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© 2003 by Futura, an imprint of Blackwell Publishing Blackwell Publishing, Inc./Futura Division, 3 West Main Street, Elmsford, New York 10523, USA Blackwell Publishing, Inc., 350 Main Street, Maiden, Massachusetts 02148-5018, USA Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Blackwell Science Asia Pty Ltd, 550 Swanston Street, Carlton South, Victoria 3053, Australia Blackwell Verlag GmbH, Kurfurstendamm 57, 10707 Berlin, Germany All rights reserved. No part of this publication may be reproduced in any form or by any electronic or mechanical means, including information storage and retrieval systems, without permission in writing from the publisher, except by a reviewer who may quote brief passages in a review. 02 03 04 05 5 4 3 2 1
ISBN: 1-4051-0387-6
Library of Congress Cataloging-in-Publication Data Vascular emergencies / edited by Alain Branchereau, Michael Jacobs. p. cm. Includes bibliographical references. ISBN 1-4051-0387-6 (alk. paper) 1. Blood vessels—Wounds and injuries. 2. Blood vessels—Wounds and injuries—Surgery. 3. Cardiovascular emergencies. I. Branchereau, Alain. II. Jacobs, Michael, M.D. RD598.5.V3462 2003 617.4'13044—dc21 2003002267 A catalogue record for this title is available from the British Library
For further information on Blackwell Publishing, visit our website: www.futuraco.com www.blackwellpublishing.com
Notice: The indications and dosages of all drugs in this book have been recommended in the medical literature and conform to the practices of the general community. The medications described do not necessarily have specific approval by the Food and Drug Administration for use in the diseases and dosages for which they are recommended. The package insert for each drug should be consulted for use and dosage as approved by the FDA. Because standards for usage change, it is advisable to keep abreast of revised recommendations, particularly those concerning new drugs.
Edited by
ALAIN BRANCHEREAU, MD University Hospital, Marseille, France
& MICHAEL JACOBS, MD University Hospital, Maastricht, The Netherlands
FUTURA, AN IMPRINT OF BLACKWELL PUBLISHING
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LIST OF CONTRIBUTORS Marko AJDUK University Hospital Merkur Zajceva ul.9 Zagreb, Croatia
Alain BRANCHEREAU Departement de Chirurgie Vasculaire Hopital Adultes La Timone 264, rue Saint Pierre 13385 Marseille Cedex 05, France
Jerome ALBERTIN Departement de Chirurgie Vasculaire Hopital Adultes La Timone 264, rue Saint Pierre 13385 Marseille Cedex 05, France
Jaap BUTH Department of Surgery Catharina Hospital, PO box 1350 5602 ZA Eindhoven, The Netherlands
RaoufAYARI Departement de Chirurgie Vasculaire Hopital Adultes La Timone 264, rue Saint Pierre 13385 Marseille Cedex 05, France Joaquim BARBOSA Vascular Unit Hospital Particular de Lisboa Rua Luis Bivar, 30 1069-142 Lisboa, Portugal Xavier BARRAL Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Nord Avenue Albert Raimond 42055 Saint-Etienne Cedex 2, France Rachel BELL Department of General and Vascular Surgery Guy's & St. Thomas' Hospital Lambeth Palace Road London SE1 7EH, United Kingdom Ramon BERGUER Division of Vascular Surgery Harper Hospital, 3990 John R Detroit, Michigan 48201, USA Ricardo BOFILL Servei d'Angiologia I Cirurgia Vascular Pg Vail d'Hebron 119-129 08035 Barcelona, Spain Didier BOURRAT Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Nord Avenue Albert Raimond 42055 Saint-Etienne Cedex 2, France Bruce BRAITHWAITE Department of Vascular and Endovascular Surgery E Floor, West Block University Hospital, Derby Road Nottingham NG7 2UH, United Kingdom
Piergiorgio CAO Unita Operativa di Chirurgia Vascolare Policlinico Monteluce, Via Brunamonti Perugia 06122, Italy Renata CASTELLANO Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy Laurent CHICHE Departement de Chirurgie Vasculaire CHU Pitie-Salpetriere, 47/83, bd de 1'Hopital 75651 Paris Cedex 13, France Roberto CHIESA Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy Efrem CIVILINI Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy Albert CLARA Servei de Cirurgia Vascular Hospital del Mar, Paseo Maritimo, 25-29 08003 Barcelona, Spain Marc COGGIA Hopital Universitaire Ambroise Pare 9, avenue Charles de Gaulle 92104 Boulogne Cedex, France Jack COLLIN Nuffield Department of Surgery John Radcliffe Hospital Oxford, OX3 9DU, United Kingdom Andreja CRKVENAC University Hospital Merkur Zajceva ul.9 Zagreb, Croatia Philippe CUYPERS Department of Surgery Catharina Hospital, PO box 1350 5602 ZA Eindhoven, The Netherlands
VII
Lourdes DEL RIO Servicio de Cirurgia Vascular Hospital Clinico Universitario 470 HValladolid, Spain
Jose Maria FUENTES Servei d'Angiologia I Cirurgia Vascular PgValld'Hebronll9-129 08035 Barcelona, Spain
Isabelle DI CENTA Hopital Universitaire Ambroise Pare 9, avenue Charles de Gaulle 92104 Boulogne Cedex, France
Mauro GARGIULO Chirurgia Vascolare Universita di Modena e Reggio Emilia Policlinico Universitario, Via del Pozzo n° 71 41100 Modena, Italy
Lucien DUIJM Department of Vascular Surgery Catharina Hospital, PO Box 1350 5602 ZA Eindhoven, The Netherlands Bertrand EDE Departement de Chirurgie Vasculaire Hopital Adultes La Timone 264, rue Saint Pierre 13385 Marseille Cedex 05, France
VIII
Philippe GERSBACH Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland Olivier GOEAU-BRISSONNIERE Hopital Universitaire Ambroise Pare 9, avenue Charles de Gaulle 92104 Boulogne Cedex, France
Ted ELENBAAS Department of Cardiac Surgery Academic Hospital Maastricht PO Box 5800 6202 AZ Maastricht, The Netherlands
Jose GONZALEZ-FAJARDO Servicio de Cirurgia Vascular Hospital Clinico Universitario 47011 Valladolid, Spain
Lidija ERDELEZ University Hospital Merkur Zajceva ul.9 Zagreb, Croatia
Daniel GRANDMOUGIN Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Nord Avenue Albert Raimond 42055 Saint-Etienne Cedex 2, France
Jose Maria ESCRIBANO Servei d'Angiologia I Cirurgia Vascular PgValld'Hebronll9-129 08035 Barcelona, Spain
George HAMILTON Department of Vascular Surgery The Royal Free Hospital NHS Trust Pond Street NWS 2QG London, United Kingdom
Jean-Noel FABIANI Departement de Chirurgie Cardiovasculaire Hopital Europeen Georges Pompidou 20, rue Leblanc, 75015 Paris, France Jean-Pierre FAVRE Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Nord Avenue Albert Raimond 42055 Saint-Etienne Cedex 2, France Maria Jose FERREIRA Vascular Unit Hospital Particular de Lisboa Rua Luis Bivar, 30 1069-142 Lisboa, Portugal
Daniel HAYOZ Departement de Medecine Vasculaire Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland Robert HINCHLIFFE Department of Vascular and Endovascular Surgery E Floor, West Block University Hospital, Derby Road Nottingham NG7 2UH, United Kingdom Brian HOPKINSON Department of Vascular and Endovascular Surgery E Floor, West Block University Hospital, Derby Road Nottingham NG7 2UH, United Kingdom
Adam FISCHER Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland
Michael HORROCKS University of Bath, Room L2.27 BA2 7AYBath, United Kingdom
Natalia de la FUENTE Servei de Cirurgia Vascular Hospital del Mar, Paseo Maritime, 25-29 08003 Barcelona, Spain
Michael JACOBS Department of Cardiovascular Surgery Academic Hospital Maastricht PO Box 5800 6202 AZ Maastricht, The Netherlands
Isabella JAVERLIAT Hopital Universitaire Ambroise Pare 9, avenue Charles de Gaulle 92104 Boulogne Cedex, France Jean Ader JULES Centre Hospitaller Universitaire Cote de Nacre 14033 Caen Cedex, France Pierre JULIA Departement de Chirurgie Cardiovasculaire Hopital Europeen Georges Pompidou 20, rue Leblanc, 75015 Paris, France Edouard KIEFFER Departement de Chirurgie Vasculaire CHU Pitie-Salpetriere, 47/83, bd de 1'Hopital 75651 Paris Cedex 13, France Mark KOELEMAY Unit of Vascular Surgery Academic Medical Center University of Amsterdam, P.O. Box 22700 1100 DE Amsterdam, The Netherlands Brandon KRIJGSMAN Department of Vascular Surgery The Royal Free Hospital NHS Trust Pond Street NWS 2QG London, United Kingdom Dink LEGEMATE Unit of Vascular Surgery Academic Medical Center University of Amsterdam, P.O. Box 22700 1100 DE Amsterdam, The Netherlands Massimo LENTI Unita Operativa di Chirurgia Vascolare Policlinico Monteluce, Via Brunamonti Perugia 06122, Italy
Bettina MARTY Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland Manuel MATAS Servei d'Angiologia I Cirurgia Vascular PgValld'Hebronll9-129 08035 Barcelona, Spain Germano MELISSANO Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy Volker MICKLEY Bereich fur Gefasschirurgie Stadtklinik Baden-Baden, Balger Strasse 50 76532 Baden-Baden, Germany Bas MOCHTAR Department of Cardiac Surgery Academic Hospital Maastricht PO Box 5800 6202 AZ Maastricht, The Netherlands Jorge MOLINA Servei de Cirurgia Vascular Hospital del Mar, Paseo Maritimo, 25-29 08003 Barcelona, Spain Lars NORGREN Department of Vascular Diseases University Hospital MAS 205 02 Malmo, Sweden William PAASKE Department of Cardiothoracic & Vascular Surgery Aarhus University Hospital Skejby Sygehus 8200 Aarhus N, Denmark
Marcelo LIBERATO DE MOURA Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy
Philippe PACHECO Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Nord Avenue Albert Raimond 42055 Saint-Etienne Cedex 2, France
Lars LONN Department of Radiology Sahlgrenska University Hospital SE 413 45 Goteborg, Sweden
Federico PAPPALARDO Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy
Carla LUCCI Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy
Gianbattista PARLANI Unita Operativa di Chirurgia Vascolare Policlinico Monteluce, Via Brunamonti Perugia 06122, Italy
Dominique MAIZA Centre Hospitalier Universitaire Cote de Nacre 14033 Caen Cedex, France
Noud PEPPELENBOSCH Department of Surgery Catharina Hospital, PO box 1350 5602 ZA Eindhoven, The Netherlands
Miguel MARTIN-PEDROSA Servicio de Cirurgia Vascular Hospital Clinico Universitario 47011 Valladolid, Spain
Gunnar PLATE Department of Surgery Helsingborg Hospital 251 87 Helsingborg, Sweden
IX
SalahQANADLI Departement de Radiologie Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland
Andrea STELLA Chirurgia Vascolare Universita di Modena e Reggio Emilia Policlinico Universitario, Via del Pozzo n° 71 41100 Modena, Italy
Paola de RANGO Unita Operativa di Chirurgia Vascolare Policlinico Monteluce, Via Brunamonti Perugia 06122, Italy
Peter TAYLOR Department of General and Vascular Surgery Guy's & St. Thomas' Hospital Lambeth Palace Road London SE1 7EH, United Kingdom
Jan RAUWERDA Department of Surgery Free University, Po Box 7057 1007 MB Amsterdam, The Netherlands Bo RISBERG Department of Surgery Sahlgrenska University Hospital SE 413 45 Goteborg, Sweden John ROBBS Nelson. R. Mandela School of Medicine Faculty of Health Sciences, Private Bag 7 Congella 4013, South Africa Begona ROMAN Faculdad de Filosofia, Departamento de Etica Universitat Ramon Llull, C/Claravall,l-3 08027 Barcelona, Spain
X
Josep ROYO Servei d'Angiologia I Cirurgia Vascular Pg Vail d'Hebron 119-129 08035 Barcelona, Spain Patrick RUCHAT Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland
Alexander TIELBEEK Department of Radiology Catharina Hospital, PO Box 1350 5602 ZA Eindhoven, The Netherlands Ivana TONKOVIC University Hospital Merkur Zajceva ul.9 Zagreb, Croatia Yamume TSHOMBA Chirurgia Vascolare IRCCS H. San Raffaele, Via Olgettina, 60 20132 Milano, Italy Carlos VAQUERO Servicio de Cirurgia Vascular Hospital Clinico Universitario 4701 IValladolid, Spain Fabio VERZINI Unita Operativa di Chirurgia Vascolare Policlinico Monteluce, Via Brunamonti Perugia 06122, Italy Francesc VIDAL-BARRAQUER Servei de Cirurgia Vascular Hospital del Mar, Paseo Maritimo, 25-29 08003 Barcelona, Spain
Geert Willem SCHURINK Department of Vascular Surgery Academic Hospital Maastricht PO Box 5800 6202 AZ Maastricht, The Netherlands
John WOLFE Regional Vascular Unit St. Mary's Hospital, Praed Street London W2 1NY, United Kingdom
Ludwig Karl von SEGESSER Departement de Chirurgie Cardiovasculaire Centre Hospitalier Universitaire Vaudois Rue du Bugnon 46 1011, Lausanne, Switzerland
Michael YAPANIS Regional Vascular Unit St. Mary's Hospital, Praed Street London W2 1NY, United Kingdom
Andrija SKOPLJANAC-MACINA University Hospital Merkur Zajceva ul.9 Zagreb, Croatia
Neval YILMAZ Department of Surgery Catharina Hospital, PO box 1350 5602 ZA Eindhoven, The Netherlands
Tomislav SOSA University Hospital Merkur Zajceva ul.9 Zagreb, Croatia
Stephane ZALINSKI Departement de Chirurgie Cardiovasculaire Hopital Europeen Georges Pompidou 20, rue Leblanc, 75015 Paris, France
FOREWORD
The subject selected for the 2003 European Vascular Course is Vascular Emergencies, and thirty one chapters in this book address the wide spectrum of urgent and emergency vascular problems. The main impetus for choosing this subject is that approximately 40% of vascular surgical practices are determined by vascular emergencies. The majority of pathologies described are applicable to every vascular surgical practice. The first chapter of the book salutes the important issue of bioethical concerns of vascular emergencies. The following three chapters focus on acute dilemmas in carotid artery disorders, including indications for emergency reconstruction. Blunt trauma of the internal carotid artery and stab wounds at the base of the neck do not occur on a daily basis in a standard vascular practice but constitute a challenging problem. Acute aortic pathology includes occlusion of the abdominal aorta as well as rupture. The latter emergency has been treated surgically for many decades and the option ofendovascular repair is appealing. While in general it is advocated that acute type B aortic dissection must be treated conservatively, new insights dictate a more surgical and endovascular attitude. Aortic emergencies also include complications of laparoscopic surgery and traumatic rupture. Acute ischemia of the upper limb is a serious problem, dictating a substantial part of our practice. Acute complications of arteriovenous fistula for hemodialysis are also addressed. Acute ischemia of the lower limb can result from embolization, thrombosis and other rare causes. Furthermore, underlying pathologies such as peripheral aneurysms and diabetes contribute to emergency situations, requiring surgical, endovascular or thrombolytic therapy. Venous emergencies are described in four chapters addressing acute thrombosis of iliocaval veins, axillary and subclavian veins, aortocaval fistula and traumatic injury of the vena cava.
XI
The last part of the book describes the subjects of acute renal artery occlusion, acute intestinal ischemia, ruptured visceral arterial aneurysms, abdominal compartment syndrome and gunshot arterial injury. We aimed for a comprehensive compilation of vascular emergencies and we could only compose this book with the crucial contribution of the authors and co-authors. Substantial editorial work has been performed by Bertrand Ede and Dirk Ubbink. We are very grateful to our secretaries Annie Barral and Claire Meertens and we appreciate the assistance of Iris Papawasiliou. The Odim team, guided by Marie-France Damia, managed once again to have both the English and French versions of this book printed in time. Blackwell Publishing/Futura contributed significantly, with editorial abetment of Joanna Levine and Jacques Strauss. The major sponsors of the biomedical industries are greatly acknowledged because the textbook and the European Vascular Course would not be possible without their continuous support and enthusiasm for this scientific assignment. Maastricht - Marseille, 2003
Michael Jacobs
Alain Branchereau
CONTENTS Contributors Foreword
VII XI
Acute complications following laparoscopic surgery Marc Coggia, IsabelleDi Centa Isabellejaverliat, Olivier Goeau-Brissonniere
Bioethical concerns in vascular emergencies Albert Clara, Begona Roman Jorje Molina, Natalia de la Fuente Francesc Vidal-Barraquer
Urgent carotid surgery Alain Branchereau, RaoufAyari Jerome Albertin, Bertrand Ede
Urgent open surgery after enaovascular AAA repair Piergiorgio Cao, Fabio Verzini, Paola De Rango Massimo Lenti, Gianbattista Parlani 71
13
Acute type B aortic dissection: surgical indications and strategy Michael Jacobs, Ted Elenbaas Geert Willem Schurink, Bas Mochtar
Blunt injury to the carotid and vertebral arteries Ramon Berguer
Endovascular treatment of aortic type B dissection Rachel Bell, Peter Taylor
Penetrating injury to the blood vessels of the nect and mediastinum John Robbs
Traumatic rupture of the thoracic aorta Roberto Chiesa, Renata Castellano Carla Lucci, Marcelo R. Liberato de Mourn Federico Pappalardo, Germano Melissano Efrem Civilini, Yamume Tshomba
87
XIII
Acute abdominal aortic occlusion Pierre Julia, Stephane Zalinski Jean-Noel Fabiani
49
Has mortality rate for ruptured abdominal aortic aneurysm changed over the last 50 years? Jack Collin
55
Ruptured AAA: should endovascular treatment be the first choice? Jaap Buth, Noud Peppelenbosch Neval Yilmaz, Philippe Cuypers Lucien Duijm, Alexander Tielbeek
81
61
107
Acute occlusion of the renal arteries Xavier Banal, Philippe Pacheco, Daniel Grandmougin, Didier Bourrat, Jean-Pierre Favre 125
Acute intestinal ischemia Brandon Krijgsman, George Hamilton
137
Rupture of splanchnic artery aneurysms Joaquim Barbosa, Maria-Jose Ferreira
149
XIV
The abdominal compartment syndrome Michael Yapanis,John Wolfe
157
Acute thrombosis of iliocaval veins Gunnar Plate, Lars Norgren
165
Endovascular treatment of blunt injury of the limbs Bo Risberg, Lars Lonn
247
Rare causes of acute ischemia of the limbs Mark Koelemay, Dink Legemate
253
Acute subclavian-axillary vein thrombosis Ramon Bofill, Josep Royo, Jose Maria Fuentes Jose Maria Escribano, Manuel Matas 173
Acute arterial thrombosis of the lower limbs William Paaske
261
Aortocaval fistula Dominique Maiza, Jean Ader Jules
Arterial emboli of the lower limbs Michael Horrocks
275
Acute thrombolysis of peripheral arterial aneurysms Ludwig Karl Von Segesser Bettina Marty, Patrick Ruchat Philippe Gersbach, Salah Quanadli Daniel Hayoz, Adam Fischer
281
Endovascular approach to acute arterial occlusions Andrea Stella, Mauro Gargiulo
287
Thrombolysis for occlusion of bypass grafts Robert Hinchliffe Bruce Braithwaite, Brian Hopkinson
295
Traumatic injury of the vena cava and its major branches Laurent Chiche, Edouard Kieffer
Acute ischemia of the upper limb Jose Gonzalez-Fajardo Miguel Martm-Pedrosa Lourdes Del Rio, Carlos Vaquero
Acute complications of arteriovenous fistula for hemodialysis VolkerMickky
Gunshot and explosive projectile vascular injuries Tomislav Sosa, Ivana Tonkovic Lidija Erdelez, Andrija Skopljanac-Macina Marko Ajduk, Andreja Crkvenac
181
193
207
217
231
Acute problems of the diabetic foot JanRauwerda 301
1 BIOETHICAL CONCERNS IN VASCULAR EMERGENCIES ALBERT CLARA, BEGONA ROMAN, JORJE MOLINA NATALIA DE LA FUENTE, FRANCESC VIDAL-BARRAQUER
The field of ethics, also called moral philosophy, involves systematizing, defending, and recommending concepts of right and wrong behavior. Although many of us would consider ourselves as trustworthy, ethical, and honest, we inevitably face choices that may hurt other people, infringe on their rights, or violate their dignity. We are always at risk of using patients as mere tools to our own ends. Ethical considerations, like diagnosis and treatment, are therefore essential features of every case of clinical care of patients. Vascular emergency patients present with problems that require quick, and sometimes immediate evaluation and intervention to save life, limb, or a serious health injury. Vascular surgeons on call have to make decisions, frequently at inconvenient hours, under circumstances of complex clinical scenarios, solitude, scarcity of hospital resources, unfamiliarity with patients, and constrained time. All these factors contribute to ethical conflicts. In the present chapter, the authors will try to provide the readers with the basic keys necessary to make a simple, reasoned, and honest analysis of ethical concerns in vascular emergencies. The reader will realize that behind the majority of our daily-practice ethical concerns, there are uncovered conflicts between moral obligations and self-interest (physician, family, or other third parties), rather than ethical dilemmas. Ethical dilemmas are infrequent and arise only if there are moral considerations for taking each of two opposing courses of action. Unfortunately, their resolution is not so easy, since determining which moral value overrides all others may reflect, at the very end, different visions of human nature.
