumours
Vascular anomalies Vascular tumours Haemangiomas and others
(syndromes) and so have eponymous names; for example, Sturge–Weber, Kasabach–Merritt and Klippel–Trenaunay syndromes. Some of these syndromes of clinical importance to the vascular surgeon are discussed separately. • The most widely accepted and complete classification is that of Hamburg 1988, which was further modified in 1989 and proposed in an international consensus document by the International Society for the Study of Vascular Anomalies (ISSVA). • Vascular anomalies are divided into two main categories: vascular tumours and vascular malformations or angiodysplasias (Table 12.1.1).
Vascular malformations Slow-flow (C/V/L) Fast-flow (A/A-VS)
• Vascular tumours can be benign or malignant. • Haemangiomasare benign tumours, the classic representative being infantile haemangioma, whose involution phase extends from 1 year until 5–7 years.
Table 12.1.2 Classification of congenital vascular malformations. Modified Hamburg 1988 classification Type
Form
Predominantly arterial defects
Truncular forms
Aplasia or obstruction Dilatation
Extratruncular forms
Infiltrating Limited
Truncular forms
Aplasia or obstruction Dilatation
Extratruncular forms
Infiltrating Limited
Truncular forms
Deep A–V fistula Superficial A–V fistula
Extratruncular forms
Infiltrating Limited
Truncular forms
Aplasia or obstruction Dilatation
Extratruncular forms
Infiltrating Limited
Truncular forms
Arterial and venous without shunt Haemolymphatic with or without shunt
Extratruncular forms
Infiltrating haemolymphatic Limited haemolymphatic
Predominantly venous defects
Predominantly A–V shunting defects
Predominantly lymphatic defects
Combined (or mixed) vascular defects
12.1.4 Aetiology
Vascular Malformations or Angiodysplasias • Vascular malformations or angiodysplasias are subdivided into slow-flow and fast-flow categories. • Malformation is first classified by its predominant component of the vascular defect (arterial, venous, or lymphatic plus the A–V shunting and combined forms); then, it is further classified into truncular or extratruncular forms depending on the embryonic stage at which pathological arrest occurred and from which it persisted. • Truncular forms represent 70% of the pathologies. These lesions arise from a maldevelopment at the stage of differentiation; they can be further separated into hypoplasia, aplasia, obstruction or dilatation; in A–V communications the superficial have to be distinguished from the deep forms, whilst the combined or mixed forms split into arterial–venous and haemolymphatic forms. • Extratruncular forms can have limited or infiltrating features, and again the combined or mixed forms are characterized by the haemolymphatic nature of the lesion. • It is important to mention that the term “angioma” is included in the limited form of extratruncular lesions. • The modified 1988 Hamburg classification (Table 12.1.2) was derived from previous classifications that used the anatomical component to distinguish among these minor or major defects. The modified 1988 Hamburg system is clinical and morphological and is crucial in that it has excellent clinical applicability and has brought a proven order to the vascular malformation chaos. • Other classification systems are those of the ISSVA Multicenter Group, who classified and treated more than 2000 patients with VMs, and the version modified according to the anatomical presentation, as used by the Mayo Clinic group.
12.1.4 Aetiology • VMs are lesions of the vascular system of unknown aetiology that are nondegenerative and noninflammatory in origin; the faulty development starts during embryogenesis. • However, familial inheritance is rare, implying that the lesions do not have a hereditary component.
• They can appear anywhere in the body and affect one or more systems, since arteries and veins both differentiate from a common capillary plexus embryologically, and blood and lymphatic vessels have a common mesenchymatic origin. • Although VMs can result in local or distal swelling, limb hypertrophy or hypotrophy, and tumour-like enlargement, they are not true neoplasias. • An important feature of these abnormal structures is the absence of endothelial cell proliferation and VMs can be distinguished from haemangiomas by their different biological behaviour: the former are an anomalous development of the primitive vascular system and their augmentation is due to enlargement of vascular channels and the recruitment of collaterals, whereas the latter are due to pathologically observable cell proliferation.
12.1.4.1 Embryology and Anatomy • The development of the blood vascular and lymphatic systems of the embryo from mesoblastic cells that are located mainly in the yolk sac begins early in the third fetal week. • During embryonic vasculogenesis and angiogenesis, the peripheral cells fuse together developing endothelial conduits which proliferate, constructing networks that conjoin in seemingly predetermined sites to form blood islands; these represent the peripheral vessels. • Central vessels are formed in a similar way, but by centrally arranged cells; eventually, the more central mesenchymal cells form many of the haemopoietic elements. • This process of the development of the primitive capillary network constitutes the first stage, which is followed by a retiform and eventually a plexiform stage. • Some vessels enlarge and remain as definitive vessels to maturity, to be joined later by other developing channels from already formed capillary plexuses. Other vessels retrogress; some disappear completely or remain as residual elements or in places as vessels of fine calibre. • Finally, some vessels that are crucially important for the circulatory needs of embryonic and fetal life become obliterated postnatally and transform into fibrous cords.
575
576
12.1 Arteriovenous Malformations
• By birth, the stronger arteries can already be differentiated from the thinner veins whilst the functionless vascular elements relent. • Thus, a complete vascular system is developed, with arteries and their branches that perfuse the capillaries with blood, controlling the blood pressure. • The exchange of gases, nutrients and other substances takes place in the arterial and venous capillaries. • The arterioles determine peripheral resistance and the venules are regulated by vasoactive amines, and are the most permeable part of the vasculature. • Development of this complex vasculature is critical; failure or error at any of the three aforementioned stages of development cause VMs that: (1) are present at birth, (2) are revealed later in life, triggered by a mechanical (e.g. trauma) or hormonal (e.g. in the menarche or pregnancy) factor, or (3) remain undetected throughout life. • The normal pattern of blood transportation is for blood to pass from the higher pressure and resistance system of the arteries to the high-capacity, lower pressure and resistance network of veins. Normally, a vascular bed exists between them which allows for control of systemic blood pressure and the exchange of gases and other substances. Any combination of abnormal structures or connections in this network can arise, creating the enigmatic puzzle of congenital VMs. These were first described in the sixteenth century and studied in detail in the nineteenth and twentieth centuries.
12.1.5 Symptoms • The general complaints about VMs are of a cosmetic nature due to dysmorphia, particularly when lesions are located on the face, and dysfunction due to either local swelling or different-sized limbs. • Other symptoms and signs include local pain, discomfort, arthralgias and mobility difficulties (especially when joints are involved), ulceration, lymph leak, stasis dermatitis, local bleeding and even severe haemorrhage. • If there is distal ischaemia, the pain is ischaemic and trophic changes may exist. • Other specific symptoms depend on the location of the defect and may be elicited from pressure in adjacent organs because of lesion growth or haemorrhage, e.g. in the brain. When located in the central nervous
system, VMs commonly lead to headaches, dizziness and seizures. • In severe cases of A–V malformations serious complications can result, such as heart insufficiency, and death due to congestive heart failure or following haemorrhage. • Disability can arise from leg length discrepancy, due to vascular bone syndrome or following therapeutic amputation. • Finally, the impact that VMs have on a person’s emotional well-being is worth mentioning, as is that on society in general, due to the degree of disability suffered by people when they might expect to be at their most productive.
12.1.5.1 Vascular Bone Syndrome • Vascular bone syndrome is distinctive in that the growth of a child’s limb can be impaired by the presence of a VM. • The altered growth is manifest as overgrowth or hypotrophy of the extremity. • Pelvic tilting and scoliosis can cause complications in the affected leg, as length discrepancy can reach 10 cm. • Vascular bone syndrome is difficult to explain, and was first described as “haemangiectatic hypertrophy” by F. Parkes–Weber. • Current suggestions indicate that tissue hypoxia due to an A–V shunt is responsible for the leg length discrepancy. • The ischaemia is thought to trigger osteoblastic activity in the bone growth zones (area of metaphyses), via a nonspecific reaction that causes mesenchymatic proliferation and hypoxic hyperostosis. • Another postulation supports the theory of increased arterial flow in the area of the epiphyseal plates, although the supply of nutrients via arteriovenous communication is diminished through a “steal” effect. • Venous stasis may be an aetiological factor, because in Klippel–Trénaunay syndrome there is venous stasis without significant A–V communication. Since the degree of involvement of arteriovenous communication in VMs correlates with the clinical picture, a separate discussion regarding this entity follows.
12.1.5 Symptoms
12.1.5.2 Specific Vascular Malformations Arteriovenous Malformations Epidemiology/Aetiology
• Among the various types of VMs, arteriovenous malformations are potentially the most harmful; they represent a pause in development at the retiform stage. • An arteriovenous malformation is a congenital communication between the arterial and the venous systems other than the pulmonary and systematic capillary beds. • Congenital A–V communications may be haemodynamically active (hyperdynamic or high flow and hypodynamic or low flow), inactive, single or multiple, in a transverse or longitudinal arrangement limited to one or occupying more anatomical structures; they can also be associated, as already mentioned, with dysplasias of other systems. • Vollmar distinguished three types of A–V malformations: (1) localized direct shunts (type I), (2) generalized multiple shunts (type II) and (3) localized tumerous shunts (type III) (Fig. 12.1.1). • The A–V malformations vary from relatively mild to life-threatening lesions with a high blood flow that stress the cardiovascular system. • The terms macrofistula and microfistula depend on the demonstration of the communication by angiography. • The vast majority of arteriovenous malformations are isolated or confined to one anatomical region, have a vascular core known as a nidus and a peripheral parasitic circulation. • Blood passes from the arteries to the veins at great pressures and often at high velocities, because there
Fig. 12.1.1 Types of A-V shunts according to Vollmar
are no capillaries between them to act as buffers; thus, elements not constructed to withstand high pressure and flow are stressed, resulting in vessel enlargement or aneurysm formation, bleeding, or local swelling, etc. A classic example is the carotidcavernous communication which presents as pulsating exophthalmia.
Localization and Symptoms
• The extent of the clinical manifestations is related to the size of the A–V communication, the duration and the precise location. • A chronic fistula is typically associated with hypertrophy, wall thickening, dilatation and elongation of the parent artery with a tortuous course. The proximal venous system is also dilated, becoming hypertrophic, fibrotic and with functional distortion such as hypertension and incompetence, causing distal swelling with wall attenuation. In large fistulas, due to the extensive shunting of the peripheral bed, the “steal” phenomenon may result in distal ischaemia and, according to the degree of steal, to loss of pulse or a decrease of Doppler signals. • The systemic consequences, as mentioned before, can lead to myocardial hypertrophy, congestive heart failure and death. • Although arteriovenous malformations can be found in many parts of the body, including the arms, legs, lungs and heart, lesions involving the lower extremity are the most frequent; lesions in the head and neck follow with less frequency. • Facial arteriovenous malformations can cause dysmorphia, mass effect or bleeding into the mouth. • Malformations in the central nervous system and in the brain, brainstem and spinal cord carry a risk of stroke, paralysis, loss of vision and speech, and even death. • In order to follow a different therapeutic management, the arteriovenous malformations of the head circulation are distinguished as intra-axial (concerning arteries of the circle of Willis that perfuse the brain directly) or extra-axial (concerning branches of the external carotid and of other arteries of the brain that perfuse not the brain but other tissues such as the dura, bone or muscles). • Arteriovenous malformations can be present in the lungs in simple or complex form and can lead to dyspnoea, palpitation and haemoptysis.
577
578
12.1 Arteriovenous Malformations
• Approximately 40% of cases are associated with hereditary haemorrhagic telangiectasia (Rendu–Osler–Weber syndrome) and are related to brain infarcts or abscesses due to paradoxical emboli. Hereditary haemorrhagic telangiectasia is also associated with lesions in the liver or spleen, although in such cases the incidence is extremely rare; this syndrome is also responsible for gastrointestinal angiomas. • In the gastrointestinal system other true arteriovenous malformations can also be found, located in the small intestine, and others due to atherosclerosis or valvular heart disease are located in the terminal ileum, caecum or ascending colon. • Arteriovenous malformations are also found in the pelvis and uterus where they are associated with menometrorrhagia, pain, anaemia and dyspareunia. • Arteriovenous malformations can also be located in the kidneys, although rarely, where they can produce haematuria and massive bleeding during pregnancy.
Simple and Associated (Syndromes) Vascular Malformations Some lesions, either simple or more complex, that have a special clinical interest are discussed separately here.
haemorrhage with headaches or seizures, or of occult repeated bleeding (intestine).
CavernousMalformations
• These are low-flow well-limited lesions composed of closely packed, large lumens embedded in fibrous tissues with incomplete septa.
BlueRubber Bleb Nevus Syndrome (BRBNS)
• This is a rare intertruncular malformation with an immature skin network, characterized by multiple cutaneous venous malformations in association with internal venous malformations (BRBNS). • It most commonly affects the gastrointestinal tract and, less often, is present in other internal organs and the brain. • Most cases are sporadic. • Some patients may have severe intestinal haemorrhage while most bleeding from the GI tract is slow, minor, chronic and occult, resulting in iron deficiency anaemia. • BRBNS has the potential to cause serious or fatal bleeding.
Rendu–OslerDisease Port-WineStains
• These are capillary malformations. • They have a pink or reddish colour in infancy, which darkens with advancing age; they are round, regular, thin-walled vessels (capillary ectasia) situated in the superficial dermis and are rarely associated (as in hypertrophic port-wine stains) with a venous-like component in the deep dermis. • They can be isolated or associated with clinical syndromes.
Telangiectasias
• They are groups of abnormally swollen capillaries; they are small lesions, usually simple, with a diameter of 1–3 mm. • In the cutaneous area they are known as nevus flammeus. • These small lesions rarely cause widespread damage to surrounding tissue. • Multiple telangiectatic angiomas, although frequently not impressive, may be the source of acute (cerebral)
• Hereditary hemorrhagic telangiectasias (HHT) of the skin and mucosa. • The disease manifestations are variable and include epistaxis, gastrointestinal bleeding, pulmonary arteriovenous malformations and cerebral arteriovenous malformations. • A higher frequency of pulmonary arteriovenous malformations has been reported for HHT1 while HHT2 is thought to be associated with a lower penetrance and milder disease manifestations. • HHT is associated with brain infarcts and abscesses due to paradoxical emboli from right to left shunts. • In young patients the disease is associated with an excessive mortality rate which is fully attributable to HHT.
Kasabach–Merritt’sSyndrome
• Large cavernous haemangiomas with anaemia and thrombocytopenia associated with haemorrhage.
12.1.5 Symptoms
Sturge–Weber–Krabbe’sSyndrome
F.P. Weber
• Cerebral and trigeminal angiomas associated with convulsions, hemiplegia or mental retardation.
• All the lesions of Klippel–Trenaunay’s syndrome may occur, but F. P. Weber syndrome is usually dominated by the symptoms of haemangiomas with multiple arteriovenous macro-shunts. • This rare fast-flow, combined vascular malformation usually involves a lower limb or the pelvis, and it is usually associated with a geographic stain (usually port-wine stain) over the enlarged limb. • Symptoms include cutaneous warmth and a bruit or thrill on clinical examination, all of which are more suggestive of a complex vascular malformation than a simple congenital malformation.
Klippel–TrenaunaySyndrome
• This is a slow-flow combined vascular anomaly (capillary-lymphatic-venous malformation) that is typically associated with marked overgrowth of the leg and geographic (i.e. well circumscribed, sharply bordered) capillary stains. • The condition may rarely be associated with hypotrophy. • Vascular alterations include: teleangiectatic nevi, usually of metameric distribution, venous or capillary haemangiomas with or without A–V microshunts and persistent embryonic veins. • Anomalous lateral veins, which are typically on the lateral aspect of the thigh, become prominent because of incompetent valves and deep venous anomalies such as agenesia/aplasia of large veins; the warning sign is when aplasia of the lower extremity’s deep venous system exists. • Other defects are: stenoses and occlusions of large veins; anomalies of the localization, course and size of large veins; varicose veins; chronic venous insufficiency due to incompetent perforators; and concomitant anomalies of lymphatic vessels, often followed by chronic lymphoedema. • Typical nonvascular alterations include hemihypertrophy or hemiatrophy of soft tissue and/or bone extremities, cephalic or caudal; syndactyly, configuration anomalies or monstrosities.
CobbSyndrome (Cutaneomeningospinal Angiomatosis)
• This syndrome consists of a high-flow capillary malformation on the posterior thorax with associated spinal involvement (arteriovenous malformation of the spine). • Sometimes the vertebral bodies are involved. • Neurological problems arise, commonly due to cord compression or spinal haemorrhage. • Spinal arteriovenous malformations are most commonly intramedullary, but may be meningeal or perimedullary. • On rare occasions, the posterior arteriovenous malformation may be seen as a port-wine stain (“pseudoport-wine stain”).
Servelleand Martorell’s Syndrome
• Same vascular alterations as in Klippel–Trenaunay’s syndrome may be present but the main symptoms are honeycomb-like telangiectatic angiomas with penetration from the soft tissues into the musculature, joint capsule and bone of a usually atrophic extremity.
ProteusSyndrome
• This is a rare complex condition, characterized by a variety of cutaneous and subcutaneous lesions including VMs, lipomas, hyperpigmentation and several types of nevi. • Males and females are equally affected. • The major clinical features of this rare vascular anomaly include verrucous nevus, lipomas and/or lipomatosis, macrocephaly, asymmetrical limbs with partial gigantism of the hands and feet, and cerebriform plantar thickening. • Partial gigantism with limb or digital overgrowth is pathognomonic. • No racial or ethnic differences in disease occurrence appear to exist. • Proteus syndrome may not be revealed in many individuals until later infancy or early childhood, depending on the degree of overgrowth or rate of cutaneous lesion appearance.
Maffucci’sSyndrome
• This is a rare condition characterized by enchondromas (benign cartilage tumours), bone deformities and venous malformations. • No racial, sexual predilection or familial pattern of inheritance has been shown.
579
580
12.1 Arteriovenous Malformations
• Maffucci’s syndrome usually manifests early in life, usually around the age of 4 or 5 years. • VMs of this syndrome manifest as blue subcutaneous nodules that are easily compressible. • Spontaneous fractures have been reported. • Malformations such as cavernous haemangiomas or lymphangioma have been reported in various areas of the body, including the leptomeninges, eyes, pharynx, tongue, trachea and intestines. • Vascular neoplasms (haemangiosarcomas, lymphangiosarcomas) may develop in a small number of patients.
Von Hippel-Lindau Syndrome
which is continuous throughout systole and diastole, with a diamond-shaped accentuation reaching a peak at the time of the second heart sound. • With palpation, a thrill or cavernous formations can be felt or the Branham-Nicoladoni “bradycardic sign” might be expressed – a decreased heart rate following compression of an arteriovenous communication. • With percussion, incompetent valves of superficial veins may be checked, but in general percussion is of limited value. Considering the complexity of VMs it is emphasized that this is a topic for a multidisciplinary approach by specialists in their field and there is no place for antagonism; additionally, as VMs are most frequently first discovered in children, a professional paediatric approach is also of paramount importance.
• Also known as oculocerebellar hemangioblastosis. Haemangioblastomas are associated with angiomas of the retina, cerebellum and other viscera.
12.1.6.2 Laboratory Investigations and Imaging
12.1.6 Diagnosis • The following should be determined when evaluating a VM: • The location of the lesion • Its severity • The presence of A–V communication • The extent of involvement of surrounding tissues such as vital organs, soft tissue or bone • The existence of other malformations elsewhere. • A sixth more practical issue, which depends on the experience of the team, may be predicting the lesion’s progression in order to decide the timing of prophylactic management. • The diagnostic approach to VMs should follow standard practice, commencing with a detailed patient history and a meticulous physical examination:
12.1.6.1 Examination • Inspection of the whole body surface looks primarily for pelvis tilt, scoliosis or differences in extremity length (e.g. limb hypertrophy), remembering that many VMs involve the skin so that discoloration, ulcers or local swelling or lesions can be observed. • Auscultation is important as an arteriovenous malformation can be revealed by a characteristic murmur often described as a “to-and-fro” or “machinery” bruit,
Following clinical suspicion, further investigation can reveal many aspects of the lesion. • Vascular laboratory methods can be used, including various types of plethysmography, thermography, Doppler flowmeter arterial study with waveform analysis, and sequential limb systolic pressure measurements, colour-coded Duplex scanning, transcranial Doppler (TCD), as well as oxygen tension of the venous blood to investigate the degree of A–V communication. Additionally, contrast echocardiography can be used to detect indocyanine green in the venous circulation following intra-arterial injection, in order to evaluate residual shunts after surgical resection. • Cardiopulmonary evaluation (chest radiography, ECG, echocardiography) are part of the routine evaluation of VMs and, in the case of bone involvement, plain bone radiographs with measurement of bone length and pelvis tilt for the assessment of growth discrepancy are necessary. • Computed tomography scans with MRI and MRA evaluation (in intracranial vessels is preferable to the three-dimensional contrast-enhanced MRA technique, with dynamic sequencing in cases of arteriovenous malformations) are indispensable for investigating the extent of the lesion; the current modality of spiral CT with the additional feature of three-dimensional reconstruction is quick and informative. • Depending on the indication, a variety of radionuclide angiographies can be performed; one method is the lung scan known as a transarterial lung perfusion scan. It is a transarterial radioisotope study with radio-
12.1.7 Treatment
nuclide-labelled with 9 9 mTc microspheres (with mean diameter of 40 μm) of human albumin. This method is useful for distinguishing microfistulous from predominantly venous lesions in diffuse-type defects. The concept behind this study is that under normal conditions these microspheres are trapped in the peripheral capillaries. The excessive concentration of the tagged microspheres in the lungs suggests an A–V shunt. The shunt volume can be estimated after a calibration procedure. Another similar study is transvenous radioisotope study with labelled red blood cells, which is called a whole body blood pool scan (WBBPS). Radioisotope lymphoscintigraphy using labelled colloids is also a valuable tool for diagnosing lymphatic system defects. • If the previous studies do not provide a definitive diagnosis or if precise mapping is necessary, then more invasive studies have to be undertaken, such as percutaneous direct puncture angiography, standard, selective, or superselective arteriography or various kinds of venography of the ascending, descending, or segmental type and/or microlymphangiography.
12.1.7 Treatment • The excellent current diagnostic methods mean that the human body has become almost transparent, and even tiny symptomless lesions can be revealed as incidental findings. • The treatment of these lesions and in particular of VMs depends on their severity, location, type and their potential for creating future problems. • The best tactic for asymptomatic lesions, especially in cases of asymptomatic arteriovenous malformations, is “to wait and see”. • This strategy is best if total resection is not feasible, because of the potential harm caused by any intervention stimulating the lesion. • An exception to this tactic may be an accessible lesion in a vital organ, such as the lungs or brain, because even there asymptomatic lesions can cause serious complications. • As a rule of thumb, symptomatic lesions should be treated when VMs enlarge and also when they are complicated by bleeding, critical distal ischaemia, disabling pain, neurological signs, tissue necrosis, ulcer or infection. • Massive haemorrhage and congestive heart failure are absolute indications for intervention.
• The treatment of VMs is complex. For the pioneers, the primary solution appeared to be to ligate the proximal feeding vessels, although it soon became obvious that this is not feasible; now it constitutes only a historical perspective and a scientific “not to do’’ as isolated praxis. • After years of analysing VMs, specialists conclude that if complete surgical excision is not feasible, combined therapy requiring a multidisciplinary approach is the best policy. • The type of malformation, the existence of arteriovenous shunting, and also an estimation of the degree of shunting should it exist (hyperdynamic, hypodynamic or nonshunting) together determine the therapeutic approach. • It is important to clarify the nature of the A–V shunt before treatment; an incidental finding of A–V shunting indicates the presence of potent mesenchymal cells, which may be stimulated by the attempted treatment. • In these situations the radical excision of the lesion is preferable, if this is feasible. • Following an international study of more than 2000 patients, the ISSVA group concluded that VM therapy must follow six principles: 1. An individualized approach for every patient. 2. Early treatment of patients aged between 3 and 7 years, better before school starts. 3. Interruption of haemodynamic dysfunction. 4. Radical surgery to be performed only when functional damage can be avoided. 5. Surgery should be staged and programmed. 6. The treatment should be interdisciplinary and combined. • Other investigators, for example the Mayo group, think that every effort should be made to achieve a one-stage operation.
12.1.7.1 Treatment According to the Type of the Malformation • Capillary malformations (for example port-wine stains) can be treated by dye laser, but sometimes tissue and orthognathic reconstructive surgery in the presence of a skeletal malformation is required. • The treatment of venous malformations is usually not surgical; sclerotherapy seems an efficient method [5]. VMs give rise to variable problems, especially in the cervicocephalic region and on the limbs and trunk, but always require a multidisciplinary approach with,
581
582
12.1 Arteriovenous Malformations
according to the site, size and repercussions, percutaneous sclerotherapy, embolization and surgery. • In arteriovenous malformations, the principal aim is to completely embolize or resect the nidus of the lesion. The ideal treatment would be complete resection of the AV malformation. As this is difficult, the usual treatment is combined therapy: surgery, which is usually preceded or followed by embolization; and reconstruction, which consists of local flaps or skin expansion in simple cases, and revascularized free flaps in difficult cases. • Lymphatic malformations (lymphangiomas) can be managed by a variety of approaches such as sclerotherapy or surgery. • Interventions for vascular bone syndrome include those for the temporary or permanent arrest of rapid bone growth (epiphysiodesis), and the corrective osteotomies to decrease the length of the bone; stapling epiphysiodesis of knee cartilage has been proposed as a solution, although the A–V malformation may worsen, so a well planned orthopaedic treatment is preferable (i.e. when length difference exceeds 2.5 cm).
•
• • •
•
slow-flow vascular anomalies, particularly for venous malformation (cavernous haemangioma) and lymphatic malformation (cystic hygroma) [5]. Various needles are used under ultrasound guidance to obtain access and then the sclerosant agent is injected into the lesion very carefully. CT-guided sclerotherapy is another option. For epistaxis, Ethibloc injections can be used. Doxycycline is an effective sclerosant agent also used for lymphatic malformations (cystic hygroma lesions) but it is not generally approved for treating patients under 8 years old. OK-432 is a lyophilized biological preparation containing the cells of Streptococcus pyogenes; this sclerosant agent is particularly useful for lymphatic malformations (cystic hygroma lesions).
LaserTherapy
• Corticosteroids can be used in cutaneous haemangiomas in children; for example, of the eyelids, the lips of the mouth, and in haemangiomas of the paratracheal region, or when surgical treatment cannot be performed. • Corticosteroids induce the regression of haemangiomas in the proliferative phase and the treatment length usually ranges from 10 to 30 days.
• Laser therapy is used for superficial cutaneous lesions, combined cutaneous-subcutaneous lesions and small localized defects. • Laser-induced interstitial thermal therapy is a minimally invasive but surgical technique for the treatment of haemangiomas and VMs, and various tumours. • The intra-lesion application of thermal energy destroys regional tissue. • This property is useful in the endoscopic treatment of gastrointestinal lesions (photocoagulation with Nd: YAG laser). • The percutaneous placement of the laser fibre for photocoagulation in deeper tissues is also possible, without the benefit of direct visual control by sonography [colour-Doppler-imaging- (CDI-) guided Nd:YAG laser therapy] or in conjunction with fused high-resolution computed tomography, and magnetic resonance image-data-based surgical navigation.
CompressionTherapy
Embolization
• Compression therapy using various types of elastic stockings is useful for compressing haemangiomas or superficial venous defects.
• Catheter-based techniques seem the ideal weapon for many vascular diseases. • Treatment of vascular anomalies with percutaneous embolization requires extreme care in addition to the selection of an appropriate embolic agent for the best therapeutic outcome; usually it is a multi-staged pre-, intra- or post-surgery treatment. • The materials used are coils, detachable balloons, microfibrillar collagen, ethiodized oil, autologous materi-
12.1.7.2 Conservative Treatment Recommended European Standard Therapeutic Steps Corticosteroids
Sclerotherapy
• The injection of a sclerosing (alcohol, sodium tetradecyl sulfate, ethanolamine oleate) substance, directly through the skin into a lesion, is used primarily for
References
als (blood clot, dura), ethylene vinyl alcohol, alginates, phosphoryl choline, sodium morrhuate, hot contrast material, 50% dextrose, gelatin sponge (gel foam), silicon spheres, polyvinyl alcohol (PVA particles), liquid thrombogenic agents and the application of covered stents. • Alcohol and cyanoacrylate glue are permanent embolic agents and both are commonly used to treat A–V lesions. • Currently, absolute alcohol (ethanol) is the most commonly used liquid agent; absolute alcohol has a direct toxic effect on the endothelium that activates the coagulation system and causes the microaggregation of red blood cells. • An experimental method used in aneurysms is embolization through a magnetically guided guidewire and catheter with a magnetic liquid embolic agent; the guidewire and catheter can be guided through the vascular system to the aneurysm. A magnetic field holds the liquid embolic agent in place while it solidifies.
iodesis) or when the lymphatic system is involved. Plastic reconstructive operations are included in this category as well as the obligatory amputations or organ resections.
12.1.8 Prognosis • The prognosis is poorer in A–V malformations when venous-arterial ulcers exist, in the case of arteriomegaly and aneurysm formation, in endocarditis-septicaemia and when congestive heart failure exists. • The prognosis in more complex multisystem syndromes is in general poor, depending on brain and CNS involvement. • Klippel–Trénaunay syndrome has the best prognosis of all syndromes with VMs, which also in objective terms is usually good. • Prompt diagnosis and early treatment by multidisciplinary specialists lead to the best feasible outcome for patients with VMs.
12.1.7.3 Surgery References Recommended European Standard Therapeutic Steps The surgical approach to VMs proposed by ISSVA takes four forms: • Reconstructive surgery (revascularization). These operations are undertaken when there is an absolute necessity to repair the vessels involved, such as in central or visceral malformations. Usual vascular techniques are performed, using autologous or synthetic patch or conduit grafts. • Surgery for improving the VM by removing the defect (devascularization). When this is feasible, it is usually performed for resection of peripheral venous defects or arteriovenous malformations, either truncular or extratruncular. • Interrupting or decreasing the haemodynamic activity of the vascular defect (non radical surgery). This is “damage control” surgery. In cases where reconstruction or removal of the defect is not feasible, minor operations are performed to reinforce the main stem by skeletizing the primary vessel, by removing the collateral web in venous defects or by reducing the shunt in arteriovenous malformations. • Other nonhaemodynamic operations may be required, such as those for vascular bone (e.g. epiphys-
1. Andre JM (1975) Les dysplasies vasculaires systématisées. Expansion Scientifique, Paris 2. Belov S, Loose DA, Weber J (1989) Vascular malformations. Periodica Angiologica Vol. 16. Einhorn Presse, Reinbeck 3. Belov ST (1990) Classification of congenital vascular defects. Int Angiol 9:141–146 4. Dimakakos PB, Arapoglou V, Katsenis K, Kotsis T, Mourikis D (2000) Therapeutic tactics and late results in predominant truncal congenital malformations. J Cardiovasc Surg 41:447–455 5. Lee BB, Kim DI, Huh S, Kim HH, Choo IW, Byun HS, Do YS (2001) New experiences with absolute ethanol sclerotherapy in the management of a complex form of congenital venous malformation. J Vasc Surg 33:764–772 6. Loose DA (2001) Die chirurgische Behandlung Angeborener Gefässfehler. Vasomed 13:96–105 7. Malan E (1974) Vascular malformations (angiodysplasias). Carlo Erba Foundation, Milan, pp 17 8. Mulliken JB (1993) Cutaneous vascular anomalies. Semin Vasc Surg 6:204–218 9. Szilagyi DE, Smith RF, Elliott JP, Hageman JH (1976) Congenital arteriovenous anomalies of the limbs. Arch Surg 111:423–429 10. Yakes WF, Parker SH (1992) Diagnosis and management of vascular anomalies. Intervent Radiol 1:152–189
583
Angioaccess Surgery
587
13.1 Vascular Access to Patients in Haemodialysis A. Kostakis, D. Mantas
13.1.1 Introduction • Patients who are in the final stage of chronic renal failure should, in order to remain alive, undergo dialysis – which may be either peritoneal dialysis or haemodialysis. • Haemodialysis may be urgent or chronic and requires venous access.
13.1.2 Urgent (Acute) Haemodialysis The application of urgent haemodialysis is indicated in cases of reversible acute renal failure, in patients with sudden decompensation of pre-existing chronic renal disease and in patients with chronic renal insufficiency who present with thrombosis of their arteriovenous shunt (A–V shunt). There are four approaches for applying urgent haemodialysis: 1. Creation of an external A–V shunt 2. Insertion of a subclavian catheter 3. Insertion of a jugular catheter 4. Insertion of a femoral catheter.
• In patients with a haemorrhagic disposition. In such conditions placing a subcutaneous catheter with a big lumen may cause a large uncontrollable haemorrhage. • In cases where it is impossible to place a catheter, such as in regions where there is inflammation. The external A–V shunt consists of two elastic tubes made of silicon which are placed in the artery and the vein. A small tube (TIP) made of Teflon is placed at the edge that enters the vessel. When the shunt is not in use for haemodialysis the outer edges are put together with a connector, which allows the circulation of blood from the artery into the vein. The usual site of placing the shunt is the radial artery and the cephalic vein, or between the posterior tibial artery or the dorsalis pedis and the saphenous vein.
Requirements for a Good Functioning Shunt The external A–V shunt needs special attention and care which includes: • careful every day cleaning of the parts of the shunt where they enter the skin • maintaining sufficient blood flow in order to avoid thrombosis • avoiding using the shunt as a pathway for medicine • avoiding measuring arterial blood pressure on the side of the shunt.
13.1.2.1 External A–V Shunt In many centres today the insertion of a shunt has decreased following the introduction of subcutaneous venous catheters of the big veins for haemodialysis. Nevertheless, an external A–V shunt is indicated in the following situations: • When there is a need for high-flow haemodialysis, such as in hypercatabolic patients.
Thrombosis of the shunt can be dealt with by: • using a no. 3 Fogarty catheter or • the administration of thrombolytic drugs.
Shunt Lifetime • The mean duration of a constantly functioning shunt is 2–15 months, although there have been cases where its function has lasted for several years.
588
13.1 Vascular Access to Patients in Haemodialysis
Disadvantages
Complications
The basic disadvantages of the shunt include: • a high rate of infection and thrombosis • danger of being extracted, especially in uncooperative patients or children.
The most common complications arising from the use of a subclavian catheter are shown in Table 13.1.1. Of these complications the most common is infection. The clinical diagnosis of an infection at the point of extraction is easy and is usually managed with the administration of antibiotics without needing to replace the catheter. Finding a positive blood culture, when there is no obvious evidence, is an indication to remove the catheter. The complications from trauma can be avoided when the catheter is placed by an experienced doctor. Haemothorax is a complication which puts the patient’s life in danger. It is necessary to take a simple chest radiograph after placing the subclavian catheter. Thrombosis of the subclavian vein is very rare and can be dealt with by removing the catheter and administering anticoagulant drugs when it is diagnosed early. It is widely believed that most of the clots which attach themselves to the catheter in the region of the superior vena cava result from damage of the intima caused by the vibration of the catheter from the machine. However, the frequency of pneumonic embolism is very low.
A nonfunctioning shunt is possible due to: • an infection or recurrence of thrombosis • a convolution of its parts or a stenosis around the lumen of the catheter due to an overgrowth of the intima. A rare complication is the creation of an aneurysm in the artery after removing the shunt.
13.1.2.2 Subclavian Catheters The manufacture of a special double-lumen catheter has enabled haemodialysis via the subclavian vein. Inserting the special catheter in the superior vena cava through the subclavian vein can be used for haemodialysis safely for many weeks. This vascular access is used when the patient is about to undergo urgent haemodialysis and there is either no A–V shunt or the existing one cannot be used. The patient can move about after the insertion, and to avoid thrombosis of the catheter between the sessions, heparin is infused through a special plastic outer edge. To remove the catheter, simply pull after removing the fixing suture and put light pressure at the point of extraction. By using this technique the vessel is not destroyed and it is thus possible to place another catheter again when needed.
13.1.2.3 Jugular Catheters During the last 5 years it has become obvious that the double-lumen catheters for haemodialysis which are inserted into the subclavian vein result in a time-dependent narrowing of its lumen. This complicates the venous Table 13.1.1 Complications of the subclavian catheter
Indications for a Subclavian Catheter • Patients in their final stage of previously undiagnosed chronic renal failure • Sudden thrombosis of the A–V shunt • Emergency transfer from peritoneal dialysis to haemodialysis • Acute irreversible renal failure • Cases where other ways of shunting prove impossible • For continuous infiltration with a double lumen • Plasmapheresis for numerous diseases.
1. Infection
Extraction point – septicaemia
2. Trauma
Pneumothorax Trauma of the subclavian artery-vein Trauma of the superior vena cava Haemothorax
3. Sudden removal
Air embolism Blood loss
4. Thrombosis
Subclavian vein Attachment of a blood clot to the catheter
13.1.3 Chronic Haemodialysis
drainage of the extremity and impaired venous blood flow is observed, which causes cyanosis and oedema. In order to avoid such complications a suggestion was made to place a catheter in the internal jugular vein. Catheters are placed in the internal jugular vein in the same way as in the subclavian, using the Seldinger technique with the ideal point of penetration being the apex of the triangle that is formed by the clavicle and sternal and clavicular heads of the sternocleidomastoid. The patient must be in the Trendelenburg position. The right internal jugular vein is preferred because it extrudes almost directly into the right innominate vein and the superior vena cava. Much care must be taken with elderly people in whom, because of their age, coiling of the carotid artery may have displaced the internal jugular vein. The jugular catheters usually have curved edges for a better and practical result.
Permanent Jugular Catheters Long-term stay in haemodialysis units, the lack of renal grafts, the stress caused to the elderly by haemodialysis as well as personal characteristics prompt us to use permanent silicon catheters with or without a cuff as a vascular access for haemodialysis. The jugular path is preferred. Permanent jugular catheters with a double lumen are most preferable.
13.1.2.4 Femoral Catheters When it is impossible to place a subclavian and jugular vein catheter and emergency haemodialysis is necessary, we use a femoral catheter with a double lumen, which is placed in the femoral and iliac vein.
13.1.3 Chronic Haemodialysis 13.1.3.1 Internal A–V Shunt (A–V Fistula) The internal A–V shunt is the access of choice in chronic haemodialysis because it entails: • easier preparation • a longer life span • a smaller percentage of infection.
