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 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)
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, p2. 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 (p5
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, 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 38°C Heart rate >90 beats/min Respiratory rate >20 breaths/min PaCO2 12,000 or 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 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