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Theories of modern biomedical ethics Biomedical ethics (or bioethics) studies the moral issues in the fields of biological and medical sciences. It traces its roots to several early codes of ethics such as the ancient Greek Hippocratic Oath, professional codes such as the one written by the English physician Thomas Percival in the 18th century, and the Nuremberg Code for research ethics on human subjects that was established in response to the gross abuses in human experimentation performed during the Second World War. Since the end of the Second World War, a remarkable amount of attention has been given to the ethics of medical practice and research as a projection of the rapidly growing concerns generated by scientific and cultural developments during the last decades [1]. In the 1960s many technical advances occurred, such as hemodialysis, major surgical procedures including organ transplantation, and the widespread development of intensive care units and use of artificial respirators. Medically safe abortions, the contraceptive pill, prenatal diagnosis, and the first steps of genetic engineering were also developed at that time. These advances seemed to alter forever the current methods of saving, improving, and extending human lives. In the mid 1960s, the traditional moral moorings of the western medical practice came into question as a result of a series of societal changes, such as a better-educated public, the spread of participatory democracy, a decline in communally shared values, and a distrust of authority and institutions of all kinds. Therefore, the patient-physician relationship changed from a paternalistic model to one in which patient autonomy in decision-making was recognized. With the erosion of the Hippocratic synthesis and the growing complexity of bioethical concerns, many physicians sought guidance in court decisions and in legislation. Most, however, recognized the dangers of confusing law or economics with ethics, and of reducing professional ethics to nothing more than personal opinion. Some philosophers began at that time to write and speak about medical ethical issues. Many bioethical theories and decision-making models were progressively proposed (principlism, casuistry, virtue ethics, narrative ethics, feminist ethics). The history of ethics,
EMERGENCIES
however, has shown humankind to be unable to reach a universally acceptable theory for guiding our actions. The wide spread of bioethical theories has also reflected this historical debate. The main questions of bioethics remain indeed among the oldest that human beings have asked themselves: the meaning of life and death, the bearing of pain and suffering, the right and power to control one's life, and our common duties to each other. PRINCIPLISM The theory of prima fade (Latin for first appearance) principles, developed by Ross, was adapted to medical ethics by Beauchamp and Childress' Principles of Biomedical Ethics [2]. W.D. Ross (The Right and the Good, 1930) believed that our moral convictions were based on duties belonging to the fundamental nature of the universe, and included the duties of fidelity, reparation, gratitude, justice, beneficence, self-improvement, and non-maleficence. The above duties are prima facie insofar as we are always under obligation unless they conflict with one another. Ross argued that there was no obvious priority among these principles, leaving our choice in the event of conflict to our own insight on a case-by-case basis. From this perspective, Beauchamp and Childress chose principles especially appropriate for medical ethics: 1 - Beneficence: duty to be of benefit to the patient, as well as to take positive steps to prevent and to remove harm from the patient. 2 - Non-maleficence: duty to not intentionally create needless harm or injury to the patient, either through acts of commission or omission. Negligence derives from not regarding this principle and includes intentionally imposing unreasonable risks as well as unintentionally imposing risks through carelessness. The debate about active euthanasia also falls within the category of non-maleficence. 3 - Respect for autonomy (self-determination): duty to leave the patient to act intentionally, with understanding, and without controlling influences that would act against a free and voluntary act. The rules of informed consent, truthfulness, privacy, and confidentiality derive from this principle. 4 - Justice: duty to provide a fair distribution of goods in society. Health resources allocation derives from this principle. These principles balance one another but often conflict. For instance, respect for autonomy can conflict with beneficence when the patient refuses
BIOETHICAL CONCERNS IN VASCULAR a recommended therapy. Beneficence can conflict with justice in the context of resource scarcity, and so on. When principles compete, no absolute hierarchy exists for choosing to follow one principle over another. Judgments about moral precedence among competing principles are made on a caseby-case basis. Critics of principlism have claimed: 1 - the lack of a system for prioritizing principles, 2 - the lack of moral justification for the chosen principles, 3 - the underestimation of character, attitude, and motives of the person performing the action as a central factor in ethics. For these reasons, even principlism's strongest supporters admit that theories incorporating virtues, personal relationships, and other elements should be used in conjunction with the framework provided by principlism.
CASUISTRY Case-based reasoning, called casuistry, is another common method of bioethical reasoning. Three clinical ethicists (a philosopher - Jonsen, a physician - Siegler, and a lawyer - Winslade) identified four "topics" that are basic and intrinsic to every clinical encounter [3]. Each topic raises questions to be answered before the ethical analysis is done [4]. 1 - Medical indications: does the treatment fulfill any of the goals of medicine? With what likelihood? If not, is the proposed treatment futile? 2 - Patient preferences: what does the patient want? Does the patient have the capacity to decide? If not, who will decide for the patient? Do the patient's wishes reflect a process that is informed, understood, and voluntary? 3 - Quality of life: describe the patient's quality of life in the patient's terms: what is the patient's subjective acceptance of likely quality of life? What are the views of the care providers about the quality of life? Is quality of life less than minimal (i.e., qualitative futility) ? 4 - Contextual features: review social, legal, economic, and institutional circumstances in the case that can influence the decision and/or be influenced by the decision. Once the details of the case have been outlined according to the four topics, it is compared with a specific case (or set of similar cases) for which a moral solution has been developed in the past with professional and/or public agreement about the resolution: does the case sound like other cases you
EMERGENCIES
may have encountered? Is there clear precedent (paradigm case)? How is the present case similar or different to the paradigm case? Is it similar, or different, in ethically significant ways? Thus, casuistry moves from clear past cases to more dubious ones, ordering them by paradigm analogy under some principle. The methodology is therefore similar to the practice of case law where precedents of previous trials are used for analyzing new cases that share similar circumstances. Whether casuistry is a complement or alternative to principlism is still under debate. Although casuistry works in the opposite direction of principlism, it does not eschew principles. Many bioethicists maintain that both theories share more similarities than not and that they complement each other in a system of bioethics. In addition, some critics have claimed casuistry be a product of the culture of the Middle Ages, when there was a consensus on certain principles, while no such consensus exists in today's morally heterogeneous society.
VIRTUE ETHICS Aristotle defined virtue as "a kind of second nature" that disposes us not only to do the right thing rightly but also to gain pleasure from what we do. Virtue ethics emphasizes the character, intentions, and motives of the moral agent rather than focusing on the agent's actions or outcomes of actions. The virtuous physician naturally will do the right thing and will not likely do the wrong thing. Until the last decades, some kind of virtue ethics had been the implicit and dominant theory in traditional medical ethics since Hippocrates. The renewed interest in virtue ethics has been stimulated by the work of Alasdair MacYntre, in particular his book After Virtue (1984). MacYntre agrees that principles and rules are important for ethics, but he rejects any attempt to justify those principles or rules that abstract them from their rootedness in the historical particularities of concrete communities. The narratives that make such communities morally coherent focuses attention on the virtues correlative to those narratives. To separate ethics from its dependence on such narratives is to lose the corresponding significance of the virtues. Critics of virtue ethics may agree that having a virtuous character may incline the physician to act ethically, but they maintain that virtues alone do not give the physician sufficiently clear action guides.
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ALGORITHM FOR ETHICAL ANALYSIS IN EMERGENCIES Iserson et al. [5] have developed a model specifically designed to be helpful in the emergency setting. It combines casuistry and deontological and utilitarian rules for decisions under time constraints. 1 - The first step is to ask the question: is this a type of ethics problem for which you have already worked out a rule or is this at least similar enough so that a rule could reasonably be extended to cover it? If so, then follow the rule. 2 - The second step is to ask the question: is there an option that will buy time for deliberation without excessive risk to the patient? If yes, buy time. 3 - If the first two steps do not yield a solution, then there are three rules to apply to any ethical decision. The three rules are the following ones. Impartiality: the decision-maker places in the position of the patient by saying: would you be willing to have this action performed if you were in the patient's place? Universalizability: would you be willing to use the same solution in all similar cases? Interpersonal justifiability: consider whether you would be willing to defend the decision to others, to share the decision in public.
Applying ethics to emergency vascular patients THE PATIENT-SURGEON RELATIONSHIP An individual patient-surgeon relationship is formed on the basis of mutual agreement on medical or surgical care for the patient. In the absence of a pre-existing relationship, the physician is not ethically obliged to provide care to an individual person unless no other physician is available, as is the case when emergency treatment is required [6]. Once the relationship is established, the surgeon has the fiduciary duty to protect and promote the patient's interest. This primary commitment holds the surgeon's self-interest (technical, scientific, economic) in check and makes it a systematically secondary consideration. This makes the fiduciary's role morally demanding [7]. Surgical ethics is based on a recognition of the rights of patients who require the care of surgeons. The patient has the negative rights not to be killed or harmed intentionally or negligently by the sur-
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geon, and not to be deceived by the surgeon. The patient has the positive rights to be adequately informed about the risks and benefits of surgery, to be treated by a knowledgeable, competent practitioner, to have his or her health and well-being more highly valued than the surgeon's own economic interest, and to decide whether to accept treatment under the conditions described. THE EMERGENCY SCENARIO The emergency department is not only a complex medical environment, but it presents complex clinical and ethical concerns. Ethical concerns will be discussed afterward on a subject-by-subject basis. Clinical complexity a) Unlike other diseases, vascular emergencies have been traditionally poorly protocolized. b) Patterns of disease have changed. c) New vascular technologies imply new emergency challenges. d) Surgical decision-making is often undertaken under data incompleteness. In emergency care, the database derived from history, examination, laboratory, and radiology is virtually always incomplete (up to 50% of the data may be inconclusive or frankly incorrect) [7]. A traditional assumption in surgical practice has been that decisions must be made taking into account the likely costs of under- and overtreating, promoting a challenging decision-making. e) Constrained time to make surgical decisions. Occasionally, some surgical procedures are undertaken under intense time constraints (i.e., drainage of a cervical hematoma and establishment of an airway in a postoperative carotid endarterectomy bleeding, staunching the bleeding from a major exsanguinating source). In these rare circumstances, surgical decision-making is usually straightforward. The perception of time constraint and the emotional sense of urgency are usually felt afterward. In contrast, time constraint may be more evident and may affect the surgeon's decisions when surgical need is not so immediate, such as the patient with a ruptured aortic aneurysm or an acute limb ischemia with neurologic involvement. Environment complexity a) Vascular surgeon solitude and loneliness. Vascular surgeons are scarce "goods" in the mass of health care providers. Unlike general surgery or trauma, in which there is frequently an on-call team, vascular surgeons on call are usually alone in their decisions, that is, outside from the daily-practice
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decision-making and supervision mechanisms of many vascular departments. b) Increasing tendency to leave on-call service to junior vascular surgeons. On-call service, although at times professionally challenging, weighs more and more with increasing age and professional activity at convenient hours. In addition, many institutions have regulated a top age for on call service. Health providers should take into consideration, however, that the decision to attempt to do everything possible in all emergency circumstances, often made by inexperienced surgeons, creates sometimes logarithmically more moral problems for subsequent health professionals. c) Scarcity of hospital human and technical resources at inconvenient hours. The extraneous environment, such as the hospital laboratory, the speed of the computed tomography (CT) scan, or the availability of operative sites, etc., logistically frustrates the surgeon, creating conflicts among the critical hospital pathways and between different clinical standards of practice or practice guidelines.
requirement. Common law, however, recognizes that the emergency treatment of incapable persons is an exception to the requirement of consent. Otherwise, competent patients have the right to make choices regarding their health care in emergencies, just as in routine care. Respect for autonomy obligates the physician to seek for the patient the greater balance of goods over harms, as those goods and harms are understood and balanced from the patient's perspective. Consent has three components: disclosure, capacity, and voluntariness.
ETHICS AND THE LAW Surgeons are morally and legally accountable, and the two may not be concordant. Physician participation in torture, for example, may be legal in some countries but is never morally defensible. Surgeons must keep in mind the distinctions and potential conflicts between legal and ethical obligations when making clinical decisions and must seek legal counsel when they are concerned about the potential legal consequences of decisions in ethical dilemmas, when initiating policy and protocols, or when updating existing procedures. The law may vary substantially between countries. While the law is limited in its ability to provide universal guidance and direction, ethical analysis should provide a framework for determining moral duty, obligation, and conduct.
Mr. EVC-2 is a 45-year-old homeless but otherwise healthy man admitted to the emergency department because of recent-onset arm swelling. A duplex scan reveals subclavian deep venous thrombosis. The vascular surgeon on call explains the conventional anticoagulant therapy and discusses comprehensively the nature, procedure, shortand long-term benefits, complementary surgical treatment, and risks of modern fibrinolytic therapy. The patient accepts lytic treatment.
Ethical issues related to patient autonomy INFORMED CONSENT Consent is the autonomous authorization of a medical intervention. The notion of consent is grounded in the ethical principles of patient autonomy and respect for people [8]. Obtaining the patient's consent to medical care is also a legal
Disclosure Mrs. EVC-1 is 80 years old and lives with her daughter in an apartment. She is fully independent and has never had a serious illness. She is admitted to the emergency department because of acute lower limb ischemia secondary to embolic disease. The vascular surgeon on call indicates prompt surgery and visits Mrs. EVC-1 to disclose benefits and risks of treatment. Before entering the emergency box, however, Mrs. EVC-1 's daughter asks the surgeon to withhold any information about risk of limb loss because her mother is very nervous.
Ethics and practice Disclosure refers to the provision of relevant information by the clinician and its comprehension by the patient. In many western countries, the prevailing standard of disclosure is that of the "reasonable person". The necessary elements of disclosure include clear information about the patient's diagnosis, the therapeutic alternatives to manage it, including surgical and nonsurgical treatment, the benefits and risks of each alternative, and a frank explanation of those factors about which the medical profession, and the individual surgeon in particular, are uncertain and cannot provide guarantees [7]. This disclosure may be adapted to a long (often the case) or short version according to emergency time constraints. Contrary to the common surgeon's belief, the majority of patients (more than 80%) want to know about the nature of their illness, the reason for surgery, and so on [9]. In
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some cultures, however, a family-centered model of decision-making is favored over one centered in the individual. "Waiver" refers to a patient's voluntary request to forego one or more elements of disclosure. In that case, the patient's reasons for waiving should be sought in order to overcome them through dialogue. If this is not possible, the patient must be informed that he can change his mind at any time or involve a family member in the decision-making process [8]. The cases EVC-1: Mrs. EVC-1 is a fully independent and capable 80-year-old woman without previous serious illnesses. Mrs. EVC-l's daughter was indeed more nervous than her mother. Withholding information during the consent process in the belief that disclosure would lead to the harm or suffering of the patient is called "therapeutic privilege" [10]. While in some cultures therapeutic privilege is widely invoked, this is not the usual case in many western countries. It is better for the surgeon to offer information and allow the patient to refuse or accept further disclosure. Accepting an inappropriate family demand to withhold information infringes on the patient's rights, violates the patient's dignity, and goes against our duty of professionalism. Conversely, there is every moral reason on the basis of confidentiality to honor requests to withhold information from family or friends if requested by the patient. EVC-2: This homeless patient is surely astonished by the surgeon's science and fine dressing. He has probably switched off his understanding after the first 100 words of the surgeon's disclosure. Mr. EVC 2 is clearly a vulnerable patient unable to understand the risks of fibrinolytic therapy in the way the surgeon has explained it. Mr. EVC-2 has probably accepted fibrinolityc therapy because of his confidence that the surgeon is looking for his best interest rather than as a consequence of personal reasoning. Although we could discuss the reasoning behind the surgeon's recommendation (patient's interest vs. surgeon-interest), there is an additional fracture in the surgeon's duty of professionalism that we must point out. Accepting consent for a risky procedure without confirming the patient's understanding of the previously cited elements of disclosure goes against respect for autonomy and is deliberately paternalistic.
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Capacity Mr: EVC-3 is a 76-year-old man subjected three weeks ago to an elective aortic aneurysm resection. His postoperative course has been troublesome since the beginning (prolonged intubation, transitory renal failure, prolonged paralitic ileus). Although extubated and conscious, he still remains in the intensive care unit and has fever and some abdominal discomfort. A CT scan performed in the evening raises the concern of a bowel perforation. The vascular surgeon on call proposes prompt surgery and the patient refuses it. He claims to be too tired to fight the disease and he wants to meet his deceased wife in Heaven. A psychiatric consultation is sought to confirm the patient's competence. Mrs. EVC-4 is a 79-year-old diabetic woman admitted to the emergency department with supurative gangrene of two toes. No abscess seems to be present in the dorsal or plantar aspects of the foot. The vascular surgeon on call recommends amputation of the toes, and the patient seems to understand the surgeon's disclosure. During the dialogue, however, she refuses treatment because, "the amputation of my toes will be just the beginning of my end". Ethics and practice Capacity refers to the patient's ability to understand the information relevant to a decision and to appreciate its consequences. Capacity is specific to particular decisions and can change over time. In common law, patients are presumed capable. The surgeon develops a general impression of a patient's capacity during the clinical encounter. In some situations, however, surgeons may be unsure about a patient's capacity. Refusal of recommended treatment usually causes the surgeon to question a person's capacity, although most refusals are caused by factors other than incapacity [11]. In case of refusal, however, the greater the cost to the patient from a false-positive determination of competence, the greater the concern should be to ascertain whether the patient is truly competent [7]. When time and opportunity permit, a psychiatric consultation should be sought, if this is likely to enhance the quality of the determination of competence. Time permitting, when the patient is not competent to consent, surrogate decision makers serve to protect the best interests of the patient by choosing among reasonable options as the patient would have chosen. Since the medical team has significant input about what would be in the patient's interest medically, a decision by a surrogate that does not adhere to this standard should not be auto-
BIOETHICAL CONCERNS IN VASCULAR matically followed and may need to be reviewed by the institutional ethics committee or legal counsel. Religious beliefs: the case of Jehovah's witnesses. Patients' religious beliefs are to be respected on the basis of respect for autonomy. The case, however, is much more troublesome when such beliefs conflict against the surgeon's perceived beneficence; as in the emergency setting, the surgeon has the duty of taking care of these patients. The standard example is the Jehovah's Witnesses, who consent to all medical interventions but refuse blood and blood product transfusions. This refusal is worthy of the surgeon's respect, since these religious beliefs are as sincere as the beliefs of any other of the world's religious traditions. The surgeon, however, does have options when confronted with a patient who refuses perioperative blood product support [7]. First, the surgeon should speak to the patient in private and assure the patient of the confidentiality of the medical records. If the patient maintains the refusal, the surgeon cannot compel a competent adult patient who is not pregnant to accept the transfusion. However, the general caveat is that while competent adults are free to make martyrs of themselves, they cannot martyr their dependent children. In addition, some American hospital policies and state laws have allowed for the imposition of a surrogate decision maker to protect the interest of a minor should a parent (especially a mother) require blood products in order to prevent death and if the death of the patient would result in the child being orphaned [7]. The cases EVC-3: The case of Mr. EVC-3 was taken to an ^urgent meeting of the hospital Ethics Committee. The surgeon presenting the case was asked whether the process of disclosure had been done with empathy and care. The answer was affirmative. The Ethics Committee considered that the adequate steps had been followed (adequate disclosure and psychiatric evaluation of competence). No additional evaluation was believed necessary since the likelihood of survival (as expressed by the surgeon) was poor. Palliative care was indicated in respect of patient's autonomy. After the meeting, the surgeon had some subjective doubts about his empathy during the consent process and revisited the patient. One hour later the patient accepted surgery. The preventive ethics approach to refusal of surgery should be respectful of the patient's reasoning, on the assumption that the patient, by his or her own
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rights, has good reason for refusal but may, with additional information and/or empathy, reconsider and accept surgery, and not on the assumption that the patient capacity is in doubt. The present case exemplifies again the morally demanding fiduciary role of the surgeon (see professionalism). EVC-4: The case of Mrs. EVC-4 shows the effects of an uncovered depression in capacity. Mrs. EVC-4 had the ability to understand her problem and the proposed treatment. The unexpected reasons of Mrs. EVC-4's refusal raised doubts about her capacity and a psychiatric consultation was requested. Mrs. EVC-4 admitted to having a persistent depressed mood and several vegetative signs of depression. She accepted treatment for depression. Her foot condition stabilized with antibiotics. Some days later, the patient accepted the proposed surgery. Had prompt surgery been needed, a surrogate decisionmaker would had been sought. Voluntariness Mrs. EVC-5 is a 65-year-old diabetic woman admitted to hospital in the morning because of a toe supurative gangrene with plantar abscess. The vascular surgeon on call (surgeon A), whose service starts at 5 pm, is in the operating room treating an elective case. Mrs. EVC-5 is evaluated by another vascular surgeon (surgeon B). There will be no operating room available until the afternoon and surgeon B considers immediate surgery unnecessary. Surgeon B insinuates surgery but leaves the complete disclosure to surgeon A, who is informed by a surgical nurse that a toe amputation has been added to the surgical emergency schedule. After ending his elective case, and without delay, surgeon A goes to eat something before reentering the operating room. When he returns, Mrs. EVC-5 is already in the operating room. Surgeon A realizes that the informed consent has been insufficient and decides to complete it in the operating room. Mr. EVC-6 is a 78 year-old-man with an 8 cm aortic aneurysm. A vascular surgeon proposes elective surgery but he refuses, claiming that he has already done all he had to do in life. He signs an advanced directive refusing emergent surgery in case of rupture. A signed copy is left in the patient's chart. Six months later the aneurysm ruptures and the patient is taken, conscious, to the hospital. The vascular surgeon on call has doubts about what to do. Ethics and practice Voluntariness refers to the patient's right to come to a decision freely, without force, coercion or
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manipulation. Internal and external factors can affect a patient's decision about treatment [8]. Internal factors arise from the patient's medical condition (i.e. pain). The surgeon's role is to minimize the potential controlling effect of these internal factors without jeopardizing the patient's capacity. External controlling factors may be related to the clinician, the health care setting, and the family or friends. Surgeons should take steps to minimize the potential for manipulation. Patients can be manipulated when the information they receive is incomplete or biased. For this reason, a useful strategy is to ask patients to review the information in their own words. Another source of manipulation is disclosing information just before a major procedure is to be performed. The setting (i.e., operating room) and the immediacy of the medical procedure militate against a patient being able to make a free or voluntary decision.