This shunt is usually placed above the wrist between the radial artery and the cephalic vein and in cases where there is no proper vein it can be done at the elbow between the humeral artery and the mesobasilic vein.
Different Kinds of A–V Fistula This kind of shunt can be done by side-to-side or by endto-side anastomosis (Fig. 13.1.1a–e). The advantages of side-to-side anastomosis are that it allows better blood flow into the hand and more than one vein can be used for this access. In 5–10% of cases it causes phlebostasis in the fingers of the hand of the adjacent arm which may require ligation of the vein peripheral to the anastomosis. This complication is usually present when there is a problem with proximal flow and the drainage of blood becomes difficult. When the vessels are far apart and do not allow side-to-side anastomosis then an end-to-side anastomosis of the vein is attempted (Fig. 13.1.2).
Problems and Complications of Arteriovenous Fistula • Insufficiency of dilated veins. This complication is usually developed in a shunt which is produced in the wrist and its origin is unknown. • Haemorrhage. This may take place immediately after the creation of the shunt and, in this case, we have to open it and ligate the vessel that is responsible. Later if there is a haemorrhage it is usually due to infection. • Thrombosis. Thrombosis is divided into early and late. Thrombosis at the early stage of the procedure is unusual and takes place at a rate of 5%. In these cases the problem is due to coagulation or hypotension. Small veins are not a contraindication for a successive shunt when the procedure is performed by an experienced surgeon. If the thrombosis takes place during the first 24–48 h then the A–V shunt must be explored in order to remove the clot with a Fogarty catheter. Thrombosis of the A–V shunt after long-lasting function is unusual but, if this is the case, we have to open the shunt as soon as possible and remove the clot with a Fogarty catheter. Then the creation of a new shunt above the old one is preferable. • Aneurysm formation. It is possible that at the point of the shunt or at the points of puncture there may be formation of an aneurysmal dilatation of the arterialized vein and creation of a clot attached to the wall of
589
590
13.1 Vascular Access to Patients in Haemodialysis
Fig. 13.1.1a–e a The site of the A–V shunt. b–e Preparation of the radial artery and the cephalic vein. Creation of the A–V fistula
the vessel, which may become detached and constrict a proximal normal vein. It is possible that the puncture at the point of the aneurysm may create problems or difficulties in haemostasis. A pseudo-aneurysm could possibly develop through the creation of a haematoma at the place of puncture of the arterialized vein. • Infection. A primary infection at the A–V fistula is very rare (1%) in contrast to the external A–V shunt, which is usually where the infection takes place. The
administration of antibiotics and avoiding puncture at the point of the infection will lead to its improvement. • Ischaemia of the hand and steal syndrome. Mass diversion of arterial blood into the vein of the anastomosis may cause ischaemia of the arm when the collateral circulation is inadequate. Clinical manifestation of the syndrome is characterized by a painful and cold arm especially in the area which receives its blood supply from the radial artery (thumb, index and middle finger) and may lead to ischaemia, ulcer or gangrene if it is not dealt with quickly. Ischaemia is more common in A–V shunts of the elbow rather than the wrist. • Cardiac failure. An increase of cardiac preload up to 10% could possibly take place after the creation of an A–V shunt but rarely produces any problems. The flow between the shunt has been calculated to vary from 300 to 500 cm3/min, rarely up to 1000 cm3/min. In
13.1.3 Chronic Haemodialysis
13.1.3.2 Arteriovenous Grafts
Fig. 13.1.2 End-to-side arteriovenous shunt
these cases the increased cardiac preload will become a problem for patients with cardiac failure. • Venous hypertension. It is possible to note an increase of pressure in the peripheral veins when a large part of arterial flow reaches them and as a result we have oedema and cyanosis of the arm. When this disorder is observed in the shunt between the radial artery and the cephalic vein of the wrist, all of the symptoms concern the thumb; this becomes extremely painful, with vein dilatation, ulcers, eczema and serous fluid secretion from the arterial bed of the nails. These manifestations form the syndrome called painful thumb. Oedema of the tissues of the wrist may cause wrist tunnel syndrome. In order to diagnose painful thumb syndrome, it must be examined clinically and possibly by angiography of the shunt.
It has been accepted worldwide that the classic internal A–V shunt in the arm constitutes ideal vascular access for performing chronic haemodialysis. When the vessels have been worn out by previous efforts or the veins are not competent, then it is necessary to use special synthetic grafts to bridge the gap between the artery and the vein as they are too far apart. These grafts cannot be the first choice for a vascular procedure in a new patient but must be used in patients who have a certified vascular problem. The A–V grafts are usually placed in the arm between the humeral artery and the axillary vein, either straight or in loop formation in the forearm between the brachial artery and the mesobasilic vein (Figs. 13.1.3–13.1.5). In rare cases the A–V grafts may be placed in the leg in loop formation between the superficial femoral artery and the major saphenous vein of the same leg (Fig. 13.1.6). They can also be placed suprapubically between the superficial femoral artery of one leg and the major saphenous vein of the other (Fig. 13.1.7). In very rare cases,
Using the A–V Shunt For functional use of the shunt two needles are needed through which two lines are passed connecting them to the filter. One is characterized by an arterial line taking the blood from a dilated vein and leading it through the artificial kidney to the filter. The other, which is called venous, returns the blood from the filter to another dilated vein of the patient. The needle of the arterial line must always be placed under that of the venous line when the puncture is at a venous branch. Placing them parallel means that the vessels do not have any collateral circulation in order to avoid dialysis of the same amount of blood constantly.
Fig. 13.1.3 Brachial–axillary A–V graft
Fig. 13.1.4 Radial-mesobasilic A–V graft of the forearm
591
592
13.1 Vascular Access to Patients in Haemodialysis
Fig. 13.1.5 Brachial-mesobasilic “en loop” A–V graft of the forearm
Fig. 13.1.7 Transversal femoral A–V graft
Fig. 13.1.8 Subclavian A–V graft
where it is not possible to place an A–V graft in either the arm or leg, the graft may be placed like a necklace between the subclavian artery of one side and the subclavian vein of the other (Fig. 13.1.8). The rate of infection is high and the average time of its function is less than that of the internal A–V shunt. In the first year, their functional time ranges from 65% to 95%. The reasons for their insufficiency are: • A high percentage of infections • Stenosis of the venous edge of the anastomosis • Aneurysm formation.
Fig. 13.1.6 Femoral-saphenous “en loop” A–V graft
The most sufficient graft is an autograft from the actual patient (whether it is the saphenous above the knee or the cephalic above the elbow). If it is impossible to use them there are other grafts from modified umbilical veins or synthetic ones from PTFE.
13.1.3 Chronic Haemodialysis
Complications of the A–V Grafts The most common complication of grafts is infection. In order to reduce or avoid infections, while placing the graft strict antiseptic rules must be followed and antibiotics administered to the patient. This tactic has significantly reduced the rate of primary infection of the graft. The puncture of the graft must be done carefully and 2–3 weeks must have passed from the date of placement to avoid haematoma. The haematoma is nutritive for the growth of microbes and contributes to the appearance of infections. During puncture of the graft, the field must be sterile, avoiding trauma (Fig. 13.1.9). Primary infection of the graft is a very serious complication which very often leads to its total removal.
Aneurysms
Aneurysm formation at the A–V graft is a very serious complication and is usually caused after continuous punctures at the same spot. Their formation is also assisted by a possible coexisting infection. These aneurysms must be dealt with surgically because their existence may endanger the patient’s life (Fig. 13.1.10). If an infection does not coexist, then the section of the graft with the aneurysm may be removed or ligated and replaced by a section of a new graft (jump graft) (Fig. 13.1.11).
Thrombosis
Thrombosis in grafts is common and is a result of: • The development of fibrosis in the intima at the point of the anastomosis of the vein • Traumatism during many unsuccessful punctures • The decrease of arterial blood pressure while using them for haemodialysis • Low arterial flow due to hypovolaemia. In such cases surgical exploration should be performed with a Fogarty catheter. When stenosis has developed a new graft is placed. The diagnosis of an occlusion of the graft demands urgent management. The administration of the anti-platelet agents dipyridamole and aspirin often helps to extend graft survival. These agents seem to lower the myointimal layer and avoid the formation of clots at the points of puncture.
Fig. 13.1.10 Arteriovenous graft with aneurysms
Fig. 13.1.9 Arteriovenous graft with infection
Fig. 13.1.11 Brachial-axillary A–V jump graft
593
594
13.1 Vascular Access to Patients in Haemodialysis
In conclusion, the best and longest life span of vascular access is the internal A–V shunt and an A–V graft should only be placed if it is completely impossible to create the former. References 1. Bell PRF, Calman KG (1974) Surgical aspects of hemodialysis. Churchill Livingstone, Edinburgh 2. Bhat DJ, Tellis VA, Kohlberg WL et al (1990) Management of sepsis involving expanded PTFE grafts for hemodialysis access. Surgery 87:445–450 3. Brescia M, Cimino J, Appel K et al (1960) Chronic hemodialysis using venepuncture and surgically created arteriovenous fistula. N Engl J Med 6:104–107 4. Dardic H, Ibrahim M, Baier R (1976) Human umbilical cord, a new source for vascular prosthesis. J Am Med Assoc 236:2859 5. Etheredge EE, Haid SD, Maeser MN et al (1993) Salvage operations for malfunctioning polytetrafluoroethylene hemodialysis access grafts. Surgery 94:464–470 6. Gakis DM (1995) Vascular access for hemodialysis. Hell Nephrol 7:692–701 7. Humphries AL Jr, Nesbit RR, Caruna RJ et al (1991) Thirty six recommendations for vascular access orientations: lessons learned from our first thousand operations. Am Surg 47:145–151 8. Johnson J, Baker LD, Williams T (1976) Expanded PTFE, a subcutaneous vascular conduit for hemodialysis. Dial Transplant 5:52–53 9. Korzets A, Changnac A, Ori Y et al (1991) Subclavian vein stenosis, permanent cardiac pacemakers and the hemodialysed patient. Nephro 58:103–105 10. Kostakis A, Bokos J, Kyriakidis S et al (1999) The use of modified umbilical vein as vascular access in chronic hemodialysis. Vasc Surg 33(4):373–379
11. Kumpe D, Cihen M (1992) Angioplasty/thrombolytic treatment of failing and failed sites: comparison with surgical treatment. Prog Cardiovasc Dis 34:263–278 12. Lazarides MK, Vasdekis SN, Arvanitis D et al (1991) The use of vein valve cutter in reverse brachiocephalic arteriovenous fistula creation. J Vasc Surg 34:263–278 13. Marx AB, Landmann J, Harder FH (1990) Vascular access for haemodialysis. Curr Prob Surg 27:150–158 14. Mattson WJ (1976) Recognition and treatment of vascular steal secondary to haemodialysis prosthesis. J Am Med Assoc 236:2859 15. May J, Tiller D, Johnson J et al (1969) Saphenous vein arteriovenous fistula in regular dialysis treatment. N Engl J Med 280:770–771 16. Middleton WD, Picus DD, Marx MV et al (1989) Color Doppler sonography of hemodialysis vascular access: comparison with angiography. Am J Roentgenol 152:633–639 17. Munda R, First R, Alexander JW et al (1993) Polytetrafluoroethylene graft survival in hemodialysis. J Am Med Assoc 249:219–222 18. Quinton WE, Dillard DH, Scribner BH (1960) Cannulation of blood vessels for prolonged hemodialysis. Trans Am Soc Artif Intern Organs 6:104–107 19. Sands J, Youngg S, Miranda C (1992) The effect of Doppler flow screening studies and elective revision on dialysis access failure. ASAIO J 38:524–527 20. Schanzer H, Sclandany M, Haimov M (1992) Treatment of angioaccess-induced ischemia by revascularization. J Vasc Surg 16:861–866 21. Tserota SO (1994) Interventional radiology in central venous stenosis and occlusion. Semin Intervent Radiol 11:291–304 22. Vlassopoulos D, Dardioti V, Chrisos D et al (1996) Influence of arteriovenous anastomosis in the cardiac function of patients in hemodialysis. Hell Nephrol 8:736–740
Multidisciplinary Vascular Issues
597
14.1 Infections in Vascular Surgery Garyphallia Poulakou, Helen Giamarellou
14.1.1 Introduction Technical advances in vascular surgery in recent years have enhanced our ability to care for patients with cardiovascular diseases. The extensive use of medical devices and prosthetic materials has resulted in longer survival of such patients and has also improved their quality of life. However, infection remains the most serious complication of prosthetic grafts and devices, because it dramatically alters the patient’s outcome. Infections are often severe and in some cases life-threatening, while their cure may be problematic if removal of the infected material is not feasible. The incidence of infection varies with the indication of implantation and the site of the implant, being more common after emergency procedures, when the prosthesis is anastomosed with the femoral artery and when placed subcutaneously. The true incidence may be higher than that reported, because many graft infections are not apparent until several years after implantation. The mortality of infected prosthetic materials remains high, despite the use of antibiotics and surgical treatment, especially if the clinical presentation comprises sepsis syndrome or anastomotic bleeding. The successful treatment of vascular implant infections requires an understanding of the pathogenesis mechanisms, identification of the infecting pathogen and adherence to surgical principles in management [7, 10].
14.1.2 Pathogenesis of Infection Exposure of vascular implants to bacteria, irrespective of source, may result in colonization and subsequent progression to clinical infection. Most commonly, microorganisms contact the graft surface directly, during surgical implantation or through the surgical wound. The most common mechanisms of infection are: break of aseptic
techniques in the operating room and contact of the graft with patient’s endogenous flora harboured in lymphatics rupturing intraoperatively, sweat glands or mucosas. Additionally, pre-existing bacterial colonization within atherosclerotic plaques, aneurysms or thrombi may act as a source of pathogens. Bacteria find their way to the host, despite careful technique and attempted sterility, and recent studies have shown that a sterile wound is almost impossible to achieve, even under laminar air flow conditions [90]. Less frequently, the implant is inoculated by bacteria through the haematogenous or lymphatic route, during bacteraemia from a remote source of infection (pneumonia, urinary tract infection, infected central catheter, infective endocarditis). In late graft infections from virulent pathogens (e.g. Staphylococcus aureus), transient bacteraemia in combination with decreased immune response of the host may play a significant role [7, 10]. The pathogenesis of vascular implant infections consists of three components: pathogen virulence, host response to medical device and physicochemical characteristics of the implanted material [7, 28].
14.1.2.1 Pathogen Virulence Bacterial adhesion is the first and most important step towards implant infection. Several tissue and foreign body adherence molecules have been described as taking part in bacterial virulence. In S. aureus isolates, adhesins, known as extracellular matrix-binding proteins or microbial surface components recognizing adhesive matrix molecules (MSCRAMM), are responsible for the binding of microorganisms to extracellular and host plasma proteins, coating the surface of indwelling medical devices. These host proteins are exposed in areas where the endothelium is denuded, by contact with or attachment to indwelling devices. Fibronectin-binding protein A and B, clumping factor A and B and collagen-binding protein are S. aureus
598
14.1 Infections in Vascular Surgery
surface proteins with proven virulence properties in an animal endocarditis model of infection [28]. Another area of interest in the pathogenesis of cardiovascular medical device infections is biofilm formation. Staphylococcus epidermidis and other coagulase-negative staphylococci, as well as S. aureus are capable of biofilm production (“slime”), which consists of infecting microorganisms and extracellular matrix covering the surface of such devices and offering a protected environment for the growth of microorganisms. In the biofilm, saprophytic colonies of bacteria are transformed to virulent forms, through a procedure described as “phenotypic phase variation”. The term describes the ability of certain microorganisms, commonly staphylococci, to express a group of genes, in a rapid and reversible manner from generation to generation, transforming to sessile, biofilmproducing populations or free-floating colonies with infectious potential [90]. Antibiotics may suppress the free floating bacteria shed from the attached population, but fail to eradicate those bacterial cells still embedded in the biofilm. Biofilm formation is associated with the chronic nature of the subsequent infection and with its inherent resistance to antimicrobial treatment [92]. The polysaccharide intercellular adhesin, encoded by the ica gene cluster, is responsible for the cellular aggregation and biofilm formation in S. epidermidis isolates. Similar genes are found in other pathogens as well [7].
14.1.2.2 Host Response The endothelium, white blood cells, platelets and microorganisms react to the special features of blood flow to which they are exposed. Normal flow at physiological shear rates is not stimulatory to the endothelium and the production of apoptotic and inflammatory mediators is suppressed. Several cardiovascular devices, including stents and grafts, are responsible for/or reside within sites of abnormal blood flow. Abnormal blood flow may be expressed as high or low shear stress with increased gradient in shear, circumferential strain alterations, abnormal boundary surfaces and turbulence. These conditions promote local endothelial activation, increase platelet aggregation and enhance platelet and microbial adherence. Neutrophil and monocyte functions have been shown to be adversely affected by contact with prosthetic surfaces. There is also evidence of suppression of T-cell function by certain devices. In addition, poor tissue vascularization around prosthetic implants results in low penetration of
antibiotics [6, 7, 28, 90, 92]. Endothelialization of an implanted device is crucial for the prevention of subsequent infection. The development of nonthrombotic fibroelastic pseudointima is observed as early as 1 month after implant deployment in animal models. In humans, although less studied, endothelialization has been described to occur by 2.7 months after the procedure [52].
14.1.2.3 Device Factors Most implant surfaces are physicochemically active and promote cellular adhesion and integration, inflammatory and immune responses. Metallic materials have high surface free energies that are potentially catalytic for chemical reactions. Hydrophobic bacterial cell surfaces (complex surface glycoprotein structures) adhere better to hydrophobic biomaterial surfaces. Synthetic prostheses favour bacterial adherence more than biomaterial ones. This applies also to irregular, textured and polymeric tubing materials when compared to regular, smooth and wire mesh ones. Stainless steel is more prone to bacterial adherence than titanium. Fibrinogen is considered to be the principal factor of adherence to prosthetic material, preceding platelet aggregation. Biomaterials with lower critical surface tension, such as Teflon and other fluorocarbon polymers, do not attract platelets, while other biomaterials with higher critical surface tension, such as Dacron, attract platelets and fibrinogen. Clumps of platelets and fibrinogen attract white blood cells with subsequent development of a surface-bound mass around the biomaterial [7, 27, 28].
14.1.3 Microbiology and Diagnosis Staphylococci (Staphylococcus aureus and coagulasenegative staphylococci) account for more than 75% of vascular device-related infections. Less frequently, microorganisms of the skin flora, such as streptococci and Propionibacterium acnes, are isolated. Other Gram-positive cocci, Gram-negative bacilli and fungi cause a minority of device-related infections. Multidrug-resistant pathogens are frequently recovered and prove the nosocomial origin of the infection, rendering the therapeutic choice of empiric antibiotic treatment difficult. Identification of the infecting pathogen is essential. Cultures of multiple blood samples and aspirates of fluid collections
14.1.5 Antimicrobial Therapy
or abscesses, performed under CT guidance or during operation, may reveal the infecting pathogen and provide optimal guidance for the antibiotic treatment. This may be the rule if the infecting pathogen is virulent enough to cause local signs of infection or systemic signs of sepsis (e.g. S. aureus). When the causative pathogen is a slimeproducing microorganism, cultures are often negative, requiring special techniques for the release of bacteria trapped in the mucopolysaccharide matrix. Mechanical disruption or sonication of the removed graft material and subsequent culture in tryptic soya broth are methods that maximize bacterial recovery from cultures and enhance the sensitivity of the microbiological studies. It is difficult to prove causality by the isolation of skin flora microorganisms if cultures are drawn from open wounds or draining sinuses. Concomitant or recent antibiotic use may also be responsible for the failure of pathogen recovery in cultures [6, 7, 10, 96]. A new diagnostic microbiologic tool has been described recently. It is an enzyme-linked immunoabsorbent assay (ELISA) which detects antibodies against staphylococcal slime polysaccharide antigens. Antibody titres of 0.4 or more ELISA units are reported to have 97% sensitivity and 100% specificity in detecting prosthetic graft infections. The assay seems promising in the noninvasive detection of late prosthetic graft infections and merits further validation in studies [89].
14.1.4 Imaging Imaging modalities are adjunctive means in the diagnosis of infections in vascular prostheses. Plain radiographs are of limited value, providing information only in the case of prosthesis misplacement or dislocation. Ultrasound has the ability to identify pseudoaneurysms, abscesses or perigraft fluid collections, and provide evidence of infection if the latter are of nonhomogenous appearance. Guided aspiration is one of the advantages of the method, while dependence on the operator’s expertise is its major drawback. Additionally, Doppler ultrasound can give indirect evidence of infection, such as turbulent blood flow through a graft or a stent, indicating lumen thrombosis. Computerized tomographic (CT) scanning can accurately image large areas, such as vascular grafts, stent grafts and perivascular tissues. Image interpretation is minimally dependent on the operator’s expertise and
new rapid techniques require minor patient cooperation. Guided aspiration of fluid collections and abscesses is a major advantage of CT, while artefacts caused by metallic prostheses are the main drawback of this modality. Findings suggestive of infection include loss of normal tissue plane in the retroperitoneal space, perigraft fluid or gas collections, false aneurysm formation, hydronephrosis, adjacent vertebral osteomyelitis and presence of a retroperitoneal abscess. Perigraft fluid or gas collection is considered normal in the early postoperative period and is indicative of infection beyond 3 months postoperatively. Magnetic resonance imaging (MRI) is the first-choice technique in the detection of vascular prosthesis infections, providing the best discriminatory ability in the evaluation of perivascular inflammatory reactions. However, it is contraindicated in patients with electrophysiological devices. The presence of metallic materials, even if they are made of material permissive for MRI imaging, may cause artefacts that compromise the use of MRI in certain patients. Radionuclide studies can be useful in the diagnosis of insidious graft infections. 9 9 mTc-labelled white blood cells, 111In or gallium scintigrams are most commonly used. False-positive results are not uncommon during the early postoperative period and low sensitivity is described in late and mild infections. High negative predictive value is considered the major advantage of the modality. Angiography is of limited value in detecting infections in vascular grafting, but it is useful in the identification of aneurysms and the evaluation of the vascular tree before scheduling revascularization surgery. Magnetic resonance angiography (MRA) may provide useful information in some cases. Contrast sinography is no longer recommended in the era of CT and MRI imaging, because of its low sensitivity and the risk of secondary contamination of the vascular prosthesis. Endoscopy is very useful in patients with suspected secondary aortoenteric erosion or fistula and is an emergency procedure in patients with recent gastrointestinal bleeding. The third and fourth part of the duodenum are the most common sites of graft-enteric fistula [3, 7, 10, 71].
14.1.5 Antimicrobial Therapy The treatment of infections in vascular procedures is based on the following principles:
599
600
14.1 Infections in Vascular Surgery
• Removal of the infected implant along with meticulous debridement of all infected tissues, to support eradication of infection and avoid re-infection of a new implant. • Appropriate antibiotic administration for an adequate time after the identification of the infecting microorganism. • Revascularization of the affected area [6]. In unstable patients with suspected vascular implant infection, empiric antimicrobial therapy covering for all possible pathogens should be started promptly and reevaluated as soon as the responsible pathogen is identified. In stable patients, treatment can be withheld until samples for cultures are processed. When cultures reveal no pathogen or there are no available specimens for culture, empiric antimicrobial treatment should target nosocomial pathogens as well as skin-colonizing organisms. Bactericidal agents are preferred and therapy should be administered parenterally if the patient is bacteraemic. The duration of therapy is individualized. Most experts recommend 4–6 weeks of treatment after the removal of the infected material. If prompt removal is not feasible, the risk of morbidity and mortality increases significantly [3, 6, 7]. Long-term suppressive therapy is a treatment option in selected patients who are not candidates for removal of the infected material and/or revascularization, due to significant comorbidities, provided that they have initially responded to induction antimicrobial therapy. There are two recent published series reporting successful treatment of such patients with long term suppressive antibiotic administration without a surgical approach. In the first study, five patients with abdominal aortic aneurysm repair infected with Gram-positive cocci received short-term parenteral therapy followed by long-term (indefinite/lifelong) oral antibiotic therapy. Good tolerance and no clinical evidence of graft infection relapse were reported after a median follow-up of 32 months [83]. In the second study, 51 patients received chronic suppressive antimicrobial therapy for cardiovascular device-related infections, including 3 aortic graft infections and 1 infected venous filter. Duration of antimicrobial therapy ranged from 3 to 120 months, with 7.3% relapse rate and 6.5% drug adverse event rate. One relapse from a Pseudomonas aeruginosa strain, which developed resistance while the patient was on long-term oral administration of ciprofloxacin as monotherapy, was reported [5]. Vancomycin is an indispensable agent in the initial empiric antimicrobial regimen, because of its excellent
anti-Gram-positive spectrum, including most staphylococci and especially the methicillin-resistant strains. Teicoplanin, a glycopeptide with a similar antimicrobial spectrum to vancomycin and can be given intramuscularly, was proven inefficient in the initially recommended dose of 6 mg/kg per day, in the treatment of vascular infections. Although in higher doses (up to 12 mg/kg per day) it may be efficacious, teicoplanin has not been evaluated in large prospective series for the treatment of infected vascular grafts, and, according to the authors, cannot replace vancomycin in the treatment of such infections [4, 37, 38, 48]. Alternative antimicrobial agents are linezolid and quinupristin/dalfopristin, which provide coverage for methicillin-resistant staphylococci (MRSA and MRSE) and vancomycin-resistant enterococci (VRE), the latter not being active against Enterococcus faecalis strains. Their use should be reserved for infections due to pathogens resistant to vancomycin, or in patients with a confirmed history of allergy to vancomycin [3, 7].
14.1.6 Prevention Prevention of infections in vascular procedures is of outstanding importance, because treatment of established infection is a labour-intensive and costly procedure with significant morbidity and mortality. Prevention measures include aseptic surgical technique, adequate postoperative management and administration of primary and secondary antibiotic prophylaxis [8].
14.1.6.1 Primary Prophylaxis Primary antibiotic prophylaxis has proven to be beneficial in the reduction of surgical site infections (SSIs) after reconstruction of the aorta, procedures on the leg that involve groin incision, lower extremity amputations for ischaemia and procedures that include implantation of a vascular prosthesis or an endoluminal stent. Single agent prophylaxis is the most commonly used regimen.
Timing of the First Dose of Antimicrobial Therapy The goal of antimicrobial prophylaxis is to provide serum and tissue antibiotic concentrations that exceed, for the duration of the operation, the minimum inhibitory concentrations (MICs) of the microorganisms likely to be en-
14.1.6 Prevention
countered during the operation. There is strong evidence that antimicrobial prophylaxis provides maximal prevention against SSIs, if administered within 60 min before incision. However, if vancomycin is indicated, the infusion should begin within 120 min before incision, to prevent drug-related reactions. When a proximal tourniquet is required, antibiotic administration should be terminated before the tourniquet is inflated [9, 16].
Duration of Antimicrobial Prophylaxis The majority of published data demonstrate no benefit from prolonged administration of antibiotics beyond wound closure, quite apart from the fact that prolonged use is associated with the emergence of resistant bacterial strains [42]. Recently published guidelines have endorsed the recommendation that prophylaxis with antimicrobials should be discontinued within 24 h after the end of surgery [16].
Antibiotic Selection Peri-operative prophylaxis should target all pathogens that could be encountered in a possible infection of the surgical site and implant, including Staphylococcus aureus and various skin colonizers. For vascular surgery of the lower extremities and in the case of groin incision, addition of an agent with coverage for Gram-negative pathogens is advisable (usually an aminoglycoside). For intra-abdominal surgery coverage for anaerobes may also be added (usually metronidazole) [54, 94]. According to the recently published consensus positions of the Surgical Infection Prevention Guideline Writers Workgroup (SIPGWW), taking part in the US Medicare National Surgical Infection Prevention Project, the recommended antimicrobials for cardiothoracic and vascular surgery include cefazolin and cefuroxime [2]. In patients with a history of serious β-lactam allergy, vancomycin is recommended as the first alternative agent. Clindamycin may serve as a second alternative, if local antimicrobial resistance patterns and institutional incidence of infections due to organisms such as Clostridium difficile are supportive of its use. For patients with known MRSA colonization, vancomycin should be preferred for prophylaxis [2, 16]. The Society for Healthcare Epidemiology of America recently recommended routine surveillance cultures on admission to hospital for patients at high risk for MRSA carriage (i.e. patients who have spent >5 days in institu-
tional settings such as long-term care facilities or acute care centres) [64]. In hospitals with high rates of MRSA or methicillin-resistant coagulase-negative staphylococci infections, vancomycin should be used as standard prophylaxis in vascular procedures. Nevertheless, there is no “consensus” about what constitutes a high prevalence of methicillin resistance [16]. In view of the rising incidence of MRSA infections in several institutions, the increased frequency of community-acquired MRSA colonization and the devastating consequences of an infected implant by a drug-resistant pathogen, the routine use of vancomycin is considered as a most advisable option in the prophylaxis of vascular surgery [42, 67, 94]. For teicoplanin, despite its advantageous pharmacokinetic properties for use as a prophylactic, there are not enough data based on randomized controlled trials. Therefore teicoplanin is not included in any published recommendation or guidelines as an alternative to vancomycin in prophylaxis regimens [37, 48, 59, 62]. For clean procedures, it is strongly recommended to treat or remove other possible sources of infection before elective surgery (e.g. control of an infected leg ulcer, or skin and soft tissue infections). If this is not possible, or if the vascular procedure is urgent, the patient should go to surgery with an antibiotic regimen appropriate both for prophylaxis and for the concurrent treatment of the infectious source [16]. Immunocompromised patients are not proven to be at higher risk of infection after vascular device implantation, therefore application of the aforementioned recommendations for prophylaxis of immunocompetent hosts is advised [6].
Antimicrobial Dosing The initial dose of the antimicrobial agent should be adequate, based on the patient’s body weight and renal function. An additional dose should be administered intraoperatively, if the operation is scheduled to last more than two serum half-life time periods of the antibiotic after the initial dose, if excessive bleeding has occurred, or if extracorporeal elimination of the antibiotic is anticipated. For patients with normal renal function, the recommended dosing intervals for cefazolin, cefuroxime, vancomycin and clindamycin are 2–5, 3–4, 3–6 and 6–12 h respectively [16, 94].
601
602
14.1 Infections in Vascular Surgery
14.1.6.2 Local Antibiotic Prophylaxis Locally administered prophylaxis targets the prevention of superficial wound infections and early bacterial colonization of the implant, which is the prelude of clinical infection. It is used as an adjuvant to systemic antibiotic prophylaxis [28]. Antimicrobial irrigation of the surgical field is hampered by variables such as volume, pressure and rhythm of irrigation, concentration of antibiotic in the solution, amount and duration of locally available antibiotic. Although vancomycin and aminoglycosides have been used among surgeons for years, the method has not been validated through prospective randomized trials. A recent randomized trial indicated that preoperatively prepared antimicrobial carriers seem to provide protection against infection. Insertion of a gentamicin-treated collagen sponge adjacent to a propylene mesh, used for repair of groin hernias, has shown a more than sixfold reduction of wound infection rate, compared to no local use of antibiotic [63]. The duration of local antimicrobial activity is reported from weeks to months but the serum and local concentration of antibiotic is highly variable and the overall efficacy depends on the local antimicrobial resistance pattern of the pathogens. Dipping of vascular grafts in antimicrobial solutions has not shown significant advantages in a prospective randomized trial with the use of rifampicin. Antimicrobial coating of implants seems to be the most promising approach for local antibiotic prophylaxis. Polytetrafluoroethylene vascular grafts coated with rifampin and minocycline showed reduced rates of staphylococcal colonization and infection when compared to uncoated grafts in an animal model [8, 29]. Silver-coated grafts seem to be effective in the prevention of graft infection in a recent experimental study, while in another recent one they do not seem to afford protection from infection. Triclosancoated grafts have a lower antimicrobial property when compared to rifampin-bonded ones, which offer maximal antimicrobial protection [13, 44]. Mupirocin intranasally was tested in heart surgery in combination with standard prophylaxis, but did not reduce the overall rate of SSIs. However, if mupirocin is selectively administered in S. aureus carriers, a benefit in infection rate may be seen [74].
14.1.6.3 Secondary Prophylaxis Secondary antibiotic prophylaxis is not recommended beyond three months after device placement for patients
who undergo dental, genitourinary, gastrointestinal and respiratory tract procedures, because there is no evidence that these procedures pose a significant risk of infection in vascular implants. However, secondary antibiotic prophylaxis is indicated in patients with vascular implants when they undergo drainage or incision of infection at another site and when they undergo replacement surgery for an infected device [8, 94].
14.1.6.4 Other Measures of Prevention Intraoperative patient temperature control within the normal range, supplemental oxygen administration and aggressive fluid resuscitation may reduce infection rates. Preoperative blood glucose control has a proven benefit in cardiac operations. The risk of SSIs was found to be related to the presence of hyperglycaemia more than the diagnosis of diabetes mellitus itself [16, 45].
14.1.7 Infections in Specific Vascular Implants 14.1.7.1 Prosthetic Graft Infections (PGI) Aortic and lower extremity prosthetic grafts are widely used in vascular surgery. PGI is an uncommon complication, ranging from 1% for aortic, to 1.5–2% for aortofemoral and 6% for infra-inguinal prosthetic grafts. It is accompanied by increased mortality (up to 75% in infections of aortic grafts) and significant morbidity (up to 70% amputation rate reported in infections of lower extremity grafts) [18, 70, 87]. Identified risk factors are groin incision, wound complications (especially incisional haematoma), diabetes mellitus, urgent procedure, prolonged operative time, multiple interventions at the same site and obesity [18, 55, 70]. The clinical symptoms and signs and the microbiology of the PGIs are related to the time of presentation after surgical implantation. Early PGI develops within 6 months (according to some surgeons within 3 or 4 months) postoperatively, more usually affecting lower extremity grafts, presents with fever, leukocytosis and is often accompanied by surgical wound infection. The clinical presentation may also include abscess or pseudoaneurysm formation, graft exposure, sepsis syndrome with bacteraemia or fungaemia, distal septic embolization and peripheral ischaemia. The most commonly encountered pathogen is S. aureus, followed by Gram-negative bacilli,
14.1.7 Infections in Specific Vascular Implants
such as Escherichia coli, Proteus spp., Pseudomonas aeruginosa, Klebsiella spp. and Enterobacter spp. [3, 6, 7]. Late PGI presents more insidiously, due to the lower virulence of the implicated microorganisms and the biofilm-based pathogenesis of the infection. Clinical presentation may include pseudoaneurysm formation, lack of graft incorporation, groin draining sinuses, abdominal pain, distal ischaemia and septic emboli, gastrointestinal haemorrhage due to graft-enteric fistula or erosion of the duodenal mucosa. In several cases of late PGI, the clinical presentation is subtle and nonspecific, leaving the diagnosis in doubt, until surgical exploration. Coagulasenegative staphylococci predominate, with S. epidermidis being the most commonly recovered pathogen. Skin flora inhabitants, such as Propionibacterium acnes and Corynebacterium spp., are less frequently recovered. Late abdominal aortic graft infections are very often polymicrobial, comprising Gram-negative bacilli of the colon flora, enterocci and anaerobes such as Bacteroides fragilis strains. Fungi are rarely encountered, but Candida spp. is an increasingly implicated pathogen in infected devices, with mechanism of virulence expressed as biofilm production [46, 51]. Mycobacteria can be the cause in a minority of infections, in selected immunocompromised hosts. Biofilm formation in late PGIs often compromises the isolation of the responsible microorganism [3, 6, 7]. The diagnosis is established with clinical criteria in the case of graft exposure, or intraoperatively by the presence of pus collection or lack of graft incorporation. Imaging modalities CT and MRI are supportive of the diagnosis of infection. CT offers the advantage of guided aspiration of fluid collections, which aids microbiological diagnosis and has a reported sensitivity of 94% and specificity of 85%, while, for MRI, sensitivity and specificity are reported to be 85% and 100% respectively. Indium-labelled white blood cells and gallium scintigraphy are a secondline imaging technique. Endoscopy is an emergency diagnostic procedure in the case of gastrointestinal bleeding, which is a life-threatening complication of PGI. The third and fourth part of the duodenum are most usually affected [3, 6, 7]. The most effective way to manage PGI is eradication of infection through total graft excision with meticulous local debridement, followed by extra-anatomical revascularization and appropriate antibiotic treatment. Graft excision is urgent when the clinical presentation includes systemic sepsis or anastomotic bleeding. Graft excision without revascularization can be attempted in the rare case of a totally thrombosed vessel with a viable limb. Early PGIs have a better outcome, but infections due to Pseudomonas
spp. carry worse prognosis. Amputation rates range from 4% to 9%. Duration of antimicrobial treatment is not well defined in controlled trials. A minimum of 6 weeks of intravenous antibiotics is recommended by some, with or without 6 weeks of additional oral treatment. Other authors recommend 3 months of therapy as minimum duration. According to each vascular centre’s expertise, a staged or sequenced procedure may be chosen. The staged approach, in which revascularization precedes and excision of the infected device follows after 2–3 days, avoids extended operative times and lowers the patient’s physiological stress. In the sequenced approach, where the two operations are performed consecutively, prompt debridement of the infectious focus provides a minimal risk of re-infection of the new implant [3, 6, 10]. Revascularization can be achieved via extra-anatomic by-pass or in situ replacement. Staged graft excision with extra-anatomic revascularization is considered the standard of care and is reported to have a 2–4.5% re-infection rate, 12–25% mortality, 0–1.4% amputation and 1.5–3% aortic stump rupture rates. These rates are significantly ameliorated when compared to the reported rates of older studies. Autologous vein grafts, with low proclivity to reinfection, are the preferred type of grafting and omental positioning should be achieved if possible [70, 87, 88]. In situ revascularization has the advantage of being a single-step procedure; in addition, it avoids local complications after saphenous vein harvesting, permits a shorter hospital stay and preserves aortic vascularization of the pelvis and limbs. It is recommended in infected grafts of the abdominal aorta that comprise the mesenteric, coeliac and renal arteries, and in local, mild infections, due to less virulent pathogens. Autogenous vein grafts are reported to have low mortality and amputation rates (8–10% and 2–3% respectively) and are probably the most indicated choice for in situ procedures [25, 97]. Good results have been recently reported with the use of prosthetic grafts for in situ replacement of 25 infected aortic grafts, followed by chronic suppressive antibiotic treatment. An 8% reduction of mortality rate and 100% improved limb salvage as compared to the extra-anatomic by-pass procedure are reported [100]. Rifampin-soaked grafts have not proven to offer protection against re-infection, whereas envelopment of the graft by autogenous tissue coverage such as omentum or muscular flaps provides significant protection [86, 97]. Rifampin-bonded grafts seem to be a safe and durable option for in situ replacement of grafts infected with S. epidermidis, but are less effective for more virulent pathogens [11, 12, 29]. Silver-coated grafts do no seem to afford protection, while triclosan-coated grafts
603
604
14.1 Infections in Vascular Surgery
Fig. 14.1.1 Axial spiral CT slice in a patient with infected bifurcated aortofemoral graft during the arterial phase post iv contrast administration. There is gas adjacent to the graft at the bifurcation (black arrow), haziness of the surrounding fat with indistinct borders and there is partial thrombosis of the left graft leg (white arrow). Calcifications of the occluded native arteries (black arrowhead) are also shown and a surgical drainage at the inflamed area (white stroked arrowhead)
display a lower prophylactic efficacy when compared to rifampin-bonded ones [44]. In situ replacement with cryopreserved or fresh allografts, although encouraging in some studies, has provided disappointing results in others and merits further evaluation [23, 36, 49, 69]. Graft preservation is advocated only in cases of aortic graft infections in patients who are not candidates for surgery, due to serious comorbidities. In these patients, long-term (sometimes lifelong) oral antimicrobial suppressive therapy is administered [19, 91]. In recent literature, a 70% rate of limb preservation is reported in PGI of the lower extremities, in the absence of haemorrhage, systemic sepsis or Pseudomonas infection, with antimicrobial regimens of 12 weeks to lifelong duration. In another study, a 7% relapse rate was reported. Partial excision is reported in recent series, with long-term antibiotic
suppression [20, 21]. Topical negative pressure therapy by use of a vacuum sponge system or vacuum assisted closure (VAC) seems to promote healing and granulation tissue formation in groin infections adjacent to prosthetic material. Its utility as an adjunct to graft preservation measures remains to be further evaluated [30, 75].
