vascular emergency

© 2003 by Futura, an imprint of Blackwell Publishing

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ISBN: 1-4051-0387-6

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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.

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2003002267

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Notice: The indications and dosages of all drugs in this book have been recommended in the medicalliterature and conform to the practices of the general community. The medications described do notnecessarily have specific approval by the Food and Drug Administration for use in the diseases and dosagesfor which they are recommended. The package insert for each drug should be consulted for use and dosageas approved by the FDA. Because standards for usage change, it is advisable to keep abreast of revisedrecommendations, particularly those concerning new drugs.

Edited by

ALAIN BRANCHEREAU, MDUniversity Hospital, Marseille, France

&MICHAEL JACOBS, MD

University Hospital, Maastricht, The Netherlands

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LIST OF CONTRIBUTORS

Marko AJDUKUniversity Hospital MerkurZajceva ul.9Zagreb, Croatia

Jerome ALBERTINDepartement de Chirurgie VasculaireHopital Adultes La Timone264, rue Saint Pierre13385 Marseille Cedex 05, France

RaoufAYARIDepartement de Chirurgie VasculaireHopital Adultes La Timone264, rue Saint Pierre13385 Marseille Cedex 05, France

Joaquim BARBOSAVascular UnitHospital Particular de LisboaRua Luis Bivar, 301069-142 Lisboa, Portugal

Xavier BARRALDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire NordAvenue Albert Raimond42055 Saint-Etienne Cedex 2, France

Rachel BELLDepartment of General and Vascular SurgeryGuy's & St. Thomas' HospitalLambeth Palace RoadLondon SE1 7EH, United Kingdom

Ramon BERGUERDivision of Vascular SurgeryHarper Hospital, 3990 John RDetroit, Michigan 48201, USA

Ricardo BOFILLServei d'Angiologia I Cirurgia VascularPg Vail d'Hebron 119-12908035 Barcelona, Spain

Didier BOURRATDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire NordAvenue Albert Raimond42055 Saint-Etienne Cedex 2, France

Bruce BRAITHWAITEDepartment of Vascular and Endovascular SurgeryE Floor, West BlockUniversity Hospital, Derby RoadNottingham NG7 2UH, United Kingdom

Alain BRANCHEREAUDepartement de Chirurgie VasculaireHopital Adultes La Timone264, rue Saint Pierre13385 Marseille Cedex 05, France

Jaap BUTHDepartment of SurgeryCatharina Hospital, PO box 13505602 ZA Eindhoven, The Netherlands

Piergiorgio CAOUnita Operativa di Chirurgia VascolarePoliclinico Monteluce, Via BrunamontiPerugia 06122, Italy

Renata CASTELLANOChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Laurent CHICHEDepartement de Chirurgie VasculaireCHU Pitie-Salpetriere, 47/83, bd de 1'Hopital75651 Paris Cedex 13, France

Roberto CHIESAChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Efrem CIVILINIChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Albert CLARAServei de Cirurgia VascularHospital del Mar, Paseo Maritimo, 25-2908003 Barcelona, Spain

Marc COGGIAHopital Universitaire Ambroise Pare9, avenue Charles de Gaulle92104 Boulogne Cedex, France

Jack COLLINNuffield Department of SurgeryJohn Radcliffe HospitalOxford, OX3 9DU, United Kingdom

Andreja CRKVENACUniversity Hospital MerkurZajceva ul.9Zagreb, Croatia

Philippe CUYPERSDepartment of SurgeryCatharina Hospital, PO box 13505602 ZA Eindhoven, The Netherlands

VII

V I I I

Lourdes DEL RIOServicio de Cirurgia VascularHospital Clinico Universitario470 HValladolid, Spain

Isabelle DI CENTAHopital Universitaire Ambroise Pare9, avenue Charles de Gaulle92104 Boulogne Cedex, France

Lucien DUIJMDepartment of Vascular SurgeryCatharina Hospital, PO Box 13505602 ZA Eindhoven, The Netherlands

Bertrand EDEDepartement de Chirurgie VasculaireHopital Adultes La Timone264, rue Saint Pierre13385 Marseille Cedex 05, France

Ted ELENBAASDepartment of Cardiac SurgeryAcademic Hospital MaastrichtPO Box 58006202 AZ Maastricht, The Netherlands

Lidija ERDELEZUniversity Hospital MerkurZajceva ul.9Zagreb, Croatia

Jose Maria ESCRIBANOServei d'Angiologia I Cirurgia VascularPgValld'Hebronll9-12908035 Barcelona, Spain

Jean-Noel FABIANIDepartement de Chirurgie CardiovasculaireHopital Europeen Georges Pompidou20, rue Leblanc, 75015 Paris, France

Jean-Pierre FAVREDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire NordAvenue Albert Raimond42055 Saint-Etienne Cedex 2, France

Maria Jose FERREIRAVascular UnitHospital Particular de LisboaRua Luis Bivar, 301069-142 Lisboa, Portugal

Adam FISCHERDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Natalia de la FUENTEServei de Cirurgia VascularHospital del Mar, Paseo Maritime, 25-2908003 Barcelona, Spain

Jose Maria FUENTESServei d'Angiologia I Cirurgia VascularPgValld'Hebronll9-12908035 Barcelona, Spain

Mauro GARGIULOChirurgia VascolareUniversita di Modena e Reggio EmiliaPoliclinico Universitario, Via del Pozzo n° 7141100 Modena, Italy

Philippe GERSBACHDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Olivier GOEAU-BRISSONNIEREHopital Universitaire Ambroise Pare9, avenue Charles de Gaulle92104 Boulogne Cedex, France

Jose GONZALEZ-FAJARDOServicio de Cirurgia VascularHospital Clinico Universitario47011 Valladolid, Spain

Daniel GRANDMOUGINDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire NordAvenue Albert Raimond42055 Saint-Etienne Cedex 2, France

George HAMILTONDepartment of Vascular SurgeryThe Royal Free Hospital NHS TrustPond StreetNWS 2QG London, United Kingdom

Daniel HAYOZDepartement de Medecine VasculaireCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Robert HINCHLIFFEDepartment of Vascular and Endovascular SurgeryE Floor, West BlockUniversity Hospital, Derby RoadNottingham NG7 2UH, United Kingdom

Brian HOPKINSONDepartment of Vascular and Endovascular SurgeryE Floor, West BlockUniversity Hospital, Derby RoadNottingham NG7 2UH, United Kingdom

Michael HORROCKSUniversity of Bath, Room L2.27BA2 7AYBath, United Kingdom

Michael JACOBSDepartment of Cardiovascular SurgeryAcademic Hospital MaastrichtPO Box 58006202 AZ Maastricht, The Netherlands

Isabella JAVERLIATHopital Universitaire Ambroise Pare9, avenue Charles de Gaulle92104 Boulogne Cedex, France

Jean Ader JULESCentre Hospitaller Universitaire Cote de Nacre14033 Caen Cedex, France

Pierre JULIADepartement de Chirurgie CardiovasculaireHopital Europeen Georges Pompidou20, rue Leblanc, 75015 Paris, France

Edouard KIEFFERDepartement de Chirurgie VasculaireCHU Pitie-Salpetriere, 47/83, bd de 1'Hopital75651 Paris Cedex 13, France

Mark KOELEMAYUnit of Vascular SurgeryAcademic Medical CenterUniversity of Amsterdam, P.O. Box 227001100 DE Amsterdam, The Netherlands

Brandon KRIJGSMANDepartment of Vascular SurgeryThe Royal Free Hospital NHS TrustPond StreetNWS 2QG London, United Kingdom

Dink LEGEMATEUnit of Vascular SurgeryAcademic Medical CenterUniversity of Amsterdam, P.O. Box 227001100 DE Amsterdam, The Netherlands

Massimo LENTIUnita Operativa di Chirurgia VascolarePoliclinico Monteluce, Via BrunamontiPerugia 06122, Italy

Marcelo LIBERATO DE MOURAChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Lars LONNDepartment of RadiologySahlgrenska University HospitalSE 413 45 Goteborg, Sweden

Carla LUCCIChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Dominique MAIZACentre Hospitalier Universitaire Cote de Nacre14033 Caen Cedex, France

Miguel MARTIN-PEDROSAServicio de Cirurgia VascularHospital Clinico Universitario47011 Valladolid, Spain

Bettina MARTYDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Manuel MATASServei d'Angiologia I Cirurgia VascularPgValld'Hebronll9-12908035 Barcelona, Spain

Germano MELISSANOChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Volker MICKLEYBereich fur GefasschirurgieStadtklinik Baden-Baden, Balger Strasse 5076532 Baden-Baden, Germany

Bas MOCHTARDepartment of Cardiac SurgeryAcademic Hospital MaastrichtPO Box 58006202 AZ Maastricht, The Netherlands

Jorge MOLINAServei de Cirurgia VascularHospital del Mar, Paseo Maritimo, 25-2908003 Barcelona, Spain

Lars NORGRENDepartment of Vascular DiseasesUniversity Hospital MAS205 02 Malmo, Sweden

William PAASKEDepartment of Cardiothoracic & Vascular SurgeryAarhus University HospitalSkejby Sygehus8200 Aarhus N, Denmark

Philippe PACHECODepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire NordAvenue Albert Raimond42055 Saint-Etienne Cedex 2, France

Federico PAPPALARDOChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Gianbattista PARLANIUnita Operativa di Chirurgia VascolarePoliclinico Monteluce, Via BrunamontiPerugia 06122, Italy

Noud PEPPELENBOSCHDepartment of SurgeryCatharina Hospital, PO box 13505602 ZA Eindhoven, The Netherlands

Gunnar PLATEDepartment of SurgeryHelsingborg Hospital251 87 Helsingborg, Sweden

IX

X

SalahQANADLIDepartement de RadiologieCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Paola de RANGOUnita Operativa di Chirurgia VascolarePoliclinico Monteluce, Via BrunamontiPerugia 06122, Italy

Jan RAUWERDADepartment of SurgeryFree University, Po Box 70571007 MB Amsterdam, The Netherlands

Bo RISBERGDepartment of SurgerySahlgrenska University HospitalSE 413 45 Goteborg, Sweden

John ROBBSNelson. R. Mandela School of MedicineFaculty of Health Sciences, Private Bag 7Congella 4013, South Africa

Begona ROMANFaculdad de Filosofia, Departamento de EticaUniversitat Ramon Llull, C/Claravall,l-308027 Barcelona, Spain

Josep ROYOServei d'Angiologia I Cirurgia VascularPg Vail d'Hebron 119-12908035 Barcelona, Spain

Patrick RUCHATDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Geert Willem SCHURINKDepartment of Vascular SurgeryAcademic Hospital MaastrichtPO Box 58006202 AZ Maastricht, The Netherlands

Ludwig Karl von SEGESSERDepartement de Chirurgie CardiovasculaireCentre Hospitalier Universitaire VaudoisRue du Bugnon 461011, Lausanne, Switzerland

Andrija SKOPLJANAC-MACINAUniversity Hospital MerkurZajceva ul.9Zagreb, Croatia

Tomislav SOSAUniversity Hospital MerkurZajceva ul.9Zagreb, Croatia

Andrea STELLAChirurgia VascolareUniversita di Modena e Reggio EmiliaPoliclinico Universitario, Via del Pozzo n°41100 Modena, Italy

71

Peter TAYLORDepartment of General and Vascular SurgeryGuy's & St. Thomas' HospitalLambeth Palace RoadLondon SE1 7EH, United Kingdom

Alexander TIELBEEKDepartment of RadiologyCatharina Hospital, PO Box 13505602 ZA Eindhoven, The Netherlands

Ivana TONKOVICUniversity Hospital MerkurZajceva ul.9Zagreb, Croatia

Yamume TSHOMBAChirurgia VascolareIRCCS H. San Raffaele, Via Olgettina, 6020132 Milano, Italy

Carlos VAQUEROServicio de Cirurgia VascularHospital Clinico Universitario4701 IValladolid, Spain

Fabio VERZINIUnita Operativa di Chirurgia VascolarePoliclinico Monteluce, Via BrunamontiPerugia 06122, Italy

Francesc VIDAL-BARRAQUERServei de Cirurgia VascularHospital del Mar, Paseo Maritimo, 25-2908003 Barcelona, Spain

John WOLFERegional Vascular UnitSt. Mary's Hospital, Praed StreetLondon W2 1NY, United Kingdom

Michael YAPANISRegional Vascular UnitSt. Mary's Hospital, Praed StreetLondon W2 1NY, United Kingdom

Neval YILMAZDepartment of SurgeryCatharina Hospital, PO box 13505602 ZA Eindhoven, The Netherlands

Stephane ZALINSKIDepartement de Chirurgie CardiovasculaireHopital Europeen Georges Pompidou20, rue Leblanc, 75015 Paris, France

FOREWORD

The subject selected for the 2003 European Vascular Course is Vascular Emergencies, andthirty one chapters in this book address the wide spectrum of urgent and emergency vascularproblems. The main impetus for choosing this subject is that approximately 40% of vascularsurgical practices are determined by vascular emergencies. The majority of pathologies describedare applicable to every vascular surgical practice.

XIThe 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 arteryand stab wounds at the base of the neck do not occur on a daily basis in a standard vascularpractice but constitute a challenging problem. Acute aortic pathology includes occlusion of theabdominal aorta as well as rupture. The latter emergency has been treated surgically for manydecades and the option ofendovascular repair is appealing. While in general it is advocated thatacute type B aortic dissection must be treated conservatively, new insights dictate a more surgicaland endovascular attitude. Aortic emergencies also include complications of laparoscopicsurgery and traumatic rupture.

Acute ischemia of the upper limb is a serious problem, dictating a substantial part of ourpractice. Acute complications of arteriovenous fistula for hemodialysis are also addressed. Acuteischemia of the lower limb can result from embolization, thrombosis and other rare causes.Furthermore, underlying pathologies such as peripheral aneurysms and diabetes contribute toemergency situations, requiring surgical, endovascular or thrombolytic therapy.

Venous emergencies are described in four chapters addressing acute thrombosis of iliocavalveins, axillary and subclavian veins, aortocaval fistula and traumatic injury of the vena cava.

The last part of the book describes the subjects of acute renal artery occlusion, acute intestinalischemia, ruptured visceral arterial aneurysms, abdominal compartment syndrome and gunshotarterial injury.

We aimed for a comprehensive compilation of vascular emergencies and we could only composethis book with the crucial contribution of the authors and co-authors. Substantial editorial workhas been performed by Bertrand Ede and Dirk Ubbink.

We are very grateful to our secretaries Annie Barral and Claire Meertens and we appreciatethe assistance of Iris Papawasiliou. The Odim team, guided by Marie-France Damia, managedonce again to have both the English and French versions of this book printed in time. BlackwellPublishing/Futura contributed significantly, with editorial abetment of Joanna Levine andJacques Strauss.

The major sponsors of the biomedical industries are greatly acknowledged because the textbookand the European Vascular Course would not be possible without their continuous support andenthusiasm for this scientific assignment.

Maastricht - Marseille, 2003

Michael Jacobs Alain Branchereau

CONTENTS

ContributorsForeword

VIIXI

Urgent open surgery afterenaovascular AAA repairPiergiorgio Cao, Fabio Verzini, Paola De RangoMassimo Lenti, Gianbattista Parlani 71

Bioethical concernsin vascular emergenciesAlbert Clara, Begona RomanJorje Molina, Natalia de la FuenteFrancesc Vidal-Barraquer

Urgent carotid surgeryAlain Branchereau, RaoufAyariJerome Albertin, Bertrand Ede 13

Acute complications followinglaparoscopic surgeryMarc Coggia, IsabelleDi CentaIsabellejaverliat, Olivier Goeau-Brissonniere 81

Acute type B aortic dissection:surgical indications and strategyMichael Jacobs, Ted ElenbaasGeert Willem Schurink, Bas Mochtar 87

Blunt injury to the carotidand vertebral arteriesRamon Berguer

Endovascular treatmentof aortic type B dissectionRachel Bell, Peter Taylor

XIII

Penetrating injury to the bloodvessels of the nect and mediastinumJohn Robbs

Acute abdominal aortic occlusionPierre Julia, Stephane ZalinskiJean-Noel Fabiani 49

Has mortality rate for rupturedabdominal aortic aneurysmchanged over the last 50 years?Jack Collin 55

Ruptured AAA: should endovasculartreatment be the first choice?Jaap Buth, Noud PeppelenboschNeval Yilmaz, Philippe CuypersLucien Duijm, Alexander Tielbeek 61

Traumatic ruptureof the thoracic aortaRoberto Chiesa, Renata CastellanoCarla Lucci, Marcelo R. Liberato de MournFederico Pappalardo, Germano MelissanoEfrem Civilini, Yamume Tshomba 107

Acute occlusion of the renal arteriesXavier Banal, Philippe Pacheco,Daniel Grandmougin, Didier Bourrat,Jean-Pierre Favre 125

Acute intestinal ischemiaBrandon Krijgsman, George Hamilton 137

Rupture of splanchnicartery aneurysmsJoaquim Barbosa, Maria-Jose Ferreira 149

The abdominalcompartment syndromeMichael Yapanis,John Wolfe 157

Endovascular treatmentof blunt injury of the limbsBo Risberg, Lars Lonn 247

Acute thrombosis of iliocaval veinsGunnar Plate, Lars Norgren 165

Rare causes of acuteischemia of the limbsMark Koelemay, Dink Legemate 253

Acute subclavian-axillaryvein thrombosisRamon Bofill, Josep Royo, Jose Maria FuentesJose Maria Escribano, Manuel Matas 173

Acute arterial thrombosisof the lower limbsWilliam Paaske 261

Aortocaval fistulaDominique Maiza, Jean Ader Jules 181

Arterial emboli of the lower limbsMichael Horrocks 275

XIVTraumatic injury of the vena cavaand its major branchesLaurent Chiche, Edouard Kieffer 193

Acute ischemia of the upper limbJose Gonzalez-FajardoMiguel Martm-PedrosaLourdes Del Rio, Carlos Vaquero 207

Acute complications of arterio-venous fistula for hemodialysisVolkerMickky 217

Gunshot and explosiveprojectile vascular injuriesTomislav Sosa, Ivana TonkovicLidija Erdelez, Andrija Skopljanac-MacinaMarko Ajduk, Andreja Crkvenac 231

Acute thrombolysis ofperipheral arterial aneurysmsLudwig Karl Von SegesserBettina Marty, Patrick RuchatPhilippe Gersbach, Salah QuanadliDaniel Hayoz, Adam Fischer 281

Endovascular approachto acute arterial occlusionsAndrea Stella, Mauro Gargiulo 287

Thrombolysis for occlusionof bypass graftsRobert HinchliffeBruce Braithwaite, Brian Hopkinson 295

Acute problems of the diabetic footJanRauwerda 301

1BIOETHICAL CONCERNS

IN VASCULAR EMERGENCIES

ALBERT CLARA, BEGONA ROMAN, JORJE MOLINANATALIA DE LA FUENTE, FRANCESC VIDAL-BARRAQUER

The field of ethics, also called moral philosophy, involves systematizing, defending, andrecommending concepts of right and wrong behavior. Although many of us would considerourselves as trustworthy, ethical, and honest, we inevitably face choices that may hurt otherpeople, infringe on their rights, or violate their dignity. We are always at risk of using patientsas mere tools to our own ends. Ethical considerations, like diagnosis and treatment, aretherefore essential features of every case of clinical care of patients.

Vascular emergency patients present with problems that require quick, and sometimesimmediate evaluation and intervention to save life, limb, or a serious health injury. Vascularsurgeons on call have to make decisions, frequently at inconvenient hours, under circum-stances of complex clinical scenarios, solitude, scarcity of hospital resources, unfamiliaritywith 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 keysnecessary to make a simple, reasoned, and honest analysis of ethical concerns in vascularemergencies. The reader will realize that behind the majority of our daily-practice ethicalconcerns, there are uncovered conflicts between moral obligations and self-interest (physician,family, or other third parties), rather than ethical dilemmas. Ethical dilemmas are infrequentand arise only if there are moral considerations for taking each of two opposing courses ofaction. Unfortunately, their resolution is not so easy, since determining which moral valueoverrides all others may reflect, at the very end, different visions of human nature.