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Advance directives document the process aimed at extending the rights of competent adults to guide their medical care through periods of decisional incapacity. Advanced directives are grounded on voluntariness. Their goals are: 1 - to maximize the likelihood that medical care serves the patient's goals (promoting respect for autonomy), 2 - to minimize the likelihood of over- and undertreatment (promoting non-maleficence), 3 - to reduce the likelihood of conflicts between family members and health care providers (promoting justice), 4 - to minimize the burden of decision-making on family members or close friends (promoting respect for autonomy). In the emergency setting, however, there are practical difficulties in having such directives function [7]. Family members may or may not be aware of such directives. Emergency medical personnel do not have access to the hospital chart at the time resuscitation and other therapeutic measures are needed. By the time it is known that an advance directive exists, the patient may already have been resuscitated, be on life support, or even be in the operating room. In general, when there is unclear evidence that a patient might have refused a particular treatment, such evidence is not binding if it goes against the clear best interests of the patient needing an emergency intervention. Most people who complete advance directives are not, at that time, suffering from a terminal or fatal disease. In
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completing an advance directive, most are expressing their wishes regarding the limitation of treatment when treatment will only prolong the process of dying. Therefore, the onus will fall on the surgeon to determine whether the conditions of advance directive apply. The cases EVC-5: The majority of readers whose practice includes on-call service will have occasionally met patients with cases similar to that of Mrs. EVC-5. The question of professionalism rises again in her case. Surgeon B should have personally informed surgeon A, especially about the incompleteness of the consent process, and surgeon A should have visited Mrs. EVC before entering the operating room. Neither surgeon A's physiological needs nor the existence of minor emergent surgical cases like toe amputations, debridements, or some A-V fistula revisions, justify the absence or incompleteness of the consent process before the patient enters the operating room. The reader should simply remember Iserson's question about impartiality: "would you be willing to have this action performed if you were in the patient's place?" EVC-6: Advanced directives take effect only in situations in which the patient is unable to participate direcdy in surgical decision-making. Appeals to living wills and surrogate decision-makers are ethically and legally inappropriate when individuals remain competent to guide their own care. The benefits and risks of surgical treatment together with the lethal condition of a nonsurgical attitude must be disclosed to the patient. If Mr. EVC-6 refuses surgery with an understanding of the consequences, his wishes should be honored. If he opts for surgery, then it should be performed promptly.
CONFIDENTIALITY AND TRUTH TELLING Confidentiality is derived from the Latin confidere, to trust. Patients confide in their physicians with the understanding that what they report will not be disclosed without explicit permission. The duty to maintain confidentiality can be viewed as a prima facie obligation that may be overridden only when it conflicts with stronger moral duties. Exceptions for confidentiality are concerns for the safety of other specific persons and for public welfare (i.e., report of certain communicable/infectious diseases) . The crisis atmosphere that often attends surgical emergencies may heighten the need of family members and loved ones for information. Sur-
BIOETHICAL CONCERNS IN VASCULAR geons, however, should not allow the exigencies of an emergency situation to undermine traditional privacy safeguards. When the patient is incapacitated, the surgeon should disclose information only to the patient's surrogate, who has a legitimate "need to know" the patient's medical status. Telling the truth may seem to be a straightforward and ancient ethical principle in health care. However, the Hippocratic oath does not make any mention of truth telling to patients, and the American Medical Association's first Code of Ethics in 1847 perpetuated this attitude. This therapeutic privilege was justified by the principle of non-maleficence, and continued into this century. Today the duty of truth telling in medicine has become an ethical issue (respect for autonomy), although in many cultures it is not the norm. There are two main situations in which it is justified to withhold the truth from the patient: 1. when the surgeon has compelling evidence that disclosure will cause real and predictable harm (i.e., make a depressed patient actively suicidal), and 2. when the patient him- or herself states an informed preference not to be told the truth.
Ethical issues related to beneficence and non-maleficence FUTILITY Medical futility refers to interventions that are unlikely to produce any significant benefit for the patient. Two kinds of medical futility are often distinguished. A treatment is quantitatively futile when the likelihood of benefit is very poor, for example when physicians conclude that it has been useless in the last 100 cases. In addition, a treatment is qualitatively futile when the question: "What sort of life is worth preserving?" is at the case core. Surgeons have no obligation to offer or provide treatments that clearly do no benefit their patients. These therapies may increase the patient's pain and discomfort (conflicts with non-maleficence) and spend finite medical resources (conflicts with justice). However, only through dialogue can the physician understand the goals of treatment and determine futility. This approach allows for exploration of the desired outcome, acceptability of burdens, and the patient's or family's willingness to gamble with the outcome.
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LIMITS TO THE AGGRESSIVE SURGICAL MANAGEMENT OF HEALTH-THREATENING EMERGENCIES A traditional assumption in surgical practice has been that emergency surgical patients should be provided rapid care at whatever level of intervention the surgeon reasonably thinks is required to preserve their lives or protect them from a serious compromise to their prior health status. Vascular surgeons on call, however, see occasional patients for whom treatment success will be very unlikely, the length of life to be secured brief, and the quality of life to be achieved marginal. These conditions create concerns as to when treatment should be characterized as futile, inappropriate, or marginally useful. In this context, surgeons look for ways of characterizing emergency patients [7]. Emergency patients for whom surgery survival is unprecedented. Vascular surgeons responding to emergency patients who are most assuredly "going," who in highest probability will very shortly die, are torn between rapid full-steamahead aggressive resuscitative measures and the recognition that interventions may succeed only in increasing the potential misery to the patient and the family. Such circumstances are represented by some patients with prolonged prehospital resuscitation following trauma and irreversible metabolic acidosis, or by patients with ruptured aortic aneurysm with certain particularities. The literature is not very prone to help to identify patients with a 100% mortality. However, the more secure surgeons are in their ability to resuscitate patients with complex surgical problems effectively, the easier it is to reach the decision not to initiate or even to terminate curative care in a patient who has an emergency surgical condition for which treatment is not reliably expected to prevent death. Vascular emergencies associated with central nervous system injury. Surgeons can be significantly frustrated when confronted with vascular surgical emergencies in patients with an associated central nervous system injury. Vascular injuries that require immediate or prompt interventions (i.e., active bleeding, acute ischemia) should be treated aggressively so long as the prognosis for the recovery of some degree of significant central nervous system function remains positive. However, especially in the postoperative period, if the most reliable prognosis is that the patient is not expected to recover to a cognitive and sapient existence, the surgeon should be willing to discontinue the trial
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of intervention, given the concurrence of the surrogate decision-maker and presuming the absence of previous binding instructions. Vascular injuries not requiring immediate treatment (i.e., many thoracic aortic pseudoaneurysms) are best delayed (and controlled) if possible until the central nervous system injury prognosis can be stated with some degree of certainty. Vascular emergency patients in whom survival with severe disability may be frequent. Traumatic vascular injuries may produce some disability by themselves (i.e., paralysis after surgical treatment of a transected aorta from blunt injury) or by associated injuries (i.e., fracture malunion, bone infection, soft tissue retraction). In the face of time constraints, surgeons can usually only imperfectly engage this process so as to prepare the patient and the patient's family for the consequences of a surgical intervention. The burden of proof needed to terminate the traditional obligation to intervene can frequently not be met because of the lack of concreteness of the data in an emergency context. Because of this softness, there are grounds to qualify in favor of intervention in all but the most well founded cases of futility.
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Emergency cases associated with a low probability of survival but with good quality of life among survivors. This may be the case for many ruptured aortic aneurysms. At stake here is the role of costs in determining the appropriateness of therapeutic interventions. While such health policies are rarely, if ever, created, bedside surgeon decision-making must be based under beneficence and respect for autonomy principles.
Ethical issues related to justice Mrs. EVC-7, a 27-year-old woman, is taken to the emergency department during the night after a motor vehicle accident. She has a femur fracture and signs of acute ischemia in the limb. The attending vascular surgeon on call, together with the orthopedic surgeon, proposes immediate surgery, however no operating room will be available in the next four hours. Because of recent hospital closures in the city, no other facility is available in which to treat this patient. Ethics and practice Resource allocation is the distribution of goods and services to programs and people. In the con-
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text of health care, macroallocations of resources are made by politics, mesoallocations are made at the level of health institutions, and microallocations are made at the level of the patient. Resource scarcity may be due to the shortage of a finite good (i.e., an organ for transplantation), or to a shortage of economic funds. While physicians have a fiduciary duty to promote the patient's best interest, their role in resource allocation is controversial. The physician can approach resource allocation in practice by choosing tests and interventions known to be beneficial, by choosing the test or intervention with the least cost among equally beneficial options, by resolving conflictive claims for scarce resources on the basis of need and benefit, and by seeking unacceptable shortages at the level of mesoand macroallocation [8]. The physician should not approach resource allocation by subordinating the primary concern of care - his or her patient's well being- to a budgetary issue. The surgeon must also pay attention when making decisions based on "quality of life." Several studies have shown that physicians often rate the patient's quality of life much lower than the patient himself does. If the patient is able to communicate, the surgeon should engage him or her in a discussion about his or her own condition assessment. The case EVC-7: The attending surgeons should provide appropriate care for Mrs. EVC-7, since a delay in vascular surgical reconstruction could result in some neurologic sequelae and in nephropatic metabolic syndrome. Surgeons should involve the administrator on call to bring in additional skilled personnel (anesthesiologist, surgical nurses, etc.) to provide care for the patient. In this way, they clarify the responsibility of the hospital to resolve the mesoallocation problem at an administrative level. Surgeons should seek resolution of unacceptable shortages at the level of emergency care.
In the pursuit of professionalism Mr. EVC-8 is a 76-year-old man with a 7 cm abdominal aortic aneurysm. He has been rejected from elective surgery because of depressed left ventricularfunction and moderate ventilatory deficit. Mr. EVC-8 comes to the emergency department with his aneurysm ruptured. The
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vascular surgeon on call wonders whether it is worth it to operate on this patient.
PROFESSION AND PROFESSIONALISM Profession has long been recognized to encompass three essential characteristics: expert knowledge, self-regulation, and a fiduciary responsibility to place the needs of the client ahead of the selfinterest of the practitioner [12]. The dominant conception of profession is sociological. Professionalism is the basis of medicine's contract with society. It demands placing the interests of patients above those of the physician, setting and maintaining standards of competence and integrity, and providing expert advise to society in matters of health. Essential to this contract is public trust in physicians, which depends on the integrity of both individual and the whole profession [13]. In this view, ethics is an important predictor for a profession, but ethics is not its essential and indispensable defining feature. Another view of profession links it to an ethical ideal without which it cannot exit. That ideal focuses on some degree of effacement of self-interest when it is required by the good of the person seeking assistance. This conception is rooted in the etymology of the word "profession," which means "a declaration, promise, or commitment publicly announced." That promise is made in every clinical encounter when the physician offers to help those who need his or her special knowledge. That promise entails competence and putting that competence at the service of the patient, even when it means some degree of sacrifice on the part of the physician [14].
CURRENT CONFUSED SCENARIO AND FUTURE PERSPECTIVES Many individual persons, groups, and institutions play a role in and are affected by medical decisionmaking in the current practice environment. Tension and competition among the interests of clinicians, insurers, patients, and institutions for available social and health care resources unavoidably influence the patient-physician relationship [6]. All these issues have raised a deep concern about the present loss of that special dedication to competence, service, and other-than-self-interest that have been associated with the ideal physician for so long. However, in its history, medicine has witnessed recurrent cycles of moral confusion-of doubts about whatever there is something special
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about the activity of medicine that imposes a higher standard of moral integrity on its practitioners. Each time this conflict has arisen in the past, it has resulted in a new infusion of moral sensitivity through successive professional codes. The reality of cycles of moral confusion must not obscure the specific dimensions of the present recurrence, some of which are unique, and some not [15]. What are not unique are the temptations of self-interest, power, prestige, pride, profit, and privilege that beset all humans, in all ages. In our times, however, there are two sources of unique conflict. 1 - There is a commodification of health care as a product like any other, left to the ethos of the marketplace, to competition, commercialization, and profit-making (today's moral imperatives). Physicians are not held to moral standards higher than those of the general society in which they live. 2 - There is an erosion of the foundations of professional ethics. Underlying these criticisms is a pervasive moral skepticism that denies the validity of any stable moral truth and even the capacity of reason to apprehend such truth were it to exist. Pellegrino expects a repetition of the historic cycle of deprofessionalization and reprofessionalization characteristic of periods of moral confusion [15]. Indeed, some have bet for a new code of professionalism [13]. However, it is not likely that any of these codes will change today's scenario if physicians do not have at the core of their beliefs the primacy of the welfare of their patients over any own self-interest (technical, scientific, academic). Only when medicine is a moral enterprise will that be possible. The case EVC-8: The perspective of a bad outcome frustrates any vascular surgeon faced with operating on a ruptured aortic aneurysm. The issues of futility (beneficence) and costs (justice) may rise. However, the mechanisms of rationalization of the surgeon's self-interest ("I'm going to waste some sleep hours, surely for nothing, while tomorrow I have a lot on my agenda") may often overcome any sincere ethical analysis. As we have seen previously, futility has very narrow margins and allocating resources is best managed while not at the bedside. Mr. EVC-8 must be offered surgical treatment and informed that, although it is the single curative choice, the probability of survival is very low. In respect of the patient's autonomy, his final decision will be honored.
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Conclusion The surgeon's fiduciary duty to protect and promote the patient's interest becomes more complex and demanding in emergencies. Vascular surgeons should face all of their clinical decisions, and specially emergencies, with bioethical reasoning. This attitude is frequently not time-consuming and may help the surgeon to unmask potential conflicts between moral obligations and self-interest (sur-
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geon, family, or other third parties) and to approach real ethical dilemmas with honesty, sense, and reasoning.
A CKNOWLEDGMENTS
The authors wish to acknowledge the valuable suggestions of Dr. F.Abel, President of the Institut Borja de Bioetica, Universitat Ramon Llull, Barcelona (Spain).
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1 Pellegrino ED. The metamorphosis of medical ethics: a 30-year retrospective. JAMA 1993; 269:1158-1162. 2 Beaucamp TL, Childress JF (eds). Principles of biomdical ethics, 5th edition. New York, Oxford University Press 1989: p 468. 3 Jonsen AR, Siegler M, Winslade W (eds). Clinical ethics: a practical approach to ethical decisions in clinical medicine, 4th edition. New York, McGraw-Hill 1998: p 202. 4 The University of Washington bioethics website: http:// eduserv.hscer.washington.edu/bioethics/credits.html 5 Iserson KV, Sanders AB, Mathieu DR, Buchanan AE (eds). Ethics in emergency medicine. Baltimore, Williams and Wilkins 1986. 6 Anonymous. Ethics manual. 4th edition. American College of Physicians. Ann Intern Med 1998; 128: 576-594. 7 McCullough LB, Jones JW, Brody BA (eds). Surgical ethics. New York, Oxford University Press 1998: p 416. 8 Singer PA (ed). Bioethics at the bedside: a clinician's guide. Ottawa, Canadian Medical Association 1999: p 154.
9 Dawes PJ, Davison P. Informed consent: what do patients want to know?/£SocMed 1994; 87:149-152. 10 Meisel A, Roth LH, Lidz CW. Toward a model of the legal doctrine of informed consent. Am J Psychiatry 1977; 134: 285-289. 11 Appelbaum PS, Roth LH. Patients who refuse treatment in medical hospitals. JAMA 1983; 250:1296-1301. 12 Sullivan WM. What is left of professionalism after managed care? Hastings Cent Rep 1999; 29: 7-13. 13 Medical professionalism in the new millennium: a physician charter. Ann Intern Med 2002; 136: 243-246. 14 Pellegrino ED. The healing relationship: the architectonics of clinical medicine. In: Shelp E (ed). The clinical encounter: the moral fabric of the patient-physician relationship. 4th edition. Boston, Reidel 1983: pp 153-172. 15 Pellegrino ED. Medical professionalism: can it, should it survive? J Am Board FamPractmO; 13:147-149.
2 URGENT CAROTID SURGERY ALAIN BRANCHEREAU, RAOUF AYARI JEROME ALBERTIN, BERTRAND EDE
Surgery of stenoses of the internal carotid artery (ICA) is intended for lesions and chronic neurologic disorders as indicated by the NASCET, ECST, and ACAS study results. Urgent surgery for an unstable neurologic condition has given rise to a considerable amount of skepticism, because of the poor results as found in the Joint Study [1]. At present, this sentiment requires reconsideration. The combined cumulative mortality and morbidity rate of carotid surgery in the years the Joint Study was performed, was 5 % to 20% [2], whereas it currently is 1% to 5% [3], At present, the urgent diagnosis of massive ischemic and hemorrhagic strokes is possible by means of computed tomography (CT) scanning and magnetic resonance (MR) imaging. Ultrasonography, sometimes in combination with angioCT or angio-MR, now allows for a sufficiently accurate appreciation of carotid stenoses, while the use of angiography of the aortic trunk is decreasing. This wins time and reduces iatrogenic neurologic morbidity. Angiography remains important in the intra-operative check-up of the reconstruction and regarding the additional therapeutic possibilities, such as intracerebral arterial thrombolysis. The introduction of stroke centers has been an essential advancement in the emergency care of these patients through an indispensable combination of a logistic platform and a multidisciplinary approach. Unfortunately, randomized controlled trials that could clarify the indications are not present at the moment. The aim of this chapter is to provide an overview of the literature and our own experience. This chapter is dedicated to urgent carotid surgery, excluding traumatic lesions, carotid dissections and postoperative strokes.
£ 13
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Pathophysiology
14
Our central nervous system has the lowest resistance to ischemia. The normal cerebral blood flow is estimated at 80 mL/100 g/min. Below 20 mL/ 100 g/min, neurologic disturbances occur, which are reversible as long as the hypoperfusion is not prolonged and the threshold of 10 mL/100 g/min is not reached. These disturbances are detected by changes in the electroencephalogram (EEC) and, the more severe ones, by changes in somatosensory evoked potentials. The allowed limits before irreversible cerebral lesions occur are a flow of 0 mL/ 100 g/min during a period of 20 minutes, 10 mL/ 100 g/min for 40 minutes, and 15 mL/100 g/min for 80 minutes. Surrounding the areas of irreversible damage there is an area of nonfunctional but still viable brain tissue, which can restore its function when normal cerebral flow is re-established. Identification of this area has led to the concept of the ischemic twilight zone. This area, which has lost its autoregulatory capacity, shows a greatly unstable pressure-sensitive metabolism. A major part of the clinical manifestations of ischemic strokes is due to the dysfunctioning of this twilight zone. The aim of urgent carotid surgery is to safeguard this ischemic twilight zone. Failure of reperfusion results in a loss or deficiency of the autoregulatory system in certain areas. Clinical symptoms can be hemorrhagic events and cerebral edema. One should discern between a cerebral hemorrhage and a hemorrhage upon a stroke. The former is due to a rupture of the blood brain barrier and penetration of blood into a previously unaffected brain area. This has a poor prognosis. The latter reflects infiltration of blood into infarcted tissue. This does not necessarily have a poor prognosis. The presence of a cerebral infarction is a well-known risk factor during carotid surgery. The wall changes in the vessels of the infarcted area may lead to vascular rupture, leading to a hemorrhagic infarction upon an ischemic event. Other risk factors of reperfusion damage are multilevel lesions causing chronic hypoperfusion and severe arterial hypertension.