14.1.7.2 Peripheral Vascular Stent Infections (PVSIs) Peripheral vascular stenting in combination with percutaneous angioplasty procedures has been the most common nonsurgical treatment of atherosclerosis in recent years, accounting for more than 400,000 implantations per year in the USA. The risk of infection is reported as being lower than 1 case per 10,000 procedures [65].
14.1.7 Infections in Specific Vascular Implants
Fig. 14.1.2 Axial spiral CT slice in a patient with infected bifurcated aortofemoral graft during the arterial phase post iv contrast administration. A fluid collection with enhancing wall (black arrows) is shown medially to the left iliopsoas muscle. Inside this fluid collection a part of the occluded infected graft (black arrowhead) is demonstrated. The occluded, calcified, native external iliac artery is recognized medially to the fluid collection. The right leg of the graft is patent (white stroke arrowhead)
The purported risk factors are: • Prolonged use of an indwelling catheter or sheath and reuse beyond 24 h postoperatively, especially in patients receiving thrombolytic therapy. • Repetitive use of the same femoral artery as vascular access within the first week of the stenting procedure. • Haematoma formation. • Increased procedural time. • Multiple surgical interventions on the same vessel or adjacent sites. The iliac artery is the most commonly affected vessel, accounting for 50% of the total cases of infections reported after peripheral vascular stenting. Clinical signs usually develop within 1 month of stent deployment, a fact that underscores the peri-operative or directly postoperative
mechanism of bacterial inoculation of the implant. Clinical picture includes fever and sepsis in the majority of cases, whereas local signs such as pain and oedema are also common [53]. In PVSIs, S. aureus typically predominates in early as well as in late infections, accounting for 83% of total reported infections being recovered from blood cultures and operative fluid specimens [3, 31]. In late PVSIs caused by S. aureus, haematogenous seeding of the stent is more probable. Groin incision, which is the commonest vascular access for stenting, and lack of chemoprophylaxis in the early years of stenting procedures are probably the cause of the overrepresentation of this pathogen in PVSIs [1]. CT scanning has a sensitivity that exceeds 90% in detecting PVSIs, especially by use of serial imaging. Primary prophylaxis for stent placement was not initially advocat-
605
606
14.1 Infections in Vascular Surgery
Fig. 14.1.3 Axial arterial phase spiral CT slice in a patient with bifurcated aortofemoral graft, thrombosis of the right graft leg and an occluded femoro-femoral graft. On the left at the site of the femoro-femoral anastomosis there is a fluid collection with enhancing wall (black arrow). Inside the collection the lumen of the graft is patent (black stroked arrowhead). The occluded femoro-femoral graft (black arrowheads) is demonstrated coursing transversely in the subcutaneous tissues
ed due to the extremely low risk of infection. Nevertheless, after identification of risk factors, there is an increasing belief that administration of primary prophylaxis, as recommended for graft implantation, is reasonable [31]. After the adoption of primary antimicrobial prophylaxis in vascular stenting, the prevalence of S. aureus in PVSIs has diminished, compared to older studies [39, 41]. Studies in animal models have proven the formation of pseudointima during stent incorporation to the vessel wall, which may be protective against bacterial invasion, thus rendering the need for secondary prophylaxis unjustified beyond the early postoperative period. In addition, dental, genitourinary, respiratory and gastrointestinal procedures have not been implicated in the mechanism of
PVSIs. Secondary prophylaxis is indicated when drainage of a remote purulent collection is performed, or before subsequent surgical manipulations in a stented vessel or surrounding tissues [16, 31, 50, 72]. Despite their rarity, PVSIs are associated with significant mortality and morbidity. The most common complications are: multiple organ dysfunction syndrome, adult respiratory distress syndrome, disseminated intravascular coagulation, osteomyelitis and amputation of the distal extremity due to embolization, vessel rupture or prolonged hypotension in the context of systemic sepsis [3, 6, 7, 17, 73, 76]. The diagnosis requires a high grade of clinical suspicion in patients with prior endovascular stent placement presenting with local and systemic signs of in-
14.1.7 Infections in Specific Vascular Implants
fection. Blood and tissue/pus cultures should be obtained and empiric antibiotic treatment against S. aureus should be initiated. Management of PVSIs includes total excision of the stent and the vessel, along with extensive perivascular debridement of the infected tissues, extra-anatomic revascularization of the affected site and appropriate antimicrobial treatment. The duration of treatment depends upon the surgeon’s expertise. Emphasis should be given to the identification of the infecting pathogen, before antibiotic treatment onset, in order to optimize antimicrobial treatment. Most experts recommend a treatment duration no shorter than 6 weeks, as described in the general part of this chapter. In patients with comorbidities who cannot tolerate surgical treatment, long-term suppressive antimicrobial treatment is a reasonable approach with acceptable results [31].
14.1.7.3 Prosthetic Carotid Patches Infections (PCPIs) The benefits of patch closure over primary arteriotomy closure in the reduction of the risk of peri-operative stroke, internal carotid artery thrombosis and recurrent stenosis have widely established the use of patches in carotid surgery. Today, available patching options include autologous (usually saphenous vein), polytetrafluoroethylene (PTFE), polyester (Dacron, DuPont, Wilmington) and bovine pericardium patches. Vein patches offer the benefit of lower risk of infection, which is outweighed by a higher risk of rupture, poor predictability of diameter size, longer operative time, groin complications and depletion of sources for future vascular reconstruction. The simplicity of a readily available prosthetic patch graft, which prevents narrowing of a small-diameter internal carotid artery and offers a shorter operative time, has led to the widespread acceptance of prosthetic patch angioplasty in carotid surgery [32]. Infection is an extremely rare complication of carotid surgery, ranging between 0.33% and 1.8% in the largest series published after the year 2000. The majority of reported cases of infections concern Dacron patches, perhaps reflecting their more frequent use compared to PTFE patches. Series in which vein patches were used report extremely low rates of infections, although few case reports concern autologous material infectious complications such as pseudoaneurysm formation. In all the aforementioned studies, antibiotic prophylaxis was administered prior to the procedure [15]. Five episodes of
infected false aneurysm formation have been reported in a series when primary closure of arteriotomy without patching was performed without primary antibiotic prophylaxis [78]. The time of presentation of the infection varies from 10 days to 41 months, but 62% of the reported infections were apparent within 3 months from surgery (early infection). Signs of early infections may be local, such as tenderness and swelling, cellulitis, abscess, pseudoaneurysm, massive haemorrhage from the vessel and patch rupture, or systemic, such as sepsis syndrome. Early carotid patch infections are often heralded by surgical wound infection [68]. S. aureus and viridans group streptococci predominate (37.5% and 31.3% of infections respectively), while Gram-negative bacilli, Propionibacterium acnes and Bacteroides fragilis are encountered less frequently. Streptococci, which are respiratory colonizers, invade the surgical site due to its proximity to the respiratory mucosa. In late patch infections, draining sinus and pseudoaneurysm formation predominate the clinical presentation. Coagulase-negative staphylococci are isolated in more than 80% of cases [31]. Diagnosis of CPI is established peri-operatively, with sampling of purulent material or fluid collection or patch material for cultures revealing the infecting pathogen in 87% of cases. Doppler ultrasound, CT, MRI, MRA and angiography are helpful in the diagnosis of CPIs [68, 82]. Treatment of PCPI requires total patch removal, extensive local debridement and, according to some specialists, use of antibiotic-impregnated sponges. Antimicrobial treatment varies in different series, from 2 to 6 weeks after prosthesis removal, but 4–6 weeks of treatment as described in the general part of this chapter is generally recommended. Replacement with autologous tissue is preferred in the majority (92%) of revascularization procedures, either as vein in situ replacement or as vein extra-anatomic by-pass. A small minority of patients cannot escape carotid artery ligation, a technique with a 50% rate of postoperative death or serious stroke [68]. The use of rifampin-bonded synthetic carotid patches has been very promising in recent studies, provided that the patient has no systemic sepsis and the affected vessel is patent. In redo carotid surgery after infection, low death or relapsing graft infection rates have been reported, but complications such as stroke, cranial nerve injury, myocardial infarct and epidural abscess may sometimes be encountered [3, 7, 15, 80].
607
608
14.1 Infections in Vascular Surgery
14.1.7.4 Arterial Closure Devices Infections Percutaneous vascular access is commonly used in the nonsurgical treatment of atherosclerosis and can be complicated by bleeding from the puncture site. Manual compression has been used, but has certain limitations: it is not always feasible in high femoral arterial punctures, it is sometimes painful for the patient and time consuming for the attending personnel and in cases where the patient receives anticoagulation it may prove inefficient. Arterial closure devices have been available since the 1990s and five types of such devices have been approved in the USA. They are classified as collagen seal devices and suture clo-
sure devices. The former type can be applied either intravascularly or extravascularly. The incidence of infection is reported as extremely low, estimated between 0.2% and 0.7% of the total number of procedures [3]. It presents most often within 1 month after the procedure (median time 10 days) and the most commonly affected site is the groin, reflecting the preference of the femoral artery as the puncture site. Clinical presentation includes local tenderness and swelling. S. aureus predominates (77% of the cases) and is recovered from blood and perioperative cultures. Gram-negative bacilli and coagulase-negative staphylococci are less often encountered (10% and 8% respectively). Purported risk factors regarding percuta-
14.1.7 Infections in Specific Vascular Implants
against skin flora may be advisable in ipsilateral repuncture [22, 24, 47, 85, 99].
14.1.7.5 Venal Caval Filter Infections Venal caval filters have been approved since the 1970s; they have been used for protection against massive pulmonary embolism in thousands of patients with thromboembolic disease in whom the use of anticoagulation is contraindicated or not tolerated. Despite their worldwide use, infectious complications are extremely rare and only five cases were described in the literature up to the end of 2004 [5, 43, 57, 61, 79]. In all five reported cases staphylococcus was the infecting pathogen, and in four cases the microorganism was recovered from blood cultures. Infection developed in four patients within 10 days after device deployment. Two patients were complicated with adjacent spondylodiskitis. One patient died due to device-related sepsis, while the three other patients survived after the removal of the device along with appropriate antibiotic administration. Finally in one patient the filter was retained with lifelong antibiotic suppression therapy [5]. Fig. 14.1.4a–c Transverse arterial phase spiral CT slices (a, b) and multiplanar reconstruction in the coronal plane (c) in a patient with infected iliofemoral graft. A fluid collection with enhancing wall (black arrows a, b and white arrowheads c) is shown surrounding the patent graft. The coronal reconstruction (c) shows to a better advance the craniocaudal extent of the fluid collection and the site of the distal anastomosis (white arrow, c). All figures are courtesy of Dr. NL Kelekis, 2nd Department of Radiology, Athens University Medical School, “ATTIKON” University Hospital
neous procedures include congestive heart failure, recannulation of the same site, difficulty in obtaining vascular access, duration of sheath retention of more than 24 h, extended procedural time (>2 h) and bleeding from the puncture site [22, 24, 47, 85, 99]. It is interesting that in the majority of the reported infections no antibiotic prophylaxis had been administered, due to the theoretically extremely low risk of infection. Treatment almost always requires total removal of the device and the pre-implanted material, extensive surgical debridement and prolonged antibiotic treatment, as in the case of graft and stent infections. Primary antibiotic prophylaxis is not routinely advocated, due to the lack of supportive evidence from prospective studies. However, in the presence of risk factors, prophylaxis directed
14.1.7.6 Infections of Haemodialysis Prosthetic Grafts and Autologous Arteriovenous Fistulas (HPGFIs) Patients that undergo chronic dialysis are at increased risk of infection, due to the immunosuppression caused by chronic renal insufficiency (CRI), the repetitive puncture of the dialysis access site and the increased rate of S. aureus nasal and skin carriage. According to the data of the national surveillance system for the infections in haemodialysis outpatients of the USA, infections and especially bacteraemia are the second cause of death in these patients. The incidence of vascular access infection, at least in the USA, was reported as 3.2 episodes per 100 patient-months, whereas for synthetic grafts the incidence was higher than that observed in autologous arteriovenous fistulas (3.6 against 0.56 episodes per 100 patientsmonths). In the case of central catheter dialysis access, the incidence of infections is even higher (8.42–11.98 episodes per patients-months, according to different types of dialysis catheters) [95]. The most frequently encountered pathogen is S. aureus, accounting for 53% of bacteraemias related to autologous or synthetic dialysis access sites, followed by
609
610
14.1 Infections in Vascular Surgery
coagulase-negative staphylococci isolated in 20% of such cases. Gram-negative bacilli are less commonly encountered and a minority of infections is polymicrobial, including Enterococcus spp. [56]. Infections caused by S. aureus are accompanied by high mortality rates (8–25%) and frequent complications, such as osteomyelitis, septic pulmonary emboli, epidural abscess, septic arthritis and endocarditis (4–44% of chronic hemodialysis patients with S. aureus infection) [26]. The skin and nasal colonization of chronic haemodialysis patients by S. aureus increases the risk of infection. Intranasal administration of mupirocin ointment was found to significantly reduce colonization and infection rates due to S. aureus [6]. However, repetitive cycles of mupirocin treatment due to relapse of colonization was described to be associated with resistance to mupirocin. Diabetes mellitus, femoral catheterization, prolonged catheterization, poor individual hygiene, immunosuppression, uncontrolled HIV infection, hypoalbuminaemia and low serum ferritin are considered as risk factors for the development of vascular dialysis access site infection accompanied by bacteraemia [6, 66]. Recently, patients undergoing chronic dialysis are the source of identification of multiresistant Gram-positive pathogens, such as MRSA, vancomycin-resistant Enterococcus (VRE), linezolid-resistant S. aureus and vancomycin-intermediate susceptibility S. aureus isolates (VISA). Interestingly, the first isolation of those strains was reported in chronic dialysis patients. The main predisposing factors for the recovery of those multiresistant cocci is the extensive antibiotic exposure of the patients and especially the overwhelming use of vancomycin, as well as the hospital stay in settings with increased antimicrobial resistance rates under circumstances that favour microbial transmission. The special requirements of dialysis render frequent contacts with the patients unavoidable and facilitate pathogen horizontal transmission through the hands of healthcare personnel. Today, the most dreadful scenario is deemed to be the isolation of a VISA strain, as has recently been described in patients under dialysis [6, 7, 14, 26, 60]. The clinical presentation commonly includes local signs of infection, but can be also expressed subclinically as bacteraemia/fungaemia or as vascular access thrombosis and dysfunction. In the case of subtle infection, the use of 111In scintigraphy can reveal the source of infection, with a reported 100% sensitivity and 75% specificity [6, 84]. Empirical initial treatment should be initiated upon suspicion of infection of dialysis vascular access,
after sampling for blood and pus cultures. Therapeutic regimens should include vancomycin plus an anti-Gramnegative active agent (aminoglycoside or third-generation cephalosporin, depending on the local surveillance antimicrobial data). It is crucial to re-evaluate the treatment as soon as the antibiogram of the infecting pathogen is available. Vancomycin is considered as the standard treatment option for MRSA infections. Linezolid and the quinupristine/dalfopristine combination are potent against VRE, VISA and MRSA, but the latter is not active against Enterococcus faecalis strains [14]. Treatment duration is not well defined through controlled trials, but in general, most specialists recommend a treatment duration no shorter than 4 weeks if S. aureus is the infecting pathogen and 3 weeks for the remaining pathogens. In cases of remote or metastatic infection, treatment is continued until the eradication of the distal focus is achieved. Eradication of the infection of the vascular dialysis access warrants removal of the synthetic graft even if it is not in use, because it may harbour bacteria and become a source of relapsing and life-threatening infections [66, 84]. Autologous arteriovenous fistulas can be treated conservatively. Not uncommonly, the depletion of alternative access sites justifies the use of parenteral antimicrobial treatment, with a view to vascular graft rescue, especially in early infections. The presence of systemic signs of sepsis, purulent exudates, abscesses or pseudoaneurysms prompts graft removal. In limited graft infection, subtotal excision has shown encouraging results according to some specialists [84]. Vacuum-assisted treatment has shown to be adjunctive to the systemic administration of antimicrobials in selected patients, in which haemodialysis access salvage through conservative treatment is the only option and merits further evaluation [98]. Efforts proposed for the prevention of dialysis access infections include: • Periodical surveillance of S. aureus colonization and intranasal administration of mupirocin [93]. • Avoidance of haemodialysis catheters and discouragement of prosthetic graft placement; dialysis through autologous arteriovenous fistula is preferable. • Use of cryopreserved allografts and antibiotic-bonded grafts for vascular dialysis access seems promising [58, 77]. • Prevention of horizontal transmission of the pathogens from patient to patient via staff hands, by adhering to contact precautions and especially hand hygiene measures, by application of hydroalcoholic antiseptic solutions.
References
• Isolation or cohorting of patients with multiresistant pathogens. • Avoidance of the unjustified use of vancomycin and prolonged administration of antibiotics (especially of cephalosporins and agents with anaerobic activity) because of the risk of resistant pathogen selection and mainly VRE [40]. • Administration of primary antimicrobial prophylaxis before the implantation of the haemodialysis graft and secondary prophylaxis after selected medical procedures, as described in the general part of this chapter, is of outstanding importance. Single-dose vancomycin is recommended due to the common colonization of this group of patients with MRSA [6, 7, 14, 26, 40, 66]. The recent development of a polysaccharide capsid vaccine is believed to provide protection against S. aureus infection. StaphVax is a phase III clinical trial product that looks to be efficacious in active and passive immunization of chronically haemodialysed patients, in terms of reducing the risk of bacteraemia. Further evaluation is needed and probably repetitive immunization is required [34, 35, 81]. References 1. Angle N (2002) Prosthetic graft infections. In: Moore WS (ed) Vascular surgery. A comprehensive review. Saunders, Philadelphia, pp 741–750 2. Anonymous (2001) Antimicrobial prophylaxis in surgery. Med Lett Drugs Ther 43:92–97 3. Antonios VS, Baddour LM (2004) Intra-arterial device infections. Curr Infect Dis Rep 6:263–269 4. Antrum RM, Galvin K, Gorst K et al (1992) Teicoplanin vs cephradine and metronidazole in the prophylaxis of sepsis following vascular surgery: an interim analysis of an ongoing trial. Eur J Surg Suppl 567:43–46 5. Baddour LM (2001) Infectious Diseases Society of America’s Emerging Infectious Network. Long-term suppressive antimicrobial therapy for intravascular device-related infections. Am J Med Sci 322:209–211 6. Baddour LM, Wilson WM (2004) Infections of prosthetic valves and other cardiovascular devices. In: Mandell GL, Bennett JE, Dolin R (eds) Principles and practice of infectious diseases, 6th edn. Churchill Livingstone, New York, pp 1022–1044 7. Baddour LM, Bettman MA, Bolger AF et al (2003) Nonvalvular cardiovascular device-related infections. Circulation 108:2015–2031
8. Baddour LM, Bettman MA, Bolger AF et al (2004) Nonvalvular cardiovascular device-related infections. Editorial Commentary Infect Dis 38:1128–1130 9. Bandyk DF (2002) Antibiotics-why so many and when should we use them? Semin Vasc Surg 15:268–274 10. Bandyk DF, Bergamini TM (1995) Infection in prosthetic vascular grafts. In Rutherford RB (ed) Vascular surgery. Saunders, Philadelphia, pp 588–596 11. Bandyk DF, Novotney ML, Back MR et al (2001) Expanded application of in situ replacement for prosthetic graft infection. J Vasc Surg 34:411–420 12. Bandyk DF, Novotney ML, Johnson BL et al (2001) Use of rifampin-soaked gelatin-sealed polyester grafts for in situ treatment of primary aortic and vascular prosthetic infections. J Surg Res 95:44–49 13. Batt M, Magne JL, Alric P et al (2003) In situ revascularization with silver-coated polyester grafts to treat aortic infection: early and midterm results. J Vasc Surg 38:983–989 14. Berns J (2003) Infection with antimicrobial-resistant microorganisms in dialysis patients. Semin Dial 16:30–37 15. Boradjani BH, Wilson SE, Fujitani RM et al (2003) Postoperative complications of carotid patching: Pseudoaneurysm and infection. Ann Vasc Surg 17:156–161 16. Bratzler DW, Houck P (2004) Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis 38:1706–1715 17. Brodman M, Stark G, Pabst E et al (2000) Osteomyelitis of the spine and abscess formation in the left thigh after stentgraft implantation in the superficial femoral artery. J Endovasc Ther 7:150–154 18. Chang JK, Calligaro KD, Ryan S et al (2003) Risk factors associated with infection of lower extremity revascularization: analysis of 365 procedures performed at a teaching hospital. Ann Vasc Surg 17:91–96 19. Calligaro KD, DeLaurentis DA, Veith FJ et al (1996) An overview of the treatment of infected prosthetic vascular grafts. Adv Surg 29:3–16 20. Calligaro KD, Veith FJ, Yuan JG et al (2003) Intra-abdominal aortic graft infections: complete or partial graft preservation in patients at very high risk. J Vasc Surg 38:1199–1205 21. Calligaro KD, Veith FJ, Valladares JA et al (2003) Prosthetic patch remnants to treat infected arterial grafts. J Vasc Surg 31:245–252 22. Cherr GS, Travis JA, Ligush J Jr. et al (2001) Infection is an unusual but serious complication of a femoral artery catheterization site closure device. Ann Vasc Surg 15:567–570 23. Chiesa R, Astore D, Frigerio S et al (2002) Vascular prosthetic graft infection: epidemiology, bacteriology, pathogenesis and treatment. Acta Chir Belg 102:238–247
611
612
14.1 Infections in Vascular Surgery
24. Culver DA, Chua J, Rehm SJ et al (2002) Arterial infection and Staphylococcus aureus bacteremia after transfemoral cannulation for percutaneous carotid angioplasty and stenting. J Vasc Surg 35:576–579 25. Daenens K, Fourneau I, Nevelsteen A (2003) Ten-year experience in autogenous reconstruction with the femoral vein in the treatment of aortofemoral prosthetic infection. Eur J Vasc Endovasc Surg 25:240–245 26. D’Agatha EMC (2002) Antimicrobial-resistant, Gram-positive bacteria among patients undergoing chronic hemodialysis. CID 35:1212–1218 27. Darouiche R (2001) Device-associated infections: a macroproblem that starts with microadherence. Clin Infect Dis 33:1567–1572 28. Darouiche R (2003) Antimicrobial approaches for preventing infections associated with surgical implants. Clin Infect Dis 36:1284–1289 29. Darouiche R, Mansouri M (2004) In vitro activity and in vivo efficacy of antimicrobial-coated vascular grafts. Ann Vasc Surg 18:497–501 30. Demaria RG, Giovannini UM, Teot L et al (2003) Topical negative pressure therapy. A very useful new method to treat severe infected vascular approaches in the groin. J Cardivasc Surg 44:757–761 31. Dosluoglu HH, Curl GR, Doerr RJ et al (2001) Stent-related iliac artery and iliac vein infections: two unreported presentations and review of the literature. J Endovasc Ther 8:202–209 32. Eikelboom BC, Ackerstaff RGA, Hoeneveld H et al (1988) Benefits of carotid patching, a randomized study. J Vasc Surg 7:240–247 33. El-Sabrout R, Reul G, Cooley DA et al (2000) Infected postcarotid endarterectomy pseudoaneurysms: retrospective review of a series. Ann Vasc Surg 14:239–247 34. Fattom A, Fuller S, Propst M et al (2004) Safety and immunogenicity of a booster dose of Staphylococcus aureus types 5 and 8 capsular polysaccharide conjugate vaccine (StaphVax) in hemodialysis patients. Vaccine 23:656–663 35. Fattom AI, Horwith G, Fuller S et al (2004) Development of StaphVax, a polysaccharide conjugate vaccine against S. aureus infection: from the lab to phase III clinical trials. Vaccine 17:880–887 36. Gabriel M, Pukacki F, Dzieciuchowicz L et al (2004) Cryopreserved arterial allografts in the treatment of prosthetic graft infections. Eur J Vasc Endovasc Surg 27:590–596 37. Giacometti A, Cirioni O, Ghiselli R et al (2001) Vascular graft infection by Staphylococcus epidermidis: efficacy of various perioperative prophylaxis protocols in an animal model. Infez Med 9:13–18
38. Gilbert DN, Wood CA, Kimbrough RC (1991) Failure of treatment with teicoplanin at 6 milligrams/kilogram/day in patients with Staphylococcus aureus intravascular infection. The Infectious Diseases Consortium of Oregon. Antimicrob Agents Chemother 35:79–87 39. Goldstone J, Moore WS (1974) Infection in vascular prostheses. Clinical manifestations and surgical management. Am J Surg 128:225–233 40. Golper TA, Schulman G, D’Agatha EMC (2000) Indications for vancomycin in dialysis patients. Semin Dial 13:389–392 41. Groschel DHM, Strain BA (1994) Arterial graft infections from a microbiologist’s view. In: Calligaro KD, Veith FJ (eds) Management of infected arterial grafts. Quality Medical, St. Louis, pp 3–15 42. Harbarth S, Samore MH, Lichtenberg D et al (2000) Prolonged antibiotic prophylaxis after cardiovascular surgery and its effect on surgical site infections and antimicrobial resistance. Circulation 27:2916–2921 43. Herbiere P, Courouble Y, Bourgeois P et al (1981) Lumbar spondylodiscitis after insertion of a Mobin-Uddin caval “umbrella” filter. Nouv Presse Med 10:3715–3716 44. Hernandez-Richter T, Schardey HM, Wittmann F et al (2003) Rifampin and triclosan but not silver is effective in preventing bacterial infection of vascular Dacron graft material. Eur J Vasc Endovasc Surg 26:550–557 45. Huang JKC, Shah EF, Vinidkumar N et al (2003) The bear hugger patient warming system in prolonged vascular surgery: an infection risk? Crit Care 7:R13–R16 46. Jabra-Rizk MA, Falkler WA, Meiller TF (2004) Fungal biofilms and drug resistance. Emerg Infect Dis 10:14–19 47. Johanning JM, Franklin DP, Elmore JR et al (2001) Femoral artery infections associated with percutaneous arterial closure devices. J Vasc Surg 34:983–985 48. Kester RC, Antrum R, Thornton CA et al (1999) A comparison of teicoplanin versus cephradine plus metronidazole in the prophylaxis of post-operative infection in vascular surgery. J Hosp Infect 41:233–243 49. Kieffer E, Gomes D, Chiche L et al (2004) Allograft replacement for infrarenal aortic graft infection: early and late results in 179 patients. J Vasc Surg 39:1009–1017 50. Kirksey L, Brener BJ, Hertz S et al (2002) Prophylactic antibiotics prior to bacteremia decrease endovascular graft infection in dogs. Vasc Endovasc Surg 66:166–177 51. Kojic EM, Darouiche RO (2004) Candida infections of medical devices. Clin Microbiol Rev 17:255–267 52. Kreutzer J, Ryan CA, Gauvreau K et al (2001) Healing response to the Clamshell device for closure of intracardiac defects in humans. Catheter Cardiovasc Interv 54:101–111
References
53. Latham JA, Irvine A (1999) Infection of endovascular stents: an uncommon but important complication. Cardiovasc Surg 7:179–273 54. Lau LL, Halliday MI, Lee B et al (2000) Intestinal manipulation during elective aortic aneurysm surgery leads to portal endotoxaemia and mucosal barrier dysfunction. Eur J Vasc Endovasc Surg 19:619–624 55. Lee ES, Olson MM (2000) Wound infection after infrainguinal bypass operations: multivariate analysis of putative risk factors. Surg Inf 1:257–263 56. Lentino JR, Baddour LM, Wray M et al (2000) Staphylococcus aureus and other bacteremias in hemodialysis patients: antibiotic therapy and surgical removal of access site. Infection 28:355–360 57. Lin M, Soo TB, Horn LC (2000) Successful retrieval of infected Günther Tulip IVC filter. J Vasc Interv Radiol 11:1341–1343 58. Maatsura JH, Rosenthal D, Wellons ED et al (2002) Hemodialysis graft infections treated with cryopreserved femoral vein. Cardiovasc Surg 10:561–565 59. Marroni M, Cao P, Fiorio M et al (1999) Prospective, randomized, double-blind trial comparing teicoplanin and cefazolin as antibiotic prophylaxis in prosthetic vascular surgery. Eur J Clin Microbiol Infect Dis 18:175–178 60. McDonald LC, Hageman JC(2004) Vancomycin intermediate and resistant Staphylococcus aureus. What the nephrologists needs to know. Nephrol News Issues 18:63–64, 66–67, 71–72 61. Millward SF, Peterson RA, Moher D et al (1994) LGM (Vena Tech) vena caval filter: experience at a single institution. J Vasc Interv Radiol 5:351–356 62. Mini E, Nobili S, Periti P (2000) Does surgical prophylaxis with teicoplanin constitute a therapeutic advance? J Chemother Suppl 5:40–55 63. Musella M, Guido A, Musella S (2001) Collagen tampons as aminoglycoside carriers to reduce postoperative infection rate in prosthetic repair of groin hernias. Eur J Surg 167:130–132 64. Muto CA, Jernigan JA, Ostrowsky BA et al (2003) SHEA Guideline for preventing nosocomial transmission of multidrug resistant strains of Staphylococcus aureus and Enterococcus. Infect Control Hosp Epidemiol 24:362–386 65. Myles O, Thomas WJ, Daniels JT et al (2000) Infected endovascular stents managed with medical therapy alone. Cath Cardiovasc Inyerv 51:471–476 66. Nassar GM, Ayus JC (2001) Infectious complications of the hemodialysis access. Kidney Int 60:1–13
67. Naylor AR, Hayes PD, Darke S on behalf of the Joint Vascular Research Group (2001) A prospective audit of complex wound and graft infections in Great Britain and Ireland: the emergence of MRSA. Eur J Vasc Endovasc Surg 21:289–294 68. Naylor AR, Payne D, London NJM et al (2002) Prosthetic patch infection after carotid endarterectomy. Eur J Vasc Endovasc Surg 23:11–16 69. Noel AA, Gloviczki P, Cherrry KJ Jr. et al (2002) Abdominal aortic reconstitution in infected fields: early results of the United states cryopreserved aortic allograft registry. J Vasc Surg 35:847–852 70. Oderich GS, Panneton JM (2002) Aortic graft infection. What have we learned during the last decade? Acta Chir Belg 102:7–13 71. Orton DE, LeVeen RF, Saigh JA et al (2000) Aortic prosthetic graft infections: radiologic manifestations and implications for management. Radiographics 20:977–993 72. Paget DS, Bukhari RH, Zayat EJ et al (1999) Infectibility of endovascular stents following antibiotic prophylaxis or after arterial wall incorporation. Am J Surg 178:219–224 73. Parry DJ, Waterworth A, Kessel D et al (1999) Endovascular repair of an inflammatory abdominal aortic aneurysm complicated by aortoduodenal fistulation with an unusual presentation. J Vasc Surg 33:874–879 74. Perl TM , Cullen JJ, Wenzel RP et al (2002) Mupirocin and the risk of Staphylococcus aureus study team: intranasal mupirocin to prevent postoperative Staphylococcus aureus infections. N Engl J Med 346:1871–1877 75. Pinocy J, Albes JM, Wicke C et al (2003) Treatment of periprosthetic soft tissue infection of the groin following vascular surgical procedures by means of polyvinyl-alcoholvacuum sponge system. Wound Repair Regen 11:104–109 76. Pruitt A, Dodson TF, Najibi S et al (2002) Distal septic emboli and fatal brachiocephalic artery mycotic pseudoaneurysm as a complication of stenting. J Vasc Surg 36:625–628 77. Raad I, Chatzinikolaou I, Chaiban G et al (2003) In vitro and ex vivo activities of minocycline and EDTA against microorganisms embedded in biofilm on catheter surfaces. Antimicrob Agents Chemother 47:3580–3585 78. Raptis S, Baker SR (1996) Infected false aneurysms of the carotid arteries after carotid endarterectomy. Eur J Vasc Endovasc Surg 11:148–152 79. Ray CE, Kaufman JA (1996) Complications of inferior vena cava filters Abdom Imaging 21:368–374 80. Rizzo A, Hertzer NR, O’Hara PJ et al (2000) Dacron carotid patch infection: A report of eight cases. J Vasc Surg 32:602–606
613
614
14.1 Infections in Vascular Surgery
81. Robbins JB, Schneerson R, Horwith G et al (2004) Staphylococcus aureus types 5 and 8 capsular polysaccharide-protein vaccines. Am Heart J 147:593–598 82. Rockman CB, Su WT, Domenig C et al (2003) Postoperative infection associated with polyester patch angioplasty after carotid endarterectomy. J Vasc Surg 38:251–256 83. Roy D, Grove DI (2000) Efficacy of long-term antibiotic suppressive therapy in proven or suspected infected abdominal aortic grafts. J Infect 40:184–204 84. Ryan SV, Calligaro KD, Scharff J et al (2004) Management of infected prosthetic dialysis arteriovenous grafts. J Vasc Surg 39:73–78 85. Samore MH. Wessolossky MA, Lewis SM et al (1997) Frequency, risk factors and outcome for bacteremia after percutaneous transluminal coronary angioplasty. Am J Cardiol 79:873–877 86. Sarac TP, Augustinos P, Lyden S et al (2003) Use of fasciaperitoneum patch as a pledget for an infected aortic stump. J Vasc Surg 38:1404–1406 87. Seeger JM (2000) Management of patients with prosthetic vascular graft infection. Am J Surg 66:166–177 88. Seeger JM, Pretus HA, Welborn MB et al (2000) Long-term outcome after treatment of aortic graft infection with staged extra-anatomic bypass grafting and aortic graft removal. J Vasc Surg 32:451–461 89. Selan L, Passariello C, Rizzo L et al (2002) Diagnosis of vascular graft infections with antibodies against staphylococcal slime antigens. Lancet 359:2166–2168 90. Schierholtz JM, Beuth J (2001) Implant infections: a haven for opportunistic bacteria. J Hosp Infect 49:87–93
91. Sladen JG, Chen JC, Reid JD (1998) An aggressive local approach to vascular graft infections. Am J Surg 176:222–225 92. Stewart PS, Costerton JW (2001) Antibiotic resistance of bacteria in biofilms. Lancet 358:135–138 93. Tacconelli E, Carmeli Y, Aizer A et al (2003) Mupirocin prophylaxis to prevent Staphylococcus aureus infection in patients undergoing dialysis: a meta-analysis. Clin Infect Dis 37:1629–1638 94. Talbot TR, Kaiser AB (2005) Postoperative infections and antimicrobial prophylaxis. In: Mandell GL, Bennett JE, Dolin R (eds) Principles and practice of infectious diseases, 6th edn. Churchill Livingstone, New York, pp 3533–3547 95. Tokars JI, Miller ER, Stein G (2002) New National Surveillance system for hemodialysis-associated infections: initial results. Am J Infect Control 30:288–295 96. Tolefson DF, Bandyk DF, Kaebnick HW et al (1987) Surface biofilm disruption. Enhanced recovery of microorganisms from vascular prostheses. Arch Surg 122:38–43 97. Valentine RJ, Clagett GP (2001) Aortic graft infections: replacement with autologous vein. Cardiovasc Surg 9:419–425 98. Vallet C, Saucy F, Haller C et al (2004) Vacuum-assisted conservative treatment for the management and salvage of exposed prosthetic hemodialysis access. Eur J Vasc Endovasc Surg 28:397–399 99. Whitton Hollis H Jr., Rehring TF (2003) Femoral endarteritis associated with percutaneous suture closure: new technology, challenging complications. J Vasc Surg 38:83–87 100. Young RM, Cherry KJ Jr., Davis PM et al (1999) The results of in situ prosthetic replacement for infected aortic grafts. Am J Surg 178:136–140
615
14.2 Vascular Problems in Urological Surgery K.G. Stravodimos, A. Giannopoulos
14.2.1 Introduction Urological surgery has evolved over time and now includes many major operations, sometimes with considerable morbidity. Procedures that were performed only in specialized centres are now considered the standard of care for many institutions all over the world. The management of renal cell carcinoma involving the inferior vena cava remains a technically challenging surgical condition, while radical pelvic surgery for bladder cancer is sometimes complicated with vascular injuries. In the last few decades we have also witnessed the evolution of laparoscopy from a diagnostic tool to a sophisticated therapeutic procedure which, in several centres, is used for advanced ablative and complex reconstructive urological procedures. However, this evolution has been accompanied by the occurrence of new types of vascular complications during laparoscopic urological surgery. Vascular surgeons probably receive more requests for intraoperative consultation than any other specialists, because iatrogenic vascular injuries are unpredictable and require immediate correction. Vascular complications may occur during many surgical procedures of different specialties (i.e. ear-nose-throat, orthopaedics, general surgery, etc.) but they perhaps are most common during pelvic procedures and especially in urological surgery. It is for this reason that all urologists should train and be familiar with the principles of vascular surgery concerning arterial and venous repair. Their role is to be able to confront minimal vascular complications or at least to control haemorrhage until the vascular surgeon arrives. There are mainly two types of interaction between vascular and urological surgeons. The usual case is when an unexpected vascular injury happens during an operation and vascular surgical consultation is needed urgently. Venous injuries are more common than arterial trauma and this is not surprising since veins are more fragile. The other is when, during the preoperative evaluation for
a urological disease, a vascular lesion is discovered and warrants consultation before any surgical procedure is scheduled. This may apply to aneurysms discovered incidentally or as a rare cause of ureteral obstruction due to retroperitoneal fibrosis or when renal tumours involve the vena cava.