VASCULAR EMERGENCIES

Theories of modernbiomedical ethics

Biomedical ethics (or bioethics) studies the moralissues in the fields of biological and medical sci-ences. It traces its roots to several early codes ofethics such as the ancient Greek Hippocratic Oath,professional codes such as the one written by theEnglish physician Thomas Percival in the 18th cen-tury, and the Nuremberg Code for research ethicson human subjects that was established in responseto the gross abuses in human experimentation per-formed during the Second World War.

Since the end of the Second World War, a remark-able amount of attention has been given to theethics of medical practice and research as a pro-jection of the rapidly growing concerns generatedby scientific and cultural developments during thelast decades [1].

In the 1960s many technical advances occurred,such as hemodialysis, major surgical proceduresincluding organ transplantation, and the wide-spread development of intensive care units and useof artificial respirators. Medically safe abortions, thecontraceptive pill, prenatal diagnosis, and the firststeps of genetic engineering were also developedat that time. These advances seemed to alter for-ever the current methods of saving, improving, andextending human lives.

In the mid 1960s, the traditional moral mooringsof the western medical practice came into questionas a result of a series of societal changes, such as abetter-educated public, the spread of participatorydemocracy, a decline in communally shared values,and a distrust of authority and institutions of allkinds. Therefore, the patient-physician relation-ship changed from a paternalistic model to one inwhich patient autonomy in decision-making wasrecognized.

With the erosion of the Hippocratic synthesis andthe growing complexity of bioethical concerns,many physicians sought guidance in court decisionsand in legislation. Most, however, recognized thedangers of confusing law or economics with ethics,and of reducing professional ethics to nothingmore than personal opinion. Some philosophersbegan at that time to write and speak about med-ical ethical issues. Many bioethical theories anddecision-making models were progressively pro-posed (principlism, casuistry, virtue ethics, narra-tive ethics, feminist ethics). The history of ethics,

however, has shown humankind to be unable toreach a universally acceptable theory for guidingour actions. The wide spread of bioethical theorieshas also reflected this historical debate. The mainquestions of bioethics remain indeed among theoldest that human beings have asked themselves:the meaning of life and death, the bearing of painand suffering, the right and power to control one'slife, and our common duties to each other.

PRINCIPLISMThe theory of prima fade (Latin for first appear-

ance) principles, developed by Ross, was adaptedto medical ethics by Beauchamp and Childress'Principles of Biomedical Ethics [2]. W.D. Ross (TheRight and the Good, 1930) believed that our moralconvictions were based on duties belonging to thefundamental nature of the universe, and includedthe duties of fidelity, reparation, gratitude, justice,beneficence, self-improvement, and non-malefi-cence. The above duties are prima facie insofar aswe are always under obligation unless they conflictwith one another. Ross argued that there was noobvious priority among these principles, leaving ourchoice in the event of conflict to our own insighton a case-by-case basis.

From this perspective, Beauchamp and Childresschose principles especially appropriate for medicalethics:1 - Beneficence: duty to be of benefit to the pa-tient, as well as to take positive steps to prevent andto remove harm from the patient.2 - Non-maleficence: duty to not intentionallycreate needless harm or injury to the patient, eitherthrough acts of commission or omission. Negli-gence derives from not regarding this principle andincludes intentionally imposing unreasonable risksas well as unintentionally imposing risks throughcarelessness. The debate about active euthanasiaalso falls within the category of non-maleficence.3 - Respect for autonomy (self-determination):duty to leave the patient to act intentionally, withunderstanding, and without controlling influencesthat would act against a free and voluntary act. Therules of informed consent, truthfulness, privacy, andconfidentiality derive from this principle.4 - Justice: duty to provide a fair distribution ofgoods in society. Health resources allocation derivesfrom this principle.

These principles balance one another but oftenconflict. For instance, respect for autonomy canconflict with beneficence when the patient refuses

BIOETHICAL CONCERNS IN VASCULAR EMERGENCIES

a recommended therapy. Beneficence can conflictwith justice in the context of resource scarcity, andso on. When principles compete, no absolute hier-archy exists for choosing to follow one principleover another. Judgments about moral precedenceamong competing principles are made on a case-by-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 acentral factor in ethics.

For these reasons, even principlism's strongest sup-porters admit that theories incorporating virtues,personal relationships, and other elements shouldbe used in conjunction with the framework pro-vided by principlism.

CASUISTRYCase-based reasoning, called casuistry, is another

common method of bioethical reasoning. Threeclinical ethicists (a philosopher - Jonsen, a physi-cian - Siegler, and a lawyer - Winslade) identifiedfour "topics" that are basic and intrinsic to every cli-nical encounter [3]. Each topic raises questions tobe answered before the ethical analysis is done [4].1 - Medical indications: does the treatment fulfillany of the goals of medicine? With what likelihood?If not, is the proposed treatment futile?2 - Patient preferences: what does the patientwant? Does the patient have the capacity to decide?If not, who will decide for the patient? Do thepatient's wishes reflect a process that is informed,understood, and voluntary?3 - Quality of life: describe the patient's quality oflife in the patient's terms: what is the patient's sub-jective acceptance of likely quality of life? What arethe views of the care providers about the quality oflife? Is quality of life less than minimal (i.e., qualita-tive futility) ?4 - Contextual features: review social, legal, eco-nomic, and institutional circumstances in the casethat can influence the decision and/or be influ-enced by the decision.

Once the details of the case have been outlinedaccording to the four topics, it is compared with aspecific case (or set of similar cases) for which amoral solution has been developed in the past withprofessional and/or public agreement about theresolution: does the case sound like other cases you

may have encountered? Is there clear precedent(paradigm case)? How is the present case similaror different to the paradigm case? Is it similar, ordifferent, in ethically significant ways? Thus, casu-istry moves from clear past cases to more dubiousones, ordering them by paradigm analogy undersome principle. The methodology is therefore sim-ilar to the practice of case law where precedents ofprevious trials are used for analyzing new cases thatshare similar circumstances.

Whether casuistry is a complement or alternativeto principlism is still under debate. Although casu-istry works in the opposite direction of principlism,it does not eschew principles. Many bioethicistsmaintain that both theories share more similaritiesthan not and that they complement each other ina system of bioethics. In addition, some critics haveclaimed casuistry be a product of the culture of theMiddle Ages, when there was a consensus on cer-tain principles, while no such consensus exists intoday's morally heterogeneous society.

VIRTUE ETHICSAristotle defined virtue as "a kind of second na-

ture" that disposes us not only to do the right thingrightly but also to gain pleasure from what we do.Virtue ethics emphasizes the character, intentions,and motives of the moral agent rather than focus-ing on the agent's actions or outcomes of actions.The virtuous physician naturally will do the rightthing and will not likely do the wrong thing. Untilthe last decades, some kind of virtue ethics had beenthe implicit and dominant theory in traditionalmedical ethics since Hippocrates. The renewedinterest in virtue ethics has been stimulated by thework of Alasdair MacYntre, in particular his bookAfter Virtue (1984). MacYntre agrees that principlesand rules are important for ethics, but he rejectsany attempt to justify those principles or rules thatabstract them from their rootedness in the histori-cal particularities of concrete communities. The nar-ratives that make such communities morally coher-ent focuses attention on the virtues correlative tothose narratives. To separate ethics from its depend-ence on such narratives is to lose the correspon-ding significance of the virtues.

Critics of virtue ethics may agree that having avirtuous character may incline the physician to actethically, but they maintain that virtues alone donot give the physician sufficiently clear actionguides.


ALGORITHM FOR ETHICAL ANALYSISIN EMERGENCIES

Iserson et al. [5] have developed a model specif-ically designed to be helpful in the emergency set-ting. It combines casuistry and deontological andutilitarian 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 outa rule or is this at least similar enough so that a rulecould reasonably be extended to cover it? If so, thenfollow the rule.

2 - The second step is to ask the question: is there anoption that will buy time for deliberation without exces-sive risk to the patient? If yes, buy time.

3 - If the first two steps do not yield a solution, thenthere are three rules to apply to any ethical deci-sion. The three rules are the following ones.

Impartiality: the decision-maker places in theposition of the patient by saying: would you be will-ing to have this action performed if you were inthe patient's place?

Universalizability: would you be willing to usethe same solution in all similar cases?

Interpersonal justifiability: consider whetheryou would be willing to defend the decision toothers, to share the decision in public.

Applying ethics toemergency vascular patients

THE PATIENT-SURGEON RELATIONSHIPAn individual patient-surgeon relationship is

formed on the basis of mutual agreement on med-ical or surgical care for the patient. In the absenceof a pre-existing relationship, the physician is notethically obliged to provide care to an individualperson unless no other physician is available, as isthe case when emergency treatment is required [6].Once the relationship is established, the surgeonhas the fiduciary duty to protect and promote thepatient's interest. This primary commitment holdsthe surgeon's self-interest (technical, scientific, eco-nomic) in check and makes it a systematically sec-ondary consideration. This makes the fiduciary'srole morally demanding [7].

Surgical ethics is based on a recognition of therights of patients who require the care of surgeons.The patient has the negative rights not to be killedor harmed intentionally or negligently by the sur-

geon, and not to be deceived by the surgeon. Thepatient has the positive rights to be adequatelyinformed about the risks and benefits of surgery,to be treated by a knowledgeable, competent prac-titioner, to have his or her health and well-beingmore highly valued than the surgeon's own eco-nomic interest, and to decide whether to accepttreatment under the conditions described.

THE EMERGENCY SCENARIOThe emergency department is not only a com-

plex medical environment, but it presents complexclinical and ethical concerns. Ethical concerns willbe discussed afterward on a subject-by-subject basis.

Clinical complexitya) Unlike other diseases, vascular emergencies havebeen traditionally poorly protocolized.b) Patterns of disease have changed.c) New vascular technologies imply new emergency chal-lenges.d) Surgical decision-making is often undertaken underdata incompleteness. In emergency care, the databasederived from history, examination, laboratory, andradiology is virtually always incomplete (up to 50%of the data may be inconclusive or frankly incor-rect) [7]. A traditional assumption in surgical prac-tice has been that decisions must be made takinginto account the likely costs of under- and overtreat-ing, promoting a challenging decision-making.e) Constrained time to make surgical decisions. Occa-sionally, some surgical procedures are undertakenunder intense time constraints (i.e., drainage of acervical hematoma and establishment of an airwayin a postoperative carotid endarterectomy bleeding,staunching the bleeding from a major exsanguinat-ing source). In these rare circumstances, surgicaldecision-making is usually straightforward. The per-ception of time constraint and the emotional senseof urgency are usually felt afterward. In contrast,time constraint may be more evident and may affectthe surgeon's decisions when surgical need is not soimmediate, such as the patient with a ruptured aor-tic aneurysm or an acute limb ischemia with neuro-logic involvement.

Environment complexitya) Vascular surgeon solitude and loneliness. Vascularsurgeons are scarce "goods" in the mass of healthcare providers. Unlike general surgery or trauma,in which there is frequently an on-call team, vascu-lar surgeons on call are usually alone in their deci-sions, that is, outside from the daily-practice


decision-making and supervision mechanisms ofmany vascular departments.b) Increasing tendency to leave on-call service to juniorvascular surgeons. On-call service, although at timesprofessionally challenging, weighs more and morewith increasing age and professional activity at con-venient hours. In addition, many institutions haveregulated a top age for on call service. Health pro-viders should take into consideration, however, thatthe decision to attempt to do everything possible inall emergency circumstances, often made by inex-perienced surgeons, creates sometimes logarithmi-cally more moral problems for subsequent healthprofessionals.c) Scarcity of hospital human and technical resources atinconvenient hours. The extraneous environment, suchas the hospital laboratory, the speed of the com-puted tomography (CT) scan, or the availability ofoperative sites, etc., logistically frustrates the sur-geon, creating conflicts among the critical hospitalpathways and between different clinical standards ofpractice or practice guidelines.

ETHICS AND THE LAWSurgeons are morally and legally accountable,

and the two may not be concordant. Physician par-ticipation in torture, for example, may be legal insome countries but is never morally defensible. Sur-geons must keep in mind the distinctions andpotential conflicts between legal and ethical obli-gations when making clinical decisions and mustseek legal counsel when they are concerned aboutthe potential legal consequences of decisions in eth-ical dilemmas, when initiating policy and protocols,or when updating existing procedures. The law mayvary substantially between countries. While the lawis limited in its ability to provide universal guidanceand direction, ethical analysis should provide aframework for determining moral duty, obligation,and conduct.

Ethical issues relatedto patient autonomy

INFORMED CONSENTConsent is the autonomous authorization of a

medical intervention. The notion of consent isgrounded in the ethical principles of patient auto-nomy and respect for people [8]. Obtaining thepatient's consent to medical care is also a legal

requirement. Common law, however, recognizesthat the emergency treatment of incapable personsis an exception to the requirement of consent. Oth-erwise, competent patients have the right to makechoices regarding their health care in emergencies,just as in routine care. Respect for autonomy obli-gates the physician to seek for the patient thegreater balance of goods over harms, as those goodsand harms are understood and balanced from thepatient's perspective. Consent has three compo-nents: disclosure, capacity, and voluntariness.

DisclosureMrs. EVC-1 is 80 years old and lives with her daugh-

ter in an apartment. She is fully independent and hasnever had a serious illness. She is admitted to the emer-gency department because of acute lower limb ischemiasecondary to embolic disease. The vascular surgeon oncall indicates prompt surgery and visits Mrs. EVC-1 todisclose benefits and risks of treatment. Before enteringthe emergency box, however, Mrs. EVC-1 's daughter asksthe surgeon to withhold any information about risk oflimb loss because her mother is very nervous.

Mr. EVC-2 is a 45-year-old homeless but otherwisehealthy man admitted to the emergency department becauseof recent-onset arm swelling. A duplex scan reveals sub-clavian deep venous thrombosis. The vascular surgeon oncall explains the conventional anticoagulant therapy anddiscusses comprehensively the nature, procedure, short-and long-term benefits, complementary surgical treatment,and risks of modern fibrinolytic therapy. The patientaccepts lytic treatment.

Ethics and practiceDisclosure refers to the provision of relevant in-

formation by the clinician and its comprehensionby the patient. In many western countries, the pre-vailing standard of disclosure is that of the "reason-able person". The necessary elements of disclosureinclude clear information about the patient's diag-nosis, the therapeutic alternatives to manage it, in-cluding surgical and nonsurgical treatment, thebenefits and risks of each alternative, and a frankexplanation of those factors about which the medi-cal profession, and the individual surgeon inparticular, are uncertain and cannot provide guar-antees [7]. This disclosure may be adapted to along (often the case) or short version according toemergency time constraints. Contrary to the com-mon surgeon's belief, the majority of patients (morethan 80%) want to know about the nature of theirillness, the reason for surgery, and so on [9]. In


some cultures, however, a family-centered model ofdecision-making is favored over one centered in theindividual. "Waiver" refers to a patient's voluntaryrequest to forego one or more elements of disclo-sure. In that case, the patient's reasons for waivingshould be sought in order to overcome themthrough dialogue. If this is not possible, the patientmust be informed that he can change his mind atany time or involve a family member in the deci-sion-making process [8].

The cases

EVC-1: Mrs. EVC-1 is a fully independent andcapable 80-year-old woman without previous seriousillnesses. Mrs. EVC-l's daughter was indeed morenervous than her mother. Withholding informationduring the consent process in the belief that dis-closure would lead to the harm or suffering of thepatient is called "therapeutic privilege" [10]. Whilein some cultures therapeutic privilege is widelyinvoked, this is not the usual case in many westerncountries. It is better for the surgeon to offer infor-mation and allow the patient to refuse or acceptfurther disclosure. Accepting an inappropriate fam-ily demand to withhold information infringes onthe patient's rights, violates the patient's dignity,and goes against our duty of professionalism. Con-versely, there is every moral reason on the basis ofconfidentiality to honor requests to withhold infor-mation from family or friends if requested by thepatient.

EVC-2: This homeless patient is surely astonishedby the surgeon's science and fine dressing. He hasprobably switched off his understanding after thefirst 100 words of the surgeon's disclosure. Mr. EVC 2is clearly a vulnerable patient unable to understandthe risks of fibrinolytic therapy in the way the sur-geon has explained it. Mr. EVC-2 has probablyaccepted fibrinolityc therapy because of his confi-dence that the surgeon is looking for his best inter-est rather than as a consequence of personalreasoning. Although we could discuss the reasoningbehind the surgeon's recommendation (patient'sinterest vs. surgeon-interest), there is an additionalfracture in the surgeon's duty of professionalismthat we must point out. Accepting consent for a riskyprocedure without confirming the patient's under-standing of the previously cited elements of disclo-sure goes against respect for autonomy and isdeliberately paternalistic.

Capacity

Mr: EVC-3 is a 76-year-old man subjected three weeksago to an elective aortic aneurysm resection. His postop-erative course has been troublesome since the beginning(prolonged intubation, transitory renal failure, prolongedparalitic ileus). Although extubated and conscious, hestill remains in the intensive care unit and has fever andsome abdominal discomfort. A CT scan performed in theevening raises the concern of a bowel perforation. Thevascular surgeon on call proposes prompt surgery and thepatient refuses it. He claims to be too tired to fight thedisease and he wants to meet his deceased wife in Heaven.A psychiatric consultation is sought to confirm thepatient's competence.

Mrs. EVC-4 is a 79-year-old diabetic woman admittedto the emergency department with supurative gangrene oftwo toes. No abscess seems to be present in the dorsal orplantar aspects of the foot. The vascular surgeon on callrecommends amputation of the toes, and the patient seemsto understand the surgeon's disclosure. During the dia-logue, however, she refuses treatment because, "the ampu-tation of my toes will be just the beginning of my end".

Ethics and practiceCapacity refers to the patient's ability to under-

stand the information relevant to a decision and toappreciate its consequences. Capacity is specific toparticular decisions and can change over time. Incommon law, patients are presumed capable. Thesurgeon develops a general impression of a patient'scapacity during the clinical encounter. In some sit-uations, however, surgeons may be unsure about apatient's capacity. Refusal of recommended treat-ment usually causes the surgeon to question a per-son's capacity, although most refusals are caused byfactors other than incapacity [11]. In case of re-fusal, however, the greater the cost to the patientfrom a false-positive determination of competence,the greater the concern should be to ascertainwhether the patient is truly competent [7]. Whentime and opportunity permit, a psychiatric consul-tation should be sought, if this is likely to enhancethe quality of the determination of competence.Time permitting, when the patient is not compe-tent to consent, surrogate decision makers serve toprotect the best interests of the patient by choos-ing among reasonable options as the patient wouldhave chosen. Since the medical team has signifi-cant input about what would be in the patient's in-terest medically, a decision by a surrogate that doesnot adhere to this standard should not be auto-


matically followed and may need to be reviewed bythe institutional ethics committee or legal counsel.

Religious beliefs: the case of Jehovah'switnesses. Patients' religious beliefs are to berespected on the basis of respect for autonomy. Thecase, however, is much more troublesome whensuch beliefs conflict against the surgeon's perceivedbeneficence; as in the emergency setting, the sur-geon has the duty of taking care of these patients.The standard example is the Jehovah's Witnesses,who consent to all medical interventions but refuseblood and blood product transfusions. This refusalis worthy of the surgeon's respect, since these reli-gious beliefs are as sincere as the beliefs of anyother of the world's religious traditions. The sur-geon, however, does have options when confrontedwith a patient who refuses perioperative blood pro-duct support [7]. First, the surgeon should speakto the patient in private and assure the patient ofthe confidentiality of the medical records. If thepatient maintains the refusal, the surgeon cannotcompel a competent adult patient who is not preg-nant to accept the transfusion. However, the gen-eral caveat is that while competent adults are freeto make martyrs of themselves, they cannot martyrtheir dependent children. In addition, some Amer-ican hospital policies and state laws have allowed forthe imposition of a surrogate decision maker to pro-tect the interest of a minor should a parent (espe-cially a mother) require blood products in order toprevent death and if the death of the patient wouldresult in the child being orphaned [7].