Definitions The modified Rankin scale is used for the clinical evaluation of neurologic deficits. This scale
EMERGENCIES
enables simple assessment of the evolution of the deficit before and after treatment as well as correct comparison of the results from the different studies. 0 - No deficit 1 - Minimal deficit with complete autonomy 2 - Minor deficit with incomplete autonomy not requiring assistance in daily activities 3 - Moderate deficit with walking ability 4 - Severe deficit with walking disability 5 - Disabling deficit leading to bed confinement 6 - Death CRESCENDO TRANSIENT ISCHEMIC ATTACK Crescendo transient ischemic attack (CTIA) is a recurrent, localized ischemic neurologic event characterized by spreading of the deficit, a lengthening of the duration of the event or shortening of the interval between each event. Despite the absence of prospective studies, the prognosis of not surgically treated CTIA is poor and it leads to a considerable number of strokes. PROGRESSIVE STROKE Progressive stroke is a severe neurologic deficit, showing a varying intensity but without disappearing. The natural history of these events shows a mortality rate of 14% to 36% and a morbidity rate of 54% to 69% [4]. The definition of progressive stroke is not unequivocal. Hence, various terminologies are used in the literature, including evolving stroke or fluctuating stroke. SEVERE STROKE IN THE ACUTE PHASE This is a severe neurologic deficit according to stages 4 and 5 of the modified Rankin scale. In the Oxfordshire Community Stroke study, an infarction of the complete anterior circulation is accompanied with a 30-day mortality of 39% and a risk of functional disability of 56%. Severe strokes of carotid origin also show a poor prognosis with a mortality between 16% and 55% and a risk of functional disability between 40% and 69% [5]. REGRESSIVE AND MODERATE STROKES IN THE EARLY PHASE These are moderate ischemic strokes according to Rankin stages 1 to 3 of which the neurologic state has reached a steady state. In case of a stroke due to partial obstruction of the anterior circulation, a mortality of 4% and a risk of functional disability
URGENT CAROTID of 39% were reported in the Oxfordshire community stroke study. Surgical treatment six months after the onset of the stroke is commonly accepted as the therapy of choice for severe carotid stenoses. This expectative policy has become questionable because of the increased risk of early stroke recurrence [6] and studies showing no risk increase after early surgery [6-10]. ANATOMICAL EMERGENCIES When the neurologic state is stable, the identification of certain carotid lesions may offer an indication for urgent surgery. The most frequent possibility is a so-called subtotal stenosis. This definition is not based on the poorly known natural history of these lesions, but on hemodynamic findings representing a reduction of the flow in the ICA and the induction of a collateral circulation (Fig. 1). The second anatomical emergency is the presence of a floating thrombus at the level of the carotid bifurcation and the extracranial ICA (Fig. 2). The literature data on this subject are contradictory [11,12]. Some advocate urgent revascu-
SURGERY
larization by means of surgery or thrombolysis, others favor medical treatment followed by secondary surgery. The last type of anatomical emergency is a carotid occlusion. For this type of lesion, the clinical presentation should determine the policy. When a neurologic deficit is absent, the carotid occlusion is virtually impossible to date and does not require urgent treatment. Nicholls et al. [13] reported an incidence of 46% for severe, initially symptomatic carotid occlusions with a yearly risk of a neurologic event of 20% after a follow-up of 39 months.
Investigation of the brain CT SCAN Ischemic lesions are characterized by a hypodensity of the cerebral tissue, but 60% of the CT scans are falsely negative. This hypodensiry generally appears only after 36 hours. However, there are early signs during the first four hours that can be identified by scrupulous analysis. These may be a hyperdense medial cerebral artery (MCA), a disappearance of the lenticular nucleus, or indirect
15
FIG. 1 Angiography of a pre-occlusive stenosis. A - The stenosis at the origin of the ICA can be estimated at more than 90%. B - The asymmetrical intracerebral contrast distribution depicts the significant hemodynamic consequences of the stenosis, which justifies the term pre-occlusive.
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signs of cerebral edema such as the disappearance of the cerebral sulci and attenuation of the cortical layer (Fig. 3). Some of these elements, like cerebral edema and a hyperdense MCA, have a poor prognosis. Hyperdensity of the MCA is an early sign, which has a sensitivity of 78% and a specificity of 93%. Disappearance of the lenticular nucleus indicates occlusion of the proximal MCA, with a sensitivity of 92% after 6 hours. Diffuse hypodensity and disappearance of the cortical sulci are correlated with a high mortality and prohibit thrombolysis.
DIFFUSION AND PERFUSION-WEIGHTED MR IMAGING Diffusion. Diffusion imaging allows the diagnosis of ischemic lesions in the hyperacute phase of a cerebrovascular event. The diagnosis is made when an area of high intensity is found on the diffusion scan after applying diffusion gradients, whereas no signal is detectable before these gradients are applied (Fig. 4). The performance of this technique in the early detection of ischemic lesions is good, with a high sensitivity and specificity of 88% and 90%, respectively
16
FIG. 2 Two angiographic examples of a floating thrombus. Small volume thrombus distal to an ICA stenosis > 90%. A - High-volume thrombus in the ICA lumen without occlusion, distal to a stenosis of 60%. B - Despite the smaller degree of stenosis, the thrombus in B is more threatening.
FIG. 3 Early sign of stroke on CT scanning: hyperdense median cerebral artery (arrow).
URGENT CAROTID [14,15]. False-positive results are rare. Detection limits are very small volume lesions, infratentorial localizations and TIAs. The volume of the ischemic lesion as measured with this technique has a prognostic value and is correlated with the initial clinical score and the situation after three months. By means of an apparent diffusion coefficient graph, any artifacts causing false-positive results can be eliminated. In emergency conditions, it is an essential investigation to confirm the diagnosis of a cerebrovascular event in the hyperacute phase and to appreciate the extent of irreversible damage. This image analysis takes only a few minutes. Thus, diffusion MR imaging is superior to CT scanning for the early detection of ischemic events and to quantify the extent of the ischemic cerebral area. Perfusion. Combining angiographic techniques with MR imaging enables investigation of the larger vessels of the brain (time of flight, phase contrast) . Investigation of the cerebral microcirculation by means of MR imaging can be performed using endogenous and exogenous tracers. A perfusion image is obtained by sequential scanning of the variation in signal intensity during passage of the contrast agent. Detection of diffusion asymmetries between cerebral areas allows assessment of the twi-
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light zones around the ischemic lesion that represent poorly perfused but viable tissue areas at the time of investigation (Fig. 5). Quantitative data, such as cerebral vascular volume, cerebral flow and transit time can also be obtained, which allow quantitative analysis of the regional hemodynamic disturbances. Subtraction of the volume of the irreversible lesions, as detected by diffusion from the volume of the area with hemodynamic disturbance as shown by perfusion, allows for the assessment of the volume of the ischemic twilight area. The volume of the area with hemodynamic disturbance as measured by perfusion MR imaging is better correlated with the clinical evolution on the short and intermediate term than the volume as measured by diffusion imaging [14,15]. Thus, diffusion- and perfusion-weighted MR imaging appears to be an essential diagnostic tool in patients presenting with a cerebrovascular event in the acute phase. CT scanning merely has a poor predictive value. However, some uncertainties remain. The reversibility of the lesions as observed with diffusion MR imaging, especially in TIAs, illustrates the limitations of diffusion MR imaging in the diagnosis of irreversible cerebral lesions.
Rapid diagnosis of carotid lesions
FIG. 4 MR imasing diffusion image of an acute phase ischemic stroke.
The occurrence of a stroke requires therapeutic action as soon as possible. Noninvasive investigation should assess the etiology of the stroke. The diagnostic arsenal comprises several possibilities. Carotid duplex scanning is the primary investigation for a quick diagnosis of extracranial carotid lesions with a high sensitivity of 80%, a high specificity of 90% and an excellent correlation with angiography [16]. Transcranial doppler (TCD) is important to evaluate the cerebral collateral circulation, the cerebral vascular reserve capacity and to detect intracerebral stenoses [17]. This technique, however, is not simple and requires know-how and expertise which limits its use in emergency situations. Furthermore, it is not yet completely evaluated. Angio-CT scanning has a high sensitivity and specificity of 90% in the diagnosis of severe carotid stenoses and allows simultaneous analysis of the cerebral tissue. By means of an angio-CT, carotid stenoses may be evaluated via two-dimensional reconstructions, measuring the residual lumen in
17
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18
FIG. 5 Development of a stroke in the territory of the median cerebral artery on diffusion and perfusion MR imagins. At the second hour, the diffusion imases show a small infarction (A) in the center of an ischemic penombra, even more visible on the perfusion MR imase (B) (arrow). At 24 hours, followins successful revascularization, the ischemic penombra has almost disappeared on the perfusion MR imase (D); the diffusion MR imase shows the clearly limited infarcted area (C).
T hemorrhagic strokes is estimated to be 15% of all strokes [22]. In general, the indications for emergency surgery are not yet clearly defined. On the one hand, surgery is able, through revascularization of the viable areas, to restore a deficit and to benefit the patient. On the other hand, surgery might also revascularize an area already lost or cause a complication due to the intervention. In other words, it may bring no benefit at all or cause deterioration. The problem is therefore to identify patients that will benefit. Today no prospective randomized trial can answer this dilemma. The data available are based on the experience of few groups and on mostly cohort studies with loose and variable inclusion criteria. Our experience is also not free from this criticism. From our medical dossiers and operation reports, we selected 15 out of 1200 cases of carotid surgery in a period of 10 years (January 1992 to December 2001), which were considered as emergency cases on the basis of an interval below 24 hours between diagnosis and intervention (Table II).
each slice, thus showing the most stenotic area of the ICA as compared with the size in a more distal, normal area (NASCET method). Angio-MR gives exact information about the carotid stenosis and the intracerebral vascularization after a few minutes of image acquisition [14]. Appreciation of the stenosis with angio-MR may overestimate the lesion. The neurologic condition of the patient allowing cooperation during the investigation is an important limitation of the outcome of the MR and CT investigations. Subtotal stenoses are difficult to discern from carotid thromboses on MR or duplex scans because of the very low flow beyond the lesion. Despite its own neurologic morbidity [18], angiography remains the reference standard, particularly in doubtful cases, to appreciate the extracranial carotid lesion and to investigate the intracranial vessels without artifacts due to the low flow state.
Indications and results In 15% to 30% of the cases with cerebral ischemia, a stenosis of the cervical ICA is found [19]. The aim of early surgery after a stroke is on the one hand to restore the cerebral vascularization of the twilight zone, and on the other to exclude the emboligenic lesion in order to avoid a recurrence. This recurrence risk was found to be 3% to 5.9% in the medical arm of the NASCET study and in natural history studies. Numerous surgical studies have found discouraging results (Table I), which has led many groups to refrain from this kind of surgery. Most of these studies were performed before the introduction of CT scanning, which in part explains the observed results, considering the incidence of
1st author [ref.]
Year of** publication
„,
I 101 n\i
Uelay
Crescendo TIA Recent series from the literature have shown encouraging results in patients with an unstable neurologic condition, selected on the basis of the clinical presentation and results of the CT scan. Table III illustrates the results of urgent carotid surgery for a crescendo TIA. The therapeutic decision is clear in this selected patient group when an accessible lesion is found. Hence, a surgical reconstruction is indicated in cases with the shortest delay, with reasonable success rates. Thus, complete healing rates of 71% to 100% can be reached. In our experience,
Improved N (%)
Unchanged N (%)
Worsened N (%}
Rob [20]
1969
74
No
A few days
21
(28)
32
(43)
Blaisdell[l]
1969
50
No
< 14 days
17
(34)
9
(18)
3
Bone [21]
1990
Yes
< 24 hours
5
(15)
10
(31)
8
Mortality N (%) 21
(28)
(6)
21
(42)
(25)
9
(28)
19
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EMERGENCIES
Number
Subtotal stenosis
Stenosis >75%
Floating thrombus
Improved neurologic state
Unchanged neurologic state
Death
CTIA
4
1
2
4
-
-
Progressive stroke
8
6
-
i» 2..
6
1
1
Severe stroke
3
3
_
.
2
_
1
Neurologic state
Subtotal stenosis + floating thrombus ** 1 subtotal stenosis + 1 stenosis >75% CTIA: crescendo transient ischemic attack
Year of publication
Number
Healing
Minor stroke
Wilson [23]
1993
12
100
-
Gertler [24]
1994
14
98
Eckstein [25]
1999
21
71
1st author [ref.]
20
Severe stroke
Mortality
2
10
19
TIA: transient ischemic attack
crescendo TIAs accounted for 27% (4/15) of the indications for urgent carotid surgery. The results are in accordance with those recently reported in the literature showing 100% healing. In our opinion, crescendo TIAs form the best indication for urgent carotid surgery.
Progressive stroke Table IV shows the results of urgent carotid surgery for progressive strokes with a normal CT scan or showing few lesions. Encouraging results compared with the natural history were reported with clinical improvement in 86% to 92% of the cases. In our experience, progressive stroke accounted for
53% (8/15) of the indications for urgent carotid surgery (Table II). The results showed clinical improvement in 75% (6/8), no change in one case (1/8), and one death (1/8). Progressive strokes form a good indication for surgery in selected patients. The aim of the selection, based on clinical and paraclinical criteria, is to identify and exclude patients in whom a revascularization is likely to have a more deleterious than beneficial effect. This may be the case in patients showing a massive lesion, a cerebral hemorrhage or a substantial impairment of their conscience. An accurate selection and preoperative work-up are necessary for a favorable outcome. For these patients, Brandl et al. [27] advise not to perform a pre-operative angiogram to reduce the neurologic morbidity and to arrange for an experienced team of carotid surgeons, with constant
URGENT CAROTID SURGERY
, r 1st author r „ [re/]
v /• ^rr , LI scan xr ,_Year ... of;. Number m publication %
~ , Delay >
Improved Unchanged Worsened ,, , ,., , • state , * neurologic i • state , , neurologic i • state , , Mortality neurologic A7 /0/, *% N (%) N N *(%) N *(%)
Greenhalgh [26]
1993
22
87
1992; 23: 486-491. 20 Rob CG. Operation for acute completed stroke due to thrombosis of the internal carotid artery. Surgery 1969; 65: 862-865. 21 Bone G, Ladurner G, Waldstein N, Rendl KH. Acute carotid artery occlusion - Operative or conservative management. Eur Neurol 1990; 30: 214-217. 22 Mead GE, O'Neill PA, McCollum CN. Is there a role for carotid surgery in acute stroke? Eur J Vase Endovasc Surg 1997; 13: 112-121. 23 Wilson SE, Mayberg MR, Yatsu F, Weiss DG. Crescendo transient ischemic attacks: a surgical imperative. Veterans Affairs trialists. /Vase Surg 1993; 17: 249-255. 24 Gertler JP, Blankensteijn JD, Brewster DC et al. Carotid endarterectomy for unstable and compelling neurologic conditions: do results justify an aggressive approach? JVasc Surg 1994; 19:32-40. 25 Eckstein HH, Schumacher H, Klemm K et al. Emergency carotid endarterectomy. Cerebrovasc Dis 1999; 9: 270-281. 26 Greenhalgh RM, Cuming R, Perkin GD, McCollum CN. Urgent carotid surgery for high risk patients. Eur J Vase Surg 1993; 7SupplA:25-32. 27 Brandl R, Brauer RB, Maurer PC. Urgent carotid endarterectomy for stroke in evolution. Vasa 2001; 30:115-121. 28 Stork JL, Levi CR, Chambers BR et al. Possible determinants of early microembolism after carotid endarterectomy. Stroke 2002; 33:2082-2085. 29 Pelz DM, Buchan A, Fox AJ et al. Intraluminal thrombus of the internal carotid arteries: angiographic demonstration of resolution with anticoagulant therapy alone. Radiology 1986; 160: 369-373. 30 Dalman JE, Beenakhaus 1C, Moll F et al. Transcanial doppler monitoring during carotid endarterectomy helps to identify patients at risk of postoperative hyperperfusion. Eur JVase Endovascular Surg 1999; 18: 222 - 227. 31 Jansen 0, Von Rummer R, Forsting M et al. Thrombolytic therapy in acute occlusion of the intracranial internal carotid artery bifurcation. AJNRAmJNeuroradiolWS; 16:1977-1986. 32 Eckstein HH, Schumacher H, Dorfler A et al. Carotid endarterectomy and intracranial thrombolysis: simultaneous and staged procedures in ischemic stroke./ Vase Surg 1999; 29: 459-471. 33 Endo S, Kuwayama N, Hirashima Y et al. Results of urgent thrombolysis in patients with major stroke and atherothrombotic occlusion of the cervical internal carotid artery. AJNR Am JNeuroradiolim; 19:1169-1175.
BLUNT INJURY TO THE CAROTID AND VERTEBRAL ARTERIES RAMON BERGUER
The incidence of blunt injury to the carotid and vertebral arteries (BICV) is low but its outcome is characterized by high mortality and morbidity. BICV constitutes 0.5% to 1.0% of all blunt trauma admissions [1-3]. The incidence is much lower in the pediatric population, where it is reported to be 0.03% [4], Such a low incidence makes it inefficient to angiographically screen every patient for vascular injury arriving to a trauma center with blunt trauma of the head and neck. However, when patients who display other markers for BICV such as cervical/skull fracture or neurologic deficits are selected for diagnostic arteriography, 29% to 44% of them will be found [1,5,6] to have BICV. The outcome of blunt vascular injuries in the neck is most serious [2,3,7,8]. The incidence of stroke following demonstrated BICV ranges from 16% to 60% for carotid injuries [9,10] to 14% for vertebral injuries [7]. The death rate for BICV ranges between 25% and 31 % [2,9], being 13% to 57% [3,7,10] for carotid injuries and 4% to 67% for vertebral injuries [3,7].
Mechanisms of injury and arterial lesions The mechanism for disruption of the extracranial carotid artery can be a direct blow, either external (Figs. 1A and IB) or transoral, hyperextension or hyper-rotation of the neck with stretching of the artery over the transverse process of Cl (Fig. 2), direct contusion by a fragment of frac-
tured mandible, and proximity involvement of the internal carotid artery in a fracture of the temporal bone. An object striking the neck from the outside can exert a direct blow to the common or internal carotid arteries (this includes the mechanism of safety belt injury). An intra-oral blow occurs when a person falls with an object (such as a toothbrush or a lollipop) in the mouth. The object strikes the internal carotid artery through the tonsillar
3_ 27
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EMERGENCIES
FIG. 1 There is a dissection of the innominate artery extending into the subclavian artery and occluding the common carotid artery. This 24-year-old man suffered a rollover car accident, crushing his anterior chest and neck against the steering wheel. A - Arteriogram showing a luminal defect in the subclavian artery and the occlusion of the common carotid artery. B - Operative view of the dissected innominate artery.
28
fossa. The internal carotid artery traverses the temporal bone through a canal in which the adventitia of the artery and the periosteum of the bone are closely connected. A fracture and displacement of the bone entails disruption of the adjacent arterial wall (Fig. 3). Following BICV by any of the mechanisms cited above, the neurologic manifestations will be delayed for hours or days in roughly one half of cases [11-13]. The vertebral artery is rarely damaged by a direct external blow, since it is protected by bone as it ascends through the neck. In its V2 segment, the vertebral artery runs in an osteomuscular canal formed by the foramina transversaria and the intertransversaria muscles. Fractures of the lateral mass of the cervical vertebrae involving the foramen transversarium, and vertebral fractures with luxation/subluxation of the cervical spine, can result in distortion of this osteomuscular conduit containing the vertebral artery (Fig. 4) and its venae comitantes and injury to these vessels (Fig. 5). This latter mechanism is frequently seen in motor vehicle accidents and in near hanging injuries. In a motor vehicle accident or during brusque chiro-
FIG. 2 False aneurysm of the internal carotid artery from contusion of the latter against the transverse process of C1.
BLUNT INJURY TO THE CAROTID AND VERTEBRAL
ARTERIES
FIG. 3 False aneurysm of the petrosal internal carotid artery found after evaluation of a 30-year-old man who suffered a skull base fracture in a car accident.
FIG. 4 Symptomatic dissection of the V2 segment of the vertebral artery in a 27-year-old woman following a fall from a horse.
practic manipulation (Fig. 6), there may be sudden rotation or hyperextension of the head. The vertebral artery has a redundant loop between Cl and C2 to accommodate the wide arc of rotation that takes place between these two vertebrae. This rotation is approximately 80 degrees or about one half of the range of rotation of the entire neck. The vertebral artery is also attached to Cl and C2 by connections between its adventitia and the periosteum of the transverse foramina. During injury, particularly with extreme head rotation, the artery is stretched between Cl and C2 beyond its normal elastic range and literally snaps, the consequence being its dissection (Fig. 7), occlusion, or rupture. If it ruptures into the surrounding tissues, a false aneurysm develops; if it ruptures into a closely adjacent and also damaged vertebral vein an arteriovenous fistula ensues (Fig. 5).
BICV may result in a wide spectrum of lesions ranging from luminal irregularities (flaps, intramural hematoma, dissection), to disruption of the arterial wall (false aneurysm, fistula), to occlusion of the lumen (Fig. 8). Brain embolization may occur from an intimal flap, from the reentry tear of a dissection or from the tail of the thrombus that forms distal to an occlusion.
Diagnosis SYMPTOMATOLOGY About one half of the patients who eventually turn out to have BICV enter the trauma unit without neurologic symptoms or signs. A substantial number (43% to 58%) of these originally asymptomatic patients will develop neurologic signs after their hospital admission [11-13].