14.2.2 Vascular Lesions on Preoperative Evaluation During the preoperative evaluation and staging for tumours of the urogenital tract, vascular lesions can be discovered incidentally. Abdominal aortic aneurysms (AAA), or to a lesser extent aortoiliac disease, may be present without any symptoms while invasion of the vena cava from a tumour of the kidney is rare (4–10%) [14, 34] but its management has proven both challenging and controversial. Vascular consultation in preoperative planning and during the surgical procedure is helpful and in many cases essential. When an AAA is discovered it is not always necessary to proceed to surgical correction, but it is significantly important to evaluate the patient before performing the appropriate urogenital operation (radical cystectomy – prostatectomy – nephrectomy). In the case of propagation of renal cell carcinoma (RCC) into the vena cava, an aggressive surgical approach with curative intent may be justified.
14.2.2.1 Abdominal Aortic Aneurysm (AAA) Incidence Several series have placed the incidence of AAA at 1.8– 6.6% [2, 29]. The frequency of both AAA and visceral malignancy increases with advancing age. At the time of AAA reconstruction, the chances of encountering intra-
616
14.2 Vascular Problems in Urological Surgery
abdominal malignancy has been estimated at up to 4% [38] while malignancy in patients with AAA is reportedly up to 12.6% [22]. The presence of invasive bladder cancer and AAA is rather rare. There are reports in the literature with up to 20 patients over a period of 6–10 years [12, 20].
Surgical Treatment Surgical treatment of these two potentially life-threatening conditions still represents the best option in many instances, but the best timing of intervention is controversial. If both conditions are diagnosed at the same time, this raises the question: should the aneurysm be repaired first, second or simultaneously with cancer resection? There are pros and cons for each approach. Simultaneous cystectomy, urinary diversion and aneurysm repair can be a difficult procedure and the main concern is the potential for graft infection due to spilled bowel contents and urine. On the other hand, the staged procedure necessitates a second anaesthesia, major surgery in a complex cicatricial territory and delay of the definitive therapy of one of two life-threatening diseases. It is reported that the risk of aneurysm rupture is higher after a major operation due to the high rate of collagen turnover observed 7–10 days after the operation [36]. In a prospective study [5] the probability of rupture of an AAA after an unrelated operative procedure averaged 3%. Still, the risk of rupture of an AAA depends on various factors, such as wall thickness, symptoms, diameter and others beyond the scope of this discussion. There is also concern that repair of the aneurysm before cancer resection potentially allows for further tumour growth in a patient weakened and possibly immunosuppressed by a major operation. There is a proposed algorithm from Lierz et al. [20] for the management of simultaneously discovered AAA and bladder cancer: • The size of the AAA is the determining factor. • Patients with aneurysms that are symptomatic, expanding or greater than 5 cm should undergo aneurysm repair with pelvic lymphadenectomy. • If nodes are microscopically positive, conservative management should be considered for the bladder cancer. If not, cystectomy should be performed at a later date. • Patients with small aneurysms should undergo cystectomy and diversion with close observation of the aneurysm.
This two-staged approach was criticized because of all the previous considerations and also the difficulties found at the time of the second operation. Other authors presented their series, in which simultaneous AAA repair and bladder cancer resection was performed. Ginsberg et al. [6] operated on the urologic neoplasm first and the AAA resection followed with the same anaesthesia. They found fewer technical problems, while the operative time and average blood loss were less when compared with the staged approach. They did not observe graft infections or vascular complications in the follow-up period either. In the most recent series [12] a prospective study was performed. Open surgery for bladder cancer and AAA was simultaneously performed in 16 patients while there were two equal-sized groups of matched control patients undergoing surgery either for AAA or bladder cancer. The AAA was always addressed first, followed by cystectomy with either orthotopic ileal bladder reconstruction or ileal loop diversion. No peri-operative mortality was noted. Systemic and urological complications were similar in patients treated for AAA and bladder cancer compared to patients treated for bladder cancer only. Simultaneous treatment did not increase the risk of vascular graft infection or other vascular complications. Simultaneous surgical treatment of coexisting AAA and bladder cancer may represent a suitable choice for intervention by both vascular and urology specialists in specialized centres.
Endovascular Treatment Another viable and attractive option is the endovascular treatment of AAA (see also Chapters 5.1–5.3). This way the prosthetic material is best protected from bowel and urinary spillage and simultaneous treatment can also be performed. This must be decided preoperatively since not all aneurysms are suitable for endovascular repair. One must also consider the possible endovascular graft complications, since if an elective or emergency open repair is needed this will be a challenging operation on a recently performed urinary diversion.
14.2.2.2 Renal Tumours Involving the Vena Cava Incidence Renal cell carcinoma (RCC), which accounts for 3% of all adult malignancies, is the most lethal of urological can-
14.2.2 Vascular Lesions on Preoperative Evaluation
cers. Traditionally, more than 40% of patients with RCC have died from their cancer, in contrast to the approximately 20% mortality rates associated with prostate and bladder carcinomas [16]. In addition, as for other relatively radioresistant solid tumours for which as yet there are no chemotherapy or immunotherapy treatments of proven and significant efficacy, surgery represents the only therapeutic option that is able to affect and favourably alter patient survival and prognosis of the disease. A subgroup of patients with special characteristics concerning prognosis and a surgically challenging condition are those where the renal tumour is associated with extension of a thrombus into the inferior vena cava (IVC) (5%), with the extension possibly reaching above the diaphragm and into the right atrium (1%) [14].
• The extension of RCC to involving the vena cava can be classified according to the position of the highest point of the thrombus as follows: • Level I: less than 5 cm above the renal vein • Level II: greater than 5 cm above the renal vein but below the hepatic veins • Level III: above the hepatic veins but below the diaphragm • Level IV: above the diaphragm [34]. • Another classification is infrahepatic (lower: the tumour thrombus protrudes into the IVC but does not extend beyond the renal veins; higher: the tumour thrombus extends into the IVC below the large hepatic veins), retrohepatic (the tumour thrombus extends into the IVC above the large hepatic veins) and atrial (the tumour thrombus reaches the right atrium) [8].
Diagnosis and Classification Prognosis and Treatment • Since RCC is primarily a radiological diagnosis, and since the presence or absence of metastasis is paramount in treatment decisions, all patients should be evaluated with an abdominal-pelvic CT scan and chest radiograph. • Magnetic resonance imaging (MRI) can be reserved for patients with locally advanced malignancy, possible venous involvement, renal insufficiency or allergy to intravenous contrast [24]. • Metastatic evaluation should also include liver function tests. • A bone scan can be reserved for patients with elevated serum alkaline phosphatase or bone pain. • A chest CT can be saved for patients with symptoms or an abnormal chest radiograph [21, 30]. • CT sensitivity for renal vein and inferior vena cava involvement is 78% and 96% respectively, with most false-negative results occurring on right kidney tumours probably due to the short length of the vein [1]. MRI is noninvasive and can provide exceptional images and useful information about the extent of thrombus. It is nowadays accepted as the first-line study for evaluation and staging of inferior vena cava thrombus [1, 3, 15]. • Venacavography was considered the standard of care for the detection of thrombus until the advent of MRI. It is now reserved only for MRI-equivocal cases. Preoperative transoesophageal ultrasound is invasive and it seems that it does not provide more information than MRI [10].
Venous involvement was once thought to be a poor prognostic finding for RCC, but more recent studies suggest that most patients with tumour thrombi can be saved with an aggressive surgical approach. In the series of Skinner et al. [31] 57% 5-year survival rates were reported when patients with metastases were excluded. There are numerous other studies in which significant 5-year survival rates (39–64%) are reported for patients with venous tumour thrombi, as long as the carcinoma is nonmetastatic [9, 32, 34, 37]. In patients without distant metastases the significance of the thrombus level for survival prognosis has been controversial. Sosa and Quek noted worse prognosis as the tumour thrombus extended higher [28, 33] although in the Sosa series the incidence of advanced locoregional or systemic disease increased with the cephalad extent of the tumour thrombus, probably accounting for the reduced survival. In contrast, more recent data found no correlation between cranial thrombus extension and survival. Recently [34] survival rates did not seem to differ significantly among patients with level I to level III thrombi, and the poor outcome in those with level IV thrombi was caused by high peri-operative mortality. Other authors compared patients with supradiaphragmatic and infradiaphragmatic tumour thrombi and found no difference in survival [19] and even patients with a tumour thrombus extending into the right atrium had a cancer-specific 5-year survival rate of almost 60% [9]. Preoperative evaluation should be meticulous in order to determine the level of the thrombus in order to allow
617
618
14.2 Vascular Problems in Urological Surgery
early involvement of the operative disciplines (urologists, liver surgeons, vascular surgeons, cardiac surgeons and anaesthesiologists) if an interdisciplinary approach is required. The primary goal of all surgical techniques should be to take control of the vena cava above the tumour thrombus to avoid embolism. All manipulations of the kidney should be kept to a minimum until the primary goal is achieved either by a tourniquet loop or a vascular clamp. For retrohepatic thrombi, techniques elaborated in liver transplantation may be useful in order to: • mobilize the liver • control the hepatocaval connection • preserve the venous collaterals • enhance the exposure • increase the safety of the resection, and • remove the tumour thrombus from IVC. This may be accomplished by a transabdominal approach [11]. This way sternotomy and cardiopulmonary by-pass can be avoided in the majority (up to 93%) of patients [4]. Extensive cardiac thrombi require cardiopulmonary by-pass. Mild hypothermia without circulatory arrest allows for controlled thrombus extraction by simultaneous atrial and caval approaches, but it can also suffer from inadequate visibility due to drainage from hepatic veins [35]. Cardiopulmonary by-pass with hypothermia and circulatory arrest offers excellent exposure and thrombus extraction under direct visualization of IVC and a bloodless field [25]. There is always the risk of peri-operative haemorrhage secondary to heparinization and platelet dysfunctions and it seems reasonable to use this method for patients with level IV thrombus or when simultaneous cardiovascular interventions are planned [34].
14.2.3 Unexpected – Iatrogenic Vascular Injuries Vascular surgeons are occasionally involved in the management of patients with vascular injuries sustained during elective operations. As interest increases in radical oncological resection, extensive lymphadenectomy, and the use of adjuvant radiation therapy, it can be expected that iatrogenic vascu-
lar injuries will continue to occur, and may become more frequent. In a recent study, over a 11-year period, 22% of vascular injuries were iatrogenic and elderly patients were more likely to suffer from iatrogenic vascular trauma [39]. Since urological procedures concern the bladder, the prostate, the kidney and the ureters and considering the proximity of iliac vessels, IVC and the aorta to these structures, it is not surprising that vascular injuries complicate urological operations. Urological operations are responsible for a small number of iatrogenic vascular traumas (3–7%) while vascular catheterization and general surgery are the predominant causes [26, 27]. Laparoscopic surgery in urology is also associated with essentially the same complications as open surgery, and the risk of bleeding is estimated to be about 0.5–1.5% [40]. Vascular injuries may refer to venous or arterial trauma. There are some factors that may be characterized as predisposing factors for iatrogenic operative injuries. Patients who undergo oncological operations, those who have distorted anatomy because of a previous operation, and those with tumour recurrence, previous radiation or inflammatory changes seem to be more prone to vascular injuries.
14.2.3.1 Venous Injuries Although serious venous injuries are relatively rare, they are associated with potential catastrophic complications and carry substantial risk for death. This is especially true of injuries located in low-pressure and high-flow veins, such as IVC and internal iliac veins. Injuries in these locations can pose a formidable challenge to the surgeon, because of difficult anatomical exposure and substantial blood loss [26]. Iatrogenic venous trauma appears to be considerably more common than arterial injury and nearly always is more difficult to control because venous bleeding pools directly in the field of repair [13]. Preventing venous trauma and avulsion of delicate venous branches is essential during urological surgery by elective ligation and division of small tributaries before traction is applied. The use of smooth forceps rather than instruments with teeth will protect larger veins from puncture wounds. A common mistake in attempting to obtain vascular control is the forceful use of clamps around the vein, resulting in additional injuries. Direct digital pres-
14.2.3 Unexpected – Iatrogenic Vascular Injuries
sure or sponge compression with “sponge sticks” proximal and distal to the injury site is a more effective and safe means of obtaining rapid vascular control. In many cases the urologist surgeon attempts to control and repair the venous trauma, which is natural since the surgeons want to repair their injuries. That is why urologists should be familiar with the principles of vascular repair. The nonvascular surgeon usually repairs minor venous injuries. Partial lacerations may be rapidly oversewn using nonabsorbable vascular suture. However, it is important to note the following: • Excessive delay in obtaining vascular surgery assistance often leads to more blood loss. It seems that most of the blood loss occurs before vascular surgeons are involved. Blood loss from injuries of the IVC or internal iliac vein may be substantial (mean 4800–7300 ml) [26]. • Most patients with operative venous injuries have partial lacerations that can be managed with relatively simple techniques, such as venorrhaphy, patch angioplasty and end-to-end anastomosis. The basic principles of venous repair are to obtain control of the laceration without tearing beyond its original dimensions and to close the defect without compromising the lumen. The surgeon should use simplicity and creativity in the repair, while avoiding tension and stenosis at the anastomosis. Continued patency is an important consideration when dealing with injuries to the IVC or the common iliac and external iliac veins in order to avoid deep venous thrombosis or venous insufficiency. Complex defects should be revised and corrected with the use of a patch. Autogenous replacement with the use of saphenous vein is considered superior to any prosthetic material but short (2–4 cm) defects may be covered by ePTFE grafts in patients with minimal or no contamination [26, 41]. Although rarely encountered, trauma to the presacral venous plexus during pelvic surgery can result in extremely serious blood loss that is refractory to local control even after ligation of both internal iliac arteries. In this desperate situation, manual compression is applied until the resection is completed. After that the presacral area is packed with gauze to continue tamponade after the abdominal incision is closed. The patient has any coagulation disturbances and thrombocytopenia corrected and 48 h later is returned to the operating room to remove the presacral packing if haemostasis is found to be satisfactory.
14.2.3.2 Arterial Injuries Iatrogenic arterial injuries comprise a significant percentage of vascular trauma treated by vascular surgeons. The most common injuries observed are caused by percutaneous vascular instrumentation while much less common injuries are observed in orthopaedic and abdominal/laparoscopic operations [23]. It seems that there has been a slow but steady increase in iatrogenic arterial trauma recently mainly due to the increasing number of percutaneous procedures performed [7]. It is reported that radical operations for cancer comprise less than 8% of the iatrogenic arterial injuries [18] and laceration of the aorta or the iliofemoral arterial segments during urological procedures is a rather unusual event. This is probably because these vessels may easily be palpated and avoided [13]. Arterial trauma may present as laceration and haemorrhage during the operation or as local thrombosis/distal embolization postoperatively due to unrecognized blunt arterial trauma. Small arterial lacerations cause pulsatile bleeding and can be repaired with fine sutures by the urologist without the assistance of a vascular surgeon. It is always important to obtain adequate exposure and to temporarily control bleeding by digital compression or by approximating the adventitia over the laceration with fine forceps. Fine (5-0 or 6-0), nonabsorbable vascular sutures should be inserted parallel to the long axis of the artery taking care not to compromise the lumen and avoid the opposite wall of the vessel. Calcified arteries with extensive lacerations should prompt the urologist to ask for the vascular surgeon. In these cases haemostasis is difficult and precise reconstruction is essential to avoid segmental arterial occlusion and distal thrombosis. Sometimes it is necessary to convert an injury to formal arteriotomy to completely inspect the lumen and repair with a patch of saphenous vein or prosthetic material in a sterile surgical field. Almost half of the cases can be repaired primarily or by simply ligating the injured artery but for the rest of the repairs vascular surgical techniques, such as interposition grafts, by-pass grafts, or patch angioplasty, are needed [7]. Complex urological procedures in the pelvis are usually performed in elderly patients with some degree of atherosclerosis of the iliac arteries. Compression of these arteries by retractors may result in local thrombosis, while intraoperative manipulation may precipitate a sud-
619
620
14.2 Vascular Problems in Urological Surgery
den occlusion of the arterial bed from atheromatous or thrombotic emboli [13]. Acute limb ischaemia in postoperative patients should alert an immediate vascular surgical consultation since surgical intervention is the most appropriate approach for salvage of the limb. Thrombectomy is usually successful in patients who do not have occlusive arterial disease. In patients with advanced iliofemoral atherosclerosis a by-pass may be necessary in order to restore satisfactory flow. Traumatic atheromatous embolization represents a more serious threat to limb viability because of the small size of the provoked emboli and the initiation of diffuse thrombotic occlusion of the plantar arch. Although not common, in some cases it may be difficult to avoid amputation. Iatrogenic arterial injuries in general may contribute to a mortality rate of 4.6–7% [7, 18], which does not significantly differ from that reported for noniatrogenic arterial injuries [17]. Permanent morbidity (defined as amputation or loss of extremity function) may vary from 2.3% to 3.5% [7, 18]. Delay in treatment contributes to this morbidity and mortality [27]. Prevention of arterial injuries by careful manipulation and retraction during urological procedures is imperative.
14.2.4 Bulleted Summary • Urologists may require vascular consultation because of either lesions discovered on preoperative evaluation or unexpected vascular injuries during an operation. • Preoperative planning is helpful and in many cases essential for dealing with cases such as abdominal aortic aneurysm coexisting with urogenital malignancy and renal tumours involving the vena cava. • Patients who undergo oncological operations, those with distorted anatomy because of previous operation, and those with tumour recurrence or radiation and inflammatory changes are more prone to iatrogenic vascular injuries. • Prevention of injuries by careful operative technique and prompt vascular consultation when they happen are the two major principles for minimizing the incidence of iatrogenic vascular trauma and avoid further complications. References 1. Bechtod RE, Zagoria RJ (1997) Imaging approach to staging of renal cell carcinoma. Urol Clin North Am 24:507–522
2. Bickerstaff LK, Hollier LH, Van Peenan HJ, Melton LJ, Pairolero PC, Cherry KJ (1984) Abdominal aortic aneurysms: the changing natural history. J Vasc Surg 1:6–12 3. Choyke PL (1997) Detection and staging of renal cancer. Magn Reson Imaging Clin N Am 5:29–47 4. Delis S, Dervenis C, Lytras D, Avgerinos C, Soloway M, Ciancio G (2004) Liver transplantation techniques with preservation of the natural venovenous bypass: effect on surgical resection of renal cell carcinoma invading the inferior vena cava. World J Surg 28:614–619 5. Durham SJ, Steed DL, Moosa HH, Makaroun MS, Webster MW (1991) Probability of rupture of an abdominal aortic aneurysm after an unrelated operative procedure: a prospective study. J Vasc Surg 13:248–252 6. Ginsberg DA, Modrall JG, Esrig D, Baek S, Yellin AE, Lieskovsky G et al (1995) Concurrent abdominal aortic aneurysm and urologic neoplasm: an argument for simultaneous intervention. Ann Vasc Surg 9:428–433 7. Giswold ME, Landry GJ, Taylor LM, Moneta GL (2004) Iatrogenic arterial injury is an increasingly important cause of arterial trauma. Am J Surg 187:590–593 8. Giuliani L, Giberti C, Martorana G, Rovida S (1990) Radical extensive surgery for renal cell carcinoma: long-term results and prognostic factors. J Urol 143:468–474 9. Glazer AA, Novick AC (1996) Long-term follow-up after surgical treatment for renal cell carcinoma extending into the right atrium. J Urol 155:448–450 10. Glazer AA, Novick AC (1997) Preoperative transesophageal echocardiography for assessment of resonance imaging. Urology 49:32–34 11. Gonzalez-Fajardo JA, Fernandez E, Rivera J, Pelaz A, Gonzalez-Zarate J, Alvarez JC, Gonzalez E, Vaquero C (2000) Transabdominal surgical approach in the management of renal tumors involving the retrohepatic inferior vena cava. Ann Vasc Surg 14:436–443 12. Grego F, Lepidi S, Bassi P, Tavolini I, Noventa F, Pagano F, Deriu GP (2003) Simultaneous surgical treatment of abdominal aortic aneurysm and carcinoma of the bladder. J Vasc Surg 37:607–614 13. Hertzer N (1985) Vascular problems in urologic patients. Urol Clin N Am 12:493–507 14. Hoehn W, Hermanek P (1983) Invasion of veins in renal cell carcinoma – frequency, correlation and prognosis. Eur Urol 9:276–280 15. Kallman DA, King BF, Hattery RR et al (1992) Renal vein and inferior vena cava tumor thrombus in renal cell carcinoma: CT, US, MRI, and venacavography. J Comput Assist Tomogr 16:240–247
References
16. Landis SH, Murray T, Bolden S, Wingo PA (1999) Cancer statistics: 1999. CA Cancer J Clin 49:8–31 17. Lazarides MK, Arvanitis DP, Liatas AC, Dayantas JN (1991) Iatrogenic and noniatrogenic arterial trauma: a comparative study. Eur J Surg 157:17–20 18. Lazarides MK, Tsoupanos SS, Georgopoulos SE, Chronopoulos AV, Arvanitis DP, Doundoulakis NJ, Dayantas JN (1998) Incidence and patterns of iatrogenic arterial injuries. A decade’s experience. J Cardiovasc Surg (Torino) 39:281–285 19. Libertino JA, Zinman L, Watkins E (1987) Long term results of resection of renal cell cancer with extension into inferior vena cava. J Urol 137:21–24 20. Lierz MF, Davis BE, Noble MJ, Wattenhofer SP, Thomas JH (1993) Management of abdominal aortic aneurysm and invasive transitional cell carcinoma of the bladder. J Urol 149:476–479 21. Lim DJ, Carter MF (1993) Computerized tomography in the preoperative staging for pulmonary metastases in patients with renal cell carcinoma. J Urol 150:1112–1114 22. Morris DM, Colquitt J (1988) Concomitant abdominal aortic aneurysm and malignant disease: a difficult management problem. J Surg Oncol 39:122–125 23. Nehler MR, Taylor LM , Porter JM (1998) Iatrogenic vascular trauma. Semin Vasc Surg 11:283–293 24. Novick AC, Campbell SC (2003) Renal tumors in Campbell’s urology,8th edn. Elsevier, Amsterdam 25. Novick AC, Kaye MC, Cosgrove DM, Angermeier K, Pontes JE, Montie JE, Streem SB, Klein E ,Stewart R ,Goormastic M (1990) Experience with cardiopulmonary bypass and deep hypothermic circulatory arrest in the management of retroperitoneal tumors with large vena caval thrombi. Ann Surg 212:472–476 26. Oderich GS, Panneton JM, Hofer J, Bower TC, Cherry KJ, Sullivan T, Noel AA, Kalra M, Gloviczki P (2004) Iatrogenic operative injuries of abdominal and pelvic veins: a potentially lethal complication. J Vasc Surg 39:931–936 27. Pedrini L, Stella A, Curti T, Paragona O, Pisano E, Saccy A (1991) Iatrogenic vascular lesions. Pathogenesis and treatment: an 18 year review. Int Angiol 10:233–237 28. Quek ML, Stein JP, Skinner DG (2001) Surgical approaches to venous tumor thrombus. Semin Urol Oncol 19:88–97 29. Reilly JM, Tilson MD (1989) Incidence and etiology of abdominal aortic aneurysms. Surg Clin N Am 69:705–711
30. Seaman E, Goluboff ET, Ross S, Sawczuk IS (1996) Association of radionuclide bone scan and serum alkaline phosphatase in patients with metastatic renal cell carcinoma. Urology 48:692–695 31. Skinner DG, Pfister RF, Colvin R (1972) Extension of renal cell carcinoma into the vena cava: the rationale for aggressive surgical management. J Urol 107:711–716 32. Skinner DG, Pritchett TR, Lieskovsky G, Boyd SD, Stiles QR (1989) Vena caval involvement by renal cell carcinoma. Surgical resection provides meaningful long-term survival. Ann Surg 210:387–392 33. Sosa RE, Muecke EC, Vaughan ED, McCarron JP Jr (1984) Renal cell carcinoma extending into the inferior vena cava: the prognostic significance of the level of vena caval involvement. J Urol 132:1097–1100 34. Staehler G, Brkovic D (2000) The role of radical surgery for renal cell carcinoma with extension into the vena cava. J Urol 163:1671–1675 35. Stewart JR, Carey JA, McDougall WS, Merrill WH, Koch MO, Bender HW et al (1991) Cavoatrial tumor thrombectomy using cardiopulmonary bypass without circulatory arrest. Ann Thorac Surg 51:717–721 36. Swanson RJ, Littooy FN, Hunt TK, Stoney RJ (1980) Laparotomy as a precipitating factor in the fracture of intraabdominal aneurysms. Arch Surg 115:299–304 37. Swierzewski DJ, Swierzewski MJ, Libertino JA (1994) Radical nephrectomy in patients with renal cell carcinoma with venous, vena caval and atrium extension. Am J Surg 168:205–209 38. Szilagyi DE, Elliot LP, Berguer R (1967) Coincidental malignancy and abdominal aortic aneurysm. Problems of management. Arch Surg 95:402–412 39. Thomson I, Muduioa G, Gray A (2004) Vascular trauma in New Zealand: an 11-year review of NZVASC, the New Zealand Society of Vascular Surgeons’ audit database. N Z Med J 117:U1048 40. Vallancien G, Cathelineau X, Baumert H, Doublet JD, Guilloneau B (2002) Complications of transperitoneal laparoscopic surgery in urology: review of 1,311 procedures at a single center. J Urol 168:23–26 41. Zamir G, Berlatzky Y, Rivkind A, Anner H, Wolf YG (1998) Results of reconstruction in major pelvic and extremity venous injuries. J Vasc Surg 28:901–908
621
623
14.3 Vascular Trauma in Orthopaedic Surgery Panayotis N. Soucacos
14.3.1 Introduction There are various situations in which the orthopaedic surgeon may be faced with vascular injuries. The most common of these are complete or incomplete nonviable amputations and open injuries/fractures of the upper or lower extremities. In addition, injuries to major vessels during trauma or reconstructive orthopaedic procedures are known to occur and need to be addressed immediately by the operating team. Prior to the development of microsurgery, vascular surgeons were usually called upon to take over and manage these very serious limb, or even life-threatening injuries. Microvascular repair by an orthopaedic team well-schooled in microsurgical techniques enhances the chances of limb salvage with satisfactory function. With the introduction of the operating microscope and other means of magnification (i.e. loupes) along with micro-instruments and micro-sutures, orthopaedic surgeons were able to achieve successful anastomoses of small vessels less than 1 mm in diameter, including the digital arteries in complete and incomplete nonviable digital amputations [29, 31, 32]. Although the use of microsurgery by orthopaedic surgeons, at least initially, was almost exclusively applied to revascularization and replantation, the growing expertise in microsurgical techniques has evolved towards a role in the management of other traumatic injuries, including type IIIb and IIIc compound fractures.
14.3.2 Basic Principles in Microvascular Surgery Fine work with reliable accuracy is made possible in microsurgery with the aid of an operating microscope or magnifying loupes, and the refined techniques and skills can be acquired only by many hours of practice. In this
regard, training in the laboratory has proven a key factor before a surgeon can make a successful clinical contribution. Before participation in complex cases of complete or incomplete nonviable amputations, surgeons need to demonstrate adequate experience and skills acquired in the laboratory, where devotion of adequate time, practice and patience are prerequisite to performing small vessel anastomosis. Microsurgical procedures are performed on small structures that require magnification. Magnification can be achieved with an operating microscope or ocular loupes. Although several types and models of operating microscopes are currently available, similar general principles apply to the use of most. In general, a magnification of 6× and 10× is used for dissection and exposure of small nerves and vessels, while microsurgical repair of vessels and nerves requires 16× and 25× magnification. While magnification from 16× to 40× is provided by the microscope and is essential when working with structures less than 1 mm in diameter, many procedures may be performed using magnifying loupes of up to 5×. Ocular loupes are invaluable tools for anastomosis of large vessels (diameter 2–3 mm) or for the initial dissection. Microvascular instruments are extraordinarily delicate so as to allow the surgeon to execute very precise procedures. Although a variety of specialized instrumentation exists, for the most part microvascular procedures require three or more straight and curved jeweller’s forceps for manipulating fragile tissues: • Fine suture, microscissors with blunt edges for fine dissection • Microscissors with serrated blades for cutting without crushing the intima of the vessel • Microvascular clamps with a closing pressure of less than 30 g per square millimetre to avoid damaging the vascular intima of small vessels and causing subsequent thrombosis. The patency rate obtained in microvascular anastomosis is dependent upon the skills learned in the laboratory and
624
14.3 Vascular Trauma in Orthopaedic Surgery
Fig. 14.3.1a,b End-to-end microvascular anastomosis. a Once the vessel ends are placed in a bar clamp, the two-stay sutures can be placed 120° apart. A suture is then placed in between the stay sutures in the anterior wall, followed by the even placement of subsequent sutures. The clamped vessel is then turned 180° to show the posterior wall. b A stitch is placed 120° from the initial stay sutures in the posterior wall, followed by evenly spaced sutures in between. Common technical errors during microvascular anastomosis include sutures catching on the back of the vessel, suturing the side wall of the vessel, sutures which are poorly placed and fail to fully penetrate the vessel wall, and uneven spacing of sutures with poor approximation of intima. The figure shows correctly placed sutures
upon careful attention and awareness of factors that influence the success of patency [64]. Minimal, no more than 1–2 mm, advential stripping is recommended in order to visualize the lumen and avoid an excess of adventitia that can invert and occlude the lumen. On the other hand, extensive stripping of the adventitia can lead to necrosis of the advential wall at the anastomosis site (Fig. 14.3.2). Interrupted suturing is the technique of choice in contrast to a running suture that can cause unacceptable constric-
tion of the lumen. A few interrupted sutures are preferable to an excessive number, as the latter may produce increased areas of vessel wall necrosis that could subsequently lead to scar formation and intimal proliferation and necrosis. Furthermore, excessive suturing may cause added deformation of the ends of the vessel, causing exposure of more collagen of the tunica media to blood flow and, in turn, producing clot aggregation and thrombus formation [1]. Suturing of the vessels must be done on healthy tissue and under no tension. In general, correct tension can be indicated by a small loop of suture visible through the opposed vessel walls. In addition, the tension should be such that the suture does not break while knotting. The diameter of this loop should be equal to the thickness of the wall [11]. Although perfusion of the lumen of the vessel is not always necessary since it may induce damage to the intima, irrigation of the edges of the vessel to remove any residual traces of blood is helpful. Once anastomosis has been achieved, patency is evaluated. A simple patency test is to inspect the fullness and pulsation of the vessel or to gently palpate the site of anastomosis. However, the most reliable patency test is the “empty-and-refill” or “milking test” performed by clamping the artery proximal to the anastomosis site with forceps and then milking the vessel distal to the anastomosis site using different forceps, thus creating an empty vessel pocket. Once an empty segment has been obtained, then the proximal forceps are released. If the vessel is patent, then the empty space should show blood flow and rapid filling.
14.3.2.1 Basic Microvascular Techniques End-to-End Microvascular Anastomosis Careful microvascular dissection under magnification is used to expose the selected vessel (Fig. 14.3.1). Magnification by a microscope is required when working with vessels less than 2 mm in diameter, while ocular loupes are valuable for the initial dissection and anastomosis of vessels greater than 2–3 mm in diameter. Proper exposure entails clearing enough room to perform the procedure and to be able to visualize enough of the proximal recipient vessel to verify its condition. Once the loose connective tissue surrounding the vessel has been removed, each end of the vessel is mobilized to obtain an adequate length to approximate both ends with no tension. This can be achieved by ligation of side branches
14.3.2 Basic Principles in Microvascular Surgery
that tether the vessel. The area is continuously irrigated with heparinized lactated Ringer solution throughout the procedure to keep the vessel moist and pliable and to prevent the suturing material from becoming sticky. Adventitia is removed from the vessel ends by circumferential trimming or applying traction to the adventitia, pulling it over the vessel stump and then transecting it (“sleeve amputation”). By doing this, all layers of the vessel wall should be exposed. Upon inspection of the intima under high magnification (25–40×), the vascular wall can be cut until the normal tissue ends appear. Afterwards, the vessel ends can be apposed with a clamp approximator. Interrupted sutures that go through the full thickness of the vessel wall are used. The first two sutures (stay
sutures) are placed about 120° apart on the vessel’s circumference and the ends are left long so that they can be used for traction. Once the clamp approximators are rotated to expose the posterior wall, a stitch 120° from the initial two stitches can be placed. Additional stitches are placed in the remaining spaces. In general, arteries 1 mm in diameter usually need five to eight stitches, while veins need 7 to 10 sutures. Once the anastomosis is complete, the clamp distal to the anastomosis is removed first, followed by the upstream clamp. Some minimal bleeding between stitches is of no concern. A patency test should be performed as described above, and soft tissues are closed over the vessels so as to avoid exposure and drying of the vascular wall.
Fig. 14.3.2a–d Histological examination of the anastomosis site has demonstrated unequivocally that extensive stripping of the adventitia or suturing under tension can seriously damage the vascular wall. a The appearance of the normal lumen in longitudinal section of an intact vessel (the femoral artery of a rabbit) as it appears under the operating microscope. b Histological appearance of the normal vascular wall cytoarchitecture (H&E, 50×). c A longitudinal section of the rabbit femoral artery following incorrect suturing technique with 8-0 suture. Anastomosis under tension and on damaged intima of the vessel result in an abnormal vessel lumen. d The histological picture of the lumen following incorrect suturing technique shows extensive (8 layers) proliferation of the intima (H&E, 50×)
625
626
14.3 Vascular Trauma in Orthopaedic Surgery
End-to-Side Microvascular Anastomosis Dissection and vessel mobilization is performed as for end-to-end anastomosis. Once dissection and mobilization has been done, a small elliptical portion is carefully excised from the recipient vessel using microscissors. The vessel that is to be connected is then cut at a 45° angle. Sutures with long suture ends for traction are placed in the proximal and distal ends of the ellipse of the receiving vessel, followed by placing sutures evenly between the traction sutures. Once anastomosis is complete, the procedures followed are similar to those described above.
Microvascular Vein Suturing and Grafting The techniques used for the suturing of a vein are similar to those applied for suturing of an artery. However, as the vessel wall of the vein is considerably thinner and more frail than that of the artery, great care is necessary in handling the vein wall to avoid tearing. In addition, finer suture material should be used when suturing veins. Vein grafting is performed when end-to-end microvascular anastomosis cannot be performed. In revascularization and replantation procedures, this may also entail bone shortening. There are several candidate veins available for grafts so that the graft can approximate the diameter of the recipient vessel. Close approximation of sizes between vein graft and recipient avoids thrombosis resulting from turbulence. Vein grafts are generally harvested from the upper and lower extremities. Upper extremity veins tend to be more flimsy because of the lower muscle content in the upper extremity vessels, but as a result they also demonstrate fewer spasm problems. The foot and forearm are sources for veins 1–2 mm in diameter, although grafts can frequently be obtained from amputated parts. The graft should be handled minimally during harvesting. When the vein is harvested, the small side branches are either ligated or cauterized with bipolar cautery far from the vein wall. A suture is placed on the proximal end. This provides an arbitrary convention for the surgeon to orient the graft knowing that the blood flow is always in the direction from the unmarked end of the graft towards the end with the suture. For arterial reconstruction using interposition graft, the vein graft should be reversed end from end in order to avoid obstruction of blood flow by the valves in the veins. This is not necessary for venous reconstruction. The suturing technique is similar to that used for end-to-end anastomosis described above, al-
though often size differences in the vessel diameters need to be overcome by cutting the vessel ends obliquely or in a fish-mouth pattern. First the proximal anastomosis is performed, once the vein graft has been gently perfused with heparinized Ringer solution. Afterwards, the distal anastomosis can be performed.
14.3.3 Application of Microvascular Surgery to Trauma Orthopaedics Orthopaedic surgery has witnessed exponential growth in the role of microsurgical techniques to a wide variety of traumatic injuries. Major contributions of microvascular surgery in orthopaedic trauma include revascularization and replantation of complete or incomplete nonviable amputated digits and extremities, type IIIb and IIIc open fractures, as well as free compound tissue transfer.
14.3.3.1 Replantation In 1968, Komatsu and Tamai [30] reported the first successful replantation of an amputated thumb. Since then, innumerable revascularization and replantation procedures for amputated digits have taken place with the indications, procedures and results being assessed in relation to complete and incomplete nonviable amputations, as well as in conjunction with the severity of the injury, the number of the amputated digits, and the various modalities and techniques included in the revascularization and replantation procedures. Today, the accumulated experience has made revascularization and replantation surgery a fairly routine procedure which can be performed in a number of hospitals worldwide, provided that they house surgeons who are well-trained in microsurgical techniques. Well-documented selection criteria have been established to assist the surgeon in screening patient eligibility for replantation. The goal of all revascularization and replantation efforts is targeted not only towards the survival of the amputated part, but mainly towards producing as close as possible normal functional ability. Well-defined selection criteria enable the surgeon to avoid procedures that lead to a surviving, but nonfunctioning part, as well as a plethora of secondary reconstructive procedures [50]. Fundamental to the success in revascularization and replantation is not only a solid microsurgical technique for vascular microanastomosis, nerve coaptation and ten-
14.3.3 Application of Microvascular Surgery to Trauma Orthopaedics
don repair, but also a clear understanding of the selection criteria. At its start, orthopaedic microsurgery focused on replantation. The tendency to replant virtually every amputated part eventually gave way to attempts to define strict selection criteria and optimize the functional results. Today, however, the major concern is not “how to replant an amputated part”, but rather “how to make it functional”. In this regard, revascularization and replantation of amputated parts without sensation and function are no longer considered acceptable [47].