The casesEVC-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 whetherthe process of disclosure had been done with empa-thy and care. The answer was affirmative. TheEthics Committee considered that the adequatesteps had been followed (adequate disclosure andpsychiatric evaluation of competence). No addi-tional evaluation was believed necessary since thelikelihood of survival (as expressed by the surgeon)was poor. Palliative care was indicated in respect ofpatient's autonomy. After the meeting, the surgeonhad some subjective doubts about his empathy dur-ing the consent process and revisited the patient.One hour later the patient accepted surgery. Thepreventive ethics approach to refusal of surgeryshould be respectful of the patient's reasoning, onthe assumption that the patient, by his or her own

rights, has good reason for refusal but may, withadditional information and/or empathy, reconsiderand accept surgery, and not on the assumption thatthe patient capacity is in doubt. The present caseexemplifies again the morally demanding fiduciaryrole of the surgeon (see professionalism).

EVC-4: The case of Mrs. EVC-4 shows the effectsof an uncovered depression in capacity. Mrs. EVC-4had the ability to understand her problem and theproposed treatment. The unexpected reasons ofMrs. EVC-4's refusal raised doubts about her capac-ity and a psychiatric consultation was requested.Mrs. EVC-4 admitted to having a persistent depressedmood and several vegetative signs of depression.She accepted treatment for depression. Her footcondition stabilized with antibiotics. Some days later,the patient accepted the proposed surgery. Hadprompt surgery been needed, a surrogate decision-maker would had been sought.

Voluntariness

Mrs. EVC-5 is a 65-year-old diabetic woman admittedto hospital in the morning because of a toe supurativegangrene with plantar abscess. The vascular surgeon oncall (surgeon A), whose service starts at 5 pm, is in theoperating room treating an elective case. Mrs. EVC-5 isevaluated by another vascular surgeon (surgeon B). Therewill be no operating room available until the afternoonand surgeon B considers immediate surgery unnecessary.Surgeon B insinuates surgery but leaves the complete dis-closure to surgeon A, who is informed by a surgical nursethat a toe amputation has been added to the surgicalemergency schedule. After ending his elective case, andwithout delay, surgeon A goes to eat something before re-entering the operating room. When he returns, Mrs. EVC-5is already in the operating room. Surgeon A realizes thatthe informed consent has been insufficient and decides tocomplete it in the operating room.

Mr. EVC-6 is a 78 year-old-man with an 8 cm aorticaneurysm. A vascular surgeon proposes elective surgerybut he refuses, claiming that he has already done all hehad to do in life. He signs an advanced directive refus-ing emergent surgery in case of rupture. A signed copyis left in the patient's chart. Six months later the aneurysmruptures and the patient is taken, conscious, to the hos-pital. The vascular surgeon on call has doubts aboutwhat to do.

Ethics and practiceVoluntariness refers to the patient's right to come

to a decision freely, without force, coercion or


8

manipulation. Internal and external factors canaffect a patient's decision about treatment [8].Internal factors arise from the patient's medicalcondition (i.e. pain). The surgeon's role is to min-imize the potential controlling effect of these inter-nal factors without jeopardizing the patient'scapacity. External controlling factors may be relatedto the clinician, the health care setting, and thefamily or friends. Surgeons should take steps tominimize the potential for manipulation. Patientscan be manipulated when the information theyreceive is incomplete or biased. For this reason, auseful strategy is to ask patients to review the infor-mation in their own words. Another source of ma-nipulation is disclosing information just before amajor procedure is to be performed. The setting(i.e., operating room) and the immediacy of themedical procedure militate against a patient beingable to make a free or voluntary decision.

Advance directives document the processaimed at extending the rights of competent adultsto guide their medical care through periods of deci-sional incapacity. Advanced directives are groundedon voluntariness. Their goals are:1 - to maximize the likelihood that medical careserves the patient's goals (promoting respect forautonomy),2 - to minimize the likelihood of over- and under-treatment (promoting non-maleficence),3 - to reduce the likelihood of conflicts between fam-ily members and health care providers (promotingjustice),4 - to minimize the burden of decision-making onfamily members or close friends (promoting respectfor autonomy).

In the emergency setting, however, there are prac-tical difficulties in having such directives function[7]. Family members may or may not be aware ofsuch directives. Emergency medical personnel donot have access to the hospital chart at the timeresuscitation and other therapeutic measures areneeded. By the time it is known that an advancedirective exists, the patient may already have beenresuscitated, be on life support, or even be in theoperating room. In general, when there is unclearevidence that a patient might have refused a par-ticular treatment, such evidence is not binding if itgoes against the clear best interests of the patientneeding an emergency intervention. Most peoplewho complete advance directives are not, at thattime, suffering from a terminal or fatal disease. In

completing an advance directive, most are expres-sing their wishes regarding the limitation of treat-ment when treatment will only prolong the processof dying. Therefore, the onus will fall on the sur-geon to determine whether the conditions ofadvance directive apply.

The casesEVC-5: The majority of readers whose practice

includes on-call service will have occasionally metpatients with cases similar to that of Mrs. EVC-5.The question of professionalism rises again in hercase. Surgeon B should have personally informedsurgeon A, especially about the incompleteness ofthe consent process, and surgeon A should havevisited Mrs. EVC before entering the operatingroom. Neither surgeon A's physiological needs northe existence of minor emergent surgical cases liketoe amputations, debridements, or some A-V fistularevisions, justify the absence or incompleteness ofthe consent process before the patient enters theoperating room. The reader should simply remem-ber Iserson's question about impartiality: "wouldyou be willing to have this action performed if youwere in the patient's place?"

EVC-6: Advanced directives take effect only in sit-uations in which the patient is unable to partici-pate direcdy in surgical decision-making. Appealsto living wills and surrogate decision-makers areethically and legally inappropriate when individu-als remain competent to guide their own care. Thebenefits and risks of surgical treatment togetherwith the lethal condition of a nonsurgical attitudemust be disclosed to the patient. If Mr. EVC-6refuses surgery with an understanding of the con-sequences, his wishes should be honored. If he optsfor surgery, then it should be performed promptly.

CONFIDENTIALITY AND TRUTH TELLINGConfidentiality is derived from the Latin con-

fidere, to trust. Patients confide in their physicianswith the understanding that what they report willnot be disclosed without explicit permission. Theduty to maintain confidentiality can be viewed as aprima facie obligation that may be overridden onlywhen it conflicts with stronger moral duties. Excep-tions for confidentiality are concerns for the safetyof other specific persons and for public welfare (i.e.,report of certain communicable/infectious dis-eases) . The crisis atmosphere that often attends sur-gical emergencies may heighten the need of familymembers and loved ones for information. Sur-


geons, however, should not allow the exigencies ofan emergency situation to undermine traditionalprivacy safeguards. When the patient is incapaci-tated, the surgeon should disclose information onlyto the patient's surrogate, who has a legitimate"need to know" the patient's medical status.

Telling the truth may seem to be a straight-forward and ancient ethical principle in healthcare. However, the Hippocratic oath does not makeany mention of truth telling to patients, and theAmerican Medical Association's first Code of Ethicsin 1847 perpetuated this attitude. This therapeuticprivilege was justified by the principle of non-mal-eficence, and continued into this century. Todaythe duty of truth telling in medicine has becomean ethical issue (respect for autonomy), althoughin many cultures it is not the norm. There are twomain situations in which it is justified to withholdthe truth from the patient: 1. when the surgeonhas compelling evidence that disclosure will causereal and predictable harm (i.e., make a depressedpatient actively suicidal), and 2. when the patienthim- or herself states an informed preference notto be told the truth.

Ethical issuesrelated to beneficenceand non-maleficence

FUTILITYMedical futility refers to interventions that are

unlikely to produce any significant benefit for thepatient. Two kinds of medical futility are often dis-tinguished. A treatment is quantitatively futile whenthe likelihood of benefit is very poor, for examplewhen physicians conclude that it has been uselessin the last 100 cases. In addition, a treatment isqualitatively futile when the question: "What sort oflife is worth preserving?" is at the case core. Sur-geons have no obligation to offer or provide treat-ments that clearly do no benefit their patients.These therapies may increase the patient's pain anddiscomfort (conflicts with non-maleficence) andspend finite medical resources (conflicts with jus-tice). However, only through dialogue can thephysician understand the goals of treatment anddetermine futility. This approach allows for explo-ration of the desired outcome, acceptability of bur-dens, and the patient's or family's willingness togamble with the outcome.

LIMITS TO THE AGGRESSIVE SURGICALMANAGEMENT OF HEALTH-THREATENINGEMERGENCIES

A traditional assumption in surgical practice hasbeen that emergency surgical patients should beprovided rapid care at whatever level of interven-tion the surgeon reasonably thinks is required topreserve their lives or protect them from a seriouscompromise to their prior health status. Vascularsurgeons on call, however, see occasional patientsfor whom treatment success will be very unlikely,the length of life to be secured brief, and the qual-ity of life to be achieved marginal. These condi-tions create concerns as to when treatment shouldbe characterized as futile, inappropriate, or mar-ginally useful. In this context, surgeons look forways of characterizing emergency patients [7].

Emergency patients for whom surgery sur-vival is unprecedented. Vascular surgeonsresponding to emergency patients who are mostassuredly "going," who in highest probability willvery shortly die, are torn between rapid full-steam-ahead aggressive resuscitative measures and therecognition that interventions may succeed only inincreasing the potential misery to the patient andthe family. Such circumstances are represented bysome patients with prolonged prehospital resusci-tation following trauma and irreversible metabolicacidosis, or by patients with ruptured aortic aneur-ysm with certain particularities. The literature is notvery prone to help to identify patients with a 100%mortality. However, the more secure surgeons arein their ability to resuscitate patients with complexsurgical problems effectively, the easier it is to reachthe decision not to initiate or even to terminatecurative care in a patient who has an emergencysurgical condition for which treatment is not reli-ably expected to prevent death.

Vascular emergencies associated with cen-tral nervous system injury. Surgeons can be sig-nificantly frustrated when confronted with vascularsurgical emergencies in patients with an associatedcentral nervous system injury. Vascular injuries thatrequire immediate or prompt interventions (i.e.,active bleeding, acute ischemia) should be treatedaggressively so long as the prognosis for the recov-ery of some degree of significant central nervoussystem function remains positive. However, espe-cially in the postoperative period, if the most reli-able prognosis is that the patient is not expectedto recover to a cognitive and sapient existence, thesurgeon should be willing to discontinue the trial


10

of intervention, given the concurrence of the sur-rogate decision-maker and presuming the absenceof previous binding instructions. Vascular injuriesnot requiring immediate treatment (i.e., many tho-racic aortic pseudoaneurysms) are best delayed(and controlled) if possible until the central nerv-ous system injury prognosis can be stated with somedegree of certainty.

Vascular emergency patients in whom sur-vival with severe disability may be frequent.Traumatic vascular injuries may produce some dis-ability by themselves (i.e., paralysis after surgicaltreatment of a transected aorta from blunt injury)or by associated injuries (i.e., fracture malunion,bone infection, soft tissue retraction). In the faceof time constraints, surgeons can usually onlyimperfectly engage this process so as to prepare thepatient and the patient's family for the conse-quences of a surgical intervention. The burden ofproof needed to terminate the traditional obliga-tion to intervene can frequently not be met becauseof the lack of concreteness of the data in an emer-gency context. Because of this softness, there aregrounds to qualify in favor of intervention in allbut the most well founded cases of futility.

Emergency cases associated with a low pro-bability of survival but with good quality oflife among survivors. This may be the case formany ruptured aortic aneurysms. At stake here isthe role of costs in determining the appropriate-ness of therapeutic interventions. While such healthpolicies are rarely, if ever, created, bedside surgeondecision-making must be based under beneficenceand respect for autonomy principles.

Ethical issues related to justice

Mrs. EVC-7, a 27-year-old woman, is taken to the emer-gency department during the night after a motor vehicleaccident. She has a femur fracture and signs of acuteischemia in the limb. The attending vascular surgeon oncall, together with the orthopedic surgeon, proposes imme-diate surgery, however no operating room will be avail-able in the next four hours. Because of recent hospitalclosures in the city, no other facility is available in whichto treat this patient.

Ethics and practiceResource allocation is the distribution of goods

and services to programs and people. In the con-

text of health care, macroallocations of resourcesare made by politics, mesoallocations are made atthe level of health institutions, and microallocationsare made at the level of the patient. Resourcescarcity may be due to the shortage of a finite good(i.e., an organ for transplantation), or to a short-age of economic funds. While physicians have afiduciary duty to promote the patient's best inter-est, their role in resource allocation is controver-sial. The physician can approach resource allocationin practice by choosing tests and interventionsknown to be beneficial, by choosing the test or inter-vention with the least cost among equally beneficialoptions, by resolving conflictive claims for scarceresources on the basis of need and benefit, and byseeking unacceptable shortages at the level of meso-and macroallocation [8]. The physician should notapproach resource allocation by subordinating theprimary concern of care - his or her patient's wellbeing- to a budgetary issue. The surgeon must alsopay attention when making decisions based on"quality of life." Several studies have shown thatphysicians often rate the patient's quality of lifemuch lower than the patient himself does. If thepatient is able to communicate, the surgeon shouldengage him or her in a discussion about his or herown condition assessment.

The caseEVC-7: The attending surgeons should provide

appropriate care for Mrs. EVC-7, since a delay invascular surgical reconstruction could result insome neurologic sequelae and in nephropatic meta-bolic syndrome. Surgeons should involve the ad-ministrator on call to bring in additional skilledpersonnel (anesthesiologist, surgical nurses, etc.) toprovide care for the patient. In this way, they clar-ify the responsibility of the hospital to resolve themesoallocation problem at an administrative level.Surgeons should seek resolution of unacceptableshortages at the level of emergency care.

In the pursuit ofprofessionalism

Mr. EVC-8 is a 76-year-old man with a 7 cm abdom-inal aortic aneurysm. He has been rejected from electivesurgery because of depressed left ventricular function andmoderate ventilatory deficit. Mr. EVC-8 comes to theemergency department with his aneurysm ruptured. The


vascular surgeon on call wonders whether it is worth it tooperate on this patient.

PROFESSION AND PROFESSIONALISMProfession has long been recognized to encom-

pass three essential characteristics: expert know-ledge, self-regulation, and a fiduciary responsibilityto place the needs of the client ahead of the self-interest of the practitioner [12].

The dominant conception of profession is socio-logical. Professionalism is the basis of medicine'scontract with society. It demands placing the inter-ests of patients above those of the physician, set-ting and maintaining standards of competence andintegrity, and providing expert advise to society inmatters of health. Essential to this contract is pub-lic trust in physicians, which depends on theintegrity of both individual and the whole profes-sion [13]. In this view, ethics is an important pre-dictor for a profession, but ethics is not its essentialand indispensable defining feature.

Another view of profession links it to an ethicalideal without which it cannot exit. That idealfocuses on some degree of effacement of self-inter-est when it is required by the good of the personseeking assistance. This conception is rooted in theetymology of the word "profession," which means"a declaration, promise, or commitment publiclyannounced." That promise is made in every clini-cal encounter when the physician offers to helpthose who need his or her special knowledge. Thatpromise entails competence and putting that com-petence at the service of the patient, even when itmeans some degree of sacrifice on the part of thephysician [14].

CURRENT CONFUSED SCENARIOAND FUTURE PERSPECTIVES

Many individual persons, groups, and institutionsplay a role in and are affected by medical decision-making in the current practice environment. Ten-sion and competition among the interests ofclinicians, insurers, patients, and institutions foravailable social and health care resources unavoid-ably influence the patient-physician relationship[6]. All these issues have raised a deep concernabout the present loss of that special dedication tocompetence, service, and other-than-self-interestthat have been associated with the ideal physicianfor so long. However, in its history, medicine haswitnessed recurrent cycles of moral confusion-ofdoubts about whatever there is something special

about the activity of medicine that imposes a higherstandard of moral integrity on its practitioners.Each time this conflict has arisen in the past, it hasresulted in a new infusion of moral sensitivitythrough successive professional codes. The realityof cycles of moral confusion must not obscure thespecific dimensions of the present recurrence, someof which are unique, and some not [15]. What arenot unique are the temptations of self-interest,power, prestige, pride, profit, and privilege thatbeset 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 aproduct like any other, left to the ethos of the mar-ketplace, to competition, commercialization, andprofit-making (today's moral imperatives). Physi-cians are not held to moral standards higher thanthose of the general society in which they live.2 - There is an erosion of the foundations of profes-sional ethics. Underlying these criticisms is a perva-sive moral skepticism that denies the validity of anystable moral truth and even the capacity of reasonto apprehend such truth were it to exist.

Pellegrino expects a repetition of the historiccycle of deprofessionalization and reprofessional-ization characteristic of periods of moral confusion[15]. Indeed, some have bet for a new code of pro-fessionalism [13]. However, it is not likely that anyof these codes will change today's scenario if physi-cians do not have at the core of their beliefs theprimacy of the welfare of their patients over anyown self-interest (technical, scientific, academic).Only when medicine is a moral enterprise will thatbe possible.

The case

EVC-8: The perspective of a bad outcome frus-trates any vascular surgeon faced with operating ona ruptured aortic aneurysm. The issues of futility(beneficence) and costs (justice) may rise. How-ever, the mechanisms of rationalization of the sur-geon's self-interest ("I'm going to waste some sleephours, surely for nothing, while tomorrow I have alot on my agenda") may often overcome any sin-cere ethical analysis. As we have seen previously,futility has very narrow margins and allocatingresources is best managed while not at the bedside.Mr. EVC-8 must be offered surgical treatment andinformed that, although it is the single curativechoice, the probability of survival is very low. Inrespect of the patient's autonomy, his final decisionwill be honored.

11


Conclusion

The surgeon's fiduciary duty to protect and pro-mote the patient's interest becomes more complexand demanding in emergencies. Vascular surgeonsshould face all of their clinical decisions, and spe-cially emergencies, with bioethical reasoning. Thisattitude is frequently not time-consuming and mayhelp the surgeon to unmask potential conflictsbetween moral obligations and self-interest (sur-

geon, family, or other third parties) and to ap-proach real ethical dilemmas with honesty, sense,and reasoning.

A CKNOWLEDGMENTS

The authors wish to acknowledge the valuable suggestions ofDr. F.Abel, President of the Institut Borja de Bioetica, UniversitatRamon Llull, Barcelona (Spain).

R E F E R E N C E S

12

1 Pellegrino ED. The metamorphosis of medical ethics: a 30-yearretrospective. 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: apractical 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). Ethicsin emergency medicine. Baltimore, Williams and Wilkins 1986.

6 Anonymous. Ethics manual. 4th edition. American College ofPhysicians. Ann Intern Med 1998; 128: 576-594.

7 McCullough LB, Jones JW, Brody BA (eds). Surgical ethics. NewYork, 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 toknow?/£SocMed 1994; 87:149-152.

10 Meisel A, Roth LH, Lidz CW. Toward a model of the legaldoctrine of informed consent. Am J Psychiatry 1977; 134:285-289.

11 Appelbaum PS, Roth LH. Patients who refuse treatment inmedical 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 physiciancharter. Ann Intern Med 2002; 136: 243-246.