29
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30
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FIG. 5 Ansiosram of a patient with a symptomatic arteriovenous vertebral fistula two years after blunt head and neck trauma. A - Arteriovenous fistula at V3. B - The venous end of the fistula has been obliterated by a detachable balloon. The vertebral artery intesrity has been preserved. Hypertrophy of the vertebral artery proximal to this chronic fistula is obvious.
The following specific findings markedly increase the likelihood that an individual that has suffered blunt trauma to the head and neck may harbor a BICV. 1 - A Horner's syndrome that occurs when there is disruption of the upper cervical ganglion by trauma (hyperextension or rotation) or of the peri-adventitial sympathetic fibers by dissection of the arterial wall. 2 - A neurologic deficit that may be the result of embolization (from the distal end of the dissection channel or from a thrombus beneath an intimal flap) or of ischemia (from low-flow compromise) due to the dissection or rupture of an artery resulting in its occlusion or near occlusion. In the setting of a trauma unit, the detection of neurologic deficits may be seriously hampered by high levels
of alcohol or drugs in blood, shock from other internal injuries, or concomitant head injuries. 3 - The finding of a skull base (Fig. 3), temporal bone, or cervical fracture (or luxation/subluxation) substantially increases the likelihood of concomitant injury to the internal carotid or vertebral arteries that are intimately associated to these bony structures. 4 - If sudden hyperextension or head rotation movement during the accident are suggested by the patient's description of the accident or by associated injuries to the head and neck. Hyperextension and hyper-rotation are the most common mechanisms for stretching injury of the carotid or vertebral arteries. In the series of Biffl et al. [11], setting up a screening protocol in their trauma unit for these
BLUNT INJURY TO THE CAROTID AND VERTEBRAL ARTERIES
FIG. 6 This 20-year-old man complained of neck pain after a basketball game. He underwent chiropractic treatments and twelve hours later developed symptoms of brain stem infarction. There is dissection of the distal vertebral artery (arrow). A ventriculostomy tube is in place. The patient eventually died.
1 31
FIG. 7 This 47-year-old woman developed a symptomatic vertebral artery dissection following a ski accident (arrow). B - This arteriogram, obtained six months later, shows the dilatation of the false lumen involving the V3 and V4 segments.
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FIG. 8 Operative photographs of a 29-year-old worker who had his neck crashed between the posts of a hydraulic case used to repair electrical cables. A - View at operation of the hematoma in the subadventitial space of the common carotid artery. B - A cylinder of intima and media that broke off and impacted into the carotid bulb. C - Open sesment of resected common carotid artery (it was replaced with a prosthesis) showing the folded layer of intima and media and the thrombus that formed distal to it.
32 markers of BICV resulted in a 10-fold increase of this diagnosis. A seatbelt sign is not considered to be a good indicator of blunt carotid injury in retrospective studies. One review of 131 patients with seatbelt sign found only one blunt carotid injury among them (0.76%) [14]. However, if the patient has a seatbelt sign and other abnormal findings (neurologic deficit, skull or cervical fractures, etc.), then there is a good indication for angiographic screening [15] and a high probability of finding a BICV.
IMAGING TECHNIQUES A few studies have analyzed the screening power of ultrasound and computed tomography (CT) angiography in the initial diagnosis of blunt vascular injury to the head and neck [1,13,16,17]. The sensitivity of the ultrasound in detecting blunt carotid injury was a remarkably high 86% in a multicenter trial [13]. Still, the study missed carotid lesions located in the distal cervical carotid and naturally the authors had no information about the intracranial carotid artery. Duplex ultrasound is not
reliable when the lesion is in the distal half of the cervical internal carotid artery, where most blunt injuries occur (skull base, infrapetrosal segment). Duplex can theoretically provide evidence of injury in the nonvisualized proximal common carotid and distal internal carotid artery by detecting abnormal flow signals. However, the noncritical stenosis created by small flaps or some dissections will go undetected while they still have a high potential for embolization and delayed occlusion. Additionally, the accuracy of duplex ultrasound of the carotid bifurcation is notoriously operator-dependent and it is unlikely that such a service will be available at all times in a trauma unit. Finally, neck swelling and associated injuries may make duplex scanning difficult and less reliable. CT angiography is not a sensitive tool to detect small defects of the arterial wall, but CT scanning of the brain is a good predictor of outcome. A large multicenter study [13] showed that those patients who showed a cerebral infarct in the admission CT of the brain had a high mortality (47%) and only
BLUNT INJURY TO THE CAROTID AND VERTEBRAL a poor chance (29%) of good neurologic recovery. On the contrary, of those patients with a normal CT of the brain on admission to the trauma unit, none died and 67% went on to a good neurologic recovery. Combined magnetic resonance imaging-magnetic resonance angiography has been advocated as a tool to simultaneously image the carotid and vertebral arteries and survey the brain parenchym. The experience with this modality is limited. As a triage tool for blunt injury it is probably not available in short notice in most trauma units. Even when available, placing the patient in a magnet may present problems because multiple trauma patients often require hardware to immobilize fractures and ventilatory support. Levy et al. [18] reported a low sensitivity of magnetic resonance for detecting discrete vascular blunt injuries. There is consensus among the authors of the largest series [11,12] that selection for arteriography within the large population of blunt trauma patients should be done on the basis of the clinical findings: stroke, Horner's syndrome, massive soft tissue injury of the neck, the mechanism of injury (severe hyperflexion-hyperextension and rotational injury), and concomitant bony findings (skull base fracture, fracture across the foramen transversarium, and temporal bone fracture). In patients with blunt injury to the head and neck, there is a strong correlation between those who present with a low Glasgow stroke score (equal to or less than six) and the finding of BICV.
Treatment The goals of treatment in emergency and semiemergency are to restore cerebral perfusion distal to an occlusive lesion and to prevent embolization from a thrombus that developed at the traumatized level. The goals during follow-up, if necessary, are to treat a false aneurysm, dissection, or arteriovenous fistula.
ANTICOAGULATION THERAPY Intravenous heparin is administered in the acute phase and followed by oral anticoagulation, the duration of which depends on residual lesions identified during follow-up. The purpose of this treatment is to prevent the formation, propagation, and/or embolization of thrombus that developed at the level of the intimal rupture.
ARTERIES
There is evidence [12] favoring anticoagulation with heparin (to be followed by Coumadin) in the treatment of BICV. The authors of the two largest series [11,12] make a good argument for systemic heparinization in the absence of centra-indications in multiple trauma patients with BCVI. Although their studies are explicidy detailed and include the largest series of BICV, they are retrospective reviews that were not analyzed using the technique of matched pairs. However, to avoid bias, they excluded patients with intracranial fistulae and those with transection or disruption of the internal carotid artery when searching by regression analyses the heparin effect on outcomes. Another retrospective review [19] of a smaller series did not find any advantage of heparin over antiplatelet therapy. It is important to weigh the advantages of anticoagulation treatment against the potential deleterious effects at the level of associated lesions. Also, cerebral infarction can be transformed in a cerebral bleeding which is most often catastrophic. Finally, some associated visceral lesions, in the case of a polytraumatic patient, mean an absolute contra-indication for anticoagulation treatment, at least in the acute phase.
SURGICAL INDICATIONS Unfortunately there is no clearly established algorithm for surgical treatment and the indications must be discussed on a case-by-case basis. The emergency indications, always very difficult, should be distinguished from the secondary, more elective surgical indications. In the acute phase, a complete rupture of a carotid or vertebral artery or a partial rupture with evident thrombus are indications for surgical intervention. However, deep coma and severe neurologic deficit with or without extensive cerebral infarction are contra-indications for surgery. In contrast, the absence of lesions at CT scanning and a fluctuating neurologic status with preserved consciousness are elements that should speed up the decision to operate. In neurologically uninjured patients, the same arterial lesions require surgical repair, however surgery can be postponed for several hours, allowing assessment of the other polytraumatic injuries and to improve the general condition of the patient. During follow-up, angiography or CT angiography can depict specific arterial lesions that might require surgery: false aneurysms, dissection, or arteriovenous fistulae. Lesions that induce transient neurologic accidents or fistulae that cause a bruit experienced by the patient and
33
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aneurysms or dissections containing thrombus despite anticoagulation, should be surgically repaired. Surgery is also indicated in case of rupture or complete thrombosis of the internal carotid artery or common carotid artery and in case of recurrent emboli resulting from arterial dissection despite anticoagulation therapy (Fig. 9). Certain aneurysms are asymptomatic. The anatomical characteristics of the infratemporal internal carotid artery and the suboccipital vertebral artery explain why false aneurysms can be surveilled because enlargement hardly occurs. As long as they behave asymptomatically, surgery is not necessary.
TECHNICAL ASPECTS This surgery is extremely difficult and challenging, requiring unusual vascular access. Additional complicating factors include the emergency setting,
EMERGENCIES
the frequently associated lesions of head and neck and extensive hematomas disturbing local anatomical landmarks. While vascular access to the common carotid artery and the bifurcation is not a problem, the majority of internal carotid artery trauma is located in the second part of the cervical region. In these circumstances it is recommended to perform nasotracheal intubation and mandible subluxation. Access to the ICA in the subparotid area requires transection of the digastric muscle and resection of the styloid apophysis. This extension allows exposure of the ICA just above the crossing of the ninth cranial nerve [20]. Access to the last centimeters of the ICA require control of the facial nerve, opening of the temporomaxillary joint, and partial ablation of the tympanal bone [21]. It must be emphasized that these complex procedures are
34
FIG. 9 A - Post-traumatic dissection of the vertebral artery that continues to be symptomatic in spite of appropriate anticoasulation. B - Exclusion bypass from the internal carotid to the vertebral artery at the level of the foramen rnasnum. The proximal vertebral artery was lisated.
BLUNT INJURY TO THE CAROTID AND VERTEBRAL ARTERIES time consuming, which is disadvantageous in these emergency settings. Surgical repair for traumatic vertebral artery injury generally requires access to the distal vertebral artery in its suboccipital segment. This can be achieved either by a cervical-lateral approach between Cl and C2 [22] or a posterior approach between Cl and the occipital foramen [23]. The latter technique is not recommended in emergency settings since the patient must be in the ventral decubitus position. In traumatic arterial lesions, venous grafts are preferred. Clamping at the distal end is always delicate because of the fragile tissue and crushing of the intima. Furthermore, the surgical field is always narrow, allowing only limited movements. Therefore, distal arterial control can be achieved by means of an occluding balloon, causing limited intimal damage and enabling manipulation of the
artery during suturing. If this technique is feasible and if 15 to 20 mm of the artery beyond the rupture are available, it is always recommended to perform an end-to-side anastomosis with closure of the transected end. This anastomotic configuration is easier to perform, allows better vision of the distal arterial segment, and provides a superior hemodynamic shape. Insertion of a shunt remains controversial. It is rarely applied because it complicates the procedure. ENDOVASCULAR TREATMENT False aneurysms can be managed with stents or stent-covered grafts. There are some initial reports of stenting as treatment for intimal flaps, proximal dissection entry points, and false aneurysms. The deployment of a stent inside a false aneurysm will not necessarily result in the thrombosis of its false lumen (Fig. 10) although such thrombosis can be
35
FIG. 10 A - This patient with BICV had two false aneurysms of the infrapetrosal internal carotid artery. B - Both false aneurysms were stented: the proximal one thrombosed; the sac of the distal false aneurysm remains patent.
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induced by filling the aneurysm sac with coils through the mesh of the stent (Fig. 11). Endovascular treatment, especially in trauma patients, is specifically appealing because it is less invasive. However, this treatment comprises two drawbacks. First, short-term and long-term results are hardly known. It cannot yet be ruled out that a stent itself or the endovascular manipulations either initiate arterial occlusion or induce cerebral emboli, as already reported [24]. Second, the advantage of endovascular repair is based on the fast procedure in a trauma patient. However, this treatment requires specific expertise and infrastructure, which is not always available in every trauma center. Occlusions or neartotal occlusions result from fracture of the wall and distal embolization of a medial-intimal fragment (Fig. 8). This kind of lesion is unlikely to be successfully managed with endovascular techniques and farther distal embolization may occur during en-
EMERGENCIES
dovascular manipulation. For this type of severe injury, open surgical techniques are advocated.
Summary BICV has a low incidence but a high morbidity and mortality. The artery may be injured by a direct external blow or by adjacent bone displaced in a fracture or a luxation. Brusque stretching of the artery is a common mechanism of injury to the carotid or vertebral arteries in motor vehicle accidents. A diagnostic angiogram is indicated when a patient presents with specific features such as neurologic symptoms or craniofacial injuries. In the absence of contra-indications from associated injuries, heparin appears to be beneficial. Endovascular and direct surgical repair are recommended for specific lesions.
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FIG. 11 A - This false aneurysm of the vertebral artery (C3 level) was stented but its false lumen did not thrombose. B - Coils were introduced into the false lumen through the mesh of the stent and eventually obliterated the false lumen.
BLUNT INJURY TO THE CAROTID AND VERTEBRAL ARTERIES R E F E R E N C E S 1 Miller PR, Fabian TC, Croce MA et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Swrg-2002; 236: 386-395. 2 McKevitt EC, Kirkpatrick AW, Vertesi L et al. Identifying patients at risk for intracranial and extracranial blunt carotid injuries. Am J Surg 2GQ2; 183: 566-570. 3 Berne JD, Norwood SH, McAuley CE et al. The high morbidity of blunt cerebrovascular injury in an unscreened population: more evidence of the need for mandatory screening protocols. JAm Coll Surg m\; 192: 314-321. 4 Lew SM, Frumiento C, Wald SL. Pediatric blunt carotid injury: a review of the National Pediatric Trauma Registry. Pediatr Neuroswrg 1999; 30: 239-244. 5 Kerwin AJ, Bynoe RP, Murray J et al. Liberalized screening for blunt carotid and vertebral artery injuries is justified. / Trauma 2001; 51: 308-314. 6 Biffl WL, Moore EE, Offher PJ et al. Optimizing screening for blunt cerebrovascular injuries. AmJSurg 1999; 178: 517-522. 7 Miller PR, Fabian TC, Bee TK et al. Blunt cerebrovascular injuries: diagnosis and treatment./ Trauma 2001; 51: 279-286. 8 Mclntyre WB, Ballard JL. Cervicothoracic vascular injuries. Semin Vase Surg 1998; 11: 232-242. 9 McKevitt EC, Kirkpatrick AW, Vertesi L et al. Blunt vascular neck injuries: diagnosis and outcomes of extracranial vessel injury. / Trauma 2002; 53: 472-476. 10 Biffl WL, Moore EE, Ryu RK et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 1998; 228: 462-470. 11 Biffl WL, Moore EE, Offner PJ, Burch JM. Blunt carotid and vertebral arterial injuries. World J Surg mi; 25: 1036-1043. 12 Fabian TC, Patton JH Jr., Croce MA et al. Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg 19%; 223:513-525. 13 Cogbill TH, Moore EE, Meissner M et al. The spectrum of blunt injury to the carotid artery: a multicenter perspective. / Trauma 1994; 37: 473-479.
14 DiPerna CA, Rowe VL, Terramani TT et al. Clinical importance of the "seat belt sign" in blunt trauma to the neck. Am Surg 2002;68:441-445. 15 Rozycki GS, Tremblay L, Feliciano DV et al. A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs. / Trauma 2002; 52: 618-624. 16 Ofer A, Nitecki SS, Braun J et al. CT angiography of the carotid arteries in trauma to the neck. EurJ Vase Endovasc Surg 2001; 21:401-407. 17 Rogers FB, Baker EF, Osier TM et al. Computed tomographic angiography as a screening modality for blunt cervical arterial injuries: preliminary results. / Trauma 1999; 46: 380-385. 18 Levy C, Laissy JP, Raveau V et al. Carotid and vertebral dissections: three-dimensional time-of-flight MR angiography and MR imaging versus conventional angiography. Radiology 1994; 190: 97-103. 19 Wahl WL, Brandt MM, Thompson BG et al. Antiplatelet therapy: an alternative to heparin for blunt carotid injury. J Trauma 2002; 52: 896-901. 20 Branchereau A, Rosset E . Carotid bifurcation. In : Branchereau A, Berguer R (eds). Vascular surgical approaches. Armonk, Futura Publishing Co, 1999 : pp 1-8. 21 Thomassin JM, Branchereau A. Intrapetrosal internal carotid artery. In : Branchereau A, Berguer R (eds). Vascular surgical approaches. Armonk, Futura Publishing Co, 1999 : pp 15-20. 22 Branchereau A, Rosset E . Distal vertebral artery (C2-C1) : anatomic features and surgical approach. In : Branchereau A, Berguer R (eds). Vascular surgical approaches. Armonk, Futura Publishing Co, 1999 : pp 27-35. 23 Berguer R . Suboccipital approach to the vertebral artery. In : Branchereau A, Berguer R (eds). Vascular surgical approaches. Armonk, Futura Publishing Co, 1999 : pp 37-41. 24 MayJ, White GH, Waugh R, Brennan J. Endoluminal repair of internal carotid artery aneurysm : a feasible but hazardous procedure. / Vase Surg 1997 ; 26 : 1055-1060.
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4 PENETRATING INJURY TO THE BLOOD VESSELS OF THE NECK AND MEDIASTINUM JOHN ROBBS
Diagnosis and particularly management of penetrating injuries to the blood vessels of the neck and mediastinum may present enormous challenges to the surgical team. The anatomical areas of the neck in the context of penetrating trauma has been arbitrarily divided into three zones. Zone 1 extends from the clavicles to the cricoid cartilage, Zone 2 extends from the cricoid cartilage to the angle of the mandible, and Zone 3 extends from the angle of the mandible to the mastoid process [1] (Fig. 1). In general terms, diagnosis and management are relatively easy in Zone 2, and the difficult areas are represented by injuries in which the trajectory goes toward the base of the skull (Zone 3) or down into the superior mediastinum (Zone 1). The morbidity and mortality associated with penetrating injuries in this region are mainly related to injuries to the blood vessels, particularly the arterial system. In this chapter, discussion will be limited to the diagnosis and management of these injuries. In terms of management, the major debate revolves around whether mandatory exploration should be done for all penetrating wounds in this region or whether a more selective policy of investigation and intervention based on clinical signs should be advocated. One could argue that the most advantageous is to fully investigate all patients with penetrating wounds; however, in extremely busy trauma units, this can be unrealistic and, based on general clinical experience, it would appear that a selective policy is safe [2]. The aim of this chapter is to provide a practical guide to diagnosis and management based on our own experience with more than 4000 major vascular injuries, of which 20% to 25% involve the cervicomediastinal region.
Tr 39
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FIG. 1
Diagram showing the Zones of the neck.
Etiology and pathology
40
In order to rationally diagnose and treat these injuries, it is essential to have a good understanding of the mechanisms of injury and pathology. Penetrating wounds may be divided into stabs, either with a knife or some other sharp implement, and missiles, which can be divided into low velocity or high velocity. High-velocity missiles are those in which the muzzle velocity exceeds 300 meters per second. This is usually associated with military weapons or hunting rifles. Low-velocity wounds such as stabs or missiles with a muzzle velocity of less than 300 meters per second, such as a standard handgun, usually produce damage that is limited to the implement or missile track. The energy transfers involved with high-velocity missiles cause a cavitation effect with tissue destruction around the actual missile track, which results in extensive associated soft tissue trauma [3]. Shotgun wounds warrant separate description. Bird shot is small caliber and densely packed within the cartridge, whereas buck shot is larger and heavier and there are fewer packed into the cartridge. The unique property of a shotgun wound is the large number of foreign bodies embedded in the tissues, particularly in the case of bird shot, with extensive associated soft tissue trauma particularly
EMERGENCIES
at close range. The blood vessels involved tend to develop multiple small perforations. An additional problem occasionally encountered when the missiles enter the vessels is distal embolization into the arterial system (Fig. 2). In general, direct injury to the artery may cause either partial or complete transection. This in turn may result in pseudoaneurysm formation or, in the case of complete transection, thrombosis of both ends of the transected vessels [4,5] (Figs. 3A and 3B). Pseudoaneurysms with expansion may lead to compression of the aerodigestive tract or the brachial plexus. Small perforations, on the other hand, may temporarily seal off and then, with dissolution of the thrombus for whatever reason whether lowgrade infection or natural fibrinolysis, develop a delayed false aneurysm. This may occur gradually with progressive enlargement or may be an acute phenomenon. These patients may then present with a large pulsating hematoma, often infected, with or without compression symptoms. Brachial plexus compression under these circumstances results in major morbidity with a very guarded prognosis for
FIG. 2 Angiogram of a young woman who sustained a shotgun wound to the neck/upper mediastinum (Zone 1). Buck shot probably entered via the venous system and embolized to the common femoral artery (arrow).