Selection Criteria The surgeon must consider various factors in determining whether to replant an amputated part, including survival of the replanted part and functional outcome. The functional outcome should be superior to that of a prosthesis or revision of the amputation. The criteria which aid the surgeon in predicting outcome can be divided into: (1) those factors related to the type of amputation and its characteristics; and (2) general factors related to the patient. Three main categories of amputations are recognized and graded, based on the viability of the amputated part. Amputations are classified as: (1) complete amputations; (2) incomplete nonviable amputations; (3) incomplete viable amputations. • Complete amputation is defined as full detachment of the amputated part from the proximal stump. • Incomplete nonviable amputation is defined as when all of the major and vital arteries and veins have been severed, however the distal amputated part is connected with the proximal stump with an islet of skin or tendon. The latter are, of course, inadequate to provide the necessary blood supply to the distal part. • Incomplete viable amputations is a grey zone type of amputation which stands true only if, after visualization under the operating microscope, a major feeding artery is intact or some venous return is present. For example, in the case of a digit, if one digital artery is intact or venous return is assisted by an intact piece of skin.
General Indications and Contraindications In addition to selection criteria related to the type, level and severity of the amputation, other general factors re-
lated to the patient need to be considered before replantation is attempted. These include: the age, mechanism of injury, interval between amputation and time of replantation (ischaemic time), patient’s general health, predicted rehabilitation and vocation.
Age
In children, an attempt should always be made to revascularize and replant almost any amputated digit or body part. If the reattached part survives, useful function can be predicted. Although digital replantation in very young patients is technically demanding regarding microanastomosis of digital vessels that are often less than 0.5 mm, we have found good functional results [7]. In contrast, poor nerve regeneration and joint stiffness pose problems for good functional outcome in the elderly. In general, good sensibility, strength and coordination are rarely achieved in the older patient, despite the satisfactory function of the replanted digit.
Mechanism of Injury
Clean-cut “guillotine” type amputations are good candidates for revascularization and replantation. Usually a satisfactory functional result can also be anticipated in minor crush or avulsion amputations that have minimal vascular injury. Severely crushed or avulsed digits or extremities have extensive vascular, nerve and soft tissue damage and the predicted outcome is usually poor. Segmental injuries at multiple levels are usually associated with severe vascular damage, often too extensive to warrant replantation.
Time of Ischaemia
Ischaemia remains a key factor in determining the success of replantation [8]. However, because the duration of ischaemia allowable varies from tissue to tissue, for didactic purposes ischaemia time is divided for digits and major limbs. Since digits consist of mostly skin, bone and subcutaneous tissue and contain no muscles, warm ischaemia is tolerated for a longer period of time. After adequate cooling, we have experienced successful replantation even up to 24 h postinjury and it has been reported up to 36 h. However, major limbs that consist of a high percentage of muscle can tolerate only 4–6 h of ischaemia following amputation. Due to the size of the amputated extremity, even when wrapped and immersed in an ice box for cooling, only the outer section of the amputated
627
628
14.3 Vascular Trauma in Orthopaedic Surgery
part is adequately cooled. The inner muscles remain in relative warm ischaemia and, thus, the allowable 6 h of ischaemia cannot be extended [24].
General Health of the Patient
If the patient has sustained other major life-threatening injuries at the time of trauma, then replantation of digits may need to be postponed or even cancelled. Certain diseases that can adversely affect peripheral circulation, such as diabetes mellitus, some autoimmune diseases, collagen vascular diseases or atherosclerosis, among others, may also produce a condition which contraindicates replantation.
Preoperative Care of the Patient and Amputated Part After other major injuries have been stabilized, bleeding from the stump should be controlled using pressure. The patient should be transported with a pressure dressing and no attempt to ligate or clamp vessels should be made. In cases where bleeding is persistent, a pneumatic tourniquet or cuff can be used. The amputated part, if contaminated during trauma, should be gently rinsed in normal saline or other physiological solutions. The part can then be wrapped with gauze, moistened in normal saline or Ringer’s lactate. The wrapped part should then be placed in a plastic bag and placed on ice. Alternatively, the part can be immersed in normal saline or Ringers lactate in a plastic bag and the bag placed on ice. The latter method is preferable as it is less likely for the part to become frozen by coming in contact with the ice or to be strangled by the wrappings. In incomplete amputations, the amputated part should be left attached to the stump with care taken to avoid rotation or pinching of the soft tissues which might further compromise any remaining flood flow. Sterile gauzes moistened in normal saline should be applied to the stump and amputated part and an ice pack applied to the amputated part. The limb may be supported with padded splints.
Surgical Sequelae and Techniques Simple reattachment of the amputated segment in patients who have sustained complete amputations does not ensure survival of the amputated part. The survival and
function of the replanted part, and in turn the success of the surgery, depend on various parameters and the appropriate management of the specific tissue components. For digit replantation, survival and function of the replanted digit are intimately related to the successful anastomosis of both of the digital arteries, as well as two dorsal veins per patent digital artery (Fig. 14.3.3). The surgical sequelae in replantation may vary somewhat according to the level of the amputation and type of injury. After thorough cleansing and debridement, structures are identified and repair is performed. Structures are repaired serially from the skeletal plane outwards, so that the deeper structures are repaired first, avoiding the sites of vascular anastomosis. In most cases, the repair of digits follows the following operative sequence: (1) tissue debridement; (2) neurovascular identification and labelling in the amputated part and stump; (3) bone shortening and stabilization; (4) extensor tendon repair for digits; (5) arterial anastomoses; (6) venous anastomoses; (7) flexor tendon repair for digits; (8) nerve repair; and (9) soft-tissue and skin coverage. All of the structures are repaired primarily, including nerves, unless a large nerve gap is present which necessitates a secondary nerve grafting procedure. Secondary reconstruction of structures would entail operating through already repaired structures of the replanted part.
Surgical Preparation of Amputated Part and Patient Revascularization and replantation procedures require two teams. One surgical team prepares the amputated part, while the other prepares the patient and the amputated stump. The amputated part is cleaned with normal saline. The part should be kept cool by placing it on a bed of ice draped by a sterile drape sheet and plastic drape. Depending on the size of the amputated part, debridement should be performed using the operating microscope or magnifying loupes. The amputated part is carefully debrided and dissected to expose and identify arteries, veins, nerves, tendons, joint capsule, periosteum and soft tissues, which will save considerable time during replantation later. Once the patient has undergone a complete clinical evaluation, the second team initiates surgical preparation of the patient. Most digital replantations can be performed under axillary brachial plexus block with bupivacaine, a long-acting local anaesthetic. Regional anaesthesia is preferred because of the increased vasodilation and periph-
14.3.3 Application of Microvascular Surgery to Trauma Orthopaedics
Fig. 14.3.3a–c Revascularization and replantation of a complete single digit amputation. a Complete amputation of the right index finger at the level of the middle phalanx slightly distal to the insertion of the flexor digitorum superficialis. b Appearance of the amputated part. c One year postoperative view showing successful revascularization and replantation. Good function of the proximal interphalangeal (PIP) joint was attributed to the intact superficialis
eral blood flow due to the peripheral autonomic block. The stump is first cleansed with an antiseptic, such as povidone-iodine solution, and irrigated with normal saline. Then the stump is debrided and neurovascular structures are identified and labelled with 8-0 or 9-0 nylon under magnification and tourniquet ischaemia. Subcutaneous veins on the stump are often very difficult to locate, but to avoid venous congestion, it is critical that an adequate number of veins are identified for later patent anastomosis. Additionally, the harvesting of veins in the digit is usually tedious, requiring meticulous and gentle dissection. However, once one good vein is located in the subcutaneous layer, it may serve to guide the surgeon to similar veins in the same plane. Another useful guide for finding veins in the stump are small red blood clots. These small thromboses form at the open ends of the veins and can be very helpful for the surgeon in pin-pointing the vein.
the best alternatives in achieving good end-to-end vessel anastomosis on healthy tissue and without tension. In general, the procedure entails the careful resection of the bone ends to ensure ease of approximation of the vessels and nerves with minimal stripping of the periosteum. The amount of bone removed varies according to the type of injury and the level of the amputation. It is usually preferable to remove bone from the amputated part, so that if the replantation fails, length of the stump has not been sacrificed. A greater amount of bone must be removed in an avulsion or crush injury until normal intimal coaptation without tension is possible, as compared to clean-cut or guillotine-type injuries. Excessive bone resection should be avoided in children, as it may result in the excision of, or potential damage to, the epiphyseal plate. Bone resection is followed by osteosynthesis, which allows for the healing of microvascular anastomoses and nerve sutures, as well as repaired tendons.
Bone Shortening and Fixation
Bone shortening almost always proceeds osteosynthesis and vessel anastomosis. Shortening of the digital skeletal framework before replantation appears to be one of
Skin Coverage
Once all of the structures have been repaired, haemostasis is imperative. Then the skin can be loosely approxi-
629
630
14.3 Vascular Trauma in Orthopaedic Surgery
Fig. 14.3.4 Revascularization and replantation of a complete amputation of the distal third of the forearm. a Preoperative view following clean-cut amputation of the distal third of the forearm. One year postoperative views showing successful revascularization and replantation (b) with good flexion (c) and extension
mated with a few interrupted nylon sutures. Potentially necrotic skin is excised and the skin is closed without tension. It is of paramount importance that the anastomosis site is covered, otherwise advential necrosis will ensue, with subsequent thromboses formation. A local flap, split thickness graft, z-plasty, two-stage pedicle flap or free flap may be required to ensure coverage of the anastomosis site, as well as the area of nerve and tendon repair. Fasciotomies are indicated if pressure or constriction occurs.
PostoperativeManagement
The wound should be covered with strips of gauze moistened with antibacterial grease. It is essential that the strips are not placed in a continuous or circumferential manner, which can potentially constrict the replanted digit. A bulky dressing is applied, with the fingertips remaining exposed for clinical observation and temperature probes. Plaster splints are usually applied to the palmar aspect of the hand so that the dorsum can be inspected, but if the flexor tendons have been repaired, the splints need to be placed dorsally to prevent pull of the flexors against the plaster. The extremity is then elevated to avoid oedema. The dressing is left in place for about 2 weeks. However, dressing changes should be done every other day to ensure that dried blood or other materials do not collect,
which can act as a constricting factor on the replanted part.
14.3.3.2 Major Limb Revascularization and Replantation Upper Limb Complete or incomplete nonviable amputations of the wrist or distal third of the forearm are ideal for revascularization and replantation because with success hand function is restored, since both flexion and extension of the digits can be achieved by the proximal uninvolved muscles (Fig. 14.3.4). Good protective sensation of the hand is also readily achieved with primary or secondary repair of the median and ulnar nerves. In contrast, amputations at the upper third of the forearm and level of the elbow are more challenging due to the severity of injury and soft tissue damage. Although above-elbow amputations are easier from the technical perspective as only one artery of large diameter (brachial) needs to be anastomosed, they are associated with extensive bone, muscle and nerve damage. This makes the preoperative evaluation and management more demanding and postoperative treatment more difficult with a high rate of infection.
14.3.3 Application of Microvascular Surgery to Trauma Orthopaedics
In addition, nerve recovery has a relatively low potential at this level, requiring multiple reconstructive procedures to provide functional use to the extremity. Amputations at the shoulder level are more severe than global brachial plexus injuries and a detailed evaluation taking into account various factors has to be considered before replantation can be attempted.
osteomyelitis, restrictive joint motion, foot deformity secondary to Volkman contracture, and plantar trophic ulcers because of inadequate nerve regeneration. For these reasons and since prosthetic devices, particularly for below-knee amputations, are able to achieve excellent rehabilitation, replantation of lower limbs should be considered carefully.
Lower Limb
Replantation in Children
In general, lower limb replantation is met with a lower rate of success compared to upper limb replantation. This is because most of these injuries are related to motor vehicle accidents which tend to be more serious in nature (Fig. 14.3.5). Severe tissue avulsion, multiple level damage and heavy contamination of the wounds usually characterize these amputations, which weaken the indications for replantation. Early complications include extensive blood loss, possible acidosis, renal insufficiency, infection and systemic toxicity. Late complications are related to considerable bone shortening, bony nonunion, chronic
The selection criteria applied to adults do not always apply to children, since in virtually all cases an attempt at revascularization and replantation in children should be made [5]. Children have a higher regenerative potential in as far as peripheral nerves are concerned. The only contraindication for attempts at replantation in children are severely damaged and/or mutilated parts, when the general condition of the child may prohibit a long surgical procedure or when other systemic injuries are present.
Postoperative Management
Fig. 14.3.5a,b Revascularization and replantation of an incomplete nonviable amputation of the foot. a Preoperative view showing relatively clean-cut incomplete nonviable amputation of the distal third of the leg. b Nine-month postoperative view showing successful revascularization and replantation
Careful postoperative management is essential for a successful outcome. The patient’s vital signs and vascularity of the area should be monitored continuously. The room should be warm, as cooling can lead to cold-induced vasospasm. In addition, the patient should be left in a quiet room with limited visitations, to avoid stress-induced vasospasm. Cigarette smoking by the patients and visitors is strictly forbidden, as nicotine is a potent inducer of vasospasm. Finally, cold drinks, as well as those with caffeine are restricted. Broad-spectrum antibiotic (cephalosporins) are generally indicated for 5–10 days for patients with open injuries. The parenteral or oral route, and the duration of antibiotic treatment depend upon the patient’s clinical situation. For vessel repair in open injuries, antibiotic administration is considered therapeutic and the duration of administration can be somewhat longer. Sharp lacerations of vessels usually require minimal anticoagulant therapy. In contrast, high energy crush or avulsion-type injuries with extensive vessel damage depend upon adequate anticoagulant therapy for better patency. Among the agents commonly used are heparin, aspirin and low molecular weight dextran (Dextran 40) [69]. Usually, heparin is administered intraoperatively from the time that the initial anastomosis is performed
631
632
14.3 Vascular Trauma in Orthopaedic Surgery
until the dressing is applied. A dose of 2500–5000 units of heparin is given immediately after removal of the clamp per anastomosed artery. The role of heparin has diminished over the years, as it has become clear that patency is more a factor of suturing on healthy tissue and without tension. The use of heparin postoperatively is also avoided because of potential excess bleeding. Several methods of monitoring after microvascular surgery have developed over time. Regardless of the method used, the most valuable and essential tool is regular clinical evaluation by the surgeon and nurses. Clinical evaluation should include colour, capillary refill, temperature and turgor. Clinical evaluation should be performed continuously for the first 3 days postoperatively. Skin temperature monitoring probes have been found the simplest and most reliable adjunct to clinical evaluation. Continuous temperature monitoring is now widely used to assess temperature changes in replanted digits and vascularized free flaps. This method, which assesses the changes in relative and absolute temperature, requires three probes, one each being placed on the revascularized area, the normal adjacent area and the dressing. If the temperature of the revascularized area drops below 30°C or differs by more than 3°C from the adjacent normal tissue, then vascular compromise is likely present.
require the vascular anastomosis to be redone or even the insertion of a vein graft. Venous congestion can be effectively relieved with the use of medicinal leeches.
Late and Chronic Complications
Although late complications due to infection are fairly frequent in digital replantations, they rarely result in the loss of the replanted part. Pin tract infections are the most common and occur about 4 weeks after surgery. They can be managed by pin removal and administration of antibiotics. The most common chronic complications include cold intolerance, tendon adhesions and malunion. • Cold intolerance is a common complaint in patients with digital replantation. It is related to the adequacy of digital reperfusion, and provides an argument for maximizing the number of arteries repaired. Cold intolerance improves over time. • Tendon adhesions are frequent, resulting in limited motion. In severe cases, tenolysis or a two-staged tendon reconstruction can be performed after a few months.
Management of Venous Congestion with Leeches
Complications Acute Complications
Inadequate perfusion is responsible for acute complications. When signs of inadequate perfusion are present, postoperative efforts must be intensified to improve the chances of survival. In difficult replantations, heparin may be beneficial. If a catheter is present, a regional sympathetic block may help alleviate vasospasm. Decreased skin temperature, loss of capillary refill, diminished turgor and or abnormal colour in the immediate postoperative period indicate that the replanted digit is in jeopardy. Following most microvascular procedures used in replantation, the rule of thumb is that when the part or area has developed pallor and loss of turgor (e.g. the area is pale with loss of capillary refill), then arterial insufficiency is present. In contrast, when the area is cyanotic, congested and turgid, then venous insufficiency is present. If the problem is minor, it sometimes can be managed without having to re-operate. Otherwise the anastomosis site needs to be evaluated surgically, to determine if there is thrombosis formation at the anastomosis site, which may
Venous congestion is a frequent and significant problem of various microsurgical procedures, including revascularization and replantation, as well as free skin flaps. Venous congestion can be the result of various factors including an inadequate anastomosis of a vein, an effect secondary to arterial insufficiency, venous spasm, venous occlusion and the absence of venous repair. It has been generally recognized that venous congestion and engorgement can potentially lead to necrosis of the replanted part or flap. In fact, clinical experience indicates that necrosis, particularly in flaps, is more frequently associated with venous congestion than arterial insufficiency. The major therapeutic effect of the leech is the relief of venous congestion. Recent recognition of the clinical efficacy of leech, in this regard, has produced a continuous increase in its use [2, 15–17, 23, 43, 49, 52, 58].Overall, venous insufficiency is the most important indication for leeching. A state of venous insufficiency can be recognized by the bluish colour of the tissue, as well as by tissue tension and oedema. In our experience, the leech was effective in the treatment of venous congestion in skin flaps and trauma, in the treatment of venous insufficiency following replantation of digits and hands, and in distal phalanx
14.3.3 Application of Microvascular Surgery to Trauma Orthopaedics
Fig. 14.3.6a–c Vascularized tensor fascia lata flap was used to cover a large pelvic defect in a young male patient. a Postoperative view showing that the flap is extremely cyanotic, oedematous, indicative of venous congestion secondary to insufficient venous drainage. b Rapid improvement of the appearance of the flap was noted after the application of leeches. c The flap was successfully salvaged over its entire surface
replantation without venous drainage due to the absence of adequate veins for anastomosis. The effectiveness of leech therapy becomes particularly apparent in view of
the extremely rapid change in colour of an engorged flap following the application of the leech (Fig. 14.3.6). Relief is accomplished both immediately with the decongestion that is produced while the leech is attached, and afterwards due to the continued flow of blood from the site of attachment. Bleeding can continue from the wound for as long as 24–48 h. Ultimately, the venous decongestion produced by leeching acts to prevent any potential arterial occlusion. The earlier that the diagnosis of venous congestion is made, the better the result. Although medicinal leeches appear to be an effective method for treating venous insufficiency following certain microsurgical procedures, it should be noted that alternative methods are also available to the surgeon. These include revision of the venous anastomoses, as well as wound decompression by incisions in patients who have undergone revascularization/replantation or by removal of the stitches in free flaps, and by maintaining egress by stimulating the flow of blood with the aid of heparinized gauzes to wipe the area. The most significant contraindication to leeching is arterial insufficiency. It should be noted that in cases of arterial insufficiency the leech does not attach. Due to the relative increased risk of bacterial infection, immunosuppressed patients are also not considered appropriate candidates for leech therapy [66]. Thus, patients who are in an immunodeficient state, either primary or secondary to immunosuppressive drug therapy, should have venous congestion treated with an alternative method. The application of leeches can potentially result in a significant loss of blood. The amount of blood lost is dependent upon the number of leeches applied and the duration of their use. However, the continuous oozing of blood from the site of attachment makes it difficult to precisely measure the total amount of blood loss due to the leech. In general, although each leech consumes only about 5–15 ml, from the subsequent oozing from the leech bite, each leech induces about 50 ml blood loss. In this regard, it is essential to closely monitor the vital signs of the patient, as well as perform frequent blood and laboratory tests, since any drop has detrimental effects not only for the patient, but also for the survival of the free flap and reattached part. Hence, the use of leeches can result in a significant loss of blood which is directly dependent upon the number of leeches applied and the duration of their use [13, 52, 55]. The use of medicinal leeches can have various complications [66]. These include persistent bleeding, anaphylaxis and local allergic reactions to biologically active
633
634
14.3 Vascular Trauma in Orthopaedic Surgery
substances within the leech‘s saliva, the transmission of viral-borne infections and excessive scaring from the leech bites. In our own experience, we have noted no significant complications that could be associated with leech therapy [52, 55]. Although the risk of infection is always there, in our experience the use of leeches has not been associated with infection in any patients. Studies indicate that Aeromonas hydrophila is a predominant leech enteric organism that is responsible for digestion [67], and that there is always the concern for infection [34, 48]. However, it should be noted that leeches have been increasingly used without report of infection problems. According to some reports, the incidence of infection ranged from 0% to 20% [40]. We have found that when patients are treated with a combination of aminoglycosides and third-generation cephalosporin antibiotics for prophylaxis infections can be effectively avoided. Another factor that may contribute to the lack of infection is the use of each leech only once [52, 55]. Furthermore, the continuous bleeding following the application of the leech may act to rinse the wound and, thus, play a role in limiting infection. Overall, leeches have been found to be effective in the treatment of venous congestion following microsurgical procedures such as replantations and free skin flaps. Since venous engorgement is a frequent cause of necrosis, the efficacy of leech therapy is of clinical significance where their application can avoid expected partial or complete loss of the replanted part or flap. The usefulness of the leech appears to be related to not only the immediate removal of congested venous blood, but also to the continuous flow of blood which ensues, as well as the local state of anticoagulation produced by the antithrombotic agent hirudin.
14.3.3.3 Open Fractures – Type IIIb and IIIc Open type IIIb and especially type IIIc fractures of the upper and lower extremities are extremely severe injuries that can often lead to amputation of a limb. These types of fractures are usually caused by high energy impact, resulting in extensive bony communition or segmental bone loss, as well as severe soft tissue injury including extensive skin loss, tendon and nerve damage, muscular and periosteal stripping from the bone, and severe circulatory compromise secondary to heavy trauma of the major vessels. The gravity of this fracture is emphasized by the high rate of amputation, which has been reported
to occur from 60% up to 100% [44, 68]. Today, efforts are no longer aimed at simply salvaging the limb that has sustained a serious compound injury, but rather at producing a functional extremity free of pain which has, at the very least, protective sensation. The functional outcome and success of preserving a limb following the treatment of these severe open fractures depends on several variables. These include the extent and severity of vascular injury, the extent of bony and soft tissue injury, the duration and type of ischaemia to the limb, the patient’s age, time since the initial injury and finally any concomitant organ injuries which may be present [20, 21]. Microsurgical techniques with the use of vein grafts are able to restore arterial blood flow in the injured limbs and, thus, contribute to salvaging the limb. On the other hand, microsurgical methods, such as free flaps, vascularized bone grafts and nerve grafting, utilized in the secondary reconstructive procedures have helped tremendously in achieving better results and in improving the functional outcome of the severely injured extremity, as well as diminishing the need for secondary amputation. Thus, microsurgery plays a decisive role in augmenting the treatment of open type IIIb and IIIc fractures by: (1) restoring the circulation of the injured extremity; and (2) improving the function of the limb using free tissue transfers such as nerve grafts, free skin flaps and vascularized bone grafts [60]. The treatment for patients with types IIIB and IIIC open fractures is an extremely demanding procedure that requires a highly specialized medical team and a hospital centre with outstanding emergency and surgical facilities. Even with today’s sophisticated scoring systems for evaluating the extent of injury, it still is difficult for the surgeon to determine which limb to preserve and which to amputate [26]. Mangled extremity syndrome and the mangled extremity severity scores are scoring systems designed to aid in the decision-making process by predicting the viability and salvageability of the mangled limb part [19, 22, 60]. For open fractures of the lower extremity, the combination of damage to both posterior and anterior tibial arteries and popliteal arteries at the trifurcation level that is often seen in open tibial fractures bears the worst prognosis [28]. In our own experience, none of our patients with open type IIIB injuries have undergone amputation [60]. This must be attributed, at least in part, to the use of microsurgical techniques which permit better restoration of arterial damage, and to the fact that most of our cases
References
involved isolated arterial injuries, which are know to have a better prognosis [39]. The use of vein grafts is a timeconsuming procedure, as it doubles the surgical time for vascular anastomosis. However, vein grafting does offer the benefit of doing the vessel anastomoses without tension and on healthy intima. Microsurgical techniques and the use of vein grafts to restore arterial blood flow in the injured extremities are also related to the relatively high rate of limb salvage in patients with type IIIC injuries. Microsurgical skills applied in secondary reconstructive procedures such as free flaps, vascularized bone grafts and nerve grafting help achieve better results and to improve the functional outcome of the severely injured extremity. Microsurgery aids the treatment of these injuries by improving the circulation of the injured extremity using fine surgical techniques, restoring limb function, and solving other complex problems such as replacing unstable scar tissue with free skin flaps.
14.3.4 Vascular Complication in Orthopaedic Patients Damage to major arterial structures during various orthopaedic procedures related to both trauma and reconstruction is well-known and has been documented extensively in the orthopaedic literature [4, 12, 14, 37, 45, 46, 57]. Injuries to the major vessels may be of several types, involving either partial or complete interruption of normal blood flow. They can be the product of continuous pressure resulting in thrombosis or false aneurysm [3] or the result of acute complete or partial laceration from a sharp instrument, such as a surgical scalpel, resulting in massive bleeding [14, 46]. These are very serious intraoperative vascular injuries that may not only jeopardize the viability of a limb, but even the life of the patient. In all cases, further injury is related to some extent to varying degrees of ischaemia and local bleeding. The orthopaedic surgeon should be aware of potential complications inherent to the procedure that they are performing. This along with solid knowledge of the anatomy of the area is the best preventive factor. In the face of these serious complications, however, the orthopaedic surgeon must have the skills to recognize and manage the emergency promptly. If there is any doubt concerning the extent of the arterial complication, a thorough clinical examination of the viability of the limb should
be performed without hesitating to use objective testing controls, such as the Doppler ultrasound or contrast media for intraoperative arteriography. No matter what the severity of the complication, if it is treated promptly and correctly, the devastating potential for limb or lift loss can be successfully avoided. There are various vulnerable anatomical sites susceptible to vascular complications during orthopaedic procedures [57]. Among these include major vessels, for example the femoral artery or popliteal artery which are susceptible to injury during reconstructive surgical procedures, such as total arthroplasties or osteotomies of the hip and knee, respectively. Surgical management of pseudoarthrosis or heterotopic ossification around the hip, knee or elbow joint is also associated with a high risk of vascular injury. Prior to the development of microsurgery, vascular surgeons were usually called upon to take over and manage these very serious intraoperative complications by repairing the damaged vessel either by end-to-end anastomosis or interposition of a vein graft. Today, these serious vascular complications during orthopaedic procedures can be met with a successful outcome when there is immediate recognition of the complication, and when there is an orthopaedic surgeon present who is well-trained in microsurgical techniques who is able to immediately mange the emergency. The presence of a vascular surgeon or an orthopaedic surgeon trained in microvascular technique represents an invaluable attribute to the orthopaedic team, and minimizes, if not eliminates, the potentially disastrous outcome from serious intraoperative vascular complications. References 1. Acland RD (1973) Thrombus formation in microvascular surgery: an experimental study of the effects of surgical trauma. Surgery 73:766–771 2. Batchelor AGG, Davison P, Sully L (1984) The salvage of congested skin flaps by application of leeches. Br J Plast Surg 37:358–360 3. Bauer R, Kershbaumer F, Poisel S (1987) Operative approaches in orthopaedic surgery and traumatology. Georg Thieme, New York, pp 90–118 4. Bergovist D, Carlsson AS, Ericsson BF (1983) Vascular complications after total hip arthroplasty. Acta Orthop Scand 54:157–163 5. Beris AE, Soucacos PN, Malizos KN, Mitsionis GJ, Soucacos PK (1994) Major limb replantation in children. Microsurgery 15:474–478
635
636
14.3 Vascular Trauma in Orthopaedic Surgery
6. Beris AE, Soucacos PN, Malizos KN, Xenakis TA (1994) Microsurgical treatment of ring avulsion injuries. Microsurgery 15:459–463 7. Beris AE, Soucacos PN, Malizos KN (1995) Microsurgery in children. Clin Orthop 314:112–121 8. Brunelli G (1988) Experimental studies of the effects of ischemia on devascularized limbs. In: Brunelli G (ed) Textbook of microsurgery. Masson, Milan, pp 89–99 9. Buncke HJ, Buncke CM, Schulz WP (1966) Immediate Nicoladoni procedure in the Rhesus monkey or halluxto-hand transplantation utilizing microminiature vascular anastomoses. Br J Plast Surg 19:332–337 10. Chen ZW, Chen LE (1987) Treatment of congenital tibial pseudarthrosis using free vascularized fibular grafts. In: Urbaniak JR (eds) Microsurgery for major limb reconstruction. Mosby, St. Louis, pp 303–307 11. Daniller A, Strauch B (1976) Symposium on microsurgery. Mosby, St. Louis 12. Dorr LD, Conaty JP, Kohl R, Harvey JP (1974) False aneurysm of the femoral artery following total hip surgery. J Bone Joint Surg 56A:1059–1062 13. Engemann JF, Hegner RW (1981) Phylum annelida, class III: Hirudo medicinalis – the medical leech. Invertebrate zoology, 3rd edn. MacMillan, New York, pp 420–426 14. Fortune WP (1994) Complication of hip and knee osteotomies. In: Eipps CH (ed) Complications in orthopaedic surgery. JP Lippincott, Philadelphia, pp 1219–1237 15. Foucher G (1980) Un vieux remede dans un pot neuf: la sangue en microchirurgie. Communication a la Siezieme Rencontre International de Microchirugie, GAM Marseille, Grance, 14–17 May 16. Foucher G, Henderson HR, Maneau M, Braun FM (1981) Distal digital replantation: one of the best indications for microsurgery. Int J Microsurg 3:263–270 17. Foucher G, Merle M, Braun JB (1981) Distal digital replantation is one of the best indications for microsurgery. Int J Microsurg 3:263–270 18. Gilbert AL, Razaboni RM (1988) Free vascularized bone transfer in children. In: Brunelli G (ed) Textbook of microsurgery. Masson, Milan, pp 361–368 19. Gregory RT, Gould RJ, Peclet M et al (1985) the mangled extremity syndrome (MES): a severity grading system for multisystem injury of the extremity. J Trauma 25:1147–1150 20. Gustilo RB, Anderson JT (1976) Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg Am 58(4):453–458
21. Gustilo RB, Mendoza RM, Williams DN (1984) Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma 24(8):742–746 22. Helfet CK, Howey T, Sanders R et al (1990) Limb salvage versus amputation: preliminary results of the mangled extremity severity score. Clin Orthop 256:80–86 23. Henderson HP, Matti B, Laing AG, Morelli S, Sully L (1983) Avulsion of the scalp treated by microvascular repair. The use of leeches for postoperative decongestion. Br J Plast Surg 36:235 24. Hidalgo DA, Shaw WW, Colen SR (1987) Upper limb replantation. In: Shaw WW, Hidalgo DA (eds) Microsurgery in trauma. Futura, New York, pp 71–88 25. Hunter JM (1984) Staged flexor tendon reconstruction. In: Hunter JM, Schneider LH, Mackin EJ, Callahan AO (eds) Rehabilitation of the hand. Mosby, St. Louis, pp 288–313 26. Ingram RR, Hunter GA (1993) Revascularization, limb salvage and or amputation in severe injuries of the lower limb Curr Orthop 7:19–25 27. Jacobson JH, Suarez EL (1960) Microsurgery in anastomosis of small vessels. Surg Forum 11:243–245 28. Katzman SS, Dickson K (1992) Determining the prognosis for limb salvage in major vascular injuries with associated open tibial fractures. Orthop Rev 21:195–199 29. Kleinert HE, Kasdan ML, Romero JL (1963) Small blood vessel anastomosis for salvage of the severely injured upper extremity. J Bone Joint Surg Am 45A:788–796 30. Komatsu S, Tamai S (1968) Successful replantation of a completely cut-off thumb: case report. Plast Reconstr Surg 42:374–377 31. Kutz JE, Hay EL, Kleinert HE (1969) Fate of small vessel repair. J Bone Joint Surg Am 51A:791 32. Lendvay PG (1968) Anastomosis of digital vessels. Med J Aust 2:723–724 33. Leung PC (1985) Thumb reconstruction using second-toe transfer. Hand Clinics 1:285–295 34. Lineaveaver WC, Hill MK, Buncke GM et al (1992) Aeromonas hydrophila infections following use of medicinal leeches in replantation and flap surgery. Ann Plast Surg 29:238–244 35. Malizos KN, Beris AE, Kabani CT, Korobilias AB, Mavrodontidis AN, Soucacos PN (1994) Distal phalanx microsurgical replantation. Microsurgery 15:464–468 36. Malizos KN, Soucacos PN, Beris AE, Korobialias A, Xenakis TA (1994) Osteonecrosis of the femoral head in immunosuppressed patients: hip salvaging with implantation of avascularised fibular graft. Microsurgery 15:485–491
References
37. Mallory TH (1972) Rupture of the common iliac vein from reaming the acetabulum during total hip replacement. A case report. J Bone Joint Surg 54A:276–277 38. Malt RA, McKhann CF (1964) Replantation of severed arms. J Am Med Assoc 189:716–722 39. McNamara MG, Heckman JD, Corley FG (1994) Severe open fractures of the lower extremity: a retrospective evaluation of the mangled extremity severity score (MESS). J Orthop Trauma 8:81–87 40. Mercer NSG, Beere DM, Bornemisza AJ, Thomas P (1987) Medicinal leeches as sources of wound infection. Br Med J 294–937 41. Merle M, Dap F, Bour C (1991) Digital replantation. In: Meyer VE, Black MJM (eds) Microsurgical procedures. Churchill Livingstone, London, pp 21–35 42. Morrison WA, O’Brien BMcC, MacLeod AM (1980) Thumb reconstruction with free neurovascular wrap around flap form the big toe. J Hand Surg 5:575–583 43. Mutimer KL, Banis J, Upton J (1987) Microsurgical reattachment of totally amputated ears. Plast Reconstr Surg 79:535–540 44. Ritchie AJ, Small JO, Hart NB, Mollan RA (1991) Type III tibial fractures in the elderly: results of 23 fractures in 20 patients. Injury 22(4):267–270 45. Scullin JP, Nelson CL, Beven EG (1975) False aneurysm of the left external iliac artery following total hip arthoplasty: report of a case. Clin Orthop 113:145–149 46. Shaw JA, Greer RB (1994) Complications of total hip replacement. In: Eipps CH (ed) Complications of orthopaedic surgery. JB Lippincott, Philadelphia, pp 1013–1056 47. Shaw WW, Hidalgo DA (1987) Replantation: general consideration. In: Shaw WW, Hidalgo DA (eds) Microsurgery in trauma. Futura, New York, pp 59–70 48. Snower DP, Ruef C, Kuritza AP, Edberg SC (1989) Aeromonas hydophila infection associated with the use of medical leeches. J Clin Microbiol 27:1421–1422 49. Song R, Gao Y (1982) The forearm flap. Clin Plast Surg 9:21–26 50. Soucacos PN (1995) Microsurgery in orthopaedics. In: Casteleyn PP, Duparc J, Fulford P (eds) European instructional course lectures, Vol. 2. Editorial, Society of Bone and Joint Surgery, London, pp 149–156 51. Soucacos PN (1995) Two-stage flexor tendon reconstruction using silicone rods. In: Vastamaki M (ed) Current trends in hand surgery. Elsevier, Amsterdam, pp 353–357
52. Soucacos PN, Beris AE (2002) Management of venous congestion in trauma and reconstructive microsurgery: the significance of medicinal leeches. In: Schuind F, de Fontaine S, Van Geertruyden J, Soucacos PN (eds). Advances in upper and lower extremity microvascular reconstruction. World Scientific, London, pp 34–40 53. Soucacos PN, Beris AE, Xenakis TA, Malizos KN, Touliatos AS (1992) Forearm flap in orthopaedic and hand surgery. Microsurgery 13:170–174 54. Soucacos PN, Beris AE, Malizos KN, Touliatos AS (1994) Bilateral thumb amputation. Microsurgery 15:454–458 55. Soucacos PN, Beris AE, Malizos KN, Kabani CT, Pakos S (1994) The use of medicinal leeches, Hirudo medicinalis, to restore venous circulation in trauma and reconstructive microsurgery. Int Angiol 13:319–325 56. Soucacos PN, Beris AE, Malizos KN, Vlastou C, Soucacos PK, Georgoulis AD (1994) Transpositional microsurgery in multiple digital amputations. Microsurgery 15:469–473 57. Soucacos PN, Beris AE, Malizos KN, Xenakis TH (1995) Vascular complications in orthopaedic patients treated by orthopaedic microsurgeons. Int Angiol 14:303–306 58. Soucacos PN, Beris AE, Touliatos AS, Korobilias AB, Gelalis J, Sakas G (1995) Complete versus incomplete nonviable amputations of the thumb: comparison of the survival rate and functional results. Acta Orthop Scand [Suppl 264] 66:16–18 59. Soucacos PN, Beris AE, Touliatos AS, Vekris M, Pakos S, Varitimidis S (1995) Current indications for single digit replantation. Acta Orthop Scand [Suppl 264] 66:12–15 60. Soucacos PN, Beris AE, Xenakis TA, Malizos KN, Vekris MD (1995) Open type IIIb and IIIc fractures as treated by an orthopaedic microsurgical team. Clin Orthop 314:59–66 61. Touliatos AS, Soucacos PN, Beris AE, Zoubos AB, Koukoubis TH, Makris H (1995) Alternative techniques for restoration of bony segments in digital replantation. Acta Orthop Scand [Suppl 264] 66:19–22 62. Urbaniak JR (1985) Wrap-around procedure for thumb reconstruction. Hand Clinics 1:259–269 63. Urbaniak JR (1987) Digital replantation: a 12-year experience. In. Urbaniak JR (ed) Microsurgery for major limb reconstruction. Mosby, St. Louis, pp 12–21 64. Urbaniak JR, Soucacos PN, Adelaar RS, Bright DS, Whitehurst LA (1977) Experimental evaluation of microsurgical techniques in small artery anastomoses. Orthop Clin N Am 8:249–263 65. Urbaniak JR, Roth JH, Nunley JA, Goldner RD, Koman A (1985) The results of replantation after amputation of a single finger. J Bone Joint Surg 67A:611–619
637
638
14.3 Vascular Trauma in Orthopaedic Surgery
66. Wells MD, Manktelow RT, Boyd JB, Bowen V (1993) The medical leech: an old treatment revisited. Microsurgery 14:183–186 67. Whitlock MR, O’Hare PM, Sanders R, Marrow NC (1983) The medicinal leech and its use in plastic surgery: a possible cause for infection. Br J Plast Surg 36:240
68. Zehntner MK, Petropoulos P, Burch H (1991) Factors determining outcome in fractures of the extremities associated with arterial injuries. J Orthop Trauma 5(1):29–31 69. Zoubos AB, Soucacos PN, Seaber AV, Urbaniak JR (1994) The effect of heparin after microvascular repair in traumatically damaged arteries. Int Angiol 13(3):245–249
639
14.4 Treatment of Aortic Arch Diseases Chris Rokkas, Dimitrios Angouras, Themistocles Chamogeorgakis, Fotios Mitropoulos, Ioannis Toumpoulis, Sotiris Stamou, Constantine Anagnostopoulos
14.4.1 Aortic Arch Aneurysms in Coarctation of the Aorta 14.4.1.1 Epidemiology/Aetiology • Aortic aneurysm formation is a well-documented complication in patients with coarctation of the aorta, whether untreated or treated. • Patients not undergoing surgical or interventional treatment may develop aneurysms of the ascending aorta, possibly involving the aortic arch. This is probably the manifestation of inherent aortic wall abnormalities. • A bicuspid aortic valve (present in 85% of these patients) is well known to be associated with aortic pathology and has been confirmed as an independent predictor of ascending aortic aneurysm in this patient population. • Moreover, coarctation patients typically have proximal arterial hypertension, which causes increased haemodynamic stress on the aortic wall and predisposes to aneurysm formation, rupture and aortic dissection. • As a result, approximately 20% of adults with coarctation will die from spontaneous rupture of the aorta if left untreated. • Close supervision of patients with bicuspid aortic valves and ascending aortic dilatation is mandatory to prevent such catastrophic complications. • Patients who have undergone surgical repair may also develop postoperative aneurysms in the region of the aortic isthmus. These aneurysms are usually asymptomatic but are associated with a 36% mortality rate if left untreated. They can be true or false and may involve the distal aortic arch. • Their incidence varies and depends on a number of factors, i.e. the time of operation, age at the time of surgery, the postoperative interval and the surgical technique employed.