14 Pellegrino ED. The healing relationship: the architectonics ofclinical medicine. In: Shelp E (ed). The clinical encounter: themoral fabric of the patient-physician relationship. 4th edition. Boston,Reidel 1983: pp 153-172.

15 Pellegrino ED. Medical professionalism: can it, should itsurvive? J Am Board FamPractmO; 13:147-149.

2URGENT CAROTID SURGERY

ALAIN BRANCHEREAU, RAOUF AYARIJEROME ALBERTIN, BERTRAND EDE

Surgery of stenoses of the internal carotid artery (ICA) is intended for lesions and chronicneurologic disorders as indicated by the NASCET, ECST, and ACAS study results. Urgentsurgery for an unstable neurologic condition has given rise to a considerable amount ofskepticism, 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 13carotid surgery in the years the Joint Study was performed, was 5 % to 20% [2], whereas itcurrently is 1% to 5% [3], At present, the urgent diagnosis of massive ischemic andhemorrhagic strokes is possible by means of computed tomography (CT) scanning andmagnetic resonance (MR) imaging. Ultrasonography, sometimes in combination with angio-CT or angio-MR, now allows for a sufficiently accurate appreciation of carotid stenoses, whilethe use of angiography of the aortic trunk is decreasing. This wins time and reduces iatrogenicneurologic morbidity. Angiography remains important in the intra-operative check-up of thereconstruction and regarding the additional therapeutic possibilities, such as intracerebralarterial thrombolysis. The introduction of stroke centers has been an essential advancement inthe emergency care of these patients through an indispensable combination of a logisticplatform and a multidisciplinary approach. Unfortunately, randomized controlled trials thatcould clarify the indications are not present at the moment. The aim of this chapter is toprovide an overview of the literature and our own experience. This chapter is dedicated tourgent carotid surgery, excluding traumatic lesions, carotid dissections and postoperativestrokes.


14

Pathophysiology

Our central nervous system has the lowest resis-tance to ischemia. The normal cerebral blood flowis estimated at 80 mL/100 g/min. Below 20 mL/100 g/min, neurologic disturbances occur, whichare reversible as long as the hypoperfusion is notprolonged and the threshold of 10 mL/100 g/minis not reached. These disturbances are detected bychanges in the electroencephalogram (EEC) and,the more severe ones, by changes in somatosensoryevoked potentials. The allowed limits before irre-versible 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/minfor 80 minutes. Surrounding the areas of irre-versible damage there is an area of nonfunctionalbut still viable brain tissue, which can restore itsfunction when normal cerebral flow is re-estab-lished. Identification of this area has led to the con-cept of the ischemic twilight zone. This area, whichhas lost its autoregulatory capacity, shows a greatlyunstable pressure-sensitive metabolism. A majorpart of the clinical manifestations of ischemicstrokes is due to the dysfunctioning of this twilightzone. The aim of urgent carotid surgery is to safe-guard this ischemic twilight zone.

Failure of reperfusion results in a loss or defi-ciency of the autoregulatory system in certain areas.Clinical symptoms can be hemorrhagic events andcerebral edema. One should discern between acerebral hemorrhage and a hemorrhage upon astroke. The former is due to a rupture of the bloodbrain barrier and penetration of blood into a pre-viously unaffected brain area. This has a poor prog-nosis. The latter reflects infiltration of blood intoinfarcted tissue. This does not necessarily have apoor prognosis. The presence of a cerebral infarc-tion is a well-known risk factor during carotid sur-gery. The wall changes in the vessels of the infarctedarea may lead to vascular rupture, leading to a hemo-rrhagic infarction upon an ischemic event.

Other risk factors of reperfusion damage are mul-tilevel lesions causing chronic hypoperfusion andsevere arterial hypertension.

Definitions

The modified Rankin scale is used for the clini-cal evaluation of neurologic deficits. This scale

enables simple assessment of the evolution of thedeficit before and after treatment as well as cor-rect comparison of the results from the differentstudies.0 - No deficit1 - Minimal deficit with complete autonomy2 - Minor deficit with incomplete autonomy not

requiring assistance in daily activities3 - Moderate deficit with walking ability4 - Severe deficit with walking disability5 - Disabling deficit leading to bed confinement6 - Death

CRESCENDO TRANSIENT ISCHEMIC ATTACKCrescendo transient ischemic attack (CTIA) is a

recurrent, localized ischemic neurologic event char-acterized by spreading of the deficit, a lengtheningof the duration of the event or shortening of theinterval between each event. Despite the absenceof prospective studies, the prognosis of not surgi-cally treated CTIA is poor and it leads to a con-siderable number of strokes.

PROGRESSIVE STROKEProgressive stroke is a severe neurologic deficit,

showing a varying intensity but without disappear-ing. The natural history of these events shows amortality rate of 14% to 36% and a morbidity rateof 54% to 69% [4]. The definition of progressivestroke is not unequivocal. Hence, various termi-nologies are used in the literature, including evol-ving stroke or fluctuating stroke.

SEVERE STROKE IN THE ACUTE PHASEThis is a severe neurologic deficit according to

stages 4 and 5 of the modified Rankin scale. In theOxfordshire Community Stroke study, an infarctionof the complete anterior circulation is accompa-nied with a 30-day mortality of 39% and a risk offunctional disability of 56%. Severe strokes ofcarotid origin also show a poor prognosis with amortality between 16% and 55% and a risk of func-tional disability between 40% and 69% [5].

REGRESSIVE AND MODERATE STROKESIN THE EARLY PHASE

These are moderate ischemic strokes accordingto Rankin stages 1 to 3 of which the neurologic statehas reached a steady state. In case of a stroke dueto partial obstruction of the anterior circulation, amortality of 4% and a risk of functional disability

URGENT CAROTID SURGERY

of 39% were reported in the Oxfordshire commu-nity stroke study.

Surgical treatment six months after the onset ofthe stroke is commonly accepted as the therapy ofchoice for severe carotid stenoses. This expectativepolicy has become questionable because of theincreased risk of early stroke recurrence [6] andstudies showing no risk increase after early surgery[6-10].

ANATOMICAL EMERGENCIESWhen the neurologic state is stable, the identifi-

cation of certain carotid lesions may offer an indi-cation for urgent surgery. The most frequentpossibility is a so-called subtotal stenosis. This def-inition is not based on the poorly known naturalhistory of these lesions, but on hemodynamic find-ings representing a reduction of the flow in theICA and the induction of a collateral circulation(Fig. 1).

The second anatomical emergency is the pres-ence of a floating thrombus at the level of thecarotid bifurcation and the extracranial ICA(Fig. 2). The literature data on this subject are con-tradictory [11,12]. Some advocate urgent revascu-

larization by means of surgery or thrombolysis, oth-ers favor medical treatment followed by secondarysurgery.

The last type of anatomical emergency is a carotidocclusion. For this type of lesion, the clinical pres-entation should determine the policy. When a neu-rologic deficit is absent, the carotid occlusion isvirtually impossible to date and does not requireurgent treatment. Nicholls et al. [13] reported anincidence of 46% for severe, initially symptomaticcarotid occlusions with a yearly risk of a neurologicevent of 20% after a follow-up of 39 months.

Investigation of the brain

CT SCANIschemic lesions are characterized by a hypo-

density of the cerebral tissue, but 60% of the CTscans are falsely negative. This hypodensiry gener-ally appears only after 36 hours. However, there areearly signs during the first four hours that can beidentified by scrupulous analysis. These may be ahyperdense medial cerebral artery (MCA), a dis-appearance 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 than90%. B - The asymmetrical intracerebral contrast distribution depicts the significant hemodynamic consequences of thestenosis, which justifies the term pre-occlusive.


16

signs of cerebral edema such as the disappearanceof the cerebral sulci and attenuation of the corti-cal layer (Fig. 3). Some of these elements, like cere-bral edema and a hyperdense MCA, have a poorprognosis. Hyperdensity of the MCA is an early sign,which has a sensitivity of 78% and a specificity of93%. Disappearance of the lenticular nucleus indi-cates occlusion of the proximal MCA, with a sensi-tivity of 92% after 6 hours. Diffuse hypodensity anddisappearance of the cortical sulci are correlatedwith a high mortality and prohibit thrombolysis.

DIFFUSION ANDPERFUSION-WEIGHTED MR IMAGING

Diffusion. Diffusion imaging allows the diag-nosis of ischemic lesions in the hyperacute phaseof a cerebrovascular event. The diagnosis is madewhen an area of high intensity is found on the dif-fusion scan after applying diffusion gradients,whereas no signal is detectable before these gradi-ents are applied (Fig. 4).

The performance of this technique in the earlydetection of ischemic lesions is good, with a high sen-sitivity and specificity of 88% and 90%, respectively

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 occlu-sion, distal to a stenosis of 60%. B - Despite the smallerdegree of stenosis, the thrombus in B is more threatening.

FIG. 3 Early sign of stroke on CT scanning: hyperdensemedian cerebral artery (arrow).


[14,15]. False-positive results are rare. Detection lim-its are very small volume lesions, infratentorial local-izations and TIAs. The volume of the ischemic lesionas measured with this technique has a prognosticvalue and is correlated with the initial clinical scoreand the situation after three months. By means ofan apparent diffusion coefficient graph, any artifactscausing false-positive results can be eliminated. Inemergency conditions, it is an essential investigationto confirm the diagnosis of a cerebrovascular eventin the hyperacute phase and to appreciate the extentof irreversible damage. This image analysis takesonly a few minutes. Thus, diffusion MR imaging issuperior to CT scanning for the early detection ofischemic events and to quantify the extent of theischemic cerebral area.

Perfusion. Combining angiographic techniqueswith MR imaging enables investigation of the lar-ger vessels of the brain (time of flight, phase con-trast) . Investigation of the cerebral microcirculationby means of MR imaging can be performed usingendogenous and exogenous tracers. A perfusion im-age is obtained by sequential scanning of the vari-ation in signal intensity during passage of the con-trast agent. Detection of diffusion asymmetriesbetween cerebral areas allows assessment of the twi-

FIG. 4 MR imasing diffusion image of an acute phaseischemic stroke.

light zones around the ischemic lesion that repre-sent poorly perfused but viable tissue areas at thetime of investigation (Fig. 5).

Quantitative data, such as cerebral vascular vo-lume, cerebral flow and transit time can also beobtained, which allow quantitative analysis of theregional hemodynamic disturbances. Subtraction ofthe volume of the irreversible lesions, as detectedby diffusion from the volume of the area with hemo-dynamic disturbance as shown by perfusion, allowsfor the assessment of the volume of the ischemictwilight area. The volume of the area with hemo-dynamic disturbance as measured by perfusion MRimaging is better correlated with the clinical evo-lution on the short and intermediate term than thevolume as measured by diffusion imaging [14,15].

Thus, diffusion- and perfusion-weighted MR imag-ing appears to be an essential diagnostic tool inpatients presenting with a cerebrovascular event inthe acute phase. CT scanning merely has a poor pre-dictive value. However, some uncertainties remain.The reversibility of the lesions as observed with dif-fusion MR imaging, especially in TIAs, illustratesthe limitations of diffusion MR imaging in the diag-nosis of irreversible cerebral lesions.

Rapid diagnosis ofcarotid lesions

The occurrence of a stroke requires therapeuticaction as soon as possible. Noninvasive investiga-tion should assess the etiology of the stroke. Thediagnostic arsenal comprises several possibilities.Carotid duplex scanning is the primary investiga-tion for a quick diagnosis of extracranial carotidlesions with a high sensitivity of 80%, a high speci-ficity of 90% and an excellent correlation withangiography [16]. Transcranial doppler (TCD) isimportant to evaluate the cerebral collateral circu-lation, the cerebral vascular reserve capacity and todetect intracerebral stenoses [17]. This technique,however, is not simple and requires know-how andexpertise which limits its use in emergency situa-tions. Furthermore, it is not yet completely evalu-ated. Angio-CT scanning has a high sensitivity andspecificity of 90% in the diagnosis of severe carotidstenoses and allows simultaneous analysis of thecerebral tissue. By means of an angio-CT, carotidstenoses may be evaluated via two-dimensionalreconstructions, measuring the residual lumen in

17


18

FIG. 5 Development of a stroke in the territory of the median cerebral artery on diffusion and perfusion MR imagins. Atthe second hour, the diffusion imases show a small infarction (A) in the center of an ischemic penombra, even more visi-ble on the perfusion MR imase (B) (arrow). At 24 hours, followins successful revascularization, the ischemic penombra hasalmost disappeared on the perfusion MR imase (D); the diffusion MR imase shows the clearly limited infarcted area (C).

T

each slice, thus showing the most stenotic area ofthe ICA as compared with the size in a more dis-tal, normal area (NASCET method). Angio-MRgives exact information about the carotid stenosisand the intracerebral vascularization after a fewminutes of image acquisition [14]. Appreciation ofthe stenosis with angio-MR may overestimate thelesion. The neurologic condition of the patientallowing cooperation during the investigation is animportant limitation of the outcome of the MR andCT investigations. Subtotal stenoses are difficult todiscern from carotid thromboses on MR or duplexscans because of the very low flow beyond the lesion.Despite its own neurologic morbidity [18], angio-graphy remains the reference standard, particularlyin doubtful cases, to appreciate the extracranialcarotid lesion and to investigate the intracranial ves-sels without artifacts due to the low flow state.

Indications and resultsIn 15% to 30% of the cases with cerebral is-

chemia, a stenosis of the cervical ICA is found [19].The aim of early surgery after a stroke is on theone hand to restore the cerebral vascularization ofthe twilight zone, and on the other to exclude theemboligenic 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 innatural history studies. Numerous surgical studieshave found discouraging results (Table I), whichhas led many groups to refrain from this kind ofsurgery.

Most of these studies were performed before theintroduction of CT scanning, which in part explainsthe observed results, considering the incidence of

hemorrhagic strokes is estimated to be 15% of allstrokes [22].

In general, the indications for emergency surgeryare not yet clearly defined. On the one hand, sur-gery is able, through revascularization of the viableareas, to restore a deficit and to benefit the patient.On the other hand, surgery might also revascular-ize an area already lost or cause a complication dueto the intervention. In other words, it may bring nobenefit at all or cause deterioration. The problemis therefore to identify patients that will benefit.Today no prospective randomized trial can answerthis dilemma. The data available are based on theexperience of few groups and on mostly cohort stud-ies 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 surgeryin a period of 10 years (January 1992 to December2001), which were considered as emergency caseson the basis of an interval below 24 hours betweendiagnosis and intervention (Table II).

Crescendo TIA

Recent series from the literature have shown en-couraging results in patients with an unstable neu-rologic condition, selected on the basis of the clinicalpresentation and results of the CT scan. Table IIIillustrates the results of urgent carotid surgery for acrescendo TIA. The therapeutic decision is clear inthis selected patient group when an accessible lesionis found. Hence, a surgical reconstruction is indi-cated in cases with the shortest delay, with reason-able success rates. Thus, complete healing rates of71% to 100% can be reached. In our experience,

19

1st author Year of**

[ref.] publication„ ,I 101 n\iUelay

Improved Unchanged Worsened MortalityN (%) N (%) N (%} N (%)

Rob [20] 1969 74 No A few days 21 (28) 32 (43) 21 (28)

Blaisdell[l] 1969 50 No < 14 days 17 (34) 9 (18) 3 (6) 21 (42)

Bone [21] 1990 Yes < 24 hours 5 (15) 10 (31) 8 (25) 9 (28)


Neurologicstate

CTIA

Progressive stroke

Severe stroke

Number

4

8

3

Subtotalstenosis

1

6

3

Stenosis>75%

2

-

_

Floatingthrombus

i »2...

Improvedneurologic

state

4

6

2

Unchangedneurologic

state

-

1

_

Death

-

1

1

Subtotal stenosis + floating thrombus** 1 subtotal stenosis + 1 stenosis >75%CTIA: crescendo transient ischemic attack

20

1st author[ref.]

Wilson [23]

Gertler [24]

Eckstein [25]

Year ofpublication

1993

1994

1999

Number

12

14

21

Healing

100

98

71

Minor stroke Severe stroke Mortality

-

2

10 19

TIA: transient ischemic attack

crescendo TIAs accounted for 27% (4/15) of theindications for urgent carotid surgery. The resultsare in accordance with those recently reported inthe literature showing 100% healing. In our opin-ion, crescendo TIAs form the best indication forurgent carotid surgery.

Progressive stroke

Table IV shows the results of urgent carotid sur-gery for progressive strokes with a normal CT scanor showing few lesions. Encouraging results com-pared with the natural history were reported withclinical improvement in 86% to 92% of the cases. Inour experience, progressive stroke accounted for

53% (8/15) of the indications for urgent carotid sur-gery (Table II). The results showed clinical improve-ment in 75% (6/8), no change in one case (1/8),and one death (1/8). Progressive strokes form agood indication for surgery in selected patients.The aim of the selection, based on clinical andparaclinical criteria, is to identify and exclude pa-tients in whom a revascularization is likely to have amore deleterious than beneficial effect. This may bethe case in patients showing a massive lesion, acerebral hemorrhage or a substantial impairmentof their conscience. An accurate selection and pre-operative work-up are necessary for a favorable out-come. For these patients, Brandl et al. [27] advisenot to perform a pre-operative angiogram to reducethe neurologic morbidity and to arrange for anexperienced team of carotid surgeons, with constant


r , v /• ^rr Improved Unchanged Worsened ,, , ,.,1st author Year of x r , LI scan ~ , , • , * i • , , i • , , Mortality

r „ ,_ ... ;. Number m Delay neurologic state neurologic state neurologic state A 7 /0/,[re/] publication % > N * % N *(%) N *(%) N (%)

Greenhalgh [26]

Gertler [24]

Brandl [27]

Eckstein [25]

1993

1994

1998

1999

22

70

12

34

87

43

100

100

< 2 4 h

A few days

< 2 4 h

24 h

19

60

11

26

(86)

(86)

(92)

(76.5)

1

5

0

0

(4)

(7)

1

3

1

6

(4)

(4)

(8)

(17.5)

1

2

0

2

(4)

(3)

(5.8)

monitoring of the hemodynamics peri-operativelyto ensure an optimal stability of the cerebralperfusion.

MODERATE AND REGRESSIVE STROKESIN THE ACUTE PHASE

The treatment of moderate ischemic strokesremains controversial. The initial attitude based on

the results of urgent carotid surgery from the 1960sand 1970s has led to the temporization of any inter-vention until after six to eight months, in whichthe cerebral tissue can recover (Fig. 6).

In our experience, acute ischemic strokes ac-counted for 20% (3/15) of the indications for ur-gent carotid surgery. The postoperative results werean improvement in two cases (2/3) and one death

21

FIG. 6 CT scan of an acute stroke with hemorrhasic petechia andedema around the lesion (A). The same patients three months later (B).


22

(1/3). Two recent prospective studies (Table V)showed encouraging results of carotid surgery aftera little disabling, ischemic stroke (Rankin scale 1to 3). These authors concluded that early carotidsurgery (within six weeks) is feasible in the acutephase of the stroke, showing a low risk of a post-operative hemorrhagic stroke and a reduction ofthe recurrence risk. The risk of a postoperativehemorrhagic stroke was below 1.2% in these stud-ies. The stroke recurrence risk in the acute phasewas 4.5% in patients scheduled for delayed surgeryafter a regressive stroke in the NASCET study. Thesedifferent series showed that there was no increasein operation risk during carotid surgery in the acutephase of a stroke. The absence of a homogeneouspatient selection in these series and the differentstudy sizes do not allow for a statistical analysis ofthe different risk factors studied.

In general, clinical and paraclinical selection ofthe patients in these series allowed exclusion ofcerebral hemorrhages, strokes with coma and majorstrokes covering more than one third of the ante-rior vascular area on CT scan.