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INJURY TO THE BLOOD VESSELS OF THE NECK AND
recovery of function [6,7]. The concept of conservative management of minimal vascular injury is not to be encouraged [8]. We believe that all perforations, even with small pseudoaneurysms that are stable, should be dealt with, as the consequences of delayed hemorrhage are highly significant in terms of morbidity. With complete transection and associated thrombosis, the thrombus tends to propagate to the first collateral. Carotid transection will propagate up to the carotid bifurcation and down to the arch of the aorta. There is also often thrombus within the lumen associated with partial lacerations (Fig. 3A). Adjacent perforations of the artery and vein will result in an arteriovenous fistula. Significant hemorrhage and the formation of a pseudoaneurysm is not an invariable feature of arteriovenous fistulae, as the arterial flow tends to take the line of least resistance into the venous system. The systemic
MEDIASTINUM
effects depend largely on the size of the arteriovenous shunt. In the acute setting when the mediastinal and neck vessels are involved, usually in fit young patients, the systemic hemodynamic effects are minimal. Undiagnosed fistulae may only present months or years later with the classic widened pulse pressure, systolic hypertension, and, rarely, congestive cardiac failure. We have on record patients presenting up to 14 years after the initial injury. In the acute setting, an important feature of arteriovenous fistulae is the development of thrombus at the fistula site and particularly in the downstream arterial segment, probably due to the diminished flow in that segment. When this occurs in the carotid artery, neurologic deficits occur quite frequently due to embolization of this thrombus. This is a major consideration in relation to interventional management (Fig. 3C).
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FIG. 3 A - Diagram showing propagation of thrombus following carotid transection. B - Lateral perforation with pseudoaneurysm formation. Note intraluminal thrombus. C - Arteriovenous fistula. Note intraluminal thrombus in distal arterial component.
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An injury that is becoming increasingly apparent in our practice is an intimal tear associated with a missile Shockwave. We have frequently noted at exploration an apparently intact carotid vessel with minimal bruising on the adventitial surface. On opening the vessel there is an intimal tear with superimposed thrombosis. It is postulated that the Shockwave causes acute lateral displacement of the vessel, causing distraction tears in the least elastic component of its wall, the intima, while the more elastic media and adventitia remain intact. The exposed media on the luminal surface is thrombogenic with resultant thrombosis that may be associated with thromboembolic phenomena (Fig. 4).
Clinical presentation The entry and exit wound may give some idea of the trajectory of the missile. However, if there is a single wound it is difficult to trace the trajectory. Probing is unreliable and is certainly not recom-
42
EMERGENCIES
mended, as thrombus may be dislodged with initiation of exsanguinating hemorrhage. We have also seen several patients in whom the stab wound has traversed the neck and caused a vascular injury on the opposite side. Presenting features may be grouped into emergency, subacute, and long-term. Emergency presentation is that of ongoing active hemorrhage whether to the exterior through the wound or concealed within the thoracic cavity, or the superior mediastinum. Subacute presentation occurs in patients who have stabilized hemodynamically. Pathognomonic signs of vascular injury are a pulsating hematoma, a pulse deficit in the upper limb, or a bruit whether systolic or of the arteriovenous type. It appears that on occasion the fistula may only develop later by the same mechanism already postulated for the development of delayed false aneurysm [9]. The communication may be sealed by thrombus and no bruit is audible in the acute phase. Within the next few days lysis occurs with the development of a manifest fistula. A systolic bruit may also result from compression resulting from pseudoaneurysm or partially occluding thrombus. More subtle signs of major vascular injury may be evidence of previous hemorrhage such as a history of major hemorrhage from the wound or a record of initial shock at presentation that has stabilized following fluid resuscitation, or when the patient presents with a low hemoglobin level. Long-term presentation may be with delayed onset of false aneurysm with or without compressive symptoms to the trachea or brachial plexus or an arteriovenous fistula that may present months or even years later with the consequences of systemic hemodynamic changes, a machinery bruit, or venous hypertension.
Diagnosis and management
FIG. 4 Diasram illustrating postulated mechanism of arterial thrombosis following proximity (Shockwave) missile injury.
Patients presenting in the emergency category with ongoing hemorrhage or acute stridor require urgent exploration in order to stop the bleeding and/or relieve the compression. This is a clinical decision requiring judgment as to where the site of the bleeding might be, and the appropriate exploration must be carried out. The hemodynamically stable patient without airway compression can be investigated appropriately. An erect, well-orientated chest film is extremely valuable. Widening of the mediastinum suggests
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INJURY TO THE BLOOD VESSELS OF THE NECK AND
that further investigation might be necessary. Computed tomography scans in the context of penetrating trauma are not as useful and give little more information than a high-quality antero-posterior chest radiograph. Duplex scanning is extremely useful for Zone 2 injuries [10,11]. It is accurate in this area for identifying intimal flaps, localizing arteriovenous fistulae, and detecting minor degrees of perforation (Fig. 5). This modality is of minimal value in Zone 1 or Zone 3 injuries because of anatomical consideration. Transesophageal echo has not proved particularly useful in our experience and we do not recommend it. Arch angiography using the Seldinger technique remains the gold standard for the diagnosis of cervicomediastinal vascular injuries. It has the additional advantage that interventional maneuvers can be performed when required. The indication for angiography is clinical suspicion of vascular injury in the hemodynamically stable patient, as previously
MEDIASTINUM
outlined. It is also recommended in our practice that routine angiography should be carried out in patients with shotgun wounds. While stab wounds can safely be observed if there is no suspicion of vascular injury on clinical grounds, our threshold for angiography is far lower with gunshot wounds, particularly those which traverse the neck, because of the possibility of a Shockwave injury. The pitfalls of interpreting angiography lie in the accurate localization of arteriovenous fistula by virtue of the rapid circulation time [7,9]. In addition, significant intraluminal thrombus may be present that is not clearly demonstrated by the radiography (Fig. 6).
Operative management It is important that the patient be positioned and draped so that access is possible from the base of the skull to the xiphisternum. The patient should be in the supine position with a bolster between
43
FIG. 5 Duplex scan showing a common carotid to internal jugular arteriovenous fistula following a stab wound in Zone 2 of the neck.
FIG. 6 Angiogram showing a carotid to jugular fistula as a result of a gunshot wound. The young male developed an acute right hemispheric neurologic deficit while awaiting operation. At surgery there was extensive thrombus formation in relation to the fistula (not clearly seen on the angiogram).
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the scapulae, the neck extended, and the head turned away from the side of the injury. It is foolish to attempt to enlarge and explore the stab wound, and the standard approach must be adapted to the blood vessels of the neck and mediastinum. The standard utility incision is placed along the anterior border of the sternomastoid muscle, which can be extended into a median sternotomy if required (Fig. 7). For Zone 2 injuries, the standard approach to the common carotid artery, the bifurcation, and the proximal internal carotid artery should be used. The aerodigestive tract can also then be explored by displacing the carotid sheath anteriorly. For lacerations of the blood vessels close to the base of the skull, access may be improved by dividing the digastric muscle. If this does not improve matters it is certainly not recommended that the temporomandibular joint be dislocated with forward displacement of the mandible, or that the ramus of the mandible be divided, as this results in unacceptable long-term morbidity.
44
FIG. 7 Incisions for exposure of cervicomediastinal blood vessels.
EMERGENCIES
Excellent access to the vessels at the base of the skull can be gained by detaching the sternomastoid muscle from its insertion on the mastoid. This can be then retracted antero-inferiorly with excellent exposure of the vessels as they enter the skull. Care must be taken not to damage the tenth and twelfth cranial nerves as well as the accessory nerve, all of which can be clearly identified [12]. For Zone 1 injuries (superior mediastinum), the optimal incision is a total median sternotomy. This provides excellent access to all the mediastinal vessels including the left subclavian artery. Under certain circumstances, a limited sternotomy down to the angle of the sternum may provide sufficient exposure. We have never found it necessary to excise the clavicle or to make trap door incisions. Division or excision of the clavicle causes major longterm morbidity particularly in manual laborers. The distal subclavian artery is best approached using a supraclavicular incision. If necessary, a separate infraclavicular incision may be made in order to tunnel a graft. Division of the clavicle invariably results in non-union and a painful pseudarthrosis, which is possibly a consequence of devascularization of the bone in the process of surgical division. The arterial injuries themselves can be repaired on their merits. The usual principles of debridement of the edges of the arterial wall back to healthy tissue pertain. The vessel can then be repaired by lateral suture, patch angioplasty, or an interposition graft [4,5]. Any prospect of narrowing the vessel by lateral suture should prompt the use of a vein patch. The through-and-through wound is best totally transected, debrided, and reconstructed in an endto-end fashion. Following excision of the damaged vessel, an endto-end anastomosis should not be attempted if there is excess tension on the suture line, as this invites occlusion. The best measure of tension is whether a single tethering stitch holds the ends together; if not, it is better to reconstruct using an interposition graft, the saphenous vein being the optimum graft. While the jugular veins have been used, they are not as satisfactory because of their thin walls and wide diameter, particularly when reconstructing the internal carotid artery. In the case of injury with an intimal tear it is best to excise the damaged segment and repair by means of an interposition graft. It is extremely important, particularly with regard to the carotid vessels, to dissect meticulously in
PENETRATING
INJURY TO THE BLOOD VESSELS OF THE NECK AND
order to avoid dislodging thrombus. It is also important to pass an embolectomy Fogarty catheter gently, both proximally and distally, to ensure that all thrombus has been extracted prior to performing repair.
Specific problems Penetrating wounds of the aortic arch that are compatible with survival are usually small puncture wounds that can be treated by digital occlusion and the insertion of mattress sutures deep to the occluding finger [12]. Wounds of the major branches close to the arch, particularly through-and-through wounds, are best treated by using a partially occluding clamp on the aorta, totally transecting the relevant vessel and oversewing its origin on the aorta. Continuity can then be restored by making an end-to-side anastomosis of a prosthetic graft to the intrapericardial portion of the ascending aorta and an end-to-end anastomosis to the relevant vessel. Attempts to reanastomose this type of injury invite disaster, as
MEDIASTINUM
it is extremely difficult to gain adequate control. It is also difficult to gain intimal apposition as the media tends to retract into the aorta. In the case of the left subclavian artery, continuity can be restored by means of a carotid to subclavian bypass if necessary (Figs. 8A and 8B). On occasion, the superior mediastinum is totally obscured by clot, which makes identification of the relevant vessels difficult. Under these circumstances, it is best to open the pericardium and expose the intrapericardiac aorta. The origins of the major vessel can then be identified by palpation and the necessary proximal control obtained prior to opening the hematoma [13]. Arch anomalies are uncommon, but they may not be identified by pre-operative angiography, and occasionally with emergency explorations they may catch the surgeon off guard (Fig. 9). In our own practice, the prevalence of some form of anomaly is 5.3%; although these anomalies are not common, this is significant [14]. The anomalies range from a common trunk from which the left common carotid and the brachiocephalic arteries arise, the so-called bouquet anomaly, to the lusorian anomaly
45
FIG. 8 Recommended sursical manasement of injuries occurring in close proximity to the aortic arch.
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EMERGENCIES
performed. Similarly, it is probably ill advised to restore continuity in a patient who is deeply comatose [16,17]. Most patients with localizing neurologic deficits improve, and we have not to our knowledge caused neurologic deterioration by following this practice.
ARTERIOVENOUS FISTULAE
FIG. 9 Arch angiogram of a young male showing a typical anomaly. There is a common origin of the brachiocephalic and left common carotid arteries (arrow). 46
in which there is a short brachiocephalic trunk from which both common carotid arteries arise and the right subclavian arises from the descending aorta and traverses the posterior mediastinum behind the esophagus [13]. Under these circumstances it would be necessary to insert a shunt from the interpericardiac aorta in order to preserve cerebral flow while repair is carried out [15].
ASSOCIATED NEUROLOGIC DEFICITS The theoretical consideration in restoring flow under these circumstances is the creation of a hemorrhagic infarct. Computed tomography scanning is notoriously unreliable within the first 24 hours of developing a neurologic deficit, and it is often not possible to obtain the necessary scan in the emergency setting. It has been our policy to restore arterial continuity in all patients with a neurologic deficit, provided that there is distal continuity, as evidenced by back bleeding following extraction of thrombus. If there is no back bleeding, ligation is
A major problem may arise if there is failure to accurately localize the fistula site particularly in the superior mediastinum. It can be very difficult to distinguish between a fistula arising from the aortic arch from one arising from major vessels close to their points of origin. In Zone 2, duplex scanning has proved sufficiently accurate in defining the exact site of fistulation. Zone 3 presents very similar problems to those in the superior mediastinum. Duplex is not helpful and angiography can indeed be misleading as to the exact site of the fistula. The veins lie in an anterior plane to the artery, and it is relatively easy to isolate the fistula by dissecting out the vein and isolating the fistula by palpation along the course of the vein. Once found, the proximal and distal arterial components can be isolated and the artery and vein repaired [5,9]. It has been stated that it is advisable to wait for fistula to mature prior to attempting repair; however, we have not found this to be advisable, as the longer one waits the more fibrosis occurs and the more difficult the procedure becomes. In the presence of extensive fibrosis and a small deficit, it may on occasion be expedient to repair the fistula transvenously but this is rarely necessary. In general, repair constitutes simple debridement and end-to-end or lateral suture. Embolism from the clot within the arterial segment just distal to the fistula is a distinct hazard. It is important to be meticulous and gentle in the dissection of the vessels and to ensure that there is no residual thrombus in the artery prior to repair and restoration of prograde flow. Back bleeding and gentle thrombectomy using a small balloon catheter should always be performed. Air embolism through the venous component has not proved to be a problem, but it is important to clamp the veins at an early stage and to fill the venous segment with saline prior to final closure. Recurrent fistulation has never proved to be a problem, but multiple fistulae do occur and it is important, particularly in the case of shotgun wounds, to ensure that all palpable thrills have disappeared on completion of the repair. It is impor-
PENETRATING INJURY TO THE BLOOD VESSELS OF THE NECK AND MEDIASTINUM tant also to attempt to trace the trajectory of the penetrating implement or missile to ensure that all injuries have been dealt with.
The use of cardiopulmonary bypass In the acute setting in most of the lesions described, cardiopulmonary bypass is unnecessary and only adds to the magnitude of the operation [18,19]. In most cases, if deemed necessary, intraluminal shunts can be during the procedure, but this is certainly not routine. Cardiopulmonary bypass may become necessary for the repair of chronic lesions presenting late in which extensive fibrosis may create major technical difficulties [20-22]. The major morbidity associated with penetrating wounds involving the extracranial cerebrovascular circulation is neurologic. In general terms, neurologic morbidity following straightforward carotid repair is negligible; however, there is a significant, approximately 5%, neurologic event rate associated with carotid arteriovenous fistulae. This, we believe, is due to thrombotic embolization. The overall mortality for mediastinal lesions is in the area of 7% and, for Zone 2 and 3 lesions, approximately 2%.
VENOUS INJURIES Frequently, particularly with gunshot trauma, there is far more extensive injury to the major veins, leaving relatively large defects that do not lend themselves to simple repair. This may be the result of increased friability of the veins and their relative inelasticity. It has been stated that repair should always be attempted in this situation. However, venous repair does not enjoy the same success that one associates with arterial reconstruction. This is the result of the friability of the vessel wall and the low intraluminal pressure. There is a high occlusion rate associated with complex repair using interposition grafts, particularly with a prosthesis. In addition, as is so often the case when attempting to repair associated complex venous injuries, it significantly increases the magnitude of the operative procedure. There is a paucity of information on the collateralization of the venous system of the head and neck. Barrett performed phlebographic studies on patients with idiopathic superior mediastinal fibrosis [23]. These studies showed extensive collateral-
ization through the anterior jugular system, the anterior communicating veins in the neck, and the superior intercostal veins that restored cardiac inflow via the azygos and hemi-azygos systems. Even when the azygos system was occluded, the superficial veins on the chest wall contributed to this collateralization. It must also be postulated that the vertebral plexus comes into play under these circumstances. It is well known with general surgical experience that interruption of one or even both internal jugular veins is well tolerated. Based on this evidence, it has been our policy for several years to repair simple lacerations or perform reanastomosis when feasible. Complex injuries with tissue loss cephalad to the azygos veins have been ligated [24,25]. If the vein is to be reconstructed, meticulous and gentle technique using a fine guage vascular suture (6/0) is absolutely essential. In a significant series of patients, we have not encountered major permanent morbidity as a result of this approach. Temporary facial and upper limb edema has been noted in several patients who have had ligation of the brachiocephalic veins but which resolved within a period of 4 to 5 days. Ligation of the distal subclavian vein has resulted in temporary upper limb edema but has not resulted in longterm morbidity. We have not seen large injuries of the superior vena cava caudad to the azygos vein, and this type of injury is probably incompatible with survival. Air embolism has not constituted a problem, although meticulous attention is paid to ensuring that significant amounts of air are not present in the major veins prior to restoring flow, and it is advisable to fill the segment with saline prior to inserting the final stitches.
INTERVENTIONAL CATHETER TECHNIQUES Embolotherapy is proving invaluable in dealing with traumatic lesions involving branches of the subclavian artery, the vertebral vessels, and branches of the external carotid [26]. In relation to the carotid system, we have had a single episode of migration of a spring coil into the internal carotid, and while the patient fortunately did not suffer any adverse sequelae, this is obviously undesirable. In relation to the vertebral vessels, particularly within the bony canal, there exists the possibility of creating a neurologic deficit with vertebral artery disruption if the posterior communicating vessels in the circle of Willis are found to be deficient [2730]. We have fortunately not encountered this problem.
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The use of covered stents to treat partial lacerations or arteriovenous fistulae is attractive. The currently available stents are polytetrafluoroethylene (PTFE) covered, and an increasing number of reports on the use of these stents, particularly in the subclavian artery, describe mixed success [3134]. The use of stents is probably not applicable within the aortic arch, and we strongly recommend
against their use in the carotid system in the context of trauma because of the thrombus frequently associated with these lesions. There is the ever-present possibility of infection, as all traumatic wounds are potentially contaminated. We have one patient on record with a proximal subclavian pseudoaneurysm that was stented; infection occurred and ultimately led to the patient's demise.
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1 RobbsJV, KeenanJ. Exploration of the neck. In: Champion HR, Robbs JV, Trunkey D (eds). Rob and Smith's operative surgery, 4th edition. London, Butterworths 1989: pp 166-172. 2 Campbell FC, Robbs JV. Penetrating injuries of the neck: a prospective study of 108 patients. flr/Swrgl980; 67: 582-586. 3 Levien LJ. Ballistics of bullet injury. In: Champion HR, RobbsJV, Trunkey D (eds). Rob and Smith's operative surgery, 4th edition. London, Butterworths 1989: pp 106-110. 4 Robbs JV. Vascular trauma. General principles of surgical management. In: Champion HR, RobbsJV, Trunkey D (eds). Rob and Smith's operative surgery, 4th edition. London, Butterworths 1989: pp 519-528. 5 Robbs JV. Basic principles in the surgical management of vascular trauma. In: Greenhalgh RM (ed). Vascular and endovascular techniques, 4th edition. London, W.B. Saunders Ltd. 2001 :pp 455-465. 6 Robbs JV, Naidoo KS. Nerve compression injuries due to traumatic false aneurysm. Ann Surg 1984; 200: 80-82. 7 Robbs JV, Baker LW. Cardiovascular trauma. Curr Probl Surg 1984; 21:1-87. 8 Frykberg ER, Crump JM, Dennis JW et al. Nonoperative observation of clinically occult arterial injuries: a prospective evaluation. Surgery 1991; 109: 85-96. 9 Robbs JV, Carrim AA, Kadwa AM, Mars M. Traumatic arteriovenous fistula: experience with 202 patients. BrJ Surg 1994; 81: 1296-1299. 10 Fry WR, Dort JA, Smith RS et al. Duplex scanning replaces arteriography and operative exploration in the diagnosis of potential cervical vascular injury. Am J Surg 1994; 168: 693-695. 11 Corr P, Abdool Carrim AT, Robbs J. Colour-flow ultrasound in the detection of penetrating vascular injuries of the neck. S Afr MedJ 1999; 80: 644 -646. 12 Robbs JV. Injuries to the vessels of the neck and superior mediastinum. In: Champion HR, RobbsJV, Trunkey D (eds). Rob and Smith's operative surgery, 4th edition. London, Butterworths 1989:pp 529-538. 13 RobbsJV. Penetrating trauma to the inlet and outlet regions of the chest. In: Westaby S, Odell J (eds). Cardiothoradc trauma. London, Arnold 1999: pp 183-195. 14 Satyapal KS, SingaramJV et al. Aortic arch branch variation case report and angiographic analysis. S Afr J Surg W02, (in press). 15 WoolgarJD, RobbsJV, Rajaruthnam P, Mohamed GS. Penetrating injuries in the innominate artery in association with abnormal aortic arch anatomy. EurJ Vase Endovasc Surg 2QQ2; 23: 462-464. 16 Perry MO, Snyder WH, Thai ER. Carotid artery injuries caused by blunt trauma. Ann Surg 1980; 192: 74-77. 17 RobbsJV, Human RR, Rajaruthnam P et al. Neurologic deficit
and injuries involving the neck arteries. Br J Surg 1983; 70: 220-222. 18 Buchan K, Robbs JV. Surgical management of penetrating mediastinal arterial trauma. Eur J Cardiothorac Surg 1995; 9:90-94. 19 Graham JM, Feliciano DV, Mattox KL, Beall AC Jr. Innominate vascular injuries. / Trauma 1982; 22: 647-655. 20 Fulton JO, de Groot KM, Buckels NJ, von Oppel UO. Penetrating injuries involving the intrathoracic great vessels. S Afr J Surg 1997; 35: 82 -86. 21 Fulton JO, de Groot MK, von Oppel UO. Stab wounds of the innominate artery. Ann Thorac Surg 1996; 61: 851-853. 22 Fulton JO, Brink JG. Complex thoracic vascular injury repair using deep hypothermia and circulatory arrest. Ann Thorac Surg 1997; 63: 557-559. 23 Barret NR. Idiopathic mediastinal fibrosis. Br } Surg 1958; 46: 207. 24 Robbs JV, Reddy E. Management options for penetrating injuries to the great veins of the neck and superium mediastinum. Surg Gynaec Obstet 1987; 165: 323-326. 25 Nair R, Robbs JV, Muckart DJ. Management of penetrating cervicomediastinal venous trauma. EurJ Vase EndovascSurg 2000; 19:65-69. 26 Naidoo NM, Corr PD, Robbs JV et al. Angiographic embolisation in arterial trauma. EurJ Vase EndovascSurg 2000; 19: 77-81. 27 Thomas GI, Anderson KN, Hain RF et al. The significance of anomalous vertebro-basilar artery communications in operations on the heart and great vessels. Surgery 1956; 46: 747-757. 28 Monson DO, Saletta JD, Freeark RJ. Carotid vertebral trauma. /Trauma 1969; 9: 987 -999. 29 Schomer DF, Marks MP, Steinberg GK et al. The anatomy of the posterior communicating artery as a risk factor for ischemic cerebral infarction. NEngJMed 1994; 330: 1565-1570. 30 Jithoo R, Nadvi SS, Robbs JV. Vertebral artery embolism post subclavian artery injury with occipital lobe infarction. EurJ Vase 31 Marin ML, Veith FJ, Panetta TF et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vase Surg 1994; 20: 466-473. 32 du Toit DF, Strauss DC, Blaszczyk M et al. Endovascular treatment of penetrating thoracic outlet arterial injuries. EurJ Vase Endavasc SurgZm-, 19: 489-495. 33 Strauss DC, du Toit DF, Warren BL. Endovascular repair of occluded subclavian arteries following penetrating trauma. JEndovasc Tfcr2001; 8: 529-533. 34 Chandler TA, Fishwick G, Bell PR. Endovascular repair of a traumatic innominate artery aneurysm. EurJ Vase Endovasc Surg 1999; 18: 80 -82.