• Although all types of surgical repair have the risk of aneurysm formation, prosthetic Dacron patch aortoplasty has been historically associated with the highest incidence (up to 39%) of this complication. • In the initial descriptions of the procedure, the posterior coarctation membrane or fibrous shelf was excised. This manoeuvre was later found to be a significant predisposing factor for development of true aneurysms and it is now discouraged. It also appears that the risk of aneurysm formation is higher for patients operated on at >13.5 years of age, for patch aortoplasty of recoarctation following resection with end-to-end anastomosis, and for patients with coarctation associated with transverse arch hypoplasia. • Recent series using PTFE for the patch have not reported any aneurysm in a short follow-up period. • Aneurysm formation also complicates balloon angioplasty. Disruption of the intima and morphologically distorted elastic media in the precoarctation and postcoarctation aortic segments are probably causally connected with this complication. • Dilatation of native adult coarctation is particularly associated with aneurysm formation, the reported incidence varying from 4% to 42%. As a result, most centres do not routinely utilize angioplasty in the management of native coarctation. Aneurysms may develop either immediately after angioplasty or after several months, hence close follow-up is essential. On the other hand, balloon angioplasty may be the preferred approach for recurrent coarctation following surgical repair. • Due to the apparent protective effect of the fibrous perivascular surgical scar, aneurysm formation is a rather infrequent complication (0–5%) in this setting.
640
14.4 Treatment of Aortic Arch Diseases
14.4.1.2 Treatment
14.4.2.4 Symptoms
• Postoperative or post-angioplasty coarctation site aneurysms are repaired with resection and insertion of a tubular prosthesis via a left thoracotomy using femoral arteriovenous or left atriofemoral by-pass. • An up to 14% in-hospital mortality rate and morbidity from paraplegia, central neurologic deficits, or bleeding should be anticipated. • Should the distal aortic arch be involved or difficulty in applying a proximal clamp be encountered, circulatory arrest allows for an accurate and safe repair. • Some patients may require additional graft repair of the left subclavian artery. • Recently, percutaneous endovascular repair with stent grafts has been applied successfully and may prove to be an effective alternative therapeutic method.
• Clinical presentation is similar to that of aortic dissection, with chest or intrascapular back pain predominating. • Patients are typically elderly (mean age, 67–72 years), older than those with aortic dissection.
14.4.2 Intramural Haematoma
14.4.2.5 Diagnosis Recommended European Standard Diagnostic Steps of Investigation The following diagnostic studies are utilized: • Transoesophageal echocardiography (TEE) • Magnetic resonance imaging (MRI) • Spiral computed tomography (CT).
Additional Useful Diagnostic Procedures
14.4.2.1 Synonyms •
Medial haematoma.
14.4.2.2 Definition • Aortic intramural haematoma (IMH) is considered a variant of aortic dissection. • It is defined as a spontaneous haematoma within the aortic wall in the absence of intimal disruption.
14.4.2.3 Epidemiology/Aetiology • Aortic IMH is apparently generated by rupture of the intramural vasa vasorum although the underlying pathogenetic process is still vague. • A history of hypertension is present in the vast majority of patients. Other traditional risk factors for aortic dissection, such as bicuspid aortic valve or Marfan’s syndrome, are uncommon. • The exact incidence is unknown, as IMH has been frequently underdiagnosed. However, with the routine utilization of newer imaging techniques, IMH has been increasingly recognized and several clinical series have shown that 13–27% of patients with a diagnosis of aortic dissection in fact have IMH.
• Aortography, rarely reveals the presence of IMH. • If intravascular ultrasound (IVUS) is used as an adjunct to aortography, diagnostic accuracy is enhanced but the exact role of this new diagnostic modality remains to be defined.
14.4.2.6 Treatment Conservative Treatment • The medical treatment should be started upon clinical suspicion and continued in the intensive care unit. • The main goals of medical treatment are the effective and immediate reduction of: (1) the mean arterial pressure and (2) the rate of myocardial fibre shortening and rise of the arterial pulse (dp/dt). • This so-called “anti-impulse” therapy consists of intravenous administration of β-blockers. Esmolol, a cardioselective β-blocker with ultrashort half-life, is frequently used in this setting, as it is very rapid and easily titratable (infusion rate 25–300 μg/kg per min). Propranolol (2–5 mg IV q4–6 h) or labetolol (α1-/β1blocker) can also be used. • If blood pressure is not adequately controlled, sodium nitroprusside can be added (0.5–5.0 μg/kg per min), but only after adequate β-blockade has been achieved
14.4.3 Obstructed Aortic Arch
because if administered alone it will increase rather than decrease dp/dt.
• Therefore, there is a tendency for more aggressive treatment of proximal IMH.
Surgery • Further management of proximal IMH is still controversial. On account of its frequent progression to aortic dissection or rupture, most authors recommend early aggressive surgical management [77]. • For arch IMH, this consists of aortic arch replacement using deep hypothermic circulatory arrest. Others, however, emphasize the feasibility of initial medical management with frequent follow-up studies, leading to timed surgical repair. • With this therapeutic strategy, only 30% of patients undergo urgent surgical repair and about 50% are treated medically alone [45]. • Initial haematoma thickness <11 mm and a normal aortic diameter in the acute phase have been identified as predictors of IMH regression without complications and such patients may benefit from a more conservative management.
14.4.3 Obstructed Aortic Arch 14.4.3.1 Synonyms •
Interrupted aortic arch.
14.4.3.2 Epidemiology/Aetiology
Differential diagnosis needs to be made from: • Aortic aneurysm with associated thrombus • Dissection with thrombosed false lumen • Severe aortic atherosclerosis, with or without penetrating aortic ulceration.
• This is a rare congenital cardiovascular defect (0.2– 1.4% of all congenital cardiac defects) characterized by complete loss of luminal continuity between ascending and descending aorta. • The male-to-female ratio is 1:1. • As originally described by Celoria and Patton [7], obstructed aortic arch (OAA) is classified into three types based on the site of obstruction in relation to the origin of the brachiocephalic vessels: (1) type A (25–35%) – obstruction distal to the left subclavian artery, (2) type B (60–70%) – obstruction between the left carotid and left subclavian artery, and (3) type C (5%) – obstruction between the brachiocephalic trunk and the left carotid artery. • OAA is almost invariably associated with other cardiac defects: ventricular septal defect, bicuspid aortic valve, left ventricular outflow obstruction, truncus arteriosus, single ventricle, aortopulmonary window and others.
14.4.2.8 Prognosis
14.4.3.3 Symptoms
• IMH may regress and disappear or may demonstrate late progression to aortic aneurysms usually over a period of several weeks or months. • IMH may also progress in the short-term to aortic dissection with an intimal tear, leading to stroke, mesenteric ischaemia, renal insufficiency, haemothorax, or cardiac tamponade and death. • The clinical course and prognosis of IMH are related to its anatomical location, with proximal IMH − i.e. IMH of the ascending aorta or arch− having a poorer prognosis. • This is partly due to the higher mortality rate associated with type A aortic dissection, should such an evolution of the IMH occur (in up to 45% of cases).
• Almost all patients develop a rather dramatic clinical picture within the first few days of life, after the ductus arteriosus begins to close. • If left untreated, 75% of patients will die within the first month of life. • Only sporadic survival to adulthood has been described.
14.4.2.7 Differential Diagnosis
14.4.3.4 Diagnosis • Historically, angiography has been used to confirm the diagnosis, assess the haemodynamics and depict intracardiac and vascular morphology.
641
642
14.4 Treatment of Aortic Arch Diseases
• More recently, the diagnosis of OAA has been based on echocardiography, which can actually be the only study to perform prior to surgical repair.
14.4.3.5 Treatment Conservative Treatment • The goal of medical management is the resuscitation of the neonate over a period of a few days before surgery. • The mainstay of medical treatment is administration of prostaglandin E1 to maintain the ductus arteriosus patent. • Other supportive measures include: • controlled ventilation with a low level of inspired oxygen and a target pCO2 of 40–50 mm Hg to increase pulmonary vascular resistance, • aggressive treatment of metabolic acidosis with sodium bicarbonate, and • inotropic support with dopamine or dobutamine. • Neonates with associated DiGeorge syndrome (also called congenital thymic hypoplasia, or third and fourth pharyngeal pouch syndrome) require irradiated blood and treatment for hypocalcaemia.
Surgery • Surgical treatment differs depending on the associated intracardiac lesions. • Herein, the surgical repair of OAA with isolated ventricular septal defect (VSD) only will be delineated, as it is by far the most common clinical scenario (70– 90%).
• In cases of graft interposition, a third stage was required at 8–12 years of age for placement of a second graft between the ascending and descending aorta to augment the flow to the lower body of the growing child. • Although some authors have reported satisfactory overall survival of 73–79%, the staged approach has been gradually supplanted by the primary one-stage correction.
One-Stage Procedure
• The one-stage procedure is performed through median sternotomy using circulatory arrest. • The ductus is ligated on the pulmonary artery side and all ductal tissue is removed from the aorta. • The descending aorta is then anastomosed tensionfree end-to-side with the ascending aorta followed by VSD closure through the right atrium or pulmonary artery. • When there is coexisting posterior deviation of the infundibular septum and important postoperative subaortic obstruction seems likely, wedge resection of the septum is performed though the VSD itself. • This is a challenging operation and continuously improving results recently reflect the overall development of the field of paediatric cardiac surgery, including advances in both peri-operative and intraoperative management. • A mortality rate of only 0–14% is reported in the recent series from experienced centres, with significant morbidity remaining as high as 10–15%. • Multi-institutional studies, however, report less favourable results with a 73%, 65% and 63% survival rate at 1 month, 1 year and 4 years, respectively. • Re-operation may be needed for recurrent obstruction at the site of the anastomosis, subaortic stenosis, VSD recurrence, or left bronchial compression.
Two-Stage Procedure
• Early surgical attempts for repair of OAA with VSD were made as a two-stage procedure. • The first stage included aortic arch repair, either with direct reconstruction or with an 8- or 10-mm PTFE graft interposition, and pulmonary artery banding through a left thoracotomy. • This was followed 2–3 months later by VSD closure, de-banding and pulmonary artery reconstruction using cardiopulmonary by-pass through median sternotomy.
14.4.4 Recurrent Obstruction of the Aortic Arch • Any patient with repaired OAA should be closely monitored for residual or recurrent arch obstruction. • Follow-up should combine clinical assessment with two-dimensional echocardiography and/or magnetic resonance angiography.
14.4.5 Takayasu’s Arteritis
• The incidence of recurrence has been reported to be as high as 41%, with younger age at primary repair and smaller absolute transverse arch diameter being independent predictors of recurrence. • Treatment is usually indicated for resting gradients in excess of 30 mmHg. • Percutaneous balloon dilatation with or without stent implantation is the initial approach for recurrent OAA, as it is effective and associated with low morbidity. The majority of cases can be successfully treated with this therapeutic modality. • Complex and tortuous lesions are not amenable to angioplasty and re-operation is required. Moreover, if prosthetic tube graft is used during the initial arch repair, re-operation is inevitable. • A popular surgical approach for recurrent OAA is the creation of an extra-anatomic ascending-to-descending aortic by-pass, after incising the posterior pericardium to gain access to the descending aorta through a median sternotomy. • If there are no defects requiring simultaneous cardiac repair, this procedure can be performed without cardiopulmonary by-pass and presents the advantages of relative simplicity, minimal mortality and efficient relief of the obstruction. • Extra-anatomic by-pass techniques were developed as a response to initial unsatisfactory results of the anatomic repair for recurrent OAA. • Extra-anatomic by-pass techniques show some disadvantages in infants and children. As by-pass grafts have no potential for growth, they may lead to deformities of the aorta, anastomotic dehiscence with development of pseudo-aneurysms at the distal suture line, and loss of elastic capacitance of the aorta leading to left ventricular hypertrophy. • Therefore, many surgeons favour anatomic repair for children. This involves a sternotomy, cardiopulmonary by-pass, repair of potential concomitant intracardiac defects, and enlargement of the aortic arch with differing techniques, such as patch reconstruction or sliding plasty. • The procedure is typically performed using deep hypothermic circulatory arrest but other approaches have also been described (e.g. moderate hypothermia with two arterial inflow cannulas, one above and one below the aortic arch). • Although this is a demanding operation associated with high incidence of operative complications, small series with acceptable operative results have been recently reported.
14.4.5 Takayasu’s Arteritis 14.4.5.1 Synonyms • Takayasu’s disease • Pulseless disease • Aortoarteritis • Nonspecific aortoarteritis • Aortitis syndrome • Occlusive thromboaortopathy • Aortic arch syndrome.
14.4.5.2 Definition • Takayasu’s arteritis (TA) is an idiopathic, systemic inflammatory disease of large arteries, affecting the aorta and its main branches, including the coronary arteries. • Pulmonary arteries may also be involved.
14.4.5.3 Epidemiology/Aetiology • Unlike atherosclerotic vascular disease, TA affects primarily, but not exclusively, women of reproductive age. • In western countries, it is a rather rare disease with an estimated incidence of 1 to 3 cases per million people. • Cell-mediated autoimmunity has been strongly implicated in its pathogenesis. Although the nature of the antigen that triggers the autoimmune process is still not known (bacterial, viral, other), the infiltrating T lymphocytes recognize self-antigens processed and presented in association with human leukocyte antigen (HLA) types. • Chemokines and proinflammatory cytokines also act in concert to bring about inflammation and necrosis of the blood vessel wall. • TA has an early active inflammatory phase and a late occlusive phase, although these two phases are not always distinct. • Active phase pathology consists of continuous or patchy inflammation of the vascular wall with mononuclear infiltration of the adventitia, perivascular cuffing of the vasa vasorum, destruction of the elastic fibres and granulomatous changes of the media. Atrophy, disappearance and replacement with fibrous tissue of the medial smooth muscle cells ensue.
643
644
14.4 Treatment of Aortic Arch Diseases
• Eventually, fibrosis and scarring of the media and acellular thickening of the intima develop, leading to multiple focal or segmental stenoses and thrombosis. • More acute progression causes destruction of the media, leading to aneurysm formation or rupture of the vessels.
14.4.5.4 Symptoms • Clinical manifestations vary according to the location of the arterial lesions. According to Ueno’s classification, there are 4 types of TA: • Type I patients have cerebral hypoperfusion attributable to aortic arch lesions. • Type II patients have systemic hypertension attributable to aortic or renal vessel involvement. • Type III patients have both cerebral hypoperfusion and systemic hypertension attributable to combined extensive lesions of the aortic arch and thoracoabdominal aorta. • Type IV patients have aneurysms. • In Europe, the aortic arch and its branches are the most common sites of involvement. • Symptoms of cerebrovascular ischemia – e.g. dizziness, syncope, transient ischaemic attack, stroke – or upper extremity ischaemia may develop. • Symptoms of vascular compromise, however, may be minimized by the development of collateral circulation due to the slow onset of stenosis. • Despite the term “pulseless disease”, the predominant finding is an asymmetrical upper extremity pulse and differences in systolic blood pressure measurements between the arms. • Absent peripheral pulses occur late in the course of the disease. • When the aortic arch itself is affected, atypical aortic coarctation with resultant hypertension, or aortic arch aneurysm may ensue. • Chronic segmental dissection of the aorta may cause recurrent chest pain for years. • Overall, stenoses occur in 90–100% of patients with TA and aneurysm formation in about 30%.
14.4.5.5 Diagnosis Recommended European Standard Diagnostic Steps of Investigation • Making the diagnosis can be extremely difficult. • TA may be asymptomatic or cause only nonspecific constitutional symptoms associated with the inflammatory phase of the illness for years. • The diagnosis is frequently not made until a major vascular complication develops. • The diagnosis is based on clinical features and vascular imaging studies – high-resolution ultrasonography, conventional or magnetic resonance arteriography − that document typical patterns of stenoses (long, smooth, tapered stenoses) or aneurysms of the aorta and its primary branches. • Tissue diagnosis is infrequently feasible.
14.5.5.6 Treatment Conservative Treatment Recommended European Standard Therapeutic Steps
• High-dose corticosteroid administration (prednisone 1–2 mg/kg per day for 4–6 weeks) is the mainstay of therapy for active inflammatory disease. • Patients not responding to corticosteroids or who relapse during corticosteroid taper require an additional agent. Methotrexate, azathioprine, cyclophosphamide, ciclosporin, mycophenolate mofetil, leflunomide or recently anti-tumour necrosis factor-alpha agents have all been used for individuals with corticosteroid-resistant disease.
Surgery Recommended European Standard Surgical Procedures
• Interventional techniques, i.e. percutaneous balloon angioplasty with or without endovascular stenting, have been utilized to treat stenotic lesions, primarily in patients with renal artery stenosis. They are safe and provide good results for short lesions. However, persistent inflammation of the vascular wall leads to a high rate of restenosis and limited long-term beneficial effect. • In most cases of vascular complications surgery is required. The surgical management of TA, however,
14.4.6 Aortic Arch Atherosclerotic Aneurysm
must be distinguished from that of atherosclerotic vascular disease. Symptomatic carotid artery disease is treated more commonly with by-pass than thromboendarterectomy. Involved subclavian arteries are also by-passed to treat ischaemic symptoms and to allow for accurate blood pressure measurement to diagnose and treat hypertension. Atypical aortic coarctation can be managed with aorto-aortic by-pass or patch reconstruction, whereas aortic arch aneurysm requires replacement with Dacron graft using hypothermic circulatory arrest. Surgical results are excellent but long-term surgery-related complications also tend to occur more frequently in these patients as a result of the underlying pathology. Anastomotic aneurysms may occur at any time after surgery and they have a cumulative incidence of 8.4%, 13.8% and 18.4% at 10, 20 and 30 years, respectively [44]. Therefore, follow-up of operated patients with appropriate imaging modalities is mandatory for life. Moreover, the overall primary 10-year cumulative patency of carotid, subclavian and aorto-aortic by-pass grafts have been reported to be 88%, 64% and 100%, respectively. The timing preferred for surgical intervention is during an inactive phase of the disease. For patients who are operated on in the clinically or histologically active stage, postoperative steroid therapy is strongly recommended.
14.4.6 Aortic Arch Atherosclerotic Aneurysm 14.4.6.1 Epidemiology/Aetiology • Aneurysms of the aortic arch represent about 10% of all thoracic aortic aneurysms. • As with aneurysms of the ascending aorta, arch aneurysms are primarily due to medial degeneration and in fact may represent the distal extension of an ascending aortic aneurysm. • In older patients, there is a frequently extensive atherosclerotic component and possible aortic calcification. Therefore, these aneurysms are usually referred to as atherosclerotic aneurysms of the aortic arch but atherosclerosis appears to be a superimposed process rather than the primary pathogenetic factor. • Distal arch aneurysms, usually acting as the proximal end of descending aortic aneurysms, may be of true atherosclerotic nature. • In general, aneurysms of the ascending aorta, aortic root and other parts of the aorta frequently coexist with aortic arch aneurysms, whereas occasionally the entire aorta may be involved (mega-aorta syndrome).
14.4.6.2 Symptoms 14.5.5.7 Prognosis • Overall prognosis of the disease, as demonstrated by Ishikawa, relates to the presence of major complications (Takayasu’s retinopathy, hypertension, aortic regurgitation, and aneurysm) and the pattern of the past clinical course [32]. • Based on these two factors, Ishikawa has formulated a prognostic classification system with three stages. Stage 3 patients, that is those with both major complications and progressive disease, have a 15-year survival rate of only 43% versus 100% survival rate of patients in stage 1. Aggressive medical and surgical treatment has been recommended for stage 3 patients. A recent study [44] using this prognostic classification system to assess the efficacy of surgery to increase long-term survival provided evidence that surgery in fact increases survival for stage 3 patients. However, surgical treatment produced surgery-related complications and decreased the survival of patients in stage 1. Therefore, conservative treatment was recommended for patients with stage 1 or 2 TA.
• Aneurysms of the aortic arch, irrespective of aetiology, can be entirely asymptomatic. • If not, they may manifest themselves with pain (usually an indicator of aneurysmal expansion) and/or a variety of symptoms resulting from compression of adjacent structures, such as trachea, bronchi, lung, left recurrent laryngeal nerve, superior vena cava, innominate veins and pulmonary artery. These symptoms include stridor, dyspnoea, wheezing, haemoptysis, cough, hoarseness, and symptoms of superior vena cava syndrome. • Erosion into the great veins, pulmonary artery, right atrium, or right ventricle results in a large arteriovenous fistula with severe haemodynamic sequelae leading to sudden and fatal heart failure. • Intraluminal friable atherosclerotic debris may embolize to the brain and cause stroke or transient ischaemic attacks. • Rupture of the aneurysm, its most dramatic and dreadful manifestation, causes death from exsanguination or cardiac tamponade.
645
646
14.4 Treatment of Aortic Arch Diseases
14.4.6.3 Diagnosis
Surgery
• Arch aneurysms can be detected on routine chest radiograph as superior mediastinal widening or prominence of the aortic knob. Further diagnostic work-up is then required, including: • Computed tomograghy (CT) scan • Magnetic resonance imaging (MRI). • Three-dimensional CT scan and MRI angiography clearly delineate the morphology of the aneurysm and arch vessels and they are usually sufficient to guide surgical intervention. • In patients over the age of 40 or in younger patients with significant risk factors for coronary artery disease, cardiac catheterization is mandatory to identify coronary lesions requiring revascularization. If angioplasty is performed, aneurysm surgery is preferably delayed for 2 weeks to avoid possible coronary thrombotic sequelae associated with the administration of heparin and protamine. Alternatively, coronary artery grafting can be carried out at the time of aneurysm repair. • Echocardiography, although not ideal for the assessment of the arch, is always performed preoperatively to establish cardiac function and to evaluate concomitant valvular abnormalities.
• Surgical treatment of aortic arch aneurysms consists of graft replacement of the diseased segment. • An element of aortic arch surgery is that cessation of blood flow to the brain may be required. Cerebral protection techniques are, therefore, an essential part of these procedures. • Since its introduction by Griepp and associates in 1975 [23], profound systemic hypothermia induced with cardiopulmonary by-pass remains the mainstay of cerebral protective strategies. • The patient is usually cooled to 15°C to 18°C core temperature to minimize brain metabolic activity and oxygen consumption and the circulation is arrested. • This gives the surgeon a theoretically safe 30 to 45-min time period to perform the necessary anastomoses in a bloodless field. • Ice packing of the head prevents passive brain rewarming during that period. • Barbiturates and/or high-dose steroids are routinely used to further decrease the metabolic rate and minimize cerebral oedema. • Sophisticated perfusion techniques are available to enhance cerebral protection and increase the safe duration of circulatory arrest. • Retrogradecerebral perfusion (RCP) consists of pumping cold oxygenated blood at low flow (≤500 ml/min) and low pressure (≤25 mmHg) via the superior vena cava “backwards” through the cerebral circulation. It appears that RCP does not provide cerebral flow sufficient to support cerebral metabolism as most of the blood is shunted through collaterals before it reaches the capillaries of the brain. Its main benefit may be in flushing air and embolic material from the cerebral circulation and in maintaining adequate cerebral hypothermia. • Antegrade cerebral perfusion supports cerebral metabolism and allows unhurried repair of more complex and extensive aneurysms. • Cannulation techniques that allow selective antegrade cerebral perfusion include: (i) cannulation of the right subclavian artery and (ii) direct cannulation of the arch branches with balloon perfusion catheters. Flow is adjusted to maintain a mean arterial pressure of 50 mm Hg usually 500–800 ml/min, at a perfusion temperature of 12–14°C. • Warm perfusion techniques have been reported to allow faster postoperative recovery, but their utility should be weighed against the risk of inadequate metabolic cerebral protection.
14.4.6.4 Treatment Indications • Although tremendous progress has been made in the intraoperative and peri-operative management of these patients, surgical repair of aortic arch aneurysms remains a difficult undertaking. • Surgical intervention should be undertaken when the risk of rupture exceeds the surgical risk but frequently this is not a clear-cut point. • In general, the onset of symptoms attributable to the aneurysm is an indication for surgery. In asymptomatic patients, surgery is usually recommended for aneurysms exceeding 6 cm in diameter or expanding more than 0.5–1.0 cm per year. • Patients with Marfan’s syndrome are treated more aggressively and should undergo surgery for aneurysms with a diameter of ≥5 cm or with an expansion rate of 0.3–0.5 cm per year. • Earlier intervention (when 3–4 cm in size) is warranted for saccular or severely asymmetric fusiform aneurysms, as these are associated with greater risk of rupture.
14.4.6 Aortic Arch Atherosclerotic Aneurysm
Recommended European Standard Surgical Procedures • The selection of the appropriate type of procedure for replacement of an arch aneurysm depends on the morphology of the aneurysm and the involvement of the adjacent aortic segments. • In patients with ascending aortic aneurysms extending to the arch but not involving the descending aorta, a hemiarch replacement is suitable. This includes a generous resection of the concave portion of the arch extending from the base of the innominate artery to 1 cm proximal to the ligamentum arteriosum and left recurrent laryngeal nerve, followed by a bevelled endto end distal anastomosis. • If all aneurysmal tissue cannot be adequately removed with hemiarch replacement, total arch replacement should be performed. In this type of repair the distal anastomosis is performed just distal to the origin of the left subclavian artery, and the arch vessels are reimplanted as a Carrel patch into the convex portion of the prosthetic graft. • When the aortic arch is heavily calcified, separate anastomoses of individual grafts to the arch vessels can be utilized. Dacron branched grafts designed for aortic arch replacement can also be used for this purpose. • In patients with aneurysmal involvement of the descending thoracic aorta, the two-staged elephant trunk technique can be employed. In the first stage of this procedure, which is carried out through a median sternotomy, the prosthetic graft utilized to replace the arch aneurysm is invaginated into itself creating a 5- to 7-cm cuff and anastomosed to the proximal descending thoracic aorta. In this fashion, the cuffed or “elephant trunk” portion of the graft dangles within the lumen of the proximal descending thoracic aorta after the completion of the first stage of the procedure. In the second stage, which usually follows 1–3 months later through a left thoracotomy, the elephant trunk is quickly grasped and clamped and the repair of the descending thoracic aortic aneurysm can be performed using only distal by-pass with a centrifugal pump, without extensive dissection and clamping of the distal arch. • Alternatively, the aortic arch and the descending thoracic aorta can be replaced in a single stage via a transverse bilateral anterior thoracotomy incision (“clamshell” incision) that allows simultaneous surgical access to the diseased aortic segments.
• In patients with aneurysms involving the distal segment of the aortic arch, repair is carried out through a left thoracotomy. Occasionally, a simple cross-clamp technique may be employed − the aorta is clamped distal to the innominate artery, whereas two separate clamps are placed upon the left common carotid and left subclavian artery. However, in most cases the distal arch is severely atherosclerotic and calcified making cross-clamping difficult and dangerous. Under these circumstances, the aneurysm repair is carried out using hypothermic circulatory arrest. This is accomplished by initiating cardiopulmonary by-pass via the femoral vessels and cooling till profound systemic hypothermia is achieved. During cooling, ventricular fibrillation occurs and if left ventricular distention develops a vent is introduced into the left ventricle either directly through its apex or via the left atrium. • Small saccular aneurysms can occasionally be treated with application of a Dacron patch to repair the aortic wall defect following excision of the aneurysm. This should not be attempted, however, if the resultant aortic defect encompasses more than 50% of the circumference of the aorta.
14.4.6.5 Prognosis • In general, replacement of the aortic arch is associated with an average mortality of 10–15% in most series, although lower mortality has been reported from a few centres. • The most frequent causes of morbidity are: postoperative neurological dysfunction, renal failure and respiratory insufficiency. • Neurological dysfunction can be transient or permanent, and focal or diffuse. Diffuse neurological dysfunction is manifest by confusion or lethargy and occurs in up to 30% of the patients. It is usually transient and associated with the duration of hypothermic circulatory arrest. On the other hand, focal neurological deficits are most often of an embolic nature and may be permanent in up to 10% of patients.
647
648
14.4 Treatment of Aortic Arch Diseases
14.4.7 Atheromas and Penetrating Atherosclerotic Ulcerations of the Aortic Arch
Laboratory tests (creatine kinase and troponin), electrocardiographic changes, and chest radiograph may help to differentiate between them.
14.4.7.1 Definition
14.4.7.3 Diagnosis
•
• The diagnosis of PAU is made with: CT, MRI or TEE. • TEE typically demonstrates an outpouching in the aortic wall in the presence of an extensive aortic atheroma with jagged edges [48, 78]. • On CT, PAU manifests as focal involvement with adjacent subintimal haematoma and is often associated with aortic wall thickening. • MRI is superior to conventional CT in differentiating acute IMH from atherosclerotic plaques [27].
Penetrating atherosclerotic aortic ulcer (PAU) describes the condition in which ulceration of an aortic atherosclerotic lesion penetrates the internal elastic lamina into the media [10, 65, 75]. • This condition is part of a clinical entity called acute aortic syndrome (AAS), which includes two other conditions: aortic intramural haematoma (IMH) and classic aortic dissection (AD).
14.4.7.2 Symptoms 14.4.7.4 Treatment • Atherosclerosis of the aortic arch has been recognized as a potential source of emboli [15, 18, 31, 34, 73, 74]. Patients with recently diagnosed stroke, TIAs and peripheral emboli may have their embolic source in the aortic arch. • The recent introduction of transoesophageal echocardiography (TEE) made the detection of protruding plaques possible when other embolic sources have been eliminated. • Plaque thickness is an independent predictor of embolic phenomena. This association is particular strong with thickness >4 mm [3]. • Cohen et al. [11] evaluated the impact of other plaque characteristics on acute vascular events. The absence of calcification on thick atheromas imparts a higher risk of recurrent embolic events. Ulceration of thick plaques defined as the presence of a disruption 2 mm in depth and width was not predictive of a higher risk for acute vascular events. • PAU may precipitate IMH. In most cases this is localized in the aortic media but occasionally it can involve the entire thoracic aorta. • These ulcers may progress in several ways: as fusiform aneurysm formation [25], as a pseudoaneurysm breaking through the adventitia [75], they may rupture in the chest [4] or they may progress to typical aortic dissection [27, 71, 75]. • PAU is often characterized by chest or back pain in a patient with coexisting hypertension. PAU pain may be confounded with that of acute coronary syndromes.
• The clinical significance of atherosclerotic ulcerations in the aortic arch is controversial. • Amarenco et al. [2] performed an autopsy bank data analysis of 500 consecutive patients with cerebrovascular and other diseases. They concluded that ulcerated plaques in the aortic arch may play a role in causing cerebral infarction, especially in patients in whom cerebral infarction has no known cause. • However, Cohen et al. [11] feel that ulceration of thick atheromatous plaques in the aortic arch are not predictive of a higher stroke risk. • Cho et al. [8], in their retrospective study of 105 patients with PAU of the aortic arch and the descending thoracic aorta, concluded that those patients can be managed nonoperatively in the acute setting with careful follow-up. The number of aortic arch PAU cases, however, was too small to make any management conclusions. • It is reasonable, however, that small aortic arch atheromatous ulcers, if asymptomatic, can be managed conservatively with blood pressure control and frequent imaging follow-up. • In conclusion, the natural history of aortic arch PAU is one of progressive aortic enlargement with saccular and fusiform aneurysm formation. Aortic dissection and rupture can occur less frequently. Surgical treatment in terms of arch replacement with circulatory arrest is mandatory if signs of impending aortic rupture, rapid aortic enlargement or inability to control pain are
14.4.8 Aortic Arch Thrombosis
evident. Large protruding aortic arch atheromas must be addressed surgically with endarterectomy or arch replacement to prevent catastrophic embolization.
14.4.8 Aortic Arch Thrombosis 14.4.8.1 Epidemiology/Aetiology • • • •
•
Thrombosisof the ascending aorta and arch rarely occurs without underlying pathology. In neonates this condition mimics aortic coarctation [12, 14, 52]. The pathogenetic mechanism includes a low-output cardiac syndrome and asphyxia. Other contributing factors are hypercoagulable state due to protein C deficiency [29] and congenital cytomegalovirus infection [38]. In adults 38 cases have been reported. Most of the patients have cardiovascular risk factors, e.g. smoking, hypertension, diabetes and hypercholesterolemia.
• Magnetic resonance angiography (MRA) and highresolution CT with intravenous contrast may be more useful in detecting thrombus in the distal aortic arch.
14.4.8.4 Treatment The treatment of aortic arch thrombosis aims to: • Restore blood flow to the ischaemic organ or extremity with emergent embolectomy. • Eliminate the embolic source from the aortic arch. Anticoagulation may paradoxically induce further embolic events by causing plaque haemorrhage, or by lysing the thin pedicle thrombus more rapidly than the thrombus itself [44, 58]. Laperche reports that 5 out of 17 patients who were treated initially with anticoagulation had recurrent embolism [39]. The incidence of embolic events is as high as 73% in patients with highly mobile thrombus as opposed to 12% when the thrombus is immobile [34].
Surgery 14.4.8.2 Symptoms • The majority of patients with aortic arch thrombosis present with cerebrovascular, mesenteric or peripheral acute ischaemia due to emboli [21]. • Asymptomatic presentation incidentally diagnosed with TEE is the exception [26, 51]. • The aortic arch is typically identified as the embolic source when other more common sources are eliminated such the heart or the descending thoracic aorta. • It is not clear why the majority of aortic thrombi originate on the lesser curvature of the arch. This may be due to the haemodynamics that predispose to the formation of atherosclerotic plaques in this location [39], or to local endothelium abnormality at the site of the ligamentum arteriosum [35]. • In most cases the atheromatous plaque acts as a thrombogenic substrate [61, 62].
14.4.8.3 Diagnosis • The diagnostic evaluation typically involves a TEE study. This modality is particularly useful for the ascending aorta and the proximal arch.
• Surgery should be considered when the thrombus is pedunculated and mobile or in medical treatment failure situations (recurrent embolic events despite optimal anticoagulation). • Surgical treatment of aortic arch thrombosis can vary from simple thrombectomy and endarterectomy of the offending atheromatous plaque [9] to more complex reconstruction of the aortic arch with graft replacement. • The arterial cannulation site of choice depends on personal preference. Femoral cannulation is acceptable, however it carries a risk of retrograde thrombus embolization to the arch vessels. • Aortic manipulations and clamping should be avoided to prevent peri-operative stroke. • Variable periods of hypothermic circulatory arrest (HCA) are necessary to perform the procedure. The low body core temperature protects the brain by decreasing its metabolism. The time spent on HCA is of paramount importance for the outcome. Cerebral ischaemic times >45 min are associated with higher stroke risk and ischaemic times >65 min are associated with higher mortality [69]. • Other brain protective strategies are:
649
650
14.4 Treatment of Aortic Arch Diseases
• administration of steroids and other neuroprotective agents and • low-flow cerebral perfusion during the HCA period. • Retrograde cerebral perfusion can be achieved from the superior vena cava [16, 28, 47, 57]. • Antegrade cerebral perfusion, an alternative technique, is technically possible when the right subclavian artery is used as the arterial in-flow site [1], or when the head vessels are attached in a graft as an island [36, 68]. Alternatively, antegrade cerebral perfusion is feasible when the innominate and the left carotid arteries are directly cannulated [33]. Discharge on oral anticoagulation or antiplatelet regimen is advised. • In conclusion, aortic arch thrombosis is associated with embolic events. TEE is a very useful diagnostic modality. An initial trial of aggressive anticoagulation for immobile thrombus is a reasonable option. Surgical treatment is reserved for mobile thrombi and anticoagulation treatment failure.
•
•
• •
• 14.4.9 Aortic Arch Trauma • 14.4.9.1 Synonyms
one in every six to ten people killed in automobile accidents sustain this injury. In his landmark paper in 1958 Parmley et al. [50] determined during autopsy the site of rupture: aortic isthmus 45%, ascending aorta 23%, descending thoracic aorta 13%, transverse aortic arch 8%, abdominal aorta 5% and multiple sites 6%. The mobility of the ascending aorta and aortic arch compared to the fixed (by the parietal pleura) distal descending aorta renders the isthmus of the aorta, which lies at the junction between the movable and fixed aspects of the aorta, the most susceptible part for rupture. Blunt traumatic aortic rupture typically involves a transverse tear in the aortic wall. In mild trauma, the injury may only be a partial circumferential tear in the intima, which may or may not occur into the media and in such a case the intact adventitia may be strong enough to contain the blood flow within the aorta. Increased arterial blood pressure can force blood between the layers of aortic wall forming a false aneurysm, which is at high risk for a subsequent rupture if untreated. In more severe traumas, the tear can extend into the adventitia causing either partial or complete aortic transection.