The indication for urgent carotid surgery insevere strokes (Rankin superior to 3) in the acutephase is very controversial because of the overallpoor results. Few series report results better thanthe natural course. Eckstein et al. [25] reported ona series of 16 patients and found a clinical improve-ment of 56.2% (9 cases) and a mortality of 19% (3cases). At present it is difficult to select from thesepatients a group that might benefit from urgentcarotid surgery. The various predictive factors stud-ied in the literature have been disputed successively

without clear evidence. The arbitrary time limit of6 hours between the stroke and surgical treatmentwas not confirmed by recent series, in which thepatients were operated within 24 hours. Further-more, the presence of emboli at the level of theMCA, which is considered as a poor prognostic fac-tor and a centra-indication for surgery [5], hasgiven rise in recent studies to combine thromboly-sis with carotid surgery, with encouraging results.This combined approach is attractive for patientswithout centra-indications for thrombolysis (Fig. 7).

ANATOMICAL EMERGENCIESSubtotal stenoses. In our experience, a subto-

tal stenosis was present in 80% (12/15) of the indi-cations for urgent carotid surgery. The results inthese patients showed clinical improvement in 75%(9/12) with a mortality of 8.3% (1/12). The natu-ral history of these carotid lesions is poorly knownbecause they are excluded from large prospectivetherapeutic trials. Therefore, this indication whichis beyond discussion for the majority of surgeons,is not supported by the literature. Based on hemo-dynamic studies by means of TCD of high-gradestenoses [28], some centers advocate investigationof the collateral circulation in order to assess thestroke risk at the time of a carotid occlusion. Thisspeculative attitude seems inappropriate to us, inview of the good surgical results obtained in thesepatients for asymptomatic carotid lesions.

Floating thrombus. In our experience, a freshcarotid thrombus was present in 20% (3/15) of thepatients undergoing urgent carotid surgery. Clini-cally one patient presented with a crescendo TIA

1st author[ref.]

Piotrowski [7]

Gasecki [6]

Ricco [8]

Ballotta [9]

Eckstein [10]

Year ofpublication

1990

1994

2000

2002

2002

Randomization

No

Yes

No

Yes

No

Number

129

100

72

86

164

Early surgeryN/CMMR%

82 / 2.5

42 / 4.8

72 / 2.8

4 5 / 2

164 / 6.7

Delayed surgeryN/CMMR%

47 / 5.3

58 / 5.2

-

4 1 / 2

-

CMMR: cumulative morbidity and mortality rate


and two patients with progressive strokes. Two pa-tients improved and one died. Literature data arecontradictory [11,12]. Concerning the treatment ofacute cerebral ischemia, some favor urgent revas-cularization by means of surgery or thrombolysis,others prefer anticoagulant therapy followed by se-condary surgery. The theoretical argument to post-pone or refrain from surgery is the considerablerisk of peroperative embolization. Pelz et al. [29]obtained results in favor of delayed surgery in acomparative study comprising 29 cases. Positiveresults for nondelayed surgery were also reported[11]. A consensus on the treatment of this pathol-ogy does not seem to show up. A pragmatic atti-tude related to the clinical situation and topo-graphic presentation of the lesion should direct thetherapeutic approach.

Principles ofsurgical treatment

INTRA-OPERATIVE MONITORINGAnticoagulant treatment should be initiated as

soon as the diagnosis of ischemic stroke is madeand centra-indications against heparin treatmentare checked. The aim of this treatment is to avoidan extended thrombosis. As to normalization of theblood pressure, one should take into account thedefense mechanisms of the cerebral perfusionwhich generate a relative hypertension. Accurateblood pressure monitoring, which is already im-portant in carotid surgery, plays a crucial role here.Sudden and/or substantial variations in blood pres-sure may cause a disturbance of the autoregulationof the cerebral circulation, which can be induced

23

FIG. 7 Urgent carotid surgery for progressive stroke. Completion angiography after ICA reconstruction shows thrombosisof the median cerebral artery (A). After 20 minutes of local thrombolysis, angiography shows patency of this artery (B).


by cerebral edema, hemorrhage or hypoperfusionof the ischemic twilight zone. Intra-operative mon-itoring by means of EEG, TCD, evoked potentialsand others is recommended by certain groups.However, the meaning of these variations observedduring the acute phase of a stroke is unknown.Moreover, the delay due to their use limits their in-dications in emergency cases. Finally, many groupsincluding ours recommend the systematic use of ashunt in case of urgent surgery when a neurologicdeficit is present, which makes cerebral monitoringredundant.

TECHNICAL ASPECTSThe carotid reconstruction does not have parti-

cular characteristics when performed urgently. Theexposition should be performed very carefullybecause of the risk of embolization. If the ICA ispatent, it should be clamped in the first place,before finishing the dissection of the carotid bifur-cation. If one suspects a carotid thrombosis of afloating thrombus at the level of the ICA, oneshould refrain from clamping it. Then it is impor-tant to clamp the common carotid artery first, fol-

lowed by the external carotid before completingthe dissection and performing the arteriotomy ofthe nonclamped ICA. In case of a thrombus, open-ing of the ICA should be done in its proximal partin order to let the thrombus come out sponta-neously, supported by the residual intracranialblood pressure. One should avoid, whenever pos-sible, any embolectomy. In our practice a shunt isplaced routinely to prevent expansion of the cere-bral ischemia in the presence of a carotid stenosis.In case of carotid thrombosis, the shunt shortensthe period of cerebral ischemia but also ensures aprogressive cerebral reperfusion, as the flow throughthe shunt is similar to an ICA stenosis of 70%. Aperfect carotid endarterectomy and a completionangiogram are required to minimize the risk of pre-operative embolization. In the series of Ballotta etal. [9] the postoperative neurologic morbidity wasdue to a postoperative embolization.

POSTOPERATIVE MONITORINGOne of the necessities for the postoperative

period is the prevention of the reperfusion risk(Fig. 8). The therapeutic arsenal comprises symp-

24

FIG. 8 Reperfusion injury. A - Massive cerebral bleedins occurring in the immediate postoperative phase, leadins topatient's death. B - Bleeding occurring at the third postoperative day for a stroke, causing temporary aggravation withadequate final outcome.


tomatic measures such as maintenance of a normalor slightly subnormal blood pressure, cerebral pro-tection by a quick recovery after general anesthe-sia, and the use of edema-preventing treatments.Monitoring the cerebral circulation by means ofTCD can identify the first signs of cerebral hyper-perfusion, which allows for symptomatic treatmentbefore reperfusion injury can occur [30].

THE PLACE OF THROMBOLYSISAND ENDOVASCULAR TREATMENT

The natural history of acute ischemic strokes withintracranial carotid thrombosis and/or thrombosisof the MCA shows a mortality greater than 53% [31].Several recent case reports showed good results ofa combination of surgery and in-situ thrombolysisin patients with extra- and intracranial carotidlesions. Eckstein et al. [32] reported eight patientswith a carotid occlusion or severe stenosis associatedwith MCA embolization treated with thrombolysisand carotid surgery. As a result, five patients suf-fered a minor stroke (62.5%), two were cured (25%)and one died (12.5%). However, despite the lowhemorrhagic complication rates reported, the pre-cise risk of an intracerebral hemorrhage after urgentthrombolysis remains to be shown.

In the literature few data are given on the endovas-cular treatment in the acute phase of a stroke. Ina series of 33 patients with a major disabling stroke,Endo et al. [33] reported four successful cases afterintra-arterial thrombolysis, three times in combina-tion with carotid angioplasty and once with surgery.The mortality was 58%. Finally, some heterogeneousand poorly documented publications show goodresults after thromboaspiration and percutaneousangioplasty of a carotid occlusion in the acute phaseof a stroke.

Comments

This general overview generates more questionsthan answers. The surgical series are mostly retro-spective and report only on highly selected cases,of which the selection criteria are quite variableand unclear. This selection has a double effect. Inthe first place, the first aid department offers onlyfew patients with a neurologic deficit with a poten-tial carotid origin to offer to the vascular surgeons.

Secondly, from these the surgeons select only thoseto investigate who may be treated surgically. Theselection criteria vary among centers and in dif-ferent time periods. It is therefore impossible toknow what the prevalence is of the indications forurgent surgery among the total of ischemic neu-rologic events, or even among the total of ischemicevents of carotid origin.

The fundamental challenge of this kind of sur-gery is therefore primarily to identify and select thesubgroups of patients for whom surgery can be ben-eficial. The second one is to organize the logisticsto perform this selection and surgery under accept-able conditions and delay.

MR imaging more than CT scanning offers pos-sibilities for basic investigations, which shouldanswer the questions raised. However, validation bymeans of prospective studies of the different qual-itative and quantitative prognostic factors as givenby MR imaging is needed. The present availabilityof this method is still limited and its use is far fromubiquitous.

Percutaneous carotid angioplasty may play aninteresting role, as it can be performed quickly.Intracerebral thrombolysis, with or without surgeryor percutaneous angioplasty, offers interesting per-spectives for the treatment of intracranial lesions.

Conclusion

Urgent carotid surgery is certainly surgery of thefuture, of which the exact indications need to befurther defined. The dogma of delayed surgeryafter a moderate stroke appears obsolete. Prospec-tive studies should be undertaken to address thefollowing essential subjects:- assess the selection criteria for carotid surgery

after moderate or regressive stroke,- accurately assess the optimum delay for surgery

after moderate or regressive stroke,- assess the arguments in favor or against surgery

for a floating thrombus and a subtotal stenosis insymptomatic and asymptomatic patients,

- assess the results of angioplasty versus surgery inacute situations.All these studies should benefit by initiating

stroke centers, which are essential for this purposeand for the treatment of the patients.

25


R E F E R E N C E S

26

1 Blaisdell WF, Clauss RH, Galbraith JG et al. Joint study ofextracranial arterial occlusion. IV. A review of surgicalconsiderations. JAMA 1969; 22; 209:1889-1895.

2 Easton JD, Sherman DG. Stroke and mortality rate in carotidendarterectomy: 228 consecutive operations. Stroke 1977; 8:565-568.

3 Hertzer NR, O'Hara PJ, Mascha EJ et al. Early outcome assess-ment for 2228 consecutive carotid endarterectomy procedures:the Cleveland Clinic experience from 1989 to 1995./ Vase Surg1997;26:1-10.

4 Toni D, Fiorelli M, Gentile M et al. Progressing neurologicaldeficit secondary to acute ischemic stroke. A study on predic-tability, pathogenesis, and prognosis. Arch Neurol 1995; 52:670-675.

5 Meyer FB, Sundt TM Jr, Piepgras DG et al. Emergency carotidendarterectomy for patients with acute carotid occlusion andprofound neurological deficits. Ann Swrg-1986; 203: 82-89.

6 Gasecki AP, Ferguson GG, Eliasziw M et al. Early endarterectomyfor severe carotid artery stenosis after a nondisabling stroke:results from the North American Symptomatic CarotidEndarterectomy Trial. / Vase Surg 1994; 20: 288 - 295.

7 Piotrowski JJ, Bernhard VM, Rubin JR et al. Timing of carotidendarterectomy after acute stroke. JVasc Surg\99Q; 11: 45-51.

8 Ricco JB, Illuminati G, Bouin-Pineau MH et al. Early carotidendarterectomy after a nondisabling stroke: a prospective study.Ann Vase Surg 2000; 14: 89 - 94.

9 Ballotta E, Da Giau G, Baracchini C et al. Early versus delayedcarotid endarterectomy after a nondisabling ischemic stroke: aprospective randomized study. Surgery 2002 ;131: 287-293.

10 Eckstein HH, Ringleb P, Dorfler A et al. The carotid surgery forischemic stroke trial: a prospective observational study oncarotid endarterectomy in the early period after ischemic stroke.J Vase Surg 2002; 36:997 -1004.

11 Christopher M. Lofthus CM. Hyperperfusion syndrome followingcarotid endarterectomy. In: Lofthus CM, Kresowik TF (eds).Carotid artery surgery, Thieme, New York, 2000 : pp 321-327.

12 Combe J, Poinsard P, BesancenotJ et al. Free-floating thrombusof the extracranial internal carotid artery. Ann Vase Surg 1990;4:558-562.

13 Nicholls SC, Bergelin R, Strandness DE. Neurologic sequelae ofunilateral carotid artery occlusion: immediate and late. J VaseSurg 1989; 10: 542 -547.

14 Grunwald I, Reith W. Non-traumatic neurological emergencies:imaging of cerebral ischemia. EurRadioim?; 12:1632-1647.

15 Cosnard G, Duprez T, Grandin C. et al. Diffusion- and perfusion-weighted MR imaging during the hyperacute phase of stroke.J Radial 2000; 81: 858 -869.

16 Long A, Lepoutre A, Corbillon E, Branchereau A. Critical reviewof non- or minimally invasive methods (duplex ultrasonography,MR- and CT-angiography) for evaluating stenosis of the proxi-mal internal carotid artery. Eur J Vase Endovasc Surg 2002;24:43-52.

17 Baumgartner RW, Baumgartner I, Mattle HP, Schroth G.Transcranial color-coded duplex sonography in the evaluation ofcollateral flow through the circle of Willis. AJNRAmJNeuroradiol1997;18:127-133.

18 Bendszus M, Koltzenburg M, Burger R et al. Silent embolism indiagnostic cerebral angiography and neurointerventional proce-dures: a prospective study. Lancet 1999 6; 354:1594-1597.

19 Timsit SG, Sacco RL, Mohr JP et al. Early clinical differentiationof cerebral infarction from severe atherosclerotic stenosis andcardioembolism. Sfrofa>1992; 23: 486-491.

20 Rob CG. Operation for acute completed stroke due to throm-bosis of the internal carotid artery. Surgery 1969; 65: 862-865.

21 Bone G, Ladurner G, Waldstein N, Rendl KH. Acute carotidartery occlusion - Operative or conservative management. EurNeurol 1990; 30: 214-217.

22 Mead GE, O'Neill PA, McCollum CN. Is there a role for carotidsurgery in acute stroke? Eur J Vase Endovasc Surg 1997; 13:112-121.

23 Wilson SE, Mayberg MR, Yatsu F, Weiss DG. Crescendo transientischemic attacks: a surgical imperative. Veterans Affairs trialists./Vase Surg 1993; 17: 249-255.

24 Gertler JP, Blankensteijn JD, Brewster DC et al. Carotid endar-terectomy for unstable and compelling neurologic conditions: doresults justify an aggressive approach? JVasc Surg 1994; 19:32-40.

25 Eckstein HH, Schumacher H, Klemm K et al. Emergency carotidendarterectomy. Cerebrovasc Dis 1999; 9: 270-281.

26 Greenhalgh RM, Cuming R, Perkin GD, McCollum CN. Urgentcarotid surgery for high risk patients. Eur J Vase Surg 1993;7SupplA:25-32.

27 Brandl R, Brauer RB, Maurer PC. Urgent carotid endar-terectomy for stroke in evolution. Vasa 2001; 30:115-121.

28 Stork JL, Levi CR, Chambers BR et al. Possible determinants ofearly microembolism after carotid endarterectomy. Stroke 2002;33:2082-2085.

29 Pelz DM, Buchan A, Fox AJ et al. Intraluminal thrombus of theinternal carotid arteries: angiographic demonstration of reso-lution with anticoagulant therapy alone. Radiology 1986; 160:369-373.

30 Dalman JE, Beenakhaus 1C, Moll F et al. Transcanial dopplermonitoring during carotid endarterectomy helps to identifypatients at risk of postoperative hyperperfusion. Eur JVase Endo-vascular Surg 1999; 18: 222 - 227.

31 Jansen 0, Von Rummer R, Forsting M et al. Thrombolytictherapy in acute occlusion of the intracranial internal carotidartery bifurcation. AJNRAmJNeuroradiolWS; 16:1977-1986.

32 Eckstein HH, Schumacher H, Dorfler A et al. Carotid endarte-rectomy and intracranial thrombolysis: simultaneous and stagedprocedures in ischemic stroke./ Vase Surg 1999; 29: 459-471.

33 Endo S, Kuwayama N, Hirashima Y et al. Results of urgentthrombolysis in patients with major stroke and atherothrom-botic occlusion of the cervical internal carotid artery. AJNR AmJNeuroradiolim; 19:1169-1175.

BLUNT INJURY TO THE CAROTIDAND VERTEBRAL ARTERIES

RAMON BERGUER

The incidence of blunt injury to the carotid and vertebral arteries (BICV) is low but itsoutcome is characterized by high mortality and morbidity. BICV constitutes 0.5% to 1.0% ofall 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 toangiographically screen every patient for vascular injury arriving to a trauma center withblunt trauma of the head and neck. However, when patients who display other markers forBICV such as cervical/skull fracture or neurologic deficits are selected for diagnosticarteriography, 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 incidenceof 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 vertebralinjuries [3,7].

3_27

Mechanisms of injuryand arterial lesions

The mechanism for disruption of the extracra-nial carotid artery can be a direct blow, eitherexternal (Figs. 1A and IB) or transoral, hyperex-tension or hyper-rotation of the neck with stretch-ing of the artery over the transverse process of Cl(Fig. 2), direct contusion by a fragment of frac-

tured mandible, and proximity involvement of theinternal carotid artery in a fracture of the tempo-ral bone. An object striking the neck from the out-side can exert a direct blow to the common orinternal carotid arteries (this includes the mecha-nism of safety belt injury). An intra-oral blow occurswhen a person falls with an object (such as a tooth-brush or a lollipop) in the mouth. The object strikesthe internal carotid artery through the tonsillar


FIG. 1 There is a dissection of the innominate artery extending into the subclavian artery and occluding the commoncarotid artery. This 24-year-old man suffered a rollover car accident, crushing his anterior chest and neck against the stee-ring wheel. A - Arteriogram showing a luminal defect in the subclavian artery and the occlusion of the common carotidartery. B - Operative view of the dissected innominate artery.

28 fossa. The internal carotid artery traverses the tem-poral bone through a canal in which the adventi-tia of the artery and the periosteum of the boneare closely connected. A fracture and displacementof the bone entails disruption of the adjacent arte-rial wall (Fig. 3). Following BICV by any of themechanisms cited above, the neurologic manifes-tations will be delayed for hours or days in roughlyone half of cases [11-13].

The vertebral artery is rarely damaged by a directexternal blow, since it is protected by bone as itascends through the neck. In its V2 segment, thevertebral artery runs in an osteomuscular canalformed by the foramina transversaria and the inter-transversaria muscles. Fractures of the lateral massof the cervical vertebrae involving the foramentransversarium, and vertebral fractures with luxa-tion/subluxation of the cervical spine, can resultin distortion of this osteomuscular conduit con-taining the vertebral artery (Fig. 4) and its venaecomitantes and injury to these vessels (Fig. 5). Thislatter mechanism is frequently seen in motor vehi-cle accidents and in near hanging injuries. In amotor vehicle accident or during brusque chiro-

FIG. 2 False aneurysm of the internal carotid artery fromcontusion 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 carotidartery found after evaluation of a 30-year-old man who suf-fered a skull base fracture in a car accident.

FIG. 4 Symptomatic dissection of the V2 segment of thevertebral artery in a 27-year-old woman following a fall froma horse.

29

practic manipulation (Fig. 6), there may be suddenrotation or hyperextension of the head. The ver-tebral artery has a redundant loop between Cl andC2 to accommodate the wide arc of rotation thattakes place between these two vertebrae. This rota-tion is approximately 80 degrees or about one halfof the range of rotation of the entire neck. Thevertebral artery is also attached to Cl and C2 byconnections between its adventitia and the perios-teum of the transverse foramina. During injury, par-ticularly with extreme head rotation, the artery isstretched between Cl and C2 beyond its normalelastic range and literally snaps, the consequencebeing its dissection (Fig. 7), occlusion, or rupture.If it ruptures into the surrounding tissues, a falseaneurysm develops; if it ruptures into a closely adja-cent and also damaged vertebral vein an arterio-venous fistula ensues (Fig. 5).