5 ACUTE ABDOMINAL AORTIC OCCLUSION PIERRE JULIA, STEPHANE ZALINSKI, JEAN-NOEL FABIANI
Acute aortic occlusion is an uncommon disease with a mortality of approximately 50%, requiring urgent treatment in a specialized center. The classic differentiation between embolus and acute thrombosis of the distal aorta remains a realistic distinction. The latter has become the most frequent etiology because of the predominance of peripheral vascular pathology in an ageing population. Other causes are more rare, such as acute thrombosis of an abdominal aortic aneurysm, an occlusion due to aortic dissection or acute hemostatic disorders. If untreated, the prognosis is poor with a mortality of 75%. The initial diagnostic failures can be explained by the associated neurologic symptoms, delaying adequate treatment and therefore aggravating the prognosis. The extent of the occlusion and associated ischemia-reperfusion syndrome can induce major metabolic disorders. Despite surgical treatment, the overall mortality of this disease is approximately 50 % in the major published series [1].
Clinical presentation The clinical features are mainly determined by the acute severe ischemia of the lower limbs, associated with bilateral pain and neurologic symptoms like numbness, paresthesias and, in the most severe state, even paralysis of both legs. Rest pain or severely deteriorated intermittent claudication have the same diagnostic value and suggest a superimposed thrombosis on pre-existing occlusive lesions. Additional abdominal complaints or renal insufficiency with oligo-anuria are reminiscent of intestinal or renal ischemia, indicating proximal extension of the thrombosis to the level of the visceral
arteries. The severity of symptoms depends on the quality of the collateral circulation, being poor in cases of embolization and more developed in aortoiliac occlusive disease. An occluding embolus causes an abrupt and severe bilateral pain often associated with low back and gluteal pain, and can subsequently induce major neurologic deficit with complete paraplegia. Skin mottling can often be impressive and involve both legs, proximally extending to the umbilicus. In contrast, an acute thrombosis in a diseased distal aorta with pre-existing severe claudication or rest pain will manifest either with aggravation of existing complaints or a neurologic deficit similar to
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spinal cord infarction. In these nonexceptional cases, the patients are referred to a neurologic or neurosurgical department, causing significant diagnostic delays. These neurologic manifestations are not induced by spinal cord infarction but by severe ischemic neuropathy, which is reversible after revascularization [2]. Physical examination reveals absence of pulsations in both groins. The degree and extent of neurologic deficit is variable and develops in time, therefore requiring initial adequate and detailed neurologic examination, which serves as a reference for subsequent assessments. Also the location and extent of the ischemic skin should be indicated and followed. Abdominal examination is usually normal; however, meteorism, pain and decrease or disappearance of peristalsis might indicate associated intestinal ischemia [3]. Urine output should also be monitored since any alteration suggests impairment of the renal arteries. Acute onset hypertension has the same diagnostic value [4].
Etiology
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The most common causes of acute distal aortic occlusion are embolization and thrombosis. Other mechanisms include traumatic occlusion, aortic dissection, metabolic disorders, and pharmacologic interactions. Acute occlusions of vascular grafts leading to the signs of aortic occlusion are very uncommon and will not be addressed in this chapter.
EMBOLI The most common source of emboli is the heart, in the past mainly from endocarditis. At present, ischemic heart disease and especially the sequelae of myocardial infarction dominate the embolic etiology [5]. Arrhythmia is often encountered, basically being atrium fibrillation, however this is rarely an isolated entity. Cardiac tumors, mainly the myxoma of the left auricle, can be the source of embolization by fragmentation of the tumor. Kao [6] reported an exceptional case of secondary acute aortic occlusion by a cardiac myxoma. Paradoxal embolization can occur in the coexistence of deep venous thrombosis, patent foramen ovale and pulmonary hypertension susceptible to cause a right-to-left shunt. Theoretically, the emboli can come from the thoracic aorta, either from an aneurysm or from an ulcerated plaque on which a
EMERGENCIES
floating thrombus developed. This mechanism, however, is unlikely to cause a complete aortic occlusion because of the size of these thrombus masses.
ACUTE THROMBOSES Acute thromboses represent the most common cause in several series [4,7], although Surowiec et al. [5] only encountered an incidence of 50%. They are often the end stage of obstructive aorto-iliac disease characterized by bilateral intermittent claudication. The severity of the initial symptoms greatly depends on the extent of the collateral system and suddenness of onset. If the collateral network is poorly developed and the pre-existing aortic stenosis is limited, the clinical picture is dramatic with acute neurologic deficits. In contrast, if the acute aortic occlusion is superimposed on a chronic extensive stenotic process, the clinical picture is often less impressive and predominantly manifests with ischemic rest pain. The occurrence of a thrombosis in diseased arteries is most often provoked by dehydration or cardiac decompensation, the latter being the result of myocardial infarction or severe arrhythmia [4]. Acute thrombosis of an abdominal aortic aneurysm only exceptionally occurs. The first case was described by Shumacker in 1959 [8] and the first revascularization was performed by Jannetta and Roberts [9]. Only 44 cases have recently been published, according to a review of the literature by Hirose et al. [10]. The clinical signs are similar to those of an acute aortic occlusion and only the palpation of an abdominal mass with transmitted pulsations might indicate the diagnosis. In approximately half of the reported series, the correct diagnosis was established during laparotomy. At present, contrast enhanced computed tomography (CT) allows rapid assessment. The following mechanisms of such an occlusion are: - coexisting bilateral severe iliac obstructive disease with iliac thrombosis and proximal extension in to the aortic aneurysm, - occlusion of the aneurysm neck by means of an embolus originating from the heart, - partial dislodgment of intra-aneurysmal mural thrombus causing obstruction of the lumen with secondary thrombosis, - hypotensive episode or low cardiac output with intravascular thrombosis in a pre-existing aneurysm largely filled by thrombus. The optimal treatment consists of emergency surgical repair, allowing simultaneous treatment of the
ACUTE ABDOMINAL AORTIC OCCLUSION aneurysm and acute thrombosis. This surgical management, however, is not always feasible because of the poor physical conditions of these patients. In these cases, distal revascularization can be established by means of an axillobifemoral graft. This technique does not prevent later rupture, as observed in 15% of the patients of Schwartz et al. [11]. The prognosis of these aortic aneurysm thromboses is poor, with a mortality rate greater than 50%. Recent progress is limited and mortality rates encountered during the last years sit at 42% [10]. Acute aortic thrombosis can also be caused by aortic dissection. In the experience of Cambria et al. [12], 10 of 325 patients with acute aortic dissection required urgent aortic replacement or fenestration because of acute aortic occlusion. The mechanism of this aortic obstruction is based on the propagation of the intimal layer until the aortic bifurcation with compression of the true lumen by the false lumen (dynamic obstruction). This mechanism rarely occurs because the dissection usually extends in a unilateral fashion, or bilateral and asymmetrical, in one or two common iliac arteries. Arterial trauma is a rare cause of aortic occlusion, in which indirect localized dissection is the mechanism. Seatbelt compression is a known cause of multiple intra-abdominal lesions, however, abdominal aortic lesions rarely occur. In general, traumatic aortic injury affects the thoracic aorta in 95% and the abdominal aorta in 5% of cases [13]. The ischemic signs are immediately severe and associated intraabdominal lesions can deteriorate the prognosis, latrogenic traumatic injuries are particularly caused by intra-aortic balloon pumps [14] or complex endovascular procedures, as applied in cases of complicated aortic dissections [15]. Aortic thromboses can also be induced by hypercoagulability syndromes. These syndromes mainly cause venous thromboses, but if arterial complications occur the prognosis is poor [4]. The clinical manifestations of aortic thrombosis in patients with nephrotic syndrome are dramatic, as reported by Imamura et al. [16]. Szychta et al. described ulcerative colitis as a result of acute aortic thrombosis [17]. Finally, lupus anticoagulants are associated with aorto-iliac occlusions and smaller caliber arteries [18,19]. Recently, DiCenta et al. [20] described a case of infrarenal aortic occlusion associated with inferior vena cava occlusion in a patient with circulating anticoagulants. Several pathologic states can be identified, including heparin-induced thrombopenia, antithrombin III, protein C, and protein S deficits. It
is therefore necessary, in case of acute aortic occlusion, to fully investigate the coagulation parameters because coagulation disorders require immediate treatment in order to prevent recurrences.
Additional investigations Duplex scanning of the lower limbs does not provide additional information to that found during physical examination. However, the technique might identify involvement of one or more visceral arteries, realizing that obesity or abdominal meteorism can limit its sensitivity. Furthermore, duplex scanning is technician dependant. Arteriography comprising aortography and arteriography of the lower limbs is debatable. In the older publications arteriography was recommended as a standard technique. There are indeed several arguments to justify this technique. It provides a perfect diagnosis and allows accurate delineation of the proximal extension of the occlusion and the status of the renal arteries, as well as the distal outflow [3]. Noteworthy to mention is the advantage of an injection in the ascending aorta which often allows better and earlier visualization of the lower limb arteries via the internal mammary and epigastric arteries. In case of embolization, arteriography might depict emboli in other regions like the superior mesenteric and renal arteries in particular but also emboli resulting from thrombus fragmentation at an arterial bifurcation, leading to a secondary shower of emboli affecting the femoral, popliteal and crural arteries. This is a relative advantage because in these ill patients the femoral bifurcation can be visualized on the initial angiography and the distal outflow can be assessed by intra-operative angiography. The disadvantages of arteriography include deterioration of renal function, delay of revascularization and the fact that it hardly modifies the surgical strategy, except in visceral involvement and aortic dissection [1,21]. CT scanning is hardly cited in the literature, probably because the majority of publications are outdated. At present, the spiral CT scanners will systematically be used, especially in the acute setting of the disease. In fact, this technique allows visualization of the total thoraco-abdominal aorta and its main visceral branches. It might also depict the cardiac cavities in the search for thrombus formation. Magnetic resonance imaging has not been applied in acute aortic occlusion
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because of its limited availability and less maneuverability in acute settings. If a cardiac embolic source is suspected, echocardiography should be performed to identify valvular disease or dyskinetic ventricular areas due to ischemic cardiopathy. Residual intracardiac thrombus mass is rarely diagnosed but is an argument for adequate and prolonged anticoagulation treatment in order to limit the risk of embolic recurrences [22].
Treatment
52
The medical treatment is similar to the management of severe acute ischemia of the lower limbs. Intravenous heparin starts with a dose of 2 000 to 3 000 IU, followed by continuous infusion of 300 to 400 lU/kg per 24 hours, frequently controlled with blood samples. The role of thrombolysis is poorly defined, but it is not applicable in acute cases in which immediate surgical revascularization is required. However, it might be considered as a first attempt in patients presenting with a subacute clinical picture. Thrombolysis can re-open at least one iliac axis, followed by an additional endovascular procedure such as thrombectomy and angioplasty [23]. At present, however, the experience with this method remains anecdotal [24]. This technique will be most effective in hypercoagulability disorders but, in severe ischemia associated with absence of collaterals and thromboses in the microcirculation, its applicability will be limited by the duration of the procedure. Surgery remains the predominant treatment to guarantee a revascularization as fast as possible. The urgency is even more obvious if neurologic deficits are present, indicating severe ischemia. If renal or mesenteric artery involvement is suspected, laparotomy is required in order to restore patency by means of thrombectomy or direct embolectomy. Bypass surgery can be performed if proximal atherosclerotic lesions are present in these arteries. In general, a large surgical field is prepared, including the abdomen, both groins and at least one axilla. The first strategy is generally a retrograde bilateral thrombectomy, which might be successful in embolization of the aortic bifurcation. Completion angiography of both legs delineates patency of the distal arteries and might indicate the need for additional embolectomy. In thromboses of diseased arteries this technique is not effective and revascularization by means of
EMERGENCIES
bypass grafting is required. A classic procedure to perform in case of failed thrombectomy is an axillobifemoral bypass, especially in order to reduce the risks associated with laparotomy [25]. Actually, the choice between a direct revascularization via abdominal access or indirect extra-anatomical bypass basically depends on age and general condition of the patient [4,26]. Emergency direct revascularization seems to offer remarkable results [27]. Extraanatomical grafts are indicated in older patients with or without cardiac insufficiency. Intra-arterial blood pressure measurement and insertion of a Swann-Ganz catheter are recommended. Acute aortic occlusion associated with severe ischemia can induce significant metabolic disorders during and after revascularization due to reperfusion of substantial tissue areas. These disorders can cause major complications in one or two legs: neurologic sequelae, compartment syndrome, extensive muscular necrosis leading to amputation or reperfusion injury with multiple organ failure and subsequent death. Controlled limb reperfusion [28,29] and systematic fasciotomies are recommended. It seems logical that, in the near future, these extremely ill patients will benefit from these controlled reperfusion methods to reduce the associated morbidity and mortality [30]. Babu et al. [4] have analyzed the main factors that determine clinical outcome. Bad left ventricular function is a major risk factor since mortality in these patients was 85% as compared to 23% in patients with an adequate left ventricular. Hypercoagulability disorders are also associated with an impressive mortality of 83%. Other risk factors for poor prognosis include suprarenal thrombosis, distal obstructive disease and direct onset extremely severe ischemia. However, neurologic deficit due to spinal cord ischemia is not a poor prognostic risk factor because all cases normalized after revascularization. Therefore, neurologic deficit is not a contra-indication, but rather an indication for prompt revascularization.
Conclusion Acute abdominal aortic occlusion is a rare phenomenon and is associated with an overall mortality of approximately 50%, mainly due to the comorbidity in the majority of patients such as cardiac pathology and extensive vascular disease of
ACUTE ABDOMINAL AORTIC OCCLUSION which the aortic occlusion is the final event. Misleading neurologic symptoms can occur in 30%, in which absence of femoral pulses should indicate cardiovascular etiology instead of lower limb paralysis. Medical treatment is still based on anticoagulation. Therapy of choice is surgical revascularization, either by embolectomy, direct grafting or extra-ana-
tomical bypass. Fasciotomy with or without controlled reperfusion should be implemented in the surgical protocol in order to limit compartment syndromes and the general consequences of revascularization. By means of such an integrated strategy, the morbidity and mortality of this severe disease can be reduced.
R E F E R E N C E S
1 Verrier C, Bertrand P, Mercier C, Piquet P. Occlusion aigue du carrefour aortique. In: Kieffer E (ed). Urgences vasculaires non tmumatiques. Paris, AERCV, 1998: pp 373-381. 2 Mozingo J, Denton 1C Jr. The neurological deficit associated with sudden occlusion of the abdominal aorta due to blunt trauma. Surgery 1975; 77: 118-125. 3 Webb KH, Jacocks MA. Acute aortic occlusion. Am] Surg 1988; 155: 405-407. 4 Babu SC, Shah PM, NitaharaJ. Acute aortic occlusion-factors that influence outcome. / Vase Surg 1995; 21: 567-575. 5 Surowiec SM, Isiklar H, Sreeram S et al. Acute occlusion of the abdominal aorta. Am J Surg 1998; 176: 193-197. 6 Kao CL, Chang JP. Abdominal aortic occlusion: a rare complication of cardiac myxoma. Tex Heart /ntf/2001; 28: 324-325. 7 Favre JP, Gay JL, Gournier JP, Barral X. Acute occlusions of the aorta. / Chir 1995; 132: 7-12. 8 Shumacker H. Surgical treatment of aortic aneurysms. Postgrad AM1959; 25:535-548. 9 Jannetta P, Roberts B. Sudden complete thrombosis of an aneurysm of the abdominal aorta. NEnglJMed 1961; 264: 434-436. 10 Hirose H, Takagi M, Hashiyada H et al. Acute occlusion of an abdominal aortic aneurysm-case report and review of the literature. Angiology 2000; 51: 515-523. 11 Schwartz RA, Nichols WK, Silver D. Is thrombosis of the infrarenal abdominal aortic aneurysm an acceptable alternative? J Vase Surg 1986; 3: 448-455. 12 Cambria RP, Brewster DC, Gertler J et al. Vascular complications associated with spontaneous aortic dissection. / Vase Surg 1988; 7: 199-209. 13 Dajee H, Richardson IW, type MO. Seat belt aorta: acute dissection and thrombosis of the abdominal aorta. Surgery 1979; 85: 263-267. 14 Sakakibara Y, Sasaki A, Nakata H et al. Acute aortic thrombosis after intra-aortic balloon pumping. Jpn J Thorac Cardiovasc Swg2000;48: 123-125. 15 Lookstein RA, Mitty H, Falk A et al. Aortic intimal dehiscence: a complication of percutaneous balloon fenestration for aortic dissection. / Vase Interv Radiol 2001; 12: 1347-1350. 16 Imamura H, Asaka M, Saito A et al. Thrombosis of the abdo-
minal aorta in a patient with nephrotic syndrome. Nippon Jinzo Gakkat Shi 2001; 43: 608-612. 17 Szychta P, Reix T, Sevestre MA et al. Aortic thrombosis and ulcerative colitis. Ann Vase Swrg-2001; 15: 402-404. 18 Setoguchi M, Fujishima Y, Abe I et al. Aorto-iliac occlusion associated with the lupus anticoagulant. Report of two cases. Angiology 1997; 48: 359-364. 19 Komori K, Okadome K, Onohara T et al. High aortic occlusion associated with lupus anti-coagulant. EurJ Vase Surg 1992; 6: 302-306. 20 DiCenta I, Fadel E, Mussot S et al. Occlusion of the aorta and inferior vena cava in a patient with circulating anticoagulants. Ann Vase Swrg2002; 16: 380-383. 21 Dossa CD, Shepard AD, Reddy DJ et al. Acute aortic occlusion. A fourty-year experience. Arch Surg 1994; 129: 603-608. 22 Busuttil RW, Keehn G, Milliken J et al. Aortic saddle embolus. A twenty-year experience. Ann Surg 1983; 197: 698-706. 23 Buth J, Cuypers P. The diagnosis and treatment of acute aortic occlusions. J Mai Vase 1996; 21: 133-135. 24 Cunningham M, May S, Tucker W, Gerlock A. Response of an abdominal aortic thrombosic occlusion to local low-dose streptokinase therapy. Surgery 1983; 93: 541-544. 25 Drager SB, Riles TS, Imparato AM. Management of acute aortic occlusion. Aw/Swig 1979; 138: 293-295. 26 Meagher AP, Lord RS, Graham AR, Hill DA. Acute aortic occlusion presenting with lower limb paralysis. J Cardiovasc Surg 1991; 32: 643-647. 27 Bradbury AW, Stonebridge PA, John TG et al. Acute thrombosis of the non-aneurysmal abdominal aorta. EurJ Vase Surg 1993; 7: 320-323. 28 Schlensak C, Doenst T, Bitu-Moreno J, Beyersdorf F. Controlled limb reperfusion with a simplified perfusion system. Thorac Cardiovasc Surg 2000; 48: 274-278. 29 Vogt PR, von Segesser LK, Fagotto E et al. Simplified, controlled limb reperfusion and simultaneous revascularization for acute aortic occlusion. / Vase Surg 1996; 23: 730-733. 30 Julia P, Fabiani JN. Ischemia-reperfusion and compartment syndrome. In: Branchereau A.Jacobs M (eds). Complications in vascular and endovascular surgery (part II). Armonk, Futura Publishing Company, 2002: pp 11-21.