• Traumatic injury of the aortic arch. • Traumatic aortic arch rupture. 14.4.9.4 Symptoms 14.4.9.2 Definition • Lesions in the aorta following penetrating or blunt trauma, including simple contusions, intramural haematomas, intimal tears, false aneurysms and rupture.
14.4.9.3 Epidemiology/Aetiology • The incidence of penetrating injuries of the aortic arch has not been estimated and it is believed to be rare. • Most penetrating injuries are due to either gunshot wounds or stab wounds with a knife. In general, blunt aortic trauma accounts for 7500–8000 victims in USA and Canada every year and by far the majority of patients diagnosed with blunt aortic trauma have suffered automobile-related trauma, while it has been concluded from the literature that
In any patient who has sustained a deceleration or acceleration injury or has had blunt chest trauma, a traumatic rupture of the aorta should be suspected. The most common symptom of traumatic aortic rupture is chest pain, while others symptoms include: • dyspnoea • back pain • hoarseness • dysphagia and • cough The triad of signs associated with acute coarctation includes: • upper limp hypertension • radio-femoral pulse delay with amplitude discrepancy and • a harsh systolic precordial or interscapular murmur (sometimes observed).
14.4.9 Aortic Arch Trauma
Occasionally, peripheral pulses may be lost, particularly if aortic dissection occurs. Certain signs and symptoms are useful indicators that an urgent investigation should begin, but their absence does not exclude the diagnosis.
14.4.9.5 Complications • Following a complete transection of the aorta, blood exsanguinates into the mediastinum and pleural cavity and the patient usually dies. • If traumatic aortic rupture is not diagnosed and treated immediately the mortality rate is as high as 86% and only 14% of the patients reach the hospital alive; of those, only 20% live longer than 1 h and 30% die within 6 h. However, examples have been published of patients suffering a complete transection of the aorta, but managing to survive for a period adequate to allow surgical intervention. • Therefore, it has now been recognized that acute mortality can be as low as 40% to 70% and patients admitted for traumatic aortic rupture fall into two categories. A small number of about 5% are haemodynamically unstable or deteriorate within 6 h of admission. Allcause mortality in this group invariably exceeds 90%. The remainders are haemodynamically stable and afford time for workup and staging of any intervention. Mortality in the haemodynamically stable patients is as low as 25% and is commonly because of a consequence of associated injuries.
14.4.9.6 Diagnosis Recommended European Standard Diagnostic Steps of Investigation • Because of the dearth of reliable clinical signs and symptoms and the frequency of traumatic aortic rupture in automobile accidents, emergency clinicians have come to rely on radiographic imaging during the management of such patients. The importance of routine chest radiograph was first emphasized in the 1960s and the most important sign was felt to be widening of the mediastinum, but this finding is not specific for aortic rupture. • Aortography has been the gold standard imaging modality for demonstrating traumatic aortic rupture and many authors suggest that this is the only way to
confirm 100% a normal aorta, while good anatomical detail is helpful for the surgical procedure. • TEE has emerged as a modality that could possibly replace arch aortography. It is less invasive, requires no contrast and can be performed quickly at the bedside. However, it may be less sensitive and specific compared to arch aortography. • Contrast-enhanced spiral CT has been established as the imaging modality of choice for stable patients at risk for aortic trauma. A negative spiral CT excludes aortic rupture. However, in the pressure of a large subadventitial hematoma it may not delineate the exact location of the intimal rupture with accuracy.
14.4.9.7 Treatment Surgery • As soon as the diagnosis of aortic rupture has been made, the patient is immediately taken to surgery because of the risk of free rupture and exsanguination. • After the aorta is clamped both proximal and distal to the haematoma, the haematoma is entered and the aortic tear is identified either on the lesser curve of the aortic arch or as a circumferential tear at this level. • Graft replacement of the ruptured segment of the aorta via a left thoracotomy incision with use of cardiopulmonary by-pass with proximal and distal aortic perfusion or with left atrial-femoral by-pass is the mainstay of the surgical treatment for acute traumatic aortic rupture. • When the aortic arch is involved, other associated injuries and the risk of deep hypothermia with circulatory arrest in the acute situation must be assessed. • An option in patients with head injuries is to first treat them medically and later to repair the aortic arch. • The evolution of endovascular stent grafting for thoracic aortic aneurysmal disease is gradually changing the management of acute thoracic aortic rupture. Endografting of the ruptured segment of the aorta may be an appropriate alternative therapy in the acute setting, particularly when multiple organ injuries coexist.
14.4.9.8 Differential Diagnosis • A widened mediastinum occurs when a traumatic pseudoaneurysm changes the contour of the medias-
651
652
14.4 Treatment of Aortic Arch Diseases
tinum or more commonly when mediastinal haemorrhage or haematoma occurs. • However, in a series of 149 patients with mediastinal haematoma, the aortic adventitia was found to be intact in 60% of cases, suggesting that the haematoma in these cases came from small arteries and veins within the mediastinum. • The use of arch angiography or spiral CT is very helpful in differential diagnosis.
• The Stanford classification distinguishes between type A and type B aortic dissection. Type A aortic dissection involves the ascending aorta whereas type B does not involve the ascending aorta. • The DeBakey classification includes three types of dissection: type I involves the entire aorta, type II involves only the ascending aorta, and type III spares the ascending aorta and arch. • The AD classification has treatment implications, because ascending aortic dissection is a surgical emergency that merits immediate surgical treatment.
14.4.9.9 Prognosis • Only 16% of patients with aortic traumatic rupture survive to reach the hospital and 99% of them will die if not treated surgically; 30% die within 6 h, 49% die within 24 h, 72% within 8 days and 90% within 4 months. • A traumatic pseudoaneurysm is formed in survivors and in most cases this undergoes secondary rupture resulting in delayed death. • The American Association of Trauma quoted an overall mortality rate of 31% in patients with traumatic aortic rupture who had surgical repair, therefore surgical treatment remains the only effective therapy for this injury.
14.4.10 Ascending Aortic Dissection 14.4.10.1 Synonyms •
Aorticdissection and dissecting aortic aneurysms are synonyms that describe the same clinical entity.
14.4.10.2 Definition • Aortic dissection is the pathological condition that is characterized by acute development of an intimal flap that separates the aortic lumen into a true and false lumen [43, 53]. • Penetrating atherosclerotic ulceration (PAU), intramural haematoma (IMH), and aortic dissection (AD) are conditions of a broader entity: the acute aortic syndromes (AAS). • Penetrating atherosclerotic ulceration may precipitate IMH or may progress to become typical AD [76].
14.4.10.3 Epidemiology/Aetiology • The incidence of AD is 2.9/100,000 per year. • Approximately 20% of patients die before admission to the hospital. • Male patients predominate in a male-to-female ratio 1.55 to 1 and the age range is 36 to 97 years with a mean age of 65.7 years [43]. • Medical management of ascending aortic dissection is associated with a mortality of 20% by 24 h after presentation, 30% by 48 h, 40% by day 7 and 50% by 1 month [49]. • The aetiology of AD includes: • several inherited connective tissue disorders as well as • acquired conditions. • The three more common connective tissue disorders that are known to affect the aortic wall media are: • Marfan’s syndrome • Ehlers–Danlos syndrome • Familial forms of thoracic aneurysm and dissection. • Marfan’s syndrome is the most prevalent connective tissue disorder with an incidence of 1 in 7000. Patients with Marfan’s demonstrate ocular, cardiovascular, skeletal as well as skin symptomatology. The common denominator is mutation on the fibrillin gene, which encodes for a defective collagen in the extracellular matrix. Marfan’s syndrome is associated with increased elastolysis [41] and enhanced expression of metalloproteinases in vascular smooth muscle cells leading to cystic medial necrosis [63]. • Ehlers–Danlos syndrome is a connective tissue disorder characterized by articular, skin and tissue fragility. Type IV Ehlers–Danlos syndrome is mainly associated with aortic involvement [67].
14.4.10 Ascending Aortic Dissection
• Familial forms of thoracic aortic dissection are associated with mutations in the fibrillin gene [20, 22]. • Acquired conditions linked to aortic dissection are hypertension and iatrogenic aortic intimal flap creation [30, 40]. Chronic hypertension causes intimal thickening and adventitial fibrosis causing vascular stiffness and vulnerability to dissection [66].
• The pathognomonic hallmark is the demonstration of the intimal flap and the false lumen. • The preferred diagnostic modality varies from one institution to another and depends on experience and availability in the emergency setting. • Coronary angiography is not essential preoperatively but it should be performed on the stable patient if it can be obtained expeditiously without delaying surgical treatment.
14.4.10.4 Symptoms • Typical presenting symptoms of aortic dissection are: acute onset of chest or back pain and syncope. • Syncope may be related to cardiac tamponade, vagal reaction to severe pain or obstruction of cerebral vessels. • Congestive heart failure may be related to acute aortic regurgitation [17]. • Other symptoms related to malperfusion of vital organs. • Paraplegia can occur if many intercostal arteries are obstructed from the false lumen. • Other presenting symptoms are: • anuria • mesenteric ischaemia or • lower extremity ischaemia. • Cerebral hypoperfusion or infarction.
14.4.10.5 Diagnosis Recommended European Standard Diagnostic Steps of Investigation The diagnostic work-up for acute aortic dissection starts with history and physical examination, a chest radiograph and progresses to more complex diagnostic tests. • The chest radiograph is abnormal in 60–90% of acute type A aortic dissection [24]. • Computed tomography. • Transthoracic or transoesophageal echocardiography are the most commonly used tests if the diagnosis is suspected [19, 24].
Additional Useful Diagnostic Options • Magnetic resonance imaging and angiography are used less commonly.
Surgery • The patient is placed on cardiopulmonary by-pass. Arterial return is preferably established via the right axilliary artery. Femoral arterial cannulation can be used alternatively. Central cannulation technique of the dissected ascending aorta has been described by Haverich et al with acceptable results but generally it is not advised due to the unpredictability of the perfusion and because safe alternative cannulation sites are usually available. Venous return is established via the right atrium. • Systemic cooling to profound hypothermia is achieved taking care to avoid cerebral and splachnic malperfusion during the period of cooling. Peripheral arterial waveforms are monitored in two sites and transcranial cerebral oxymetry is used to assure adequate cerebral perfusion. • During the period of circulatory arrest at 15 to 18°C with or without selective antegrade cerebral perfusion, the aortic arch is inspected and open distal anastomosis is performed to the selected Dacron tube graft. The entire ascending aorta is replaced. • The extent of aortic resection is guided by the presence of the intimal tear, not the extent of dissected aortic wall. Segments of the aorta that include the intimal tear are resected. If there is obstruction of the head vessels by the false lumen it may be necessary to resect the proximal portion of the obstructed head vessels and reimplant them to the tube graft via interposition grafts or replace that segment of the arch with a branched aortic arch graft. Routine replacement of the aortic arch for acute type A aortic dissection regardless of the extent of the dissection is not advisable. • Concurrent aortic valve incompetence is usually adequately treated with resuspension of the dissected commisures, usually the ones between the left and the non-coronary sinus and between the right and
653
654
14.4 Treatment of Aortic Arch Diseases
the non-coronary sinus. Circumferential dissection of the aortic root or extension of the intimal tear into it, requires aortic root replacement with a composite valved graft or occasionally reimplantation of the aortic valve into the graft utilizing an aortic valve preservation technique as described by David. Patients with the Marfan syndrome should undergo composite graft replacement of the aortic root. • Operative mortality varies between 15% and 30% [13, 37, 54, 70, 78] and relates mainly to preoperative morbidity caused by malperfusion phenomena or coexistent coronary artery disease.
14.4.11.3 Epidemiology/Aetiology • Marfan’s syndrome affects about 1 in 10,000 individuals. • The syndrome is caused by mutations in the fibrillin-1 gene located on chromosome 15q21.1. • Abnormalities involving microfibrils weaken the aortic wall. • In almost all patients with Marfan’s syndrome progressive aortic dilatation that can progress to valvular incompetence and dissection eventually occur because of tension caused by left ventricular ejection impulses. • Marfan’s syndrome accounts for 5–9% of all aortic dissections.
14.4.10.6 Differential Diagnosis The differential diagnosis includes other pathologic conditions such as: • Acute coronary syndrome when the false lumen causes compression of the coronary ostia. • Oesophageal spasm. • Pneumothorax.
14.4.11 Marfan’s Syndrome 14.4.11.1 Synonyms • Arachnodactyly • Contractural arachnodactyly • Dolichostenomelia • Marfanoid hypermobility syndrome.
14.4.11.2 Definition • Marfan’s syndrome is an inherited connective tissue disorder that results in characteristic cardiovascular, ocular and skeletal abnormalities. • Cardinal features of the disorder include tall stature, ectopia lentis, mitral valve prolapse, aortic root dilatation and aortic dissection. • Symptoms vary greatly among affected individuals. • Marfan’s syndrome is inherited as an autosomal dominant trait.
14.4.11.4 Symptoms • Involvement of the aortic arch in patients with Marfan’s syndrome may manifest as abrupt onset of thoracic pain, which occurs in more than 90% of patients with aortic dissection. • Other signs include syncope, shock, pallor, pulselessness and paraesthesia or paralysis in the extremities. • Acute aortic dissection may also cause superior vena cava syndrome, vocal cord paralysis, haematemesis, Horner’s syndrome, haemoptysis and airway compression as a result of local compression and mass effect. • Onset of hypotension may indicate aortic rupture.
14.4.11.5 Complications • The risk of dissection increases with the size of the aorta and fortunately occurs infrequently below a diameter of 55 mm in the adult. • Aortic dissection in patients with Marfan’s syndrome usually begins just above the coronary ostia (type A in the Stanford classification) and extends the entire length of the aorta (type I in DeBakey classification). • About 10% of dissections begin distal to the left subclavian (type B or III). • Pregnant women with Marfan’s syndrome have an increased risk of dissection because of the haemodynamic stresses that pregnancy places on the aorta. Several case reports attest to the heightened incidence of dissection during the third trimester, parturition and the first month post partum [55, 64]. However, in the majority of instances, serious
14.4.12 Ehlers–Danlos Syndrome
aortic dilatation was present. Prospective evaluation of 21 women through 45 pregnancies suggests that the cardiovascular risks are relatively low if the aortic diameter does not exceed 40 mm and cardiac function is not compromised [60].
14.4.11.6 Diagnosis Recommended European Standard Diagnostic Steps of Investigation • Angiography, MRI and TEE all have a role in the diagnosis of acute dissection in Marfan’s syndrome. • Transthoracic echocardiography is sufficient for detecting and monitoring changes in diameter, because in the absence of dissection dilatation is limited to the proximal ascending aorta, and the rate of change is slow, measured in millimetres per year. • Patients with dilatation less than 1.5 times the mean diameter predicted for their body size can be observed annually; as the diameter increases, more frequent evaluation is necessary.
stage replacement of the thoracic aorta, both distal (lower descending aorta) and proximal (arch) anastomoses are performed under hypothermic circulatory arrest. • The arch-first technique, which modifies the perfusion strategy in order to minimize the period of brain ischaemia, was introduced by Rokkas and Kouchoukos and is a good option for patients with Marfan’s syndrome and subacute type A dissection [42, 59]. According to this technique, the arch anastomosis is constructed first with a custom-made Dacron T-graft and the brain is perfused with cold blood through the side branch of the graft while performing reconstruction of the descending thoracic aorta.
14.4.11.8 Differential Diagnosis • Ehlers–Danlos syndrome • Osteogenesis imperfecta • Pseudoxanthoma elasticum • MASS phenotype.
14.4.11.9 Prognosis 14.4.11.7 Treatment Surgery • The key question is one of timing of the operation in the life of the Marfan’s patient. • The purpose of operating is to prevent dissection. • In most instances, any region of the aorta should be repaired when complications of further dissection, branch vessel occlusion, or aortic dilatation beyond a diameter of 50 mm occur. • Composite graft replacement of the aortic root is the procedure of choise for aortic • root aneurysm with or without coexisting aortic insufficiency. • Mitral valve regurgitation frequently develops and requires replacement with • mechanical prosthetic valve. • A staged approach to total replacement of the Marfan aorta is now both feasible and successful. • Single-stage replacement has been preferred in certain situations, such as extensive involvement of the arch or impending rupture of the descending component of a thoracic aortic aneurysm. During traditional single-
• Prognosis depends on the severity of cardiovascular complications. • Early diagnosis, timely and improved surgical techniques, and prophylactic use of β-blockers all are helping to prolong survival. • Pharmalogical interventions with angiotensin-II inhibitors at a young age may prevent or delay the onset of cardiovascular complications. • The average life expectancy is now about 70 years. • Aortic dissection is the most common cause of early death in Marfan patients. • Aortic dimension, rate of increase and family history are the best predictors of occurrence [8].
14.4.12 Ehlers–Danlos Syndrome 14.4.12.1 Synonyms • Hypermobility syndrome • Acrogeria.
655
656
14.4 Treatment of Aortic Arch Diseases
14.4.12.2 Definition • The Ehlers–Danlos family of disorders is a group of related conditions that share a common decrease in the tensile strength and integrity of the skin, joints and other tissues. • Inheritance is usually autosomal dominant.
14.4.12.3 Epidemiology/Aetiology • Ehlers–Danlos syndrome is a connective tissue disorder of the proα1(III) chain of type III collagen with an incidence of 1 in 5000. • Many mutations in the COL3A1 gene have been found to account for the deficiency of type III procollagen.
• Sutures must be managed delicately, the use of rough clamps and instruments should be avoided, and thin arterial layers must be supported with the extensive use of pledged Teflon sutures and biological glue [6].
14.4.12.8 Differential Diagnosis • Cutis laxa (elastolysis) and pseudoxanthoma elasticum.
14.4.12.9 Prognosis • Patients with type IV Ehlers–Danlos syndrome die young, and most deaths result from arterial rupture.
14.4.12.4 Symptoms • Patients may present with symptoms of rupture of the aorta and its branches.
14.4.13 Noonan Syndrome 14.4.13.1 Synonyms •
Hypertelorism, “male Turner”,Turner-like syndrome.
14.4.12.5 Complications • In the type IV form (vascular form) of Ehlers–Danlos syndrome extreme fragility of the arteries is associated with multiple aneurysm formation, spontaneous rupture and dissection. • Most prone are the abdominal aorta and its branches, the great vessels of the aortic arch and the large arteries of the limbs. • False aneurysms and fistulas may form in those patients who do not die of the initial rupture.
14.4.13.2 Definition • Noonan syndrome is an autosomal dominant disorder that is characterized by dysmorphic facial features, proportionate short stature (in about 50% of cases) and heart disease (most commonly valvular pulmonic stenosis and hypertrophic cardiomyopathy).
14.4.13.3 Epidemiology/Aetiology 14.4.12.6 Diagnosis • Analysis of collagen production by cultured skin fibroblasts should be used to confirm the diagnosis.
• The syndrome is relatively common, with an estimated incidence of 1:1000–2500 live births. • Linkage analysis performed on a Dutch family with autosomal dominant Noonan syndrome suggested that a gene for Noonan syndrome is on chromosome arm 12q.
14.4.12.7 Treatment • The operative mortality is high because of the friable nature of the vascular tissue. • The sutures cut the arteries, the ties can cut through the branches and clamps may tear the vessels.
14.4.13.4 Symptoms • Patients with Noonan syndrome may present with symptoms of aortic dissection.
References
14.4.13.5 Complications • Noonan syndrome is associated with bleeding diathesis and aortic dissection. • Other characteristic lesions include dysplastic/stenotic pulmonic valve, and hypertrophic cardiomyopathy.
14.4.13.6 Diagnosis • Any patient suspected of having Noonan syndrome requires a detailed cardiac work-up including echocardiogram to rule out aortic dissection.
14.4.13.7 Treatment • Before any patient with Noonan syndrome can undergo aortic surgery, a full haematological work-up must be performed. • The most frequent abnormality is factor XI deficiency.
14.4.13.8 Differential Diagnosis • • • • •
Fetal hydantoin syndrome LEOPARD syndrome Cardio-facial-cutaneous syndrome XO/XY mosaicism Turner’s syndrome.
References 1. Aebert H, Reber D, Kobuch R et al (2001) Aortic arch surgery using moderate systemic hypothermia and antegrade cerebral perfusion via the right subclavian artery. Thorac Cardiovasc Surg 49:283–286 2. Amarenco P, Duyckaerts C, Tzourio C et al (1992) The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med 326:221–225 3. Amarenco P, Cohen A, Tzourio C et al (1994) Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 331:1474–1479 3a. Anagnostopoulos CE (1975) Acute Aortic Dissections. Baltimore, London, Tokyo: University Park Press; 255 pages 3b. Anagnostopoulos CE (1976) Lethal Diseases of the Ascending Aorta. Baltimore: University Park Press; 150 pages 3c. Anagnostopoulos CE Prabhakar MJ, Kittle CF. (1972) Aortic dissections and dissecting aneurysms. Am J Cardiol 30:263–273
4. Ando Y, Minami H, Muramoto H et al (1994) Rupture of the thoracic aorta caused by penetrating aortic ulcer. Chest 106:624–626 5. Apaydin AZ, Posacioglu H, Yagdi T, Islamoglu F, Calkavur T, Buket S (2002) Arch-first technique used with commercial T-graft to treat subacute type-A aortic dissection in patient with Marfan syndrome. Tex Heart Inst J 29:26–29 6. Ascione R, Gomes WJ, Bates M, Shannon JL, Pope FM, Angelini GD (2000) Emergency repair of type A aortic dissection in type IV Ehlers-Danlos syndrome. Cardiovasc Surg 8:75–78 7. Celoria GC, Patton RB (1959) Congenital absence of the aortic arch. Am Heart J 58:407–413 8. Cho KR, Stanson AW, Potter DD et al (2004) Penetrating atherosclerotic ulcer of the descending thoracic aorta and arch. J Thorac Cardiovasc Surg 127:1393–1401 9. Choukroun EM, Labrousse LM, Madonna FP et al (2002) Mobile thrombus of the thoracic aorta: diagnosis and treatment in 9 cases. Ann Vasc Surg 16:714–722 10. Coady MA, Rizzo JA, Hammond GL et al (1998) Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it? J Vasc Surg 27:1006–1016 11. Cohen A, Tzourio C, Bertrand B et al (1997) Aortic plaque morphology and vascular events: a follow up study in patients in patients with ischemic stroke Circulation 96:3838–3841 12. Conti VR, Bilfinger TV, Wolf W (1988) Aortic arch thrombosis in the neonate. J Thorac Cardiovasc Surg 95:138–140 13. Crawford ES, Kirklin JW, Naftel DC et al (1992) Surgery for acute dissection for ascending aorta. Should the arch be included? J Thorac Cardiovasc Surg 104:46–59 14. Das BB, Sahoo S, Ivy DD (2004) Neonatal aortic arch thrombosis masquerading as coarctation of the aorta. Pedriatr Cardiol 25:80–83 15. Davila-Roman VG, Barzilai B, Wareing TH et al (1994) Atherosclerosis of the ascending aorta: prevalence and role as an independent predictor of cerebrovascular events in cardiac patients. Stroke 25:2010–2016 16. Deeb GM, Jenkins E, Bolling SF et al (1995) Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity. J Thorac Cardiovasc Surg 109:259–268 17. DeSanctis RW, Doroghazi RM, Austen WG et al (1987) Aortic dissection. N Engl J Med 317:1060–1067 18. Di Tullio MR, Sacco RL, Gersony D et al (1996) Aortic atheromas and acute ischemic stroke: a transesophageal echocardiographic study in an ethnically mixed population. Neurology 46:1560–1566
657
658
14.4 Treatment of Aortic Arch Diseases
19. Eagle KA (1999) Current management of aortic dissection: data from the international registry for aortic dissection (IRAD). Eur Heart J 20 [Suppl]:A3287 20. Furthmayr H, Francke U (1997) Ascending aortic aneurysm with or without features of Marfan‘s syndrome and other fibrillinopathies: new insights. Semin Thorac Cardiovasc Surg 9:191–205 21. Geha AS, El-Zein C, Massad MG et al (2004) Surgery for aortic arch thrombosis. Thorac Cardiovasc Surg 52:187–190 22. Glesby M, Pyeritz R (1989) Association of mitral valve prolapse and systemic abnormalities of connective tissue: a phenotypic continuum. J Am Med Assoc 262:523–528 23. Griepp RB, Stinson EB, Oyer PE, Copeland JG, Shumway NE (1975) The superiority of aortic cross-clamping with profound local hypothermia for myocardial protection during aorta-coronary bypass grafting. J Thorac Cardiovasc Surg 70:995–1009 24. Hagan PG, Nienaber CA, Isselbacher EM et al (2000) The international registry of acute aortic dissection (IRAD): new insights into an old disease. J Am Med Assoc 283:897–903 25. Harris JA, Bis KG, Glover JL et al (1994) Penetrating atherosclerotic ulcers of the aorta. J Vasc Surg 19:90–99 26. Hassan I, Zehr K, Firek B et al (2001) A case of asymptomatic thoracic aorta mural thrombi. Ann Thorac Surg 72:1735–1737 27. Hayashi H, Matsuoka Y, Sakamoto I et al (2000) Penetrating atherosclerotic ulcer of the aorta: imaging features and disease concept. Radiographics 20:995–1005 28. Hilgenberg AD, Logan DL (2001) Results of aortic arch repair with hypothermic circulatory arrest and retrograde cerebral perfusion. J Card Surg 16:246–251 29. Istvan H, Krisztina K, Eva B et al (1996) Successful surgical management of cardiovascular thrombosis and aortic coarctation , caused by protein C deficiency, in a newborn infant. Orv Hetil 137:251–253 30. Januzzi J, Sabatine MS, Eagle KA et al (2002) Iatrogenic aortic dissection. Am J Cardiol 89:623–626 31. Jones EJ, Kalman JM, Calafiore P et al (1995) Proximal aortic atheroma: an independent risk factor for cerebral ischemia. Stroke 26:218–224 32. Ishikawa K, Maetani S (1994) Long-term outcome for 120 Japanese patients with Takayasu‘s disease. Clinical and statistical analyses of related prognostic factors. Circulation 90:1855–1860 33. Kalangos A, Vala D, Bednarkiewicz M et al (1999) Technical implications regarding surgical removal of a floating thrombus located in the ascending aorta or aortic arch. Ann Vasc Surg 13:115–120
34. Karalis DG, Chandrasekaran K, Victor MF et al (1991) Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 17:73–78 34a. Kolff J, Bates RJ, Balderman SC, Shenkoya K, Anagnostopoulos CE (1977) Acute aortic arch dissection: reevaluation of the indications for medical and surgical therapy. Am J Cardiol 39:727–733 35. Kolvekar SK, Chaubey S, Firmin R (2001) Floating thrombus in the aorta. Ann Thorac Surg 72:925–927 35a. Kotsis VN, Connery CP, Azariades P, Prappas S, Galanos O, Drossos G, Anagnostopoulos CE (2001) Prevention of aortic anastomotic hemorrhage. A simplified intraoperative testing technique. J Cardiovasc Surg (Torino) 42:481–484 35b. Kouchoukos NT, Masetti P, Rokkas CK, Murphy SF (2002) Hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 74:S1885–1887 35c. Kouchoukos NT, Masetti P, Rokkas CK, Murphy SF (2002) Single-stage reoperative repair of chronic type A aortic dissection using the arch-first technique. Ann Thorac Surg 74: S1800–1802 36. Kouchoukos NT, Masetti P (2004) Total aortic arch replacement with a branched graft and limited circulatory arrest of the brain. J Thorac Cardiovasc Surg 128:233–237 37. Lai D, Robbins R, Mitchell S et al (2002) Does profound hypothermic circulatory arrest improve survival with acute type A aortic dissection? Circulation 106:1–218 38. Lanari M, Lazzarotto T, Papa I et al (2001) Neonatal aortic arch thrombosis as a result of congenital cytomegalovirus infection. Pediatrics. 108:E114 39. Laperche T, Laurian C, Roudaut R et al (1997) Mobile thrombus of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. Circulation 96:288–294 40. Larson EW, Edwards WD (1984) Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 53:849–855 41. Lesauskaite V, Tanganelli P, Sassi P et al (2001) Smooth muscle cells of the media in the dilatative pathology of ascending thoracic aorta: morphology, immunoreactivity for osteopontin, matrix metalloproteinases, and their inhibitors. Hum Pathol 32:1003–1011 42. Lipscomb KJ, Clayton-Smith J, Clarke B et al (1997) Outcome of pregnancy in women with Marfan‘s syndrome. Br J Obstet Gynaecol 104:210–216 42a. Matsagas MI, Anagnostopoulos CE, Papakostas JC, DeRose JJ, Siminelakis S, Katsouras CS, Toumpoulis IK, Drossos GE, Michalis LK (2006) Endovascular stentgraft repair as a late secondary procedure after previous aortic grafts. Cardiovasc Intervent Radiol 29:655–658
References
43. Meszaros I, Moroez J, Szlavi J et al (2000) Epidemiology and clinicopathology of aortic dissection. Chest 117:1271–1278 44. Miyata T, Sato O, Koyama H, Shigematsu H, Tada Y (2003) Long-term survival after surgical treatment of patients with Takayasu‘s arteritis. Circulation 108:1474–1480 45. Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K (2002) Management of patients with intramural hematoma involving the ascending aorta. J Thorac Cardiovasc Surg 124:918–924 46. Moldveen-Gerominus M, Meriam JC (1967) Cholesterol embolization: from pathologic curiosity to clinical entity. Circulation 35:946–953 47. Moshkovitz Y, David TE, Caleb M et al (1998) Circulatory arrest under moderate systemic hypothermia and cold retrograde cerebral perfusion. Ann Thorac Surg 66:1179–1184 48. Movsowitz HD, David M, Movsowitz C et al (1993) Penetrating atherosclerotic aortic ulcers: the role of transesophageal echocardiography in diagnosis and clinical management. Am Heart J 126:745–747 49. Nienaber C, Kim E (2003) Aortic dissection: new frontiers in diagnosis and management. Part I: From etiology to diagnostic strategies Circulation 108(5):628–635 50. Parmley LF, Mattingly TW, Manion WC (1958) Penetrating wounds of the heart and aorta. Circulation 17(5):953–973 51. Pasierski T, Jasek S, Firek B et al (1996) Resolution of an aortic mobile mass with anticoagulation without evidence of arterial embolism. Clin Cardiol 19:151–152 52. Pilossoff W, Schober JG, Muller KD et al (1988) Complete thrombotic obliteration of the ascending aorta and the aortic arch as a cause of complete heart failure in a newborn. Eur J Pediatr 148:11–14 52a. Prabhakar MJ, Redding ME, Anagnostopoulos CE, Kittle CF (1971) Gas gangrene complicating aortic dissection. Report of a case. Arch Surg 103:96–97 53. Pretre R, von Segesser LK (1997) Aortic dissection. Lancet 349:1461–1464 54. Pugliese P, Pessotto R, Santini F et al (1998) Risk of late reoperations in patients with acute type A aortic dissection: impact of a more radical surgical approach. Eur J Cardiothorac Surg 13:576–580 55. Pyeritz RE (1981) Maternal and fetal complications of pregnancy in the Marfan syndrome. Am J Med 71:784 56. Ramirez F (1996) Fibrillin mutations in Marfan‘s syndrome and related phenotypes. Curr Opin Genet Dev 6:309–315 57. Reich DL, Uysal S, Ergin MA et al (2001) Retrograde cerebral perfusion as a method of neuroprotection during thoracic aortic surgery. Ann Thorac Surg 72:1774–1782 58. Ridker PM, Michel T (1989) Streptokinase therapy in cholesterol embolization. Am J Med 87:357–358
59. Rokkas CK, Kouchoukos NT (1999) Single-stage extensive replacement of the thoracic aorta: the arch-first technique. J Thorac Cardiovasc Surg 117:99–105 59a. Rokkas CK, Murphy SF, Kouchoukos NT (2002) Aortic coarctation in the adult: management of complications and coexisting arterial abnormalities with hypothermic cardiopulmonary bypass and circulatory arrest. J Thorac Cardiovasc Surg 124:155–161 60. Rossiter JP, Morales AJ, Repke JT et al (1995) A prospective longitudinal evaluation of pregnancy in the Marfan syndrome. Am J Obstet Gynecol 173:1599 61. Ruhlmann C, Walther T, Walter T et al (1997) The aortic arch as the source of a peripheral arterial embolism. Dtsch Med Wochenschr 122:287–292 62. Sadony V, Walz M, Lohr E et al (1988) Unusual cause of recurrent arterial embolism: floating thrombus in the aortic arch surgically removed under hypothermic circulatory arrest. Eur J Cardiothorac Surg 2:469–471 62a. Sanderson CJ, Cote RJ, Levett JM, Beere P, Anagnostopoulos CE (1982) Acute aortic dissection. An historical review. J R Coll Surg Edinb 27:195–199 62b. Sanderson CJ, Rich S, Beere PA, Anagnostopoulos CE, Levett JM, Lawrence JM (1981) Clotted False Lumen – A Reapprasial of Indications for Medical Management of Acute Aortic Dissection. Thorax 36:194–199 63. Segura AM, Luna RE, Horiba K et al (1998) Immunohistochemistry of matrix metalloproteinases and their inhibitors in thoracic aortic aneurysms and aortic valves of patients with Marfans syndrome. Circulation 98 [Suppl II]: II331–II337 64. Spittell PC, Spittell JA Jr, Joyce JW et al (1993) Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990). Mayo Clin Proc 68:642 65. Stanson AW, Kazmier FJ, Hollier LH et al (1986) Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg 1:15–23 66. Stefanadis CI, Karayannacos PE, Boudoulas HK et al (1993) Medial necrosis and acute alterations in aortic distensibility following removal of vasa vasorum of canine ascending aorta. Cardiovasc Res 27:951–956 67. Steinmann B, Royce P, Superti-Furga A (1993) The EhlersDanlos syndrome. In: Royce PM, Steinmann B (eds) Connective tissue and its heritable disorders. Wiley-Liss, New York, pp 351–407 68. Strauch JT, Spielvogel D, Lauten A et al (2004) Technical advances in total aortic arch replacement. Ann Thorac Surg 77:581–590
659
660
14.4 Treatment of Aortic Arch Diseases
69. Svensson LG, Crawford ES, Hess KR et al (1993) Deep hypothermia with circulatory arrest: determinants of stroke and early mortality in 656 patients. J Cardiovasc Surg 106:19–31 70. Tan ME, Dossche KM, Morshuis WJ et al (2003) Is extended arch replacement for acute type a aortic dissection an additional risk factor for mortality? Ann Thorac Surg 76:1209–1214 71. Tisnado J, Cho S, Beachley MC et al (1980) Ulcerlike projections: a precursor angiographic sign to thoracic aortic dissection. AJR Am J Roentgenol 135:719–722 71a. Toumpoulis IK, Papakostas JC, Matsagas MI, MalamouMitsi VD, Pappa LS, Drossos GE, DeRose JJ, Anagnostopoulos CE (2004) Superiority of early relative to late ischemic preconditioning in spinal cord protection after descending thoracic aortic occlusion. J Thorac Cardiovasc Surg 128:724–730 71b. Toumpoulis IK, Anagnostopoulos CE, Drossos GE, Malamou-Mitsi VD, Pappa LS, Katritsis DG (2003) Early ischemic preconditioning without hypotension prevents spinal cord injury caused by descending thoracic aortic occlusion. J Thorac Cardiovasc Surg 125:1030–1036 71c. Toumpoulis IK, Anagnostopoulos CE, Drossos GE, Malamou-Mitsi VD, Pappa LS, Katritsis DG (2003) Does ischemic preconditioning reduce spinal cord injury because of descending thoracic aortic occlusion? J Vasc Surg 37:426–432