BICV may result in a wide spectrum of lesionsranging from luminal irregularities (flaps, intra-mural hematoma, dissection), to disruption of thearterial wall (false aneurysm, fistula), to occlusionof the lumen (Fig. 8). Brain embolization mayoccur from an intimal flap, from the reentry tearof a dissection or from the tail of the thrombusthat forms distal to an occlusion.

DiagnosisSYMPTOMATOLOGY

About one half of the patients who eventuallyturn out to have BICV enter the trauma unit with-out neurologic symptoms or signs. A substantialnumber (43% to 58%) of these originally asymp-tomatic patients will develop neurologic signs aftertheir hospital admission [11-13].


30

FIG. 5 Ansiosram of a patient with a symptomatic arteriovenous vertebral fistula two years after blunt headand neck trauma. A - Arteriovenous fistula at V3. B - The venous end of the fistula has been obliterated bya detachable balloon. The vertebral artery intesrity has been preserved. Hypertrophy of the vertebral arteryproximal to this chronic fistula is obvious.

The following specific findings markedly increasethe likelihood that an individual that has sufferedblunt trauma to the head and neck may harbor aBICV.1 - A Horner's syndrome that occurs when there isdisruption of the upper cervical ganglion by trauma(hyperextension or rotation) or of the peri-adven-titial sympathetic fibers by dissection of the arterialwall.2 - A neurologic deficit that may be the result ofembolization (from the distal end of the dissectionchannel or from a thrombus beneath an intimalflap) or of ischemia (from low-flow compromise)due to the dissection or rupture of an artery result-ing in its occlusion or near occlusion. In the set-ting of a trauma unit, the detection of neurologicdeficits may be seriously hampered by high levels

of alcohol or drugs in blood, shock from otherinternal injuries, or concomitant head injuries.3 - The finding of a skull base (Fig. 3), temporalbone, or cervical fracture (or luxation/subluxation)substantially increases the likelihood of concomi-tant injury to the internal carotid or vertebral arter-ies that are intimately associated to these bonystructures.4 - If sudden hyperextension or head rotation move-ment during the accident are suggested by thepatient's description of the accident or by associ-ated injuries to the head and neck. Hyperextensionand hyper-rotation are the most common mecha-nisms for stretching injury of the carotid or verte-bral arteries.

In the series of Biffl et al. [11], setting up ascreening protocol in their trauma unit for these


FIG. 6 This 20-year-old man complainedof neck pain after a basketball game. Heunderwent chiropractic treatments andtwelve hours later developed symptoms ofbrain stem infarction. There is dissection ofthe distal vertebral artery (arrow). A ven-triculostomy tube is in place. The patienteventually died.

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FIG. 7 This 47-year-old woman developed a symptomatic vertebral artery dissection following aski accident (arrow). B - This arteriogram, obtained six months later, shows the dilatation of thefalse lumen involving the V3 and V4 segments.


FIG. 8 Operative photographs of a 29-year-old worker who had his neck crashed between the posts of a hydraulic caseused to repair electrical cables. A - View at operation of the hematoma in the subadventitial space of the common caro-tid artery. B - A cylinder of intima and media that broke off and impacted into the carotid bulb. C - Open sesment ofresected common carotid artery (it was replaced with a prosthesis) showing the folded layer of intima and media andthe thrombus that formed distal to it.

32

markers of BICV resulted in a 10-fold increase ofthis diagnosis. A seatbelt sign is not considered to bea good indicator of blunt carotid injury in retro-spective studies. One review of 131 patients with seat-belt sign found only one blunt carotid injury amongthem (0.76%) [14]. However, if the patient has aseatbelt sign and other abnormal findings (neuro-logic deficit, skull or cervical fractures, etc.), thenthere is a good indication for angiographic screen-ing [15] and a high probability of finding a BICV.

IMAGING TECHNIQUESA few studies have analyzed the screening power

of ultrasound and computed tomography (CT)angiography in the initial diagnosis of blunt vascu-lar injury to the head and neck [1,13,16,17]. Thesensitivity of the ultrasound in detecting blunt ca-rotid injury was a remarkably high 86% in a mul-ticenter trial [13]. Still, the study missed carotidlesions located in the distal cervical carotid and nat-urally the authors had no information about theintracranial carotid artery. Duplex ultrasound is not

reliable when the lesion is in the distal half of thecervical internal carotid artery, where most bluntinjuries occur (skull base, infrapetrosal segment).Duplex can theoretically provide evidence of injuryin the nonvisualized proximal common carotid anddistal internal carotid artery by detecting abnormalflow signals. However, the noncritical stenosis cre-ated by small flaps or some dissections will go unde-tected while they still have a high potential forembolization and delayed occlusion. Additionally,the accuracy of duplex ultrasound of the carotidbifurcation is notoriously operator-dependent andit is unlikely that such a service will be available atall times in a trauma unit. Finally, neck swellingand associated injuries may make duplex scanningdifficult and less reliable.

CT angiography is not a sensitive tool to detectsmall defects of the arterial wall, but CT scanningof the brain is a good predictor of outcome. A largemulticenter study [13] showed that those patientswho showed a cerebral infarct in the admission CTof the brain had a high mortality (47%) and only


a poor chance (29%) of good neurologic recovery.On the contrary, of those patients with a normalCT of the brain on admission to the trauma unit,none died and 67% went on to a good neurologicrecovery.

Combined magnetic resonance imaging-magneticresonance angiography has been advocated as atool to simultaneously image the carotid and ver-tebral arteries and survey the brain parenchym. Theexperience with this modality is limited. As a triagetool for blunt injury it is probably not available inshort notice in most trauma units. Even when avail-able, placing the patient in a magnet may presentproblems because multiple trauma patients oftenrequire hardware to immobilize fractures and ven-tilatory support. Levy et al. [18] reported a low sen-sitivity of magnetic resonance for detecting discretevascular blunt injuries.

There is consensus among the authors of thelargest series [11,12] that selection for arteriogra-phy within the large population of blunt traumapatients should be done on the basis of the clini-cal findings: stroke, Horner's syndrome, massivesoft tissue injury of the neck, the mechanism ofinjury (severe hyperflexion-hyperextension androtational injury), and concomitant bony findings(skull base fracture, fracture across the foramentransversarium, and temporal bone fracture). Inpatients with blunt injury to the head and neck,there is a strong correlation between those whopresent with a low Glasgow stroke score (equal toor less than six) and the finding of BICV.

Treatment

The goals of treatment in emergency and semi-emergency are to restore cerebral perfusion distalto an occlusive lesion and to prevent embolizationfrom a thrombus that developed at the traumatizedlevel. The goals during follow-up, if necessary, areto treat a false aneurysm, dissection, or arteriove-nous fistula.

ANTICOAGULATION THERAPYIntravenous heparin is administered in the acute

phase and followed by oral anticoagulation, theduration of which depends on residual lesions iden-tified during follow-up. The purpose of this treat-ment is to prevent the formation, propagation,and/or embolization of thrombus that developedat the level of the intimal rupture.

There is evidence [12] favoring anticoagulationwith heparin (to be followed by Coumadin) in thetreatment of BICV. The authors of the two largestseries [11,12] make a good argument for systemicheparinization in the absence of centra-indicationsin multiple trauma patients with BCVI. Althoughtheir studies are explicidy detailed and include thelargest series of BICV, they are retrospective reviewsthat were not analyzed using the technique ofmatched pairs. However, to avoid bias, they excludedpatients with intracranial fistulae and those withtransection or disruption of the internal carotidartery when searching by regression analyses theheparin effect on outcomes. Another retrospectivereview [19] of a smaller series did not find anyadvantage of heparin over antiplatelet therapy.

It is important to weigh the advantages of anti-coagulation treatment against the potential delete-rious effects at the level of associated lesions. Also,cerebral infarction can be transformed in a cerebralbleeding which is most often catastrophic. Finally,some associated visceral lesions, in the case of a poly-traumatic patient, mean an absolute contra-indica-tion for anticoagulation treatment, at least in theacute phase.

SURGICAL INDICATIONSUnfortunately there is no clearly established algo-

rithm for surgical treatment and the indicationsmust be discussed on a case-by-case basis. The emer-gency indications, always very difficult, should bedistinguished from the secondary, more electivesurgical indications. In the acute phase, a completerupture of a carotid or vertebral artery or a partialrupture with evident thrombus are indications forsurgical intervention. However, deep coma and se-vere neurologic deficit with or without extensivecerebral infarction are contra-indications for sur-gery. In contrast, the absence of lesions at CT scan-ning and a fluctuating neurologic status with pre-served consciousness are elements that should speedup the decision to operate. In neurologically unin-jured patients, the same arterial lesions require sur-gical repair, however surgery can be postponed forseveral hours, allowing assessment of the other poly-traumatic injuries and to improve the general con-dition of the patient. During follow-up, angiogra-phy or CT angiography can depict specific arteriallesions that might require surgery: false aneurysms,dissection, or arteriovenous fistulae. Lesions thatinduce transient neurologic accidents or fistulaethat cause a bruit experienced by the patient and

33


aneurysms or dissections containing thrombus de-spite anticoagulation, should be surgically repaired.Surgery is also indicated in case of rupture or com-plete thrombosis of the internal carotid artery orcommon carotid artery and in case of recurrentemboli resulting from arterial dissection despite an-ticoagulation therapy (Fig. 9).

Certain aneurysms are asymptomatic. The ana-tomical characteristics of the infratemporal internalcarotid artery and the suboccipital vertebral arteryexplain why false aneurysms can be surveilled be-cause enlargement hardly occurs. As long as they be-have asymptomatically, surgery is not necessary.

TECHNICAL ASPECTSThis surgery is extremely difficult and challeng-

ing, requiring unusual vascular access. Additionalcomplicating factors include the emergency setting,

the frequently associated lesions of head and neckand extensive hematomas disturbing local anatom-ical landmarks.

While vascular access to the common carotid ar-tery and the bifurcation is not a problem, the ma-jority of internal carotid artery trauma is locatedin the second part of the cervical region. In thesecircumstances it is recommended to perform na-sotracheal intubation and mandible subluxation.Access to the ICA in the subparotid area requirestransection of the digastric muscle and resectionof the styloid apophysis. This extension allows ex-posure of the ICA just above the crossing of theninth cranial nerve [20]. Access to the last cen-timeters of the ICA require control of the facialnerve, opening of the temporomaxillary joint, andpartial ablation of the tympanal bone [21]. It mustbe 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 appro-priate anticoasulation. B - Exclusion bypass from the internal carotid to the vertebral artery at the level of theforamen rnasnum. The proximal vertebral artery was lisated.


time consuming, which is disadvantageous in theseemergency settings.

Surgical repair for traumatic vertebral arteryinjury generally requires access to the distal verte-bral artery in its suboccipital segment. This can beachieved either by a cervical-lateral approach be-tween Cl and C2 [22] or a posterior approach be-tween Cl and the occipital foramen [23]. The lattertechnique is not recommended in emergency set-tings since the patient must be in the ventral decu-bitus position.

In traumatic arterial lesions, venous grafts arepreferred. Clamping at the distal end is always del-icate because of the fragile tissue and crushing ofthe intima. Furthermore, the surgical field is alwaysnarrow, allowing only limited movements. There-fore, distal arterial control can be achieved bymeans of an occluding balloon, causing limited inti-mal damage and enabling manipulation of the

artery during suturing. If this technique is feasibleand if 15 to 20 mm of the artery beyond the rup-ture are available, it is always recommended to per-form an end-to-side anastomosis with closure of thetransected end. This anastomotic configuration iseasier to perform, allows better vision of the distalarterial segment, and provides a superior hemody-namic shape. Insertion of a shunt remains contro-versial. It is rarely applied because it complicatesthe procedure.

ENDOVASCULAR TREATMENTFalse aneurysms can be managed with stents or

stent-covered grafts. There are some initial reportsof stenting as treatment for intimal flaps, proximaldissection entry points, and false aneurysms. Thedeployment of a stent inside a false aneurysm willnot necessarily result in the thrombosis of its falselumen (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 aneurysmremains patent.


induced by filling the aneurysm sac with coilsthrough the mesh of the stent (Fig. 11). Endovas-cular treatment, especially in trauma patients, isspecifically appealing because it is less invasive. How-ever, 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 theendovascular manipulations either initiate arterialocclusion or induce cerebral emboli, as already re-ported [24]. Second, the advantage of endovascu-lar repair is based on the fast procedure in a traumapatient. However, this treatment requires specificexpertise and infrastructure, which is not alwaysavailable in every trauma center. Occlusions or near-total occlusions result from fracture of the wall anddistal embolization of a medial-intimal fragment(Fig. 8). This kind of lesion is unlikely to be suc-cessfully managed with endovascular techniques andfarther distal embolization may occur during en-

dovascular manipulation. For this type of severeinjury, open surgical techniques are advocated.

Summary

BICV has a low incidence but a high morbidityand mortality. The artery may be injured by a directexternal blow or by adjacent bone displaced in afracture or a luxation. Brusque stretching of the ar-tery is a common mechanism of injury to the carotidor vertebral arteries in motor vehicle accidents.

A diagnostic angiogram is indicated when a pa-tient presents with specific features such as neuro-logic symptoms or craniofacial injuries. In the ab-sence of contra-indications from associated injuries,heparin appears to be beneficial. Endovascular anddirect surgical repair are recommended for specificlesions.

^36

FIG. 11 A - This false aneurysm of the vertebral artery (C3 level) was stented but its false lumendid not thrombose. B - Coils were introduced into the false lumen through the mesh of the stentand eventually obliterated the false lumen.


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4PENETRATING INJURY

TO THE BLOOD VESSELS OF THENECK AND MEDIASTINUM

JOHN ROBBS

Diagnosis and particularly management of penetrating injuries to the blood vessels of the Trneck and mediastinum may present enormous challenges to the surgical team. The 39anatomical areas of the neck in the context of penetrating trauma has been arbitrarily dividedinto three zones. Zone 1 extends from the clavicles to the cricoid cartilage, Zone 2 extends fromthe cricoid cartilage to the angle of the mandible, and Zone 3 extends from the angle of themandible to the mastoid process [1] (Fig. 1). In general terms, diagnosis and managementare relatively easy in Zone 2, and the difficult areas are represented by injuries in which thetrajectory 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 aremainly 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 ofmanagement, the major debate revolves around whether mandatory exploration should bedone for all penetrating wounds in this region or whether a more selective policy ofinvestigation and intervention based on clinical signs should be advocated. One could arguethat 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 generalclinical experience, it would appear that a selective policy is safe [2]. The aim of this chapteris to provide a practical guide to diagnosis and management based on our own experiencewith more than 4000 major vascular injuries, of which 20% to 25% involve thecervicomediastinal region.


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FIG. 1 Diagram showing the Zones of the neck.

Etiology and pathology

In order to rationally diagnose and treat theseinjuries, it is essential to have a good understand-ing 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 veloc-ity or high velocity. High-velocity missiles are thosein which the muzzle velocity exceeds 300 metersper second. This is usually associated with militaryweapons or hunting rifles. Low-velocity woundssuch as stabs or missiles with a muzzle velocity ofless than 300 meters per second, such as a standardhandgun, usually produce damage that is limitedto the implement or missile track. The energy trans-fers involved with high-velocity missiles cause a cavi-tation effect with tissue destruction around theactual missile track, which results in extensive asso-ciated soft tissue trauma [3].

Shotgun wounds warrant separate description.Bird shot is small caliber and densely packed withinthe cartridge, whereas buck shot is larger and heav-ier and there are fewer packed into the cartridge.The unique property of a shotgun wound is thelarge number of foreign bodies embedded in thetissues, particularly in the case of bird shot, withextensive associated soft tissue trauma particularly

at close range. The blood vessels involved tend todevelop multiple small perforations. An additionalproblem occasionally encountered when the mis-siles enter the vessels is distal embolization into thearterial system (Fig. 2).

In general, direct injury to the artery may causeeither partial or complete transection. This in turnmay result in pseudoaneurysm formation or, in thecase of complete transection, thrombosis of bothends of the transected vessels [4,5] (Figs. 3A and3B).

Pseudoaneurysms with expansion may lead tocompression of the aerodigestive tract or the bra-chial plexus. Small perforations, on the other hand,may temporarily seal off and then, with dissolutionof the thrombus for whatever reason whether low-grade infection or natural fibrinolysis, develop adelayed false aneurysm. This may occur graduallywith progressive enlargement or may be an acutephenomenon. These patients may then present witha large pulsating hematoma, often infected, with orwithout compression symptoms. Brachial plexuscompression under these circumstances results inmajor morbidity with a very guarded prognosis for

FIG. 2 Angiogram of a young woman who sustained ashotgun wound to the neck/upper mediastinum (Zone 1).Buck shot probably entered via the venous system andembolized to the common femoral artery (arrow).

PENETRATING INJURY TO THE BLOOD VESSELS OF THE NECK AND MEDIASTINUM

recovery of function [6,7]. The concept of conser-vative management of minimal vascular injury isnot to be encouraged [8]. We believe that all per-forations, even with small pseudoaneurysms that arestable, should be dealt with, as the consequencesof delayed hemorrhage are highly significant interms of morbidity.

With complete transection and associated throm-bosis, the thrombus tends to propagate to the firstcollateral. Carotid transection will propagate up tothe carotid bifurcation and down to the arch of theaorta. There is also often thrombus within thelumen associated with partial lacerations (Fig. 3A).

Adjacent perforations of the artery and vein willresult in an arteriovenous fistula. Significant hemo-rrhage and the formation of a pseudoaneurysm isnot an invariable feature of arteriovenous fistulae,as the arterial flow tends to take the line of leastresistance into the venous system. The systemic

effects depend largely on the size of the arteriove-nous shunt.

In the acute setting when the mediastinal andneck vessels are involved, usually in fit youngpatients, the systemic hemodynamic effects are min-imal. Undiagnosed fistulae may only presentmonths or years later with the classic widened pulsepressure, systolic hypertension, and, rarely, conges-tive cardiac failure. We have on record patients pre-senting up to 14 years after the initial injury. In theacute setting, an important feature of arteriovenousfistulae is the development of thrombus at the fis-tula site and particularly in the downstream arte-rial segment, probably due to the diminished flowin that segment. When this occurs in the carotidartery, neurologic deficits occur quite frequentlydue to embolization of this thrombus. This is amajor consideration in relation to interventionalmanagement (Fig. 3C).

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FIG. 3 A - Diagram showing propagation of thrombus following carotid transection. B - Lateral perforation with pseudo-aneurysm formation. Note intraluminal thrombus. C - Arteriovenous fistula. Note intraluminal thrombus in distal arterialcomponent.


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An injury that is becoming increasingly apparentin our practice is an intimal tear associated with amissile Shockwave. We have frequently noted atexploration an apparently intact carotid vessel withminimal bruising on the adventitial surface. Onopening the vessel there is an intimal tear withsuperimposed thrombosis. It is postulated that theShockwave causes acute lateral displacement of thevessel, causing distraction tears in the least elasticcomponent of its wall, the intima, while the moreelastic media and adventitia remain intact. Theexposed media on the luminal surface is throm-bogenic with resultant thrombosis that may be asso-ciated with thromboembolic phenomena (Fig. 4).

Clinical presentation

The entry and exit wound may give some idea ofthe trajectory of the missile. However, if there is asingle wound it is difficult to trace the trajectory.Probing is unreliable and is certainly not recom-

FIG. 4 Diasram illustrating postulated mechanism of arte-rial thrombosis following proximity (Shockwave) missileinjury.

mended, as thrombus may be dislodged with initi-ation of exsanguinating hemorrhage. We have alsoseen several patients in whom the stab wound hastraversed the neck and caused a vascular injury onthe opposite side.