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6 HAS MORTALITY RATE FOR RUPTURED ABDOMINAL AORTIC ANEURYSM CHANGED OVER THE LAST 50 YEARS? JACK COLLIN
Annual rates of abdominal aortic aneurysm (AAA) rupture continue to increase with the ageing of populations throughout the developed world (Figure). Deaths from AAA represent the rates of tobacco smoking over the previous 60 years. Only a third of patients with ruptured AAA have emergency surgery, and operative mortality is around 50%. Intra-operative mortality rates have not changed for a generation but postoperative mortality rates have decreased by 3.5% per decade with improved management of organ failure. Most patients with AAA rupture die without surgery. Consequently, small improvements in operative mortality have negligible impact on overall AAA mortality. In the short term early detection of AAA by population screening and elective repair of aneurysms greater than 55 mm diameter offer the best chance to reduce AAA mortality. In the long term current low rates of tobacco smoking among the higher socio-economic groups of North America and Europe presage the progressive disappearance of AAA as a major cause of premature death.
National statistical data AAA is a disease of the elderly. Rupture of an AAA is uncommon in men under age 55 years or women younger than 60 years. It becomes increasingly common with advancing age. The incidence of death from AAA as a percentage of all deaths peaks in men aged between 70 and 75 years. There
is, however, no peak in the incidence of deaths from AAA per thousand at risk with increasing age. The older the cohort studied, the more deaths from AAA are seen to occur per thousand at risk [1]. The relative risk of death from AAA is 10 times greater in men than in women at age of 60 years. Among those who survive into their late 80s, men are only three times more likely to die from AAA
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56
than women of the same age. Since among the very elderly, women outnumber men by more than three to one, the false perception has sometimes arisen that the disease is more common in elderly women than men. Throughout the developed world the proportion of elderly men and women in the population has been increasing since the agricultural revolution. In the United Kingdom, data from the 2001 census show that for the first time in history those over 65 years of age are more numerous than those under 16 years. In addition to being old and male, in order to be at high risk of developing an AAA it is necessary to have smoked a substantial quantity of tobacco over a number of years. To be at high risk of AAA rupture, a patient with a known AAA should be a current smoker with poorly controlled hypertension [2]. In Europe, cigarette smoking became increasingly common in men during and after the First World War of 1914 to 1918. European women began to smoke in large numbers from the Second World War (1939 to 1945) onward. In Northern Europe and North America, smoking rates among adult males have been slowly declining for the last 30 years, particularly in the higher socio-economic groups, but smoking rates among women have increased. With all the above information in mind, it comes as no surprise to discover that over the last 20 years deaths from AAA in the United Kingdom have continued to increase [3]. Unless cigarette smoking significantly declines as a European addiction, there are sound reasons to predict that the number of patients presenting with AAA will continue to increase.
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Has elective AAA surgery reduced overall AAA mortality? Data from the United Kingdom Multicentre Abdominal Aortic Aneurysm Screening Study (MASS) [4] have shown that for patients with AAA diameters greater than 55 mm measured by ultrasonography, the number needed to treat (NNT) with elective AAA repair to prevent one death from AAA over the following four years is five. For patients with AAA diameters of 50 to 55 mm, the NNT is unknown but likely to be at best very substantially larger. At worst it may be replaced by a number needed to harm (NNH). The United Kingdom Small Aneurysm Trial [5] showed that patients with AAA antero-posterior diameters of 40 to 54 mm measured by ultrasonography randomized to elective surgical treatment were more likely to die from an AAA-related cause than those randomized to best medical treatment. Not surprisingly, after elective surgery fewer deaths occurred from AAA rupture but the number of rupture deaths prevented was exceeded by the number of operative deaths from elective AAA repair. It is clearly inadequate to use death rates from ruptured AAA alone as the measure of successful management of AAA. Scrutiny of death certification in the MASS study revealed that for many patients who died within 30 days of elective surgery, AAA was not mentioned as a cause of death and was not therefore recorded in national statistics.
HAS MORTALITY RATE FOR RUPTURED AAA Present evidence supports the conclusion that for patients with AAA diameter less than 55 mm, elective AAA repair is likely to do more harm than good. Until the publication of data from the Small Aneurysm Trial, it had become common to perform elective repair on AAAs of modest size. The current fashion for transluminal graft insertion has ensured that many patients at low risk of AAA rupture continue to have surgical treatment for small AAAs. The advocates for these internal fashion accessories justify their enthusiasm by claims that the risks of insertion are low and that they protect the wearer from subsequent AAA rupture. Neither claim currently withstands evidence-based analysis.
What treatment do patients with ruptured AAA receive? For practical purposes without surgical repair, rupture of an AAA has a mortality of 100%. Whether death occurs within minutes, hours, or days is determined by the site of rupture and the strength of the peri-aortic retroperitoneal connective tissue. Anterior free rupture into the peritoneal cavity results in exsanguination within minutes. Posterior or lateral contained rupture permits transportation of the patient to a hospital. If the patient is fortunate, the hospital will have a vascular surgeon available who can perform emergency AAA repair. If the patient is unfortunate, interhospital transfer will have to be arranged if judged to be appropriate. Finally, both the patient and the vascular surgeon need to agree that an attempt to repair the AAA rupture is sensible and worthwhile. Fewer than 50% of patients with AAA rupture have sufficient initial containment of hemorrhage to survive long enough to reach the hospital alive. Those who do are further reduced in number by delayed diagnosis, unnecessary diagnostic imaging, lack of a vascular surgeon, dilatory transfer arrangements, patient choice, and clinical selection based on age, coexistent disease, and estimated probability of operative survival. Overall, around one third of patients who have AAA rupture currently undergo an operation for its attempted repair. In individual hospitals, operation rates on those admitted range from less than 50% to almost 100%. Patel et al. [6] have shown that ruptured AAA repair is cost-effective provided the operative mor-
CHANGED OVER THE LAST 50 YEARS? tality is less than 85%. It is likely therefore that some reduction in overall mortality from ruptured AAA could be achieved by better access to specialist vascular surgical services. Most published data on AAA mortality are difficult to interpret. Clarity is obscured by misuse and inappropriate interchange of the distinctly different terms peri-operative, peroperative (intra-operative), and postoperative. Additional fog is created by often-deliberate confusion of emergency and even urgent AAA surgery with repair of ruptured AAA. Bown et al. [7] have made a valiant attempt to penetrate this obfuscation with a recent metaanalysis of 171 articles covering 50 years of ruptured AAA surgery. They have shown that after allowance for publication bias, the intra-operative mortality for ruptured AAA surgery has remained constant at 20%. They deduce that when analysis of retrospective data from individual institutions reveal a high intra-operative mortality rate, authors tend not to report it but instead disclose only the overall 30-day operative or in-hospital mortality. Operative mortality for urgent or emergency operations undertaken in the belief that an AAA has ruptured or is about to rupture (acute AAA surgery) is around a third of that for ruptured AAA surgery and three times that for elective AAA repair. Inclusion of acute AAA surgical data with that for ruptured AAA has the remarkable property of improving the operative mortality figures for both elective and ruptured AAA surgery. In the author's experience, local audit of data often reveals large differences in intra-operative mortality rates between individual surgeons. Part of the difference can be explained by the relative willingness or reluctance of different surgeons to operate on moribund patients with little or no chance of survival. Operative technique and skill play an additional part. Surgery for ruptured AAA is difficult and unforgiving of inexperience or carelessness. The most important principle underlying success is to lose as little blood as possible during the operation additional to that which has already and inevitably been lost to the circulation by pre-operative bleeding. The common causes of unnecessary pre-operative blood loss are listed in the Table. Most intra-operative deaths tend to be attributed to a cardiac cause, which has the advantage of making the surgeon feel better. The reality is different. In almost all cases, the proximate cause of the myocardial ischemia and resultant arrhythmia, asystole, or
57
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Postoperative mortality after ruptured AAA repair 1
Failure to occlude the neck of the AAA before incising the posterior peritoneum.
2
Injury to renal, gonadal or adrenal veins by blind clamping of the AAA neck.
3
Injury to iliac veins by unnecessary dissection behind the common iliac arteries.
4
Delayed recognition of aorto-caval fistula.
5
Inadequate control of inferior mesenteric, lumbar and median sacral arteries.
6
Heparin administration to a patient already fully anticoagulated by massive blood loss and hypothermia.
7
Reperfusion back-bleeding through already oversewn common iliac artery origins.
8
Closure of the abdomen before coagulation has been restored by administration of fresh frozen plasma, platelets, cryoprecipitate and rewarming.
58
pump failure is blood loss and inadequate blood replacement. The learning curve for successful repair of ruptured AAA is long for this most difficult of vascular surgical operations. In major tertiary referral centers in the US, ruptured AAA may represent as little as 5% of all AAA operations performed [8,9]. In the United Kingdom in some regional vascular centers [10], they account for more than 50% of all AAA operations. Most surgeons currently operating on patients with ruptured AAA perform fewer than five such operations per annum. Even in major referral centers, few individual surgeons operate on more than 10 patients with ruptured AAA each year. In such circumstances it is no surprise that intraoperative mortality remains around 20% as it has done since the early days of the operation fifty years ago. It is improbable that intra-operative mortality rates will improve in the foreseeable future.
In contrast to intra-operative surgical skill-based mortality there is evidence that postoperative 30-day mortality has progressively fallen by approximately 3.5% per decade [7]. This steady fall in postoperative death rates is attributable to the development of the specialty of intensive care medicine and improvements in the management of organ failure. Numerous authors have attempted to devise predictive scoring systems for postoperative death based on both pre-operative and early postoperative evaluation of the function of different organ systems [11-13]. In order of relative importance, survival is determined by control of cardiac, respiratory, renal, and hepatic failure. To date, most success has been achieved by expert management of renal and cardiac failure and least impact has been made on deaths from hepatic and respiratory failure. It is now unusual for a patient to succumb from renal failure alone without coexistent failure of at least one other organ system. The cynical view is sometimes expressed that, with profligate use of intensive care unit facilities, it is now possible to keep many patients alive for 30 days postoperatively who have little if any prospect of independent survival. It is certainly the case that beyond five days intensive care the rule of diminishing returns begins to apply. Few patients who are not fit for discharge from an intensive care unit five days after surgery will ultimately leave the hospital alive. With healthcare systems around the world in financial crisis, the cost effectiveness of long-term intensive care is increasingly being challenged.
Overall mortality for ruptured AAA At present only a third of patients who rupture an AAA will have an operation. Thirty-day operative mortality rates are around 50%, with wide variations in reported rates from different centers. Two fifths of all operative deaths occur during the operation and intra-operative mortality has remained unchanged for decades. It is reassuring to learn that while today's surgeons are no better than their
HAS MORTALITY RATE FOR RUPTURED AAA CHANGED OVER THE LAST 50 YEARS? mentors, at least they are no worse. The overall mortality from ruptured AAA remains stubbornly between 80% and 85%. The apparent 3.5% reduction per decade in postoperative mortality attributable to the growth of the expensive and laborintensive specialty of intensive care medicine has had a negligible and undetectable effect on AAA mortality statistics.
Can AAA mortality be reduced? Beyond any shadow of doubt, the most important factor underlying the current high incidence of death from AAA was the 20th century phenomenon of cigarette smoking by at its peak up to 75% of the adult male population. Primary prevention of this disease is likely to be much more effective than any imaginable cure. Fashions in human habits and addictions change and the emotional props of one century are prone to disappear in the next as quickly as they appeared in the last.
The most hopeful sign that tobacco smoking in the developed world may be in terminal decline is that it has now been largely abandoned by the trend-setting intellectual elite of Northern Europe and North America. Target growth areas for tobacco sales are now largely third world countries. Secondary prevention is directed at reducing the risk of AAA rupture in those who already have the disease. The proven interventions are smoking cessation and control of hypertension. Specific therapies with drugs to reduce growth rates of AAA at present are unproven. Recently the United Kingdom MASS study [4] established the value of a screening program for AAA detection in men aged 65 to 74 years. Elective surgical repair of AAAs with a diameter greater than 55 mm reduces the incidence of death from AAA-related causes, although all cause mortality is not affected. It is probable that current AAA-specific mortality could be reduced by restricting elective AAA surgery to those patients with AAA antero-posterior diameters measured by ultrasonography of at least 55 mm.
R E F E R E N C E S 1 Anonymous. Office for National Statistics. Mortality by cause (24). Series DH2, London. The Stationery Office 1999. 2 Brown LC, Powell JT. Risk factors for aneurysm rupture in patients kept under ultrasound surveillance. United Kingdom Small Aneurysm Trial Participants. Ann Surg 1999; 230: 289-297. 3 Anonymous. Office for National Statistics. Mortality by cause (5-24). Series DH2, London. The Stationery Office (1981 -1999). 4 Anonymous. Multicentre Aneurysm Screening Study Group. The Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet m% 360:1531-1539. 5 Anonymous. The United Kingdom Small Aneurysm Trial Participants. Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet 1998; 352:1649-1655. 6 Patel ST, Korn P, Haser PB et al. The cost-effectiveness of repairing ruptured abdominal aortic aneurysms. / Vase Surg 2000:32;247-257. 7 Bown MJ, Sutton AJ, Bell PRF, Savers RD. A meta-analysis of
50 years of ruptured abdominal aortic aneurysm repair. Br J Surg 2002; 89: 71 4 -730. 8 Cooley DA, Carmichael MJ. Abdominal aortic aneurysm. 9 Lawrie GM, Morris GC Jr, Crawford ES et al. Improved results of operation for ruptured abdominal aortic aneurysms. Surgery 1979: 85; 483 -488. 10 Collin J, Murie J, Morris PJ. Two year prospective analysis of the Oxford experience with surgical treatment of abdominal aortic aneurysm. Surg Gymcol Obstet 1989: 169; 527-531. 11 Davies MJ, Murphy WG, Murie JA et al. Pre-operative coagulopathy in ruptured abdominal aortic aneurysm predicts poor outcome, fir/ Swrg 1993; 80: 974-976. 12 Meesters RC, van der Graaf Y, Vos A, Eikelboom BC. Ruptured aortic aneurysm: early postoperative prediction of mortality using an organ system failure score. 5r/Swrgl994; 81: 512-516. 13 Brady AR, Fowkes FG, Greenhalgh RM et al. Risk factors for postoperative death following elective surgical repair of abdominal aortic aneurysm: results from the United Kingdom Small Aneurysm Trial. On behalf of the United Kingdom Small Aneurysm Trial participants, fir/ Surg 2000; 87: 742-749.
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7 RUPTURED AAA: SHOULD ENDOVASCULAR TREATMENT BE THE FIRST CHOICE? JAAP BUTH, NOUD PEPPELENBOSCH, NEVAL YILMAZ PHILIPPE CUYPERS, LUCIEN DUIJM, ALEXANDER TIELBEEK
Rupture of an abdominal aortic aneurysm (AAA) remains lethal despite rapid prehospital transport, early diagnosis and resuscitations, expeditious surgical repair and progress in anesthesia and intensive care. Mortality rates remain between 32% and 70% with significant associated morbidity [1-5]. Most centers quote rates near 50 % [6-8]. These high operative mortality rates reflect the magnitude of the physiologic stress of patients following rupture. Hemorrhage, prolonged hypotension, laparotomy and prolonged lower limb ischemia because of aortic clamping all contribute to the risk of cardiac complications, multiple organ failure and death. In addition, the patients are usually elderly and often have pre-existing comorbidities. Hypotension following rupture is often controlled at first by tamponade within the retroperitoneum, but the relaxation of the abdominal tone at induction of general anesthesia often precipitates cardiovascular collapse. Exposure of the neck of the aneurysm together with the dissection through the hematoma causes disruption of retroperitoneal veins and small arteries, resulting in further hemorrhage that is often difficult to control in coagulopathic patients. In the presence of large retroperitoneal hematoma, the aorta is frequently clamped at the supraceliac segment. This renders the viscera and lower extremities ischemic, which contributes to the establishment of a fibrinolytic state [9,10] and has a dramatic effect on cardiac afterload and lactic acid production. Subsequent reperfusion of the lower limbs adds further physiologic injury. Secondary bleeding episodes and other complications such as renal failure, adult respiratory distress syndrome, and colonic and gallbladder ischemia are ultimately responsible for most of the deaths.
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The excessive operative mortality also has important resource implications since most patients will spend many days in the intensive care unit before finally succumbing to the complications of rupture and emergency surgery [11]. In general,, patients who undergo open surgery represent a relatively favorable subset, as a considerable number are not operated at all because of significant comorbid factors. These patients inevitably will die without a surgical option [12].
Endovascular approach
62
Endovascular repair of ruptured AAA (rAAA) offers the possibility of a significant reduction in operative mortality. This approach relies on the intravascular deployment of an aortic stent graft, introduced via the femoral arteries to exclude the aneurysm from the circulation [13,14]. Laparotomy is avoided and the procedure can be performed under local anesthesia. It is likely that the risk of turning a contained rupture into intraperitoneal hemorrhage by the induction of general anesthesia would be significantly reduced. Additional blood loss due to opening of the retroperitoneal hematoma is avoided, while prolonged infra- or suprarenal aortic clamping is not necessary. Additionally, cardiac stress and duration of lower limb ischemia will be minimized. There is no ample evidence that endovascular aortic repair (EVAR) is technically feasible and safe in patients scheduled for elective AAA repair [1518]. In this chapter we will describe the results of a consecutive cohort study, comparing the impact of a protocol of preferential management by EVAR. The study group includes patients who were mostly, but not all, treated by EVAR. The study group will be compared with a historical control group consisting of patients treated routinely by open surgery for symptomatic or ruptured AAA (rAAA).
Methods From May 2001 onward, patients with symptomatic nonruptured AAA (snrAAA) and rAAA of the abdominal aorta presenting at the Catharina Hospital in Eindhoven were treated according to a well-defined management protocol involving intentto-treat by emergency (e)-EVAR. Patients were considered symptomatic nonruptured AAA if there were
no signs of hemorrhage outside the wall of the aneurysm on computed tomography (CT), but they had acute pain in the abdomen and an abdominal aneurysm that was painful at palpation. Aneurysms were defined ruptured AAA if there was extravasation of blood surrounding the aneurysm at CT examination. In patients who did not undergo CT examination, a retroperitoneal hematoma at open surgery was the criterion for rupture of the aneurysm. Within the study period, all patients who were referred to our hospital with a symptomatic aneurysm of the abdominal aorta were prospectively analyzed and included in this study. On arrival in the emergency ward, the intravenous fluid infusion rate was minimized. The protocol dictated that patients were taken to the radiology department for emergency CT examination with intravenous contrast infusion to opacity the aorta. An exception was made for patients in profound shock or those who had a cardiac arrest during transportation to the hospital. Diameter and length of the infrarenal neck of the aneurysm were measured and the decision whether endovascular repair was feasible was taken and communicated with the operating room staff. Exclusion criteria for e-EVAR were a short neck (less than 10 mm length), a wide neck (more than 30 mm in diameter), and inaccessible iliac arteries. Following CT examination, patients were quickly transported to the operating room for the selected emergency procedure, or taken to the intensive care unit (ICU) for further optimization (only in snrAAA). Patients with rupture of their aneurysm were preferentially treated with an aorto-uni-iliac (AUI) endograft (Fig. 1) combined with a crossover bypass. The study group described above was compared with a control group of patients with symptomatic aneurysms, who were treated by open procedure, between January 1999 and May 2001. This historical control group was retrospectively analyzed by hospital chart review. Primary outcome events that
RUPTURED AAA: SHOULD ENDOVASCULAR TREATMENT BE THE FIRST CHOICE?
63
FIG. 1 A - Intra-operative angiogram demonstrating rAAA B - Intra-operative angiogram demonstrating deployment of proximal component of AUI device C - Intra-operative angiogram demonstrating bilateral iliac arteries D - Postoperative CT examination demonstrating functioning AUI device with complete exclusion of the aneurysm.
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Results
were compared included: 30-day or in-hospital mortality, morbidity, length of hospital and ICU stay, intra-operative blood loss, requirement of blood products and overall fluid infusion during operation. Statistical analysis was performed using SPSS® for Windows® version 9.0. Chi-square and Fisher tests were used for the comparison of discrete variables and the Mann-Whitney test was used for continuous variables. Continuous variables are presented as the mean range. A p value of smaller than 0.05 was considered significant.
Group I Study group (40 patients)
Group n Control group
64
PATIENTS From May 2001 until June 2002, 40 consecutive patients in the study group were admitted and treated in our hospital because of a ruptured or symptomatic infrarenal abdominal aneurysm (group I, Table I). Fourteen patients had snrAAA and 26 rAAA. Twenty-six patients received endovascular repair (EVAR subgroup) and 14 patients conventional open surgery (COS [conventional open surgery] subgroup, Table II). While there was a trend that
a/ , //• ; Male/female 'J _
Mean , age v (range) Years
SnrAAA/ AAA rAAA N
^Mean ., , 0 AAA (range) cm
Systolic -.^ u