72. Treasure T (2000) Cardiovascular surgery for Marfan syndrome. Heart 84:674–678 73. Tunick PA, Kronzon I (1990) Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography. Am Heart J 120:658–660 74. Tunick PA, Perez JL, Kronzon I (1991) Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 115:423–427 75. Vilacosta I, San Roman JA, Aragoncillo P et al (1998) Penetrating atherosclerotic aortic ulcer: documentation by transesophageal echocardiography. J Am Coll Cardiol 32:83–89 76. Vilacosta I, San Roman JA (2001) Acute aortic syndrome. Heart 85:365–368 77. von Kodolitsch Y, Csosz SK, Koschyk DH et al (2003) Intramural hematoma of the aorta: predictors of progression to dissection and rupture. Circulation 107:1158–1163 78. Yucel EK, Steinberg FL, Egglin TK et al (1990) Penetrating aortic ulcers: diagnosis with MR imaging. Radiology 177:779–781 79. Yun KL, Glower DD, Miller DC et al (1991) Aortic dissection resulting from tear of transverse arch: is concomitant arch repair warranted? J Thorac Cardiovasc Surg 102:355–368
661
Subject Index
α2-agonists 98 β-blockers 97, 98, 132 A abciximab 133 abdominal angina 407, 417 abdominal aortic aneurysm 317 – aetiology 317, 333 – bladder cancer and 615, 616 – definition 317 – diagnosis 89, 321, 334 – endovascular repair 327, 343–347 – epidemiology 317, 332 – inflammatory 320, 331–341 – open repair 325 – risk of rupture 319 – rupture 320, 334 – screening 321 – symptoms 320, 333 – therapy 89, 322, 336 – treatment options 325 abdominal aortic reconstruction, quality control 119 acetylsalicylic acid 168 acidosis, after acute limb ischaemia 452 acrocyanosis 242 acrogeria 655 acute aortic syndromes 652 acute leg/limb/lower extremity ischaemia 449–457 – diagnostic procedures 90 – therapy 91 acute peripheral arterial occlusion 449–457 acute renal ischaemia 422 adhesion molecules 26 Adson’s manoeuvre 251 adventitial cystic disease 479 algodystrophy 245 Allen test 219, 247 amaurosis fugax 140
amputation 438, 476, 485, 494, 497, 501, 502, 525–535, 583, 602, 603, 627 – above-knee 533 – below-knee 532 – classification 627 – complications 535 – level of 527 – ray 529 – rehabilitation 534 – Syme’s 531 – toe 528 – transmetatarsal 530 – upper extremity 534 amputation, for upper extremity vascular trauma 259 anaesthesia 95 anastomosis 624 – end-to-end microvascular 624 – end-to-side microvascular 626 anastomotic aneurysms 463–465 aneurysms, upper extremity 232 angiodysplasias 573 angiography 117, 121, 124, 175, 188 – for aortic dissection 285 – in acute intestinal ischaemia 418 – in Buerger’s disease 473 – in chronic splanchnic ischaemia 402 – in obstructed aortic arch 641 – in trauma of the thoracic aorta 303 angioplasty 211, 364, 427, 431 – cutting balloon 431 – for aortoiliac disease 210 – for aortoiliac occlusive disease 210, 360, 364, 438 – for Buerger’s disease 476 – for carotid stenosis 149, 181–197, 213, 214 – for chronic splanchnic ischaemia 406 – for coarctation of the aorta 639 – for coronary artery disease 212–214 – for coronary stenosis 214
662
Subject Index
– for fibromuscular dysplasia 168, 169 – for lower limb ischaemia 427 – for subclavian artery stenosis 226 – for Takayasu’s arteritis 644 – for thoracic outlet syndrome 255 – laser 431 – patch 259, 454, 455 – subintimal 427 – ultrasonic 431 angioscopy 118, 123, 159, 440 angiotensin 28, 168 angiotensin-converting enzyme 24 angiotensin converting enzyme inhibitors 112, 114 angiotensin II receptor blockers 114 ankle brachial pressure index 12, 51, 509 – for lower extremity vascular trauma 486 antibiotic-bonded grafts 610 antibiotic prophylaxis 100, 600 – local 602 – primary 600 – secondary 602 antibiotics 597–611 antibiotic suppressive treatment 603 anticardiolipin antibodies 45 anticholinergic therapy 242 anticoagulants 552 anticoagulant therapy, for subclavian vein thrombosis 255 anticoagulation, for extracranial carotid aneurysms 176, 178 antimicrobial therapy 599 antiperspirants 241 antiphospholipid antibodies 45 antiplatelet agents 32, 114, 593 – for aortic arch thrombosis 650 – for carotid stenosis 133, 139, 145, 181 – for extracranial carotid aneurysms 178 antithrombin III deficiency 44 aortic arch aneurysms 639 aortic arch atherosclerotic aneurysm 645–648 aortic arch syndrome 222, 643 aortic arch thrombosis 649 aortic arch trauma 650 aortic dissection 277, 652 – aetiology 277 – classification 278, 652 – complications 283, 293 – diagnosis 285 – epidemiology 277 – prognosis 289
– symptoms 282 – therapy 289 aortic stump 327, 366, 379, 603 aortitis syndrome 643 aortoarteritis 643 aortocaval fistula 320, 327, 334 aortoenteric fistula 320, 323, 327 – primary 320 – secondary 323 aortography, in aortic intramural hematoma 640 aortoiliac endarterectomy 368 aortoiliac occlusive disease 355 – aetiology 357 – classification 356 – differential diagnosis 363 – epidemiology 357 – prognosis 363 – symptoms 358 – treatment 360 aortorenal by-pass 169 arachnodactyly 654 arterial closure devices infections 608 arterial embolism 449 arterial embolus, treatment 453 arterial injuries 451 arterial prostheses 11 arterial thrombosis 450 arterial thrombosis, treatment 454 arteriography 7, 12, 67–72 – complications 70 – for upper extremity vascular trauma 258 – in carotid stenosis 141 – in extracranial carotid aneurysms 176 arteriovenous fistula 6, 232, 589–591 – posttraumatic 494 arteriovenous grafts 591–594 arteriovenous malformations 573 – classification 574 arteriovenous shunt 587, 589–591 – external 587 – internal 589 ascites 566 – chylous 566 aspirin 133, 145 atherectomy 431 – directional 431 – vibrational 431 atherosclerosis 23, 209 atherosclerosis, upper extremity 222 atherosclerotic plaque 23–32
Subject Index
– classification 30 atorvastatin 35, 36 atropine 132 autotransfusion 99 axillary artery 369 B bacterial colonization, of atherosclerotic plaques 597 bacterial colonization, of graft 602 block matching 80 blue rubber bleb nevus syndrome 578 blue toe syndrome 356, 358, 450 botulinum A toxin–haemagglutin complex 242 brachial artery 220, 221, 222, 226, 232 brachial artery, trauma to 257 brain protection devices 184 – distal occlusion balloon 184 – filters 184 – proximal occlusion system 186 Buerger’s disease 471–477 – upper extremity 226–228 bupivacaine 97 by-pass 226, 267, 289, 307, 361, 362, 365, 366, 367, 368, 369, 371, 372, 375, 404, 422, 427, 428, 437, 454, 482 – aortobifemoral laparoscopy-assisted 375 – aortobifemoral totally laparoscopic 375 – aortobifemoral totally laparoscopic, with Coggia’s technique 372 – aortobifemoral video-assisted 371 – aortofemoral 365 – aortoiliac 366 – aortorenal 422 – aortovisceral 404 – axillobifemoral 361 – axillofemoral 362, 369 – cardiopulmonary 289, 307 – carotid-subclavian 226 – extracranial-intracranial 178 – femoro-distal 427, 482 – femoro-femoral 362, 368 – femoro-popliteal 428 – femorodistal 437–446 – for Buerger’s disease 476 – graft thrombectomy 454 – iliofemoral 368 – left heart 267, 307 – subclavian–subclavian 226 – thoracoiliofemoral 367 by-pass graft thrombosis, treatment 454
C C-reactive protein 36, 37, 111 calcium channel blockers 98, 239 calcium channel blockers, in Buerger’s disease 476 capillaroscopy 220 capillary microscopy 53 captopril 239 cardiac catheterization, in aortic arch aneurysms 646 cardiac ischaemia 97 – monitoring 96 – prevention 97 carotid-subclavian by-pass 226 carotid artery 11 carotid body tumour 201–208 – aetiology 201 – complications 202 – diagnosis 203 – differential diagnosis 208 – epidemiology 201 – Shamblin classification 202 – symptoms 202 – therapy 206 carotid disease – diagnostic procedures 91 – treatment 91 carotid dissection 174 carotid endarterectomy 146, 212 – anaesthesia 132 – cerebral monitoring 132 – cerebral protection 132 – quality control 124 – shunt 132 carotid procedures 131 – adjuvant medical therapy 133 – cerebral embolization 133 – complications 131 – transcranial doppler 131 carotid stenosis 181, 212–214 – atheroembolization 138 – clinical manifestation 140 – diagnosis 56–59, 141 – endovascular treatment 149 – indications for angioplasty 181 – indications for surgery 181 – medical treatment 145 – noninvasive diagnosis 56–59 – plaque activity 138 – surgical treatment 145 carotid stenting 183 – complications 193
663
664
Subject Index
– follow-up 195 – peri-operative monitoring 193 – preoperative evaluation 187 – technique 190 catecholamines, in carotid body tumour 201 catheters 588 – angiographic 70 – femoral 589 – jugular 588 – subclavian 588 causalgia 244, 245 cavernous malformations 578 cellulitis 512 cerebrospinal fluid drainage 268 Charcot arthropathy 506 Charles reduction 569 chemodectoma 201 chest radiography – in aortic arch aneurysms 646 – in trauma of the thoracic aorta 303 cholesterol 35, 36, 37 chronic lower limb ischaemia – diagnostic procedures 89–90 – treatment 90 clopidogrel 133, 145, 168 clotting disorders 41 coagulation factor 45 coarctation of the aorta 639 Cobb syndrome 579 Cockett’s perforators 12 coeliac artery aneurysms 411 coeliac axis compression syndrome 401 cold hypersensitivity 243 collagen, in aneurysm wall 317 colon ischaemia – after abdominal aortic aneurysm repair 322 – after endovascular aneurysm repair 327 common femoral artery aneurysms 462–466 compartment syndrome 455, 493 complex regional pain syndrome 245 compression devices, for lymphoedema 568 compression stockings, for lymphoedema 562, 568 compression therapy 545, 552, 556 – for arteriovenous malformations 582 computed tomographic angiography – in carotid stenosis 58 – in peripheral arterial disease 54 – in upper extremity vascular trauma 258 computed tomography 189 – in abdominal aortic aneurysm 321
– in aortic arch aneurysms 646 – in aortic dissection 285 – in carotid stenosis 144 – in extracranial carotid aneurysms 175 – in inflammatory abdominal aortic aneurysm 335 – in trauma of the thoracic aorta 304 computer-aided diagnosis 77–82 congenital anomalies, upper extremity 225 connective tissue disorders 230 continuous wave (CW) doppler 117 contrast encephalopathy 193 contrast media 69 coronary artery by-pass grafting 211–213 coronary artery disease 209–214 corticosteroids – for arteriovenous malformations 582 – for inflammatory abdominal aortic aneurysm 336 – for Takayasu’s arteritis 644 cranial nerve injury 177 cranial nerves – in carotid body tumour 202, 206, 208 – in carotid endarterectomy 146, 148 creatinine 113 crescendo TIAs 140 CREST syndrome 231 critical limb ischaemia 427, 438 crossover by-pass 226 cryoglobulinemia 226, 229 cryoplasty 432 cryptogenic emboli 450 cutaneomeningospinal angiomatosis 579 cutaneous livedo 450 cystic medial necrosis 652 cytomegalovirus, in inflammatory abdominal aortic aneurysms 333 D D-dimer assay 61 D-dimers 114, 418, 552 Dacron graft 308 – for abdominal aortic aneurysm 317 – for thoracoabdominal aneurysms 267, 271 – for trauma of the thoracic aorta 307, 308 – properties affecting infection risk 598 Dacron patch infection 607 deep vein thrombosis 551–557 – noninvasive diagnosis 61, 551 – prophylaxis 100, 556 devascularization, for arteriovenous malformations 583 dextran 133
Subject Index
diabetes – aortography in 68 – aortoiliac occlusive disease and 357, 360 – fibrinolytic activity in 45 – infection and 602, 610 – preoperative evaluation 85, 86, 90 – vascular disease and 29, 111–114 diabetic foot 501 – aetiology 503 – complications 506 – definition 501 – diagnosis 507 – epidemiology 501 – infections 510–517 diabetic neuropathy 503 diabetics, femorodistal by-pass and 442–443 digital arteritis 229 digital artery aneurysm 232 digital ischaemia, in Raynaud’s syndrome 237–239 digital pressure 52 dilatation of the internal carotid artery 170 diltiazem 239 dipyridamole 593 dissection, as complication of arteriography 71 distal artery aneurysms 468 distichiasis 563 diverticulum of Kommerel 226 dobutamine 231, 642 dobutamine stress echocardiography 266 dolichostenomelia 654 dopamine 98, 102, 132, 231, 642 doppler 122 – in carotid stenosis 56 – in chronic venous insufficiency 61 – in peripheral arterial disease 52 – ultrasonography 12 drug injection 231 Drummond’s marginal arch 355 duplex 54, 56, 118, 122, 125, 188 – in aortic dissection 285 – in aortoiliac occlusive disease 359 – in Buerger’s disease 473 – in carotid stenosis 141 – in chronic splanchnic ischaemia 402 – in extracranial carotid aneurysms 175 – in intestinal ischaemia 418 – in periphal arterial disease 54 – in upper extremity vascular trauma 258 – in venous insufficiency 544 – in venous thrombosis 552
dysfibrinogenemia 41 dysphagia lusoria 225 E echocardiography – in aortic arch aneurysms 646 – in aortic dissection 285 – in obstructed aortic arch 642 Ehlers–Danlos syndrome 277, 327, 411, 655 Ekk’s fistula 6 elastin, in aneurysm wall 317 elephantiasis 566 elephant trunk technique 647 embolectomy 6, 7, 369, 454 – balloon 454 – catheter 454 – femoral 369 – percutaneous aspiration 454 embolectomy, complications of 455 embolectomy, upper extremity 221 embolism 5, 220 – aetiology 221 Embolism, upper extremity 220 embolization, for arteriovenous malformations 582 endarterectomy 432 – radiologically guided 432 endarterectomy, for femoro-popliteal occlusions 432 endoaneurysmorraphy 6 endoleakage 323, 328 endoprostheses 14 endotension 323 endothelial cells 23–32 endothelium 113 endovascular repair – of abdominal aortic aneurysms 322, 327–329 – of aortic arch aneurysm 347 – of aortic bronchial fistula 349 – of aortic dissection 347 – of aortoenteric fistula 349 – of difficult aortic aneurysms 343–347 – of extracranial carotid aneurysms 178 – of inflammatory abdominal aortic aneurysms 338 – of lower limb ischaemia 427–433 – of thoracoabdominal aneurysms 269 – of trauma of the thoracic aorta 309 – of upper extremity vascular trauma 258 – of visceral artery aneurysms 414 – using aortouniiliac endoprothesis 387–395 endovascular surgery 101 – peri-operative care 101
665
666
Subject Index
– training 107 epinephrine 231 eversion carotid endarterectomy 155–159 – advantages 159 – disadvantages 159 – technique 155–158 extracranial carotid aneurysms 173–179 – aetiology 173 – complications 175 – definition 173 – diagnosis 175 – epidemiology 173 – symptoms 175 – treatment 176 extraperitoneal exposure – of abdominal aorta 366 – of iliac arteries 367 – of thoracoabdominal aorta 367 F F. P. Weber syndrome 579 facial nerve 206 factor V Leiden 44 false aneurysm 7 – after carotid surgery 174 – iatrogenic 491 – of abdominal aorta 321 – posttraumatic 277, 279, 494 fasciotomy 455, 493, 496 fatty streak 25 femoral artery – anastomotic parietal circulation and 355 – in aortic dissection 282 – in aortofemoral by-pass 366, 376 – in aortoiliac occlusive disease 356, 365 – in endovascular aneurysm repair 322 – in femorofemoral by-pass 369 – in left heart by-pass 267 fibrinogen 112 fibrinolysis 114 fibrinolytic factors 41 fibromuscular dysplasia 231 – classification 161 – complications 168 – diagnosis 168 – differential diagnosis 169 – pathophysiology 161 – prognosis 169 – treatment 168 filariasis 566
filter – for cerebral protection 133, 178, 184 – infection 609 – vena cava 72 first-order statistics 78 flavonoids 545 flowmetry 119, 124, 132 foam cells 26 fondaparinux 556 fractal dimension 79 G gadolinium 285 gangrene – after acute limb ischaemia 452 – in arteriovenous fistula 590 – in Buerger’s disease 473 – in diabetics 502, 508–512 – in popliteal entrapment 480 – of foot 438 gastroduodenal artery aneurysm 411 giant cell aortitis 277 giant cell arteritis 226 global cerebral ischaemia 140 glossopharyngeal nerve 201, 208 Gott shunt 293 graft 439, 440 – composite 440 – for peripheral arterial occlusive disease 437–444 – in abdominal aortic aneurysm 322 – in aortic dissection 289–294 – in aortoiliac occlusive disease 361, 362 – in carotid body tumour resection 207 – in eversion endarterectomy 159 – in extracranial aneurysm repair 177 – in situ vein 440 – in superior mesentric artery disease 405 – in thoracic outlet syndrome 253 – in thoracoabdominal aortic aneurysm repair 267– 272 – in trauma of the thoracic aorta 307 – in upper extremity vascular trauma 259 – in visceral aneurysm repair 414 – nonreversed vein 440 – reversed vein 439 – surveillance 443 graft infection 327, 597–611 graft thrombectomy 454 graft thrombosis 449, 450 granulocyte colony-stimulating factor 517
Subject Index
grey level difference statistics 79 Gsell–Erdheim syndrome 277 H Hach classification 543 haemangiectatic hypertrophy 576 haemangiomas 574 haematoma, as complication of arteriography 68, 71 haemodialysis 587–594 haemodialysis prosthetic graft infection 609 haemodynamic forces 26 haemoglobin A1c 32 haemorrheological drugs 361 hammer syndrome 233 hemiarch replacement 647 heparin 12, 45, 99, 133, 145, 646 hepatic artery aneurysms 412–415 high-resolution ultrasonography 143 Hollenhorst plaque 144 Holter monitoring 98 Homans procedure 569 homocysteine 111 homocysteinemia 28 Horner’s syndrome 167, 175 hybrid procedure, for thoracoabdominal aneurysm repair 269 hybrid procedures, for lower limb ischaemia 428 hyperbaric oxygen 12, 517 hypercoagulation states 41 hyperhidrosis 240 hyperhomocysteinemia 44 hyperlipidaemia 35 hypermobility syndrome 655 hyperperfusion syndrome 131, 193 hypersensitivity vasculitis 230 hypertelorism 656 hypertension 28 – in coarctation of the aorta 639 – in renal artery fibromuscular dysplasia 161–169 – in Takayasu’s arteritis 644 – intra-abdominal 421 hyperviscosity syndromes 450 hypoglossal nerve 202, 208 hypothenar hammer syndrome 231, 232, 233 hypothermia – in aortic arch repair 643, 646, 651 – in aortic dissection repair 289 – in thoracoabdominal aneurysm repair 268 – perioperative 96 hypothermic circulatory arrest 268
I iatrogenic aneurysms 462, 464, 465 iatrogenic ischaemia, upper extremity 233 iatrogenic ischemic accidents 233 iliac artery 270, 283, 322, 325–328 – laparoscopic exposure 378 – retroperitoneal exposure 376 iliac compression syndrome 12 iloprost, in Buerger’s disease 476 image analysis 78 impotence, in aortoiliac occlusive disease 356, 358 infection 597–611 – antibiotic selection 601 – classification 515 – imaging 599 – microbiology 598 – of diabetic foot 510–517 – pathogenesis 597 – prevention 600 innominate artery 283, 647 instrumental recanalization 427 insulin resistance 114 interrupted aortic arch 641 intestinal angina 168 intestinal ischaemia 168, 403, 417, 420 – acute 417 – after aortoiliac surgery 420 – after endovascular aneurysm repair 420 intimal fibroplasia 161, 164 intimal hyperplasia – after embolectomy 455 – at the anastomotic site 450, 454 – in fibromuscular dysplasia 161, 164, 167 intramural haematoma 640 intramural haemorrhage 277 intravascular ultrasonography 118 – in aortic dissection 285 – in aortic intramural hematoma 640 iontophoresis 241 ischaemia-inducing agents 231 ischaemic penumbra 138 J juxtarenal aortic occlusion 366 K Kasabach–Merritt’s syndrome 578 kidney 326, 343, 350, 591 – arteriovenous malformation 578 – artificial 591
667
668
Subject Index
– horseshoe 326, 343, 350 – hypothermic protection 268 – ischaemic injury 99 – revascularization 88 – tumour 615, 617 Klippel–Trenaunay syndrome 579 L labetolol 640 laminar flow 27 laparoscopic surgery 371 laparoscopy-assisted aortic procedures – complications 382 – indications 383 – retroperitoneal route 376 – transperitoneal route 375 Laplace’s law 343 laser doppler fluxmetry 53 laser therapy, for arteriovenous malformations 582 laws’ texture energy 79 Leriche’s syndrome 8, 355 ligation, of the carotid 178 limb oedema, etiology 562 livedo reticularis 243 losartan 239 low density lipoproteins 28 lower extremity aneurysms 459 lower extremity by-pass, quality control 120 low molecular weight heparin 552, 556 lupus anticoagulant 45 lymph–venous anastomosis 12 lymphangiography 11, 567 lymphangiosarcoma 566 lymphangitis 568 lymphatic by-pass 569 lymphocytes 25, 26 – in artherogenesis 29 – in Takayasu’s arteritis 643 lymphoedema 11, 12, 561–570 – aetiology 563 – definition 563 – diagnosis 566 – epidemiology 563 – primary 563 – secondary 565 – symptoms 566 – treatment 568 lymphography 568 lymphorrhoea 394, 395
M Maffucci’s syndrome 579 magnetic resonance angiography 58, 189 – for aortic dissection 285 – in carotid stenosis 57 – in chronic splanchnic ischaemia 403 – in extracranial carotid aneurysms 175 – in peripheral arterial disease 55 magnetic resonance imaging – in abdominal aortic aneurysm 321 – in aortic arch aneurysms 646 – in aortic intramural hematoma 640 – in carotid stenosis 144 malignant tumours, upper extremity 226 mangled extremity syndrome 634 mannitol 98, 455 Marfan’s syndrome 277, 640, 654 marfanoid hypermobility syndrome 654 markers of inflammation 114 matrix metalloproteinases 517 medial degeneration 645 medial fibrodysplasia 162, 164 medial haematoma 640 medial hyperplasia 161 median arcuate ligament syndrome 401 Meige disease 563 mesenteric artery – acute ischaemia 417 – anastomotic circulation 355 – duplex 402 – fibromuscular dysplasia 161, 164 – in abdominal aortic aneurysm repair 326 – in visceral hybrid procedure 269 – ischaemia 401 – revascularization 119 mesenteric bridge 569 mesenteric steal 358, 359 mesenteric venous thrombosis 419 metabolic syndrome 37, 114 metalloproteinases 318 metaraminol 231 methylenetetrahydrofolate reductase 677T 44 microalbuminuria 114 microvascular surgery 623 – basic principles 623 migration of endograft 323, 328 Milroy disease 563 mimocausalgia 245 minimally invasive surgery 370 motion analysis 80
Subject Index
multifocal arterial disease 209–214 multiple myeloma 229 mural thrombus 30, 31, 251, 449 mycotic aneurysm 232, 463–465 myeloma 239 myeloproliferative disorders 450 myocardial infarction, embolization from 417, 449 N neck, aortic aneurysm 101, 118, 266, 321, 323, 325–328, 343–345, 388 neck, hostile 150 neck coefficient 345 necrotizing fasciitis 515 necrotizing infections 511, 512 neighbourhood grey tone difference matrix 79 nephrectomy, in renovascular hypertension 423 neuro-osteoarthropathy 506 neuropathic ulcer 503 neuropathy 363, 503 – diabetic 363, 433, 503 nicotinic acid 112 nifedipine 239, 244, 245 nitroglycerin 99 nitroprusside 99, 132 nonspecific aortoarteritis 643 nonsteroidal anti-inflammatory drug 100, 422 Noonan syndrome 656 norepinephrine 131, 231 nuclear medicine investigations 204 O obstructed aortic arch 641 – classification 641 occlusive disease 401 occlusive thromboaortopathy 643 OctreoScan® 205 optical flow 80 osteomyelitis 512, 513, 516 oximetry 132 P Paget–Schroetter syndrome 254 Palmaz stent 183, 345 pancreatoduodenal artery aneurysm 411 papaverine 100, 119, 122, 123, 124 paragangliomas 201 paraplegia 308–312 – after aortic aneurysm endovascular repair 395 – after aortic arch repair 640
– – – –
after aortic dissection repair 293 after thoracic aortic trauma repair 307–312 after thoracoabdominal aneurysm repair 268 after thoracoabdominal aortic aneurysm repair 99, 266, 268, 273 – in aortic dissection 283, 653 Parkes–Weber syndrome 576 patch angioplasty, for carotid stenosis 148 patch infection 607 penetrating atherosclerotic aortic ulcer 648 pentoxifylline 239 percutaneous transluminal angioplasty 13 peri-operative monitoring 96, 100 perimedial dysplasia 162 peripheral arterial disease 111 – noninvasive diagnosis 51–55 – risk factors 111 peroneal artery – by-pass to 441 – exposure of 442 phenoxybenzamine 245 phlebodynamometry 544 phlebography 12, 65, 72–74 phlegmasia cerulea dolens 220, 452, 457 photocoagulation 582 photoplethysmography 60, 544 plantar arch 441, 620 plaque – activity 138 – bacterial colonization 597 – characteristics 54, 77–80, 133, 139, 143, 182, 648 – complicated 30 – cryoplasty of 432 – embolization from 133, 138, 140, 212, 222, 648 – in carotid endarterectomy 146–148, 156–159 – instability 30 – motion 80 – stabilization 37, 95, 145 – thrombosis on 90, 138, 358, 450 – ulceration 223 plasminogen 45 plasminogen activator inhibitor 24, 43, 95, 114 platelet-derived growth factor 24, 506 platelet aggregation 23, 133, 138, 145, 212, 598 platelets 114 plethysmography 12, 52, 60–61, 238, 475, 509, 580 polyarteritis nodosa 231 polyarthritis nodosa 411 polycythaemia 226, 239, 420 popliteal aneurysm 4, 6, 452, 459–462
669
670
Subject Index
popliteal artery entrapment 479 – classification 480 Port-Wine stains 578 positron emission tomography 131, 132, 146 post-thrombotic syndrome 557 postoperative gut function 101 postoperative ileus 102 postoperative pain treatment 100 prazosin 239 pregnancy – clotting disorders 41–43, 45–46 – Marfan’s syndrome and 654 – visceral artery aneurysm and 414 preoperative planning 95 propranolol 102, 640 prostacyclin 23, 24, 26, 28, 506 prostaglandin 23, 24, 231, 239 – for obstructed aortic arch 642 prostaglandin analogue 476 prostaglandin analogues 228 prostanoids 90 prosthetic carotid patches infections 607 prosthetic graft infections 602 protamine 99, 133, 646 protein C deficiency 44 protein S deficiency 44 Proteus syndrome 579 prothrombin gene mutation 20210A 44 prothrombin time 96, 193 pseudo-allergic reactions, after arteriography 71 pseudoaneurysm – after AAA repair 323 – after endovascular AAA repair 327, 393 – as complication of arteriography 71 – as complication of carotid patch infection 607 – as complication of haemodialysis prosthetic graft infection 610 – as complication of prosthetic graft infection 602, 603 – as complication of thrombolysis 456 – of the carotid arteries 178 – of the thoracic aorta 301, 303, 304, 648, 651, 652 – of the upper extremity arteries 233, 258 – of vascular access 590 pseudointima 598 pseudoxanthoma elasticum 655, 656 pulmonary arteriovenous malformations 578 pulmonary artery catheterization 96 pulmonary artery reconstruction 642 pulmonary complications 86, 100 pulmonary embolectomy 7, 10
pulmonary embolism 41, 46, 254, 327, 364, 420, 551, 552, 553, 609 pulmonary wedge pressure 366 pulseless disease 643 pulse volume recording 52 Q quality of life, after femorodistal by-pass 445 quality of life, after lower limb arterial recenalization 430 R radial artery – Allen test 219, 247 – angiography access 190, 191 – in vascular access surgery 587, 589–591 radiation arteritis 150, 226, 401 radicular artery 283 Raeder’s paratrigeminal syndrome 175 Raynaud’s disease 237 Raynaud’s phenomenon 219, 237 – in Buerger’s disease 472 Raynaud’s syndrome 237 – aetiology 239 – in Buerger’s disease 227 – in thoracic outlet syndrome 251 – in upper extremity vascular trauma 233 recombinant human tissue plasminogen activator 455 recurrent obstruction of the aortic arch 642 refenestration 290 reflex sympathetic dystrophy 245 region tracking 80 renal artery – aneurysms 411–414 – angiography 120 – CT angiography 54 – embolectomy 422 – embolism 422 – fibromuscular disease 161 – in aortic dissection 278, 283 – in thoracoabdominal aneurysms 265–273 – MR angiography 55 – stenosis 88 – thrombosis 422 renal autotransplantation 169 renal cell carcinoma 615, 616 – involving the vena cava 616 renal failure 587, 588 – in renal artery fibromuscular dysplasia 167, 169
Subject Index
renal function impairment, as complication of arteriography 71 renal insufficiency 51, 69, 88, 98–100, 113, 114, 609 – after AAA repair 323 – after aortic dissection 641 – after lower limb replantation 631 – femorodistal by-pass and 442 – in inflammatory abdominal aortic aneurysms 332 renal revascularization 88, 168 – duplex 120 – quality control 120 renal tubular necrosis 455 renal vein 325, 376 Rendu–Osler disease 578 renin 131, 168, 423 renovascular hypertension 13, 283, 423 reperfusion injury 102, 268, 364, 405, 419, 454, 455, 485, 493 reperfusion syndrome 455 replantation 626 – complications 632 – in children 631 – postoperative management 630 – preoperative care 628 – selection criteria 627 – surgical preparation 628 – surgical techniques 628 resistance to activated protein C 44 restenosis – after by-pass 440 – in Takayasu’s arteritis 644 – of carotid arteries 124–127, 133, 148, 149, 155, 195–197 – of renal arteries 120 – of visceral arteries 119 – postangioplasty 112 retroesophageal subclavian artery 225 retrograde cerebral perfusion, in aortic arch aneurysms 646 revascularization 419, 630 – for arteriovenous malformations 583 – for chronic splanchnic ischaemia 404 – for upper extremity vascular trauma 259 – lower limb 631 – of the superior mesenteric artery 419 – upper limb 630 reversible cerebral ischaemia 140 rheumatoid arthritis 219, 231 Riolan’s arch 355 risk stratification
– cardiovascular system 85–86 – renal system 88 – respiratory system 86–88 rupture, of visceral artery aneurysms 412 S “steal” phenomenon 233 saphenous vein graft – for Buerger’s disease 476, 477 – for carotid artery repair 159, 169, 177, 207 – for femorodistal by-pass 439, 440, 443, 444 – for renal artery revascularization 170 – for thoracic outlet syndrome 253–254 – for vascular trauma repair 259, 496 Schwan-Ganz catheter 96 scimitar sign 481 scleroderma 219, 231 sclerotherapy 93, 545 – for arteriovenous malformations 582 second-order statistics 78 segmental limb systolic pressure 52 Seldinger 12, 13 Seldinger’s technique 69, 72, 364, 365, 388, 589 serotonin 102, 471 Servelle and Martorell’s syndrome 579 shear stress 26, 27, 30, 174, 598 shunt – arteriovenous 587–594 – carotid 132, 146, 159, 177, 207 – for vascular trauma repair 307, 308, 489, 495, 497 – in arteriovenous malformations 573–583 simvastatin 36 single photon emission computed tomography 205 Sistrunk procedure 569 Sjögren’s syndrome 219 slime 598, 599 small aortic syndrome 355, 356 smoking 25, 28 – abdominal aortic aneurysm and 318, 319, 325 – atherosclerosis and 28, 31, 32 – Buerger’s disease and 471, 476, 477 – carotid restenosis and 125 – carotid stenosis and 145, 222, 228 – coronary artery disease and 85 – fibrinogen levels and 112 – fibromuscular dysplasia and 167 – peripheral arterial disease and 88, 90, 95, 101, 102, 111, 357, 437 – pulmonary complications and 86 – Raynaud’s syndrome and 237
671
672
Subject Index
smooth muscle cells 23–32 sodium bicarbonate, for reperfusion syndrome 455 somatosensory-evoked potentials 269 somatostatin receptor scintigraphy 205 spinal cord 268, 269 – monitoring 269 – protection 268 spinal cord ischaemia 99, 283, 293, 307 spinal cord stimulation 90, 226, 228, 231 – for Buerger’s disease 477 spiral computed tomography, in aortic intramural hematoma 640 splenic artery aneurysms 411 staphylokinase 455 statins 32, 35–38, 133, 145 steal phenomenon 402, 576, 577 steal syndrome, in arteriovenous fistula 590 stent infections 604 – risk factors 605 stents 427 – covered 429 – drug-eluting 429 streptokinase 455, 456 stress tests 480 stroke 137–141, 146 – after CABG 212 – after carotid stenting 194, 196 – carotid endarterectomy for 124–127 – epidemiology of 137 – fibromuscular dysplasia and 165, 167, 170 – imaging studies for 57, 58, 65, 144 – in aortic arch disease 641, 644, 645, 648, 649 – in evolution 140 – pathogenesis 138 – perioperative 133, 148, 155, 175–178, 212, 607 – prevention of 36 – risk factors for 28, 111–113 stump pressure – carotid 132, 148 – inferior mesenteric artery 421 Sturge–Weber–Krabbe’s syndrome 579 subclavian–axillary vein thrombosis 254 subclavian artery 222 – aortic dissection and 282, 283 – coverage by endovascular graft 270, 311, 347 – injury of 249, 258, 259 – occlusive disease 222–226 subclavian steal 222 subintimal angioplasty 14
Sudeck’s atrophy 245 superficial femoral artery aneurysms 466–467 superior laryngeal nerve 202, 208 superior mesenteric artery – aneurysms 411 – occlusive disease 401 superior vena cava syndrome 302, 645, 654 surgical techniques 628 Swan Ganz catheter 366 sympathectomy 90, 226, 231, 239, 242, 476 – for cold hypersensitivity 245 – for complex regional pain syndrome 246 – for hyperhidrosis 242 – for livedo reticularis 243 – lumbar 90, 476 – thoracic 239, 242, 476 – thoracocervical 226 sympathetic blockade, for complex regional pain syndrome 245 syncope, in aortic dissection 653 systemic inflammatory vasculopathy 174 systemic lupus erythematosus 230 T Takayasu’s arteritis 226, 643–645 – classification 644 – prognostic classification system 645 TcpO2 53 telangiectasias 578 temperature control 96 texture analysis 78 thoracic outlet decompression 255 thoracic outlet syndrome 247 – arterial 251 – combined supra-clavicular and infra-clavicular approach 252 – neurogenic 247 – transaxillary resection of the first rib 248 thoracoabdominal aneurysm 265 – classification 265 – imaging 266 – treatment 267 thoracotomy 307 – posterolateral 307 thrombangiitis obliterans 226, 471 – upper extremity 226 thrombectomy – for deep venous thrombosis 553 – of aortic arch 649
Subject Index
– of carotid artery 148 – of graft 328, 394, 454 – of subclavian vein 255 thrombo-endarterectomy 10 thrombocytopenia 578, 619 thrombolysis 14, 455–457 – for acute renal ischaemia 422 – for deep venous thrombosis 553 – for intestinal ischaemia 419 – for subclavian vein thrombosis 255 thrombophilia 41–47, 420 – definition 41 – diagnosis 45, 46 – treatment 46, 47 thrombosis 5, 12 – after vascular trauma 257, 485, 489, 491 – aortic arch 649 – aortoiliac 356–365 – arterial 90, 221, 449 – arteriovenous shunt 587, 588 – Buerger’s disease and 471 – carotid artery 138, 185, 206, 207 – deep vein 41, 61, 220 – graft 390, 391, 443, 450 – mesenteric vein 419, 420 – mesentric artery 417 – subclavian-axillary vein 254, 255, 588 – ulnar artery 231 – venous 12 – visceral artery aneurysm 412 thromboxane 24, 25, 506 tibial artery, by-pass to 441, 442 tibio-peroneal angioplasty 428 ticlopidine 145 tissue plasminogen activator 24, 327 tonometry, in chronic splanchnic ischaemia 403 total arch replacement 647 totally laparoscopic aortic procedures 377 – combined transperitoneal and retroperitoneal procedures 379 – complications 382 – direct transperitoneal procedure 380 – indications 383 – retrocolic or prerenal transperitoneal procedure 377 – retroperitoneal operation 380 transaortic endarterectomy 404 transcranial doppler 132, 133, 144 transcutaneous oxygen measurements 53 transient cerebral ischaemia 140
transient ischaemic attack – aortic arch aneurysms and 645 – carotid stenosis and 91, 138–140, 181 – extracranial carotid aneurysms and 175 – fibromuscular carotid disease and 165, 167 – Takayasu’s arteritis and 644 translumbar aortography 68 transoesophageal echocardiography – in aortic dissection 285 – in aortic intramural hematoma 640 – in trauma of the thoracic aorta 306 transposition 226 transthoracic echocardiography, in aortic dissection 655 transthoracic endoscopic sympathectomy 242 trauma of the thoracic aorta 299 traumatic 233 traumatic dystrophy 245 treadmill exercise 53, 90, 209, 359 Turner-like syndrome 656 Turner’s syndrome 277 U ulcer 503, 505, 509, 510 – classification 509 – diagnosis 509 – ischaemic 505 – neuroischaemic 510 – neuropathic 503, 510 ulnar artery – Allen test 219, 247 – aneurysm 232 – thrombosis 231 ultrasonography – in abdominal aortic aneurysm 321 – in chronic venous insufficiency 61 – in inflammatory abdominal aortic aneurysm 335 umbilical vein, as allograft 440, 592 upper extremity – deep vein thrombosis 254, 255 – embolization 450 – fibromuscular dysplasia 164 – occlusive disease 219, 222 – vascular trauma 257–262 urate 113 ureteral involvement, in inflammatory abdominal aortic aneurysm 332, 338 urokinase 45, 122, 455, 457
673
674
Subject Index
V vagus nerve – carotid body tumour and 201, 202, 206, 208 – in carotid endarterectomy 146 varicose veins 3, 5, 7, 92, 539–549 – in arteriovenous malformations 579 – phlebography for 72 vasa vasorum 318 vascular access 69 – for haemodialysis 587–594 – in endovascular aneurysm repair 343 vascular bone syndrome 576 vascular complications – in urological surgery 618 – orthopaedic patients 635 vascular malformations 12, 573 vascular trauma 257, 485, 623 – blunt 257, 488 – iatrogenic 490 – in orthopaedic surgery 623 – lower limb 485 – of the carotids 174 – of the upper extremity 233, 257 – penetrating 257 – sharp 488 vascular tumours 574 vasculitis 169, 229 vasculogenic impotence 12 vasopressin 102, 131, 231 vasospasm 95, 102, 476, 631 – due to carotid filters 185 vasospastic disorders of the upper extremities 237 vein transposition, for subclavian vein thrombosis 255 velocity waveform 52 vena cava 327 – duplicated 327 – filter 72 – filter infections 609 – left-sided 327 – renal cell carcinoma and 615–620 venography – in venous insufficiency 544 – in venous thrombosis 552
venous anomalies 327 venous by-pass 10, 11 venous compression, in inflammatory abdominal aortic aneurysms 332 venous disease – diagnostic procedures 92 – treatment 92 venous gangrene 5 venous hypertension 254, 485, 495, 496 – in arteriovenous fistula 233, 591 venous insufficiency 539–549, 632, 633 – noninvasive diagnosis 59–61 venous thrombosis 5, 41, 551–557 – diagnosis 551 – differential diagnosis 556 – prevention 556 – prognosis 557 – risk factors 41–47, 551 – symptoms 551 – treatment 552 video-assisted surgery 370 Virchow’s triad 5, 551 visceral arteries 411, 417 – acute ischaemia 417 – aneurysms 411 – occlusive disease 401 – revascularization, quality control 119 vitamin K 420 Volkman contracture 631 volume plethysmography – in chronic venous insufficiency 60 – in deep vein thrombosis 61 von Hippel-Lindau syndrome 580 von Willebrand factor 24, 113 W warfarin 45, 69, 145, 552 waveform 52, 80, 238, 359, 360, 580 wrist-brachial index 258 X ximelagatran 556