Presenting features may be grouped into emer-gency, subacute, and long-term. Emergency presen-tation is that of ongoing active hemorrhage whetherto the exterior through the wound or concealedwithin the thoracic cavity, or the superior medias-tinum. Subacute presentation occurs in patients whohave stabilized hemodynamically. Pathognomonicsigns of vascular injury are a pulsating hematoma,a pulse deficit in the upper limb, or a bruit whethersystolic or of the arteriovenous type. It appears thaton occasion the fistula may only develop later bythe same mechanism already postulated for the de-velopment of delayed false aneurysm [9]. The com-munication may be sealed by thrombus and no bruitis audible in the acute phase. Within the next fewdays lysis occurs with the development of a mani-fest fistula. A systolic bruit may also result from com-pression resulting from pseudoaneurysm or partial-ly occluding thrombus.

More subtle signs of major vascular injury maybe evidence of previous hemorrhage such as a his-tory of major hemorrhage from the wound or arecord of initial shock at presentation that has sta-bilized following fluid resuscitation, or when thepatient presents with a low hemoglobin level.

Long-term presentation may be with delayedonset of false aneurysm with or without compres-sive symptoms to the trachea or brachial plexus oran arteriovenous fistula that may present monthsor even years later with the consequences of sys-temic hemodynamic changes, a machinery bruit, orvenous hypertension.

Diagnosis and management

Patients presenting in the emergency categorywith ongoing hemorrhage or acute stridor requireurgent exploration in order to stop the bleedingand/or relieve the compression. This is a clinicaldecision requiring judgment as to where the site ofthe bleeding might be, and the appropriate explo-ration must be carried out.

The hemodynamically stable patient without air-way compression can be investigated appropriately.An erect, well-orientated chest film is extremelyvaluable. Widening of the mediastinum suggests


that further investigation might be necessary. Com-puted tomography scans in the context of pene-trating trauma are not as useful and give little moreinformation than a high-quality antero-posteriorchest radiograph.

Duplex scanning is extremely useful for Zone 2injuries [10,11]. It is accurate in this area for iden-tifying intimal flaps, localizing arteriovenous fistu-lae, and detecting minor degrees of perforation(Fig. 5). This modality is of minimal value in Zone 1or Zone 3 injuries because of anatomical consid-eration. Transesophageal echo has not proved par-ticularly useful in our experience and we do notrecommend it.

Arch angiography using the Seldinger techniqueremains the gold standard for the diagnosis of cer-vicomediastinal vascular injuries. It has the addi-tional advantage that interventional maneuvers canbe performed when required. The indication forangiography is clinical suspicion of vascular injuryin the hemodynamically stable patient, as previously

outlined. It is also recommended in our practicethat routine angiography should be carried out inpatients with shotgun wounds. While stab woundscan safely be observed if there is no suspicion ofvascular injury on clinical grounds, our thresholdfor angiography is far lower with gunshot wounds,particularly those which traverse the neck, becauseof the possibility of a Shockwave injury. The pitfallsof interpreting angiography lie in the accuratelocalization of arteriovenous fistula by virtue of therapid circulation time [7,9]. In addition, significantintraluminal thrombus may be present that is notclearly demonstrated by the radiography (Fig. 6).

Operative management

It is important that the patient be positioned anddraped so that access is possible from the base ofthe skull to the xiphisternum. The patient shouldbe in the supine position with a bolster between

FIG. 5 Duplex scan showing a common carotid to inter-nal jugular arteriovenous fistula following a stab wound inZone 2 of the neck.

FIG. 6 Angiogram showing a carotid to jugular fistula asa result of a gunshot wound. The young male developedan acute right hemispheric neurologic deficit while await-ing operation. At surgery there was extensive thrombus for-mation in relation to the fistula (not clearly seen on theangiogram).

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the scapulae, the neck extended, and the head turn-ed away from the side of the injury. It is foolish toattempt to enlarge and explore the stab wound,and the standard approach must be adapted to theblood vessels of the neck and mediastinum. Thestandard utility incision is placed along the ante-rior border of the sternomastoid muscle, which canbe extended into a median sternotomy if required(Fig. 7).

For Zone 2 injuries, the standard approach to thecommon carotid artery, the bifurcation, and theproximal internal carotid artery should be used.The aerodigestive tract can also then be exploredby displacing the carotid sheath anteriorly.

For lacerations of the blood vessels close to thebase of the skull, access may be improved by divid-ing the digastric muscle. If this does not improvematters it is certainly not recommended that thetemporomandibular joint be dislocated with for-ward displacement of the mandible, or that theramus of the mandible be divided, as this resultsin unacceptable long-term morbidity.

FIG. 7 Incisions for exposure of cervicomediastinal bloodvessels.

Excellent access to the vessels at the base of theskull can be gained by detaching the sternomastoidmuscle from its insertion on the mastoid. This canbe then retracted antero-inferiorly with excellentexposure of the vessels as they enter the skull. Caremust be taken not to damage the tenth and twelfthcranial nerves as well as the accessory nerve, all ofwhich can be clearly identified [12].

For Zone 1 injuries (superior mediastinum), theoptimal incision is a total median sternotomy. Thisprovides excellent access to all the mediastinal ves-sels including the left subclavian artery. Under cer-tain circumstances, a limited sternotomy down tothe angle of the sternum may provide sufficient ex-posure. We have never found it necessary to excisethe clavicle or to make trap door incisions. Divi-sion or excision of the clavicle causes major long-term morbidity particularly in manual laborers.The distal subclavian artery is best approachedusing a supraclavicular incision. If necessary, a sep-arate infraclavicular incision may be made in orderto tunnel a graft. Division of the clavicle invariablyresults in non-union and a painful pseudarthrosis,which is possibly a consequence of devasculariza-tion of the bone in the process of surgical division.

The arterial injuries themselves can be repairedon their merits. The usual principles of debride-ment of the edges of the arterial wall back tohealthy tissue pertain. The vessel can then be re-paired by lateral suture, patch angioplasty, or an in-terposition graft [4,5].

Any prospect of narrowing the vessel by lateralsuture should prompt the use of a vein patch.

The through-and-through wound is best totallytransected, debrided, and reconstructed in an end-to-end fashion.

Following excision of the damaged vessel, an end-to-end anastomosis should not be attempted if thereis excess tension on the suture line, as this invitesocclusion. The best measure of tension is whethera single tethering stitch holds the ends together; ifnot, it is better to reconstruct using an interposi-tion graft, the saphenous vein being the optimumgraft. While the jugular veins have been used, theyare not as satisfactory because of their thin wallsand wide diameter, particularly when reconstruct-ing the internal carotid artery. In the case of injurywith an intimal tear it is best to excise the dam-aged segment and repair by means of an interpo-sition graft.

It is extremely important, particularly with regardto the carotid vessels, to dissect meticulously in


order to avoid dislodging thrombus. It is also impor-tant to pass an embolectomy Fogarty catheter gen-tly, both proximally and distally, to ensure that allthrombus has been extracted prior to performingrepair.

Specific problems

Penetrating wounds of the aortic arch that arecompatible with survival are usually small puncturewounds that can be treated by digital occlusion andthe insertion of mattress sutures deep to the occlud-ing finger [12].

Wounds of the major branches close to the arch,particularly through-and-through wounds, are besttreated by using a partially occluding clamp on theaorta, totally transecting the relevant vessel andoversewing its origin on the aorta. Continuity canthen be restored by making an end-to-side anasto-mosis of a prosthetic graft to the intrapericardialportion of the ascending aorta and an end-to-endanastomosis to the relevant vessel. Attempts toreanastomose this type of injury invite disaster, as

it is extremely difficult to gain adequate control. Itis also difficult to gain intimal apposition as themedia tends to retract into the aorta. In the caseof the left subclavian artery, continuity can berestored by means of a carotid to subclavian bypassif necessary (Figs. 8A and 8B).

On occasion, the superior mediastinum is totallyobscured by clot, which makes identification of therelevant vessels difficult. Under these circumstances,it is best to open the pericardium and expose the in-trapericardiac aorta. The origins of the major vesselcan then be identified by palpation and the necess-ary proximal control obtained prior to opening thehematoma [13].

Arch anomalies are uncommon, but they may notbe identified by pre-operative angiography, andoccasionally with emergency explorations they maycatch the surgeon off guard (Fig. 9). In our ownpractice, the prevalence of some form of anomalyis 5.3%; although these anomalies are not common,this is significant [14]. The anomalies range froma common trunk from which the left commoncarotid and the brachiocephalic arteries arise, theso-called bouquet anomaly, to the lusorian anomaly

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FIG. 8 Recommended sursical manasement of inju-ries occurring in close proximity to the aortic arch.


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FIG. 9 Arch angiogram of a young male showing a typi-cal anomaly. There is a common origin of the brachioce-phalic and left common carotid arteries (arrow).

in which there is a short brachiocephalic trunkfrom which both common carotid arteries arise andthe right subclavian arises from the descendingaorta and traverses the posterior mediastinumbehind the esophagus [13]. Under these circum-stances it would be necessary to insert a shunt fromthe interpericardiac aorta in order to preserve cere-bral flow while repair is carried out [15].

ASSOCIATED NEUROLOGIC DEFICITSThe theoretical consideration in restoring flow

under these circumstances is the creation of a hem-orrhagic infarct. Computed tomography scanningis notoriously unreliable within the first 24 hoursof developing a neurologic deficit, and it is oftennot possible to obtain the necessary scan in theemergency setting. It has been our policy to restorearterial continuity in all patients with a neurologicdeficit, provided that there is distal continuity, asevidenced by back bleeding following extraction ofthrombus. If there is no back bleeding, ligation is

performed. Similarly, it is probably ill advised torestore continuity in a patient who is deeply com-atose [16,17]. Most patients with localizing neuro-logic deficits improve, and we have not to ourknowledge caused neurologic deterioration by fol-lowing this practice.

ARTERIOVENOUS FISTULAEA major problem may arise if there is failure to

accurately localize the fistula site particularly in thesuperior mediastinum. It can be very difficult todistinguish between a fistula arising from the aor-tic arch from one arising from major vessels closeto their points of origin. In Zone 2, duplex scan-ning has proved sufficiently accurate in definingthe exact site of fistulation. Zone 3 presents verysimilar problems to those in the superior medi-astinum. Duplex is not helpful and angiographycan indeed be misleading as to the exact site ofthe fistula.

The veins lie in an anterior plane to the artery,and it is relatively easy to isolate the fistula by dis-secting out the vein and isolating the fistula by pal-pation along the course of the vein. Once found,the proximal and distal arterial components can beisolated and the artery and vein repaired [5,9].

It has been stated that it is advisable to wait forfistula to mature prior to attempting repair; how-ever, we have not found this to be advisable, as thelonger one waits the more fibrosis occurs and themore difficult the procedure becomes. In the pres-ence of extensive fibrosis and a small deficit, it mayon occasion be expedient to repair the fistula trans-venously but this is rarely necessary.

In general, repair constitutes simple debridementand end-to-end or lateral suture. Embolism fromthe clot within the arterial segment just distal tothe fistula is a distinct hazard. It is important to bemeticulous and gentle in the dissection of the ves-sels and to ensure that there is no residual throm-bus in the artery prior to repair and restoration ofprograde flow. Back bleeding and gentle thrombec-tomy using a small balloon catheter should alwaysbe performed. Air embolism through the venouscomponent has not proved to be a problem, but itis important to clamp the veins at an early stageand to fill the venous segment with saline prior tofinal closure. Recurrent fistulation has never provedto be a problem, but multiple fistulae do occur andit is important, particularly in the case of shotgunwounds, to ensure that all palpable thrills have dis-appeared on completion of the repair. It is impor-


tant also to attempt to trace the trajectory of thepenetrating implement or missile to ensure that allinjuries have been dealt with.

The use ofcardiopulmonary bypass

In the acute setting in most of the lesionsdescribed, cardiopulmonary bypass is unnecessaryand only adds to the magnitude of the operation[18,19]. In most cases, if deemed necessary, intra-luminal shunts can be during the procedure, butthis is certainly not routine. Cardiopulmonary bypassmay become necessary for the repair of chroniclesions presenting late in which extensive fibrosismay create major technical difficulties [20-22]. Themajor morbidity associated with penetrating woundsinvolving the extracranial cerebrovascular circula-tion is neurologic. In general terms, neurologic mor-bidity following straightforward carotid repair isnegligible; however, there is a significant, approxi-mately 5%, neurologic event rate associated withcarotid arteriovenous fistulae. This, we believe, isdue to thrombotic embolization. The overall mor-tality for mediastinal lesions is in the area of 7%and, for Zone 2 and 3 lesions, approximately 2%.

VENOUS INJURIESFrequently, particularly with gunshot trauma,

there is far more extensive injury to the majorveins, leaving relatively large defects that do notlend themselves to simple repair. This may be theresult of increased friability of the veins and theirrelative inelasticity. It has been stated that repairshould always be attempted in this situation. How-ever, venous repair does not enjoy the same suc-cess that one associates with arterial reconstruction.This is the result of the friability of the vessel walland the low intraluminal pressure. There is a highocclusion rate associated with complex repair usinginterposition grafts, particularly with a prosthesis.In addition, as is so often the case when attempt-ing to repair associated complex venous injuries, itsignificantly increases the magnitude of the opera-tive procedure.

There is a paucity of information on the collat-eralization of the venous system of the head andneck. Barrett performed phlebographic studies onpatients with idiopathic superior mediastinal fibro-sis [23]. These studies showed extensive collateral-

ization through the anterior jugular system, theanterior communicating veins in the neck, and thesuperior intercostal veins that restored cardiacinflow via the azygos and hemi-azygos systems. Evenwhen the azygos system was occluded, the superfi-cial veins on the chest wall contributed to this col-lateralization. It must also be postulated that thevertebral plexus comes into play under these cir-cumstances. It is well known with general surgicalexperience that interruption of one or even bothinternal jugular veins is well tolerated. Based onthis evidence, it has been our policy for several yearsto repair simple lacerations or perform reanasto-mosis when feasible. Complex injuries with tissueloss cephalad to the azygos veins have been ligated[24,25]. If the vein is to be reconstructed, meticu-lous and gentle technique using a fine guage vas-cular suture (6/0) is absolutely essential. In a sig-nificant series of patients, we have not encounteredmajor permanent morbidity as a result of this ap-proach. Temporary facial and upper limb edemahas been noted in several patients who have hadligation of the brachiocephalic veins but which re-solved within a period of 4 to 5 days. Ligation ofthe distal subclavian vein has resulted in temporaryupper limb edema but has not resulted in long-term morbidity. We have not seen large injuries ofthe superior vena cava caudad to the azygos vein,and this type of injury is probably incompatible withsurvival. Air embolism has not constituted a prob-lem, although meticulous attention is paid to ensur-ing that significant amounts of air are not presentin the major veins prior to restoring flow, and it isadvisable to fill the segment with saline prior toinserting the final stitches.

INTERVENTIONAL CATHETER TECHNIQUESEmbolotherapy is proving invaluable in dealing

with traumatic lesions involving branches of thesubclavian artery, the vertebral vessels, and bran-ches of the external carotid [26]. In relation to thecarotid system, we have had a single episode ofmigration of a spring coil into the internal carotid,and while the patient fortunately did not suffer anyadverse sequelae, this is obviously undesirable. Inrelation to the vertebral vessels, particularly withinthe bony canal, there exists the possibility of cre-ating a neurologic deficit with vertebral artery dis-ruption if the posterior communicating vessels inthe circle of Willis are found to be deficient [27-30]. We have fortunately not encountered thisproblem.

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The use of covered stents to treat partial lacera-tions or arteriovenous fistulae is attractive. The cur-rently available stents are polytetrafluoroethylene(PTFE) covered, and an increasing number ofreports on the use of these stents, particularly inthe subclavian artery, describe mixed success [31-34]. The use of stents is probably not applicablewithin the aortic arch, and we strongly recommend

against their use in the carotid system in the con-text of trauma because of the thrombus frequentlyassociated with these lesions. There is the ever-pres-ent possibility of infection, as all traumatic woundsare potentially contaminated. We have one patienton record with a proximal subclavian pseudoa-neurysm that was stented; infection occurred andultimately led to the patient's demise.

R E F E R E N C E S

48

1 RobbsJV, KeenanJ. Exploration of the neck. In: Champion HR,Robbs JV, Trunkey D (eds). Rob and Smith's operative surgery, 4thedition. London, Butterworths 1989: pp 166-172.

2 Campbell FC, Robbs JV. Penetrating injuries of the neck: aprospective 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 surgicalmanagement. 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 ofvascular trauma. In: Greenhalgh RM (ed). Vascular andendovascular techniques, 4th edition. London, W.B. Saunders Ltd.2001 :pp 455-465.

6 Robbs JV, Naidoo KS. Nerve compression injuries due totraumatic false aneurysm. Ann Surg 1984; 200: 80-82.

7 Robbs JV, Baker LW. Cardiovascular trauma. Curr Probl Surg1984; 21:1-87.

8 Frykberg ER, Crump JM, Dennis JW et al. Nonoperativeobservation of clinically occult arterial injuries: a prospectiveevaluation. Surgery 1991; 109: 85-96.

9 Robbs JV, Carrim AA, Kadwa AM, Mars M. Traumatic arterio-venous fistula: experience with 202 patients. BrJ Surg 1994; 81:1296-1299.

10 Fry WR, Dort JA, Smith RS et al. Duplex scanning replacesarteriography and operative exploration in the diagnosis ofpotential cervical vascular injury. Am J Surg 1994; 168: 693-695.

11 Corr P, Abdool Carrim AT, Robbs J. Colour-flow ultrasound inthe detection of penetrating vascular injuries of the neck. S AfrMedJ 1999; 80: 644 -646.

12 Robbs JV. Injuries to the vessels of the neck and superiormediastinum. In: Champion HR, RobbsJV, Trunkey D (eds). Roband Smith's operative surgery, 4th edition. London, Butterworths1989:pp 529-538.

13 RobbsJV. Penetrating trauma to the inlet and outlet regions ofthe 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 casereport and angiographic analysis. S Afr J Surg W02, (in press).

15 WoolgarJD, RobbsJV, Rajaruthnam P, Mohamed GS. Penetratinginjuries in the innominate artery in association with abnormalaortic arch anatomy. EurJ Vase Endovasc Surg 2QQ2; 23: 462-464.

16 Perry MO, Snyder WH, Thai ER. Carotid artery injuries causedby 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 penetratingmediastinal arterial trauma. Eur J Cardiothorac Surg 1995;9:90-94.

19 Graham JM, Feliciano DV, Mattox KL, Beall AC Jr. Innominatevascular injuries. / Trauma 1982; 22: 647-655.

20 Fulton JO, de Groot KM, Buckels NJ, von Oppel UO. Penetra-ting injuries involving the intrathoracic great vessels. S Afr J Surg1997; 35: 82 -86.

21 Fulton JO, de Groot MK, von Oppel UO. Stab wounds of theinnominate artery. Ann Thorac Surg 1996; 61: 851-853.

22 Fulton JO, Brink JG. Complex thoracic vascular injury repairusing deep hypothermia and circulatory arrest. Ann Thorac Surg1997; 63: 557-559.

23 Barret NR. Idiopathic mediastinal fibrosis. Br } Surg 1958;46: 207.

24 Robbs JV, Reddy E. Management options for penetrating inju-ries 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 penetratingcervicomediastinal venous trauma. EurJ Vase EndovascSurg 2000;19:65-69.

26 Naidoo NM, Corr PD, Robbs JV et al. Angiographic embolisa-tion in arterial trauma. EurJ Vase EndovascSurg 2000; 19: 77-81.

27 Thomas GI, Anderson KN, Hain RF et al. The significance ofanomalous vertebro-basilar artery communications in opera-tions 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 theposterior communicating artery as a risk factor for ischemiccerebral infarction. NEngJMed 1994; 330: 1565-1570.

30 Jithoo R, Nadvi SS, Robbs JV. Vertebral artery embolism postsubclavian artery injury with occipital lobe infarction. EurJ Vase

31 Marin ML, Veith FJ, Panetta TF et al. Transluminally placedendovascular stented graft repair for arterial trauma. J Vase Surg1994; 20: 466-473.

32 du Toit DF, Strauss DC, Blaszczyk M et al. Endovascular treat-ment of penetrating thoracic outlet arterial injuries. EurJ VaseEndavasc SurgZm-, 19: 489-495.

33 Strauss DC, du Toit DF, Warren BL. Endovascular repair ofoccluded subclavian arteries following penetrating trauma.JEndovasc Tfcr2001; 8: 529-533.

34 Chandler TA, Fishwick G, Bell PR. Endovascular repair of atraumatic innominate artery aneurysm. EurJ Vase Endovasc Surg1999; 18: 80 -82.

5ACUTE 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 embolusand acute thrombosis of the distal aorta remains a realistic distinction. The latter has becomethe most frequent etiology because of the predominance of peripheral vascular pathology in anageing population. Other causes are more rare, such as acute thrombosis of an abdominalaortic aneurysm, an occlusion due to aortic dissection or acute hemostatic disorders. Ifuntreated, the prognosis is poor with a mortality of 75%. The initial diagnostic failures canbe explained by the associated neurologic symptoms, delaying adequate treatment and thereforeaggravating the prognosis. The extent of the occlusion and associated ischemia-reperfusionsyndrome can induce major metabolic disorders. Despite surgical treatment, the overallmortality of this disease is approximately 50 % in the major published series [1].

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The clinical features are mainly determined bythe acute severe ischemia of the lower limbs, asso-ciated with bilateral pain and neurologic symptomslike numbness, paresthesias and, in the most severestate, even paralysis of both legs. Rest pain or se-verely deteriorated intermittent claudication havethe same diagnostic value and suggest a superim-posed thrombosis on pre-existing occlusive lesions.Additional abdominal complaints or renal insuffi-ciency with oligo-anuria are reminiscent of intesti-nal or renal ischemia, indicating proximal exten-sion of the thrombosis to the level of the visceral

arteries. The severity of symptoms depends on thequality of the collateral circulation, being poor incases of embolization and more developed in aorto-iliac occlusive disease.

An occluding embolus causes an abrupt andsevere bilateral pain often associated with low backand gluteal pain, and can subsequently inducemajor neurologic deficit with complete paraplegia.Skin mottling can often be impressive and involveboth legs, proximally extending to the umbilicus.In contrast, an acute thrombosis in a diseased dis-tal aorta with pre-existing severe claudication or restpain will manifest either with aggravation of exist-ing complaints or a neurologic deficit similar to


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spinal cord infarction. In these nonexceptionalcases, the patients are referred to a neurologic orneurosurgical department, causing significant diag-nostic delays. These neurologic manifestations arenot induced by spinal cord infarction but by severeischemic neuropathy, which is reversible after revas-cularization [2].

Physical examination reveals absence of pulsa-tions in both groins. The degree and extent of neu-rologic deficit is variable and develops in time,therefore requiring initial adequate and detailedneurologic examination, which serves as a referencefor subsequent assessments. Also the location andextent of the ischemic skin should be indicated andfollowed.

Abdominal examination is usually normal; how-ever, meteorism, pain and decrease or disappearanceof peristalsis might indicate associated intestinal is-chemia [3]. Urine output should also be monitoredsince any alteration suggests impairment of therenal arteries. Acute onset hypertension has thesame diagnostic value [4].

Etiology

The most common causes of acute distal aorticocclusion are embolization and thrombosis. Othermechanisms include traumatic occlusion, aortic dis-section, metabolic disorders, and pharmacologicinteractions. Acute occlusions of vascular grafts lead-ing to the signs of aortic occlusion are very uncom-mon and will not be addressed in this chapter.

EMBOLIThe most common source of emboli is the heart,

in the past mainly from endocarditis. At present,ischemic heart disease and especially the sequelaeof myocardial infarction dominate the embolic eti-ology [5]. Arrhythmia is often encountered, basi-cally being atrium fibrillation, however this is rarelyan isolated entity. Cardiac tumors, mainly the myx-oma of the left auricle, can be the source ofembolization by fragmentation of the tumor. Kao[6] reported an exceptional case of secondary acuteaortic occlusion by a cardiac myxoma.

Paradoxal embolization can occur in the coexis-tence of deep venous thrombosis, patent foramenovale and pulmonary hypertension susceptible tocause a right-to-left shunt. Theoretically, the embolican come from the thoracic aorta, either from ananeurysm or from an ulcerated plaque on which a

floating thrombus developed. This mechanism,however, is unlikely to cause a complete aortic occlu-sion because of the size of these thrombus masses.

ACUTE THROMBOSESAcute thromboses represent the most common

cause in several series [4,7], although Surowiec etal. [5] only encountered an incidence of 50%. Theyare often the end stage of obstructive aorto-iliacdisease characterized by bilateral intermittent clau-dication. The severity of the initial symptoms greatlydepends on the extent of the collateral system andsuddenness of onset. If the collateral network ispoorly developed and the pre-existing aortic steno-sis is limited, the clinical picture is dramatic withacute neurologic deficits. In contrast, if the acuteaortic occlusion is superimposed on a chronic exten-sive stenotic process, the clinical picture is oftenless impressive and predominantly manifests withischemic rest pain. The occurrence of a thrombo-sis in diseased arteries is most often provoked bydehydration or cardiac decompensation, the latterbeing the result of myocardial infarction or severearrhythmia [4].

Acute thrombosis of an abdominal aortic aneur-ysm only exceptionally occurs. The first case wasdescribed by Shumacker in 1959 [8] and the firstrevascularization was performed by Jannetta andRoberts [9]. Only 44 cases have recently been pub-lished, according to a review of the literature byHirose et al. [10]. The clinical signs are similar tothose of an acute aortic occlusion and only the pal-pation of an abdominal mass with transmitted pulsa-tions might indicate the diagnosis. In approximatelyhalf of the reported series, the correct diagnosiswas established during laparotomy. At present, con-trast enhanced computed tomography (CT) allowsrapid assessment. The following mechanisms of suchan occlusion are:- coexisting bilateral severe iliac obstructive disease

with iliac thrombosis and proximal extension in tothe aortic aneurysm,

- occlusion of the aneurysm neck by means of anembolus originating from the heart,

- partial dislodgment of intra-aneurysmal muralthrombus causing obstruction of the lumen withsecondary thrombosis,

- hypotensive episode or low cardiac output withintravascular thrombosis in a pre-existing aneur-ysm largely filled by thrombus.The optimal treatment consists of emergency sur-

gical repair, allowing simultaneous treatment of the

ACUTE ABDOMINAL AORTIC OCCLUSION

aneurysm and acute thrombosis. This surgical man-agement, however, is not always feasible because ofthe poor physical conditions of these patients. Inthese cases, distal revascularization can be estab-lished by means of an axillobifemoral graft. Thistechnique does not prevent later rupture, as ob-served in 15% of the patients of Schwartz et al. [11].The prognosis of these aortic aneurysm thrombosesis poor, with a mortality rate greater than 50%. Re-cent progress is limited and mortality rates encoun-tered during the last years sit at 42% [10]. Acuteaortic thrombosis can also be caused by aortic dis-section. In the experience of Cambria et al. [12], 10of 325 patients with acute aortic dissection requiredurgent aortic replacement or fenestration becauseof acute aortic occlusion. The mechanism of thisaortic obstruction is based on the propagation ofthe intimal layer until the aortic bifurcation withcompression of the true lumen by the false lumen(dynamic obstruction). This mechanism rarely oc-curs because the dissection usually extends in a uni-lateral fashion, or bilateral and asymmetrical, in oneor two common iliac arteries.

Arterial trauma is a rare cause of aortic occlusion,in which indirect localized dissection is the mecha-nism. Seatbelt compression is a known cause of mul-tiple intra-abdominal lesions, however, abdominalaortic lesions rarely occur. In general, traumatic aor-tic injury affects the thoracic aorta in 95% and theabdominal aorta in 5% of cases [13]. The ischemicsigns are immediately severe and associated intra-abdominal lesions can deteriorate the prognosis,latrogenic traumatic injuries are particularly causedby intra-aortic balloon pumps [14] or complex en-dovascular procedures, as applied in cases of com-plicated aortic dissections [15]. Aortic thrombosescan also be induced by hypercoagulability syn-dromes. These syndromes mainly cause venousthromboses, but if arterial complications occur theprognosis is poor [4]. The clinical manifestationsof aortic thrombosis in patients with nephrotic syn-drome are dramatic, as reported by Imamura et al.[16]. Szychta et al. described ulcerative colitis as aresult of acute aortic thrombosis [17]. Finally, lupusanticoagulants are associated with aorto-iliac occlu-sions and smaller caliber arteries [18,19]. Recently,DiCenta et al. [20] described a case of infrarenalaortic occlusion associated with inferior vena cavaocclusion in a patient with circulating anticoagu-lants. Several pathologic states can be identified,including heparin-induced thrombopenia, anti-thrombin III, protein C, and protein S deficits. It

is therefore necessary, in case of acute aortic occlu-sion, to fully investigate the coagulation parame-ters because coagulation disorders require imme-diate treatment in order to prevent recurrences.

Additional investigations

Duplex scanning of the lower limbs does not pro-vide additional information to that found duringphysical examination. However, the techniquemight identify involvement of one or more visceralarteries, realizing that obesity or abdominal mete-orism can limit its sensitivity. Furthermore, duplexscanning is technician dependant.

Arteriography comprising aortography and arte-riography of the lower limbs is debatable. In theolder publications arteriography was recommendedas a standard technique. There are indeed severalarguments to justify this technique. It provides aperfect diagnosis and allows accurate delineationof the proximal extension of the occlusion and thestatus of the renal arteries, as well as the distal out-flow [3]. Noteworthy to mention is the advantageof an injection in the ascending aorta which oftenallows better and earlier visualization of the lowerlimb arteries via the internal mammary and epi-gastric arteries. In case of embolization, arterio-graphy might depict emboli in other regions likethe superior mesenteric and renal arteries in par-ticular but also emboli resulting from thrombusfragmentation at an arterial bifurcation, leading toa secondary shower of emboli affecting the femoral,popliteal and crural arteries. This is a relative advan-tage because in these ill patients the femoral bifur-cation can be visualized on the initial angiographyand the distal outflow can be assessed by intra-oper-ative angiography. The disadvantages of arteriogra-phy include deterioration of renal function, delayof revascularization and the fact that it hardly mod-ifies the surgical strategy, except in visceral involve-ment and aortic dissection [1,21]. CT scanning ishardly cited in the literature, probably because themajority 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 tho-raco-abdominal aorta and its main visceral branches.It might also depict the cardiac cavities in the searchfor thrombus formation. Magnetic resonance imag-ing has not been applied in acute aortic occlusion

_51


52

because of its limited availability and less maneu-verability in acute settings. If a cardiac embolicsource is suspected, echocardiography should beperformed to identify valvular disease or dyskineticventricular areas due to ischemic cardiopathy. Re-sidual intracardiac thrombus mass is rarely diag-nosed but is an argument for adequate and pro-longed anticoagulation treatment in order to limitthe risk of embolic recurrences [22].

Treatment

The medical treatment is similar to the manage-ment of severe acute ischemia of the lower limbs.Intravenous heparin starts with a dose of 2 000 to3 000 IU, followed by continuous infusion of 300to 400 lU/kg per 24 hours, frequently controlledwith blood samples.

The role of thrombolysis is poorly defined, but itis not applicable in acute cases in which immediatesurgical revascularization is required. However, itmight be considered as a first attempt in patientspresenting with a subacute clinical picture. Throm-bolysis can re-open at least one iliac axis, followed byan additional endovascular procedure such as throm-bectomy and angioplasty [23]. At present, however,the experience with this method remains anecdotal[24]. This technique will be most effective in hyper-coagulability disorders but, in severe ischemia as-sociated with absence of collaterals and thrombosesin the microcirculation, its applicability will be lim-ited by the duration of the procedure.

Surgery remains the predominant treatment toguarantee a revascularization as fast as possible. Theurgency is even more obvious if neurologic deficitsare present, indicating severe ischemia. If renal ormesenteric artery involvement is suspected, laparo-tomy is required in order to restore patency bymeans of thrombectomy or direct embolectomy.Bypass surgery can be performed if proximal ath-erosclerotic lesions are present in these arteries.

In general, a large surgical field is prepared,including the abdomen, both groins and at leastone axilla. The first strategy is generally a retro-grade bilateral thrombectomy, which might be suc-cessful in embolization of the aortic bifurcation.Completion angiography of both legs delineatespatency of the distal arteries and might indicate theneed for additional embolectomy.

In thromboses of diseased arteries this techniqueis not effective and revascularization by means of

bypass grafting is required. A classic procedure toperform in case of failed thrombectomy is an axil-lobifemoral bypass, especially in order to reducethe risks associated with laparotomy [25]. Actually,the choice between a direct revascularization via ab-dominal access or indirect extra-anatomical bypassbasically depends on age and general condition ofthe patient [4,26]. Emergency direct revasculariza-tion seems to offer remarkable results [27]. Extra-anatomical grafts are indicated in older patientswith or without cardiac insufficiency. Intra-arterialblood pressure measurement and insertion of aSwann-Ganz catheter are recommended.

Acute aortic occlusion associated with severeischemia can induce significant metabolic disordersduring and after revascularization due to reperfu-sion of substantial tissue areas. These disorders cancause major complications in one or two legs: neu-rologic sequelae, compartment syndrome, extensivemuscular necrosis leading to amputation or reper-fusion injury with multiple organ failure and sub-sequent death. Controlled limb reperfusion [28,29]and systematic fasciotomies are recommended. Itseems logical that, in the near future, these extre-mely ill patients will benefit from these controlledreperfusion methods to reduce the associated mor-bidity and mortality [30].

Babu et al. [4] have analyzed the main factorsthat determine clinical outcome. Bad left ventricu-lar function is a major risk factor since mortality inthese patients was 85% as compared to 23% inpatients with an adequate left ventricular. Hyper-coagulability disorders are also associated with animpressive mortality of 83%. Other risk factors forpoor prognosis include suprarenal thrombosis, dis-tal obstructive disease and direct onset extremelysevere ischemia. However, neurologic deficit due tospinal cord ischemia is not a poor prognostic riskfactor because all cases normalized after revascu-larization. Therefore, neurologic deficit is not acontra-indication, but rather an indication forprompt revascularization.

Conclusion

Acute abdominal aortic occlusion is a rare phe-nomenon and is associated with an overall mortal-ity of approximately 50%, mainly due to thecomorbidity in the majority of patients such as car-diac pathology and extensive vascular disease of

ACUTE ABDOMINAL AORTIC OCCLUSION

which the aortic occlusion is the final event. Mis-leading neurologic symptoms can occur in 30%, inwhich absence of femoral pulses should indicate car-diovascular 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 con-trolled reperfusion should be implemented in thesurgical protocol in order to limit compartment syn-dromes and the general consequences of revascu-larization. By means of such an integrated strategy,the morbidity and mortality of this severe diseasecan be reduced.

R E F E R E N C E S

1 Verrier C, Bertrand P, Mercier C, Piquet P. Occlusion aigue ducarrefour aortique. In: Kieffer E (ed). Urgences vasculaires nontmumatiques. Paris, AERCV, 1998: pp 373-381.

2 Mozingo J, Denton 1C Jr. The neurological deficit associatedwith sudden occlusion of the abdominal aorta due to blunttrauma. 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-factorsthat influence outcome. / Vase Surg 1995; 21: 567-575.

5 Surowiec SM, Isiklar H, Sreeram S et al. Acute occlusion of theabdominal aorta. Am J Surg 1998; 176: 193-197.

6 Kao CL, Chang JP. Abdominal aortic occlusion: a rare compli-cation of cardiac myxoma. Tex Heart /ntf/2001; 28: 324-325.

7 Favre JP, Gay JL, Gournier JP, Barral X. Acute occlusions ofthe aorta. / Chir 1995; 132: 7-12.

8 Shumacker H. Surgical treatment of aortic aneurysms. PostgradAM1959; 25:535-548.

9 Jannetta P, Roberts B. Sudden complete thrombosis of an aneur-ysm of the abdominal aorta. NEnglJMed 1961; 264: 434-436.

10 Hirose H, Takagi M, Hashiyada H et al. Acute occlusion of anabdominal aortic aneurysm-case report and review of the lit-erature. Angiology 2000; 51: 515-523.

11 Schwartz RA, Nichols WK, Silver D. Is thrombosis of the infra-renal abdominal aortic aneurysm an acceptable alternative?J Vase Surg 1986; 3: 448-455.

12 Cambria RP, Brewster DC, Gertler J et al. Vascular complicationsassociated with spontaneous aortic dissection. / Vase Surg 1988;7: 199-209.

13 Dajee H, Richardson IW, type MO. Seat belt aorta: acute dis-section and thrombosis of the abdominal aorta. Surgery 1979;85: 263-267.

14 Sakakibara Y, Sasaki A, Nakata H et al. Acute aortic thrombo-sis after intra-aortic balloon pumping. Jpn J Thorac CardiovascSwg2000;48: 123-125.

15 Lookstein RA, Mitty H, Falk A et al. Aortic intimal dehiscence:a complication of percutaneous balloon fenestration for aorticdissection. / 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 JinzoGakkat Shi 2001; 43: 608-612.

17 Szychta P, Reix T, Sevestre MA et al. Aortic thrombosis andulcerative colitis. Ann Vase Swrg-2001; 15: 402-404.

18 Setoguchi M, Fujishima Y, Abe I et al. Aorto-iliac occlusion asso-ciated with the lupus anticoagulant. Report of two cases. Angi-ology 1997; 48: 359-364.

19 Komori K, Okadome K, Onohara T et al. High aortic occlu-sion 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 andinferior 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 aor-tic occlusions. J Mai Vase 1996; 21: 133-135.

24 Cunningham M, May S, Tucker W, Gerlock A. Response of anabdominal aortic thrombosic occlusion to local low-dose strep-tokinase therapy. Surgery 1983; 93: 541-544.

25 Drager SB, Riles TS, Imparato AM. Management of acute aor-tic occlusion. Aw/Swig 1979; 138: 293-295.

26 Meagher AP, Lord RS, Graham AR, Hill DA. Acute aortic occlu-sion presenting with lower limb paralysis. J Cardiovasc Surg 1991;32: 643-647.

27 Bradbury AW, Stonebridge PA, John TG et al. Acute thrombo-sis of the non-aneurysmal abdominal aorta. EurJ Vase Surg 1993;7: 320-323.

28 Schlensak C, Doenst T, Bitu-Moreno J, Beyersdorf F. Controlledlimb reperfusion with a simplified perfusion system. Thorac Car-diovasc Surg 2000; 48: 274-278.

29 Vogt PR, von Segesser LK, Fagotto E et al. Simplified, control-led limb reperfusion and simultaneous revascularization foracute aortic occlusion. / Vase Surg 1996; 23: 730-733.

30 Julia P, Fabiani JN. Ischemia-reperfusion and compartmentsyndrome. In: Branchereau A.Jacobs M (eds). Complicationsin vascular and endovascular surgery (part II). Armonk, FuturaPublishing Company, 2002: pp 11-21.

5_53

6HAS MORTALITY RATE FOR RUPTURED

ABDOMINAL AORTIC ANEURYSMCHANGED OVER THE LAST 50 YEARS?

JACK COLLIN

Annual rates of abdominal aortic aneurysm (AAA) rupture continue to increase with theageing of populations throughout the developed world (Figure). Deaths from AAA representthe rates of tobacco smoking over the previous 60 years. Only a third of patients with rupturedAAA have emergency surgery, and operative mortality is around 50%. Intra-operativemortality rates have not changed for a generation but postoperative mortality rates havedecreased by 3.5% per decade with improved management of organ failure. Most patientswith AAA rupture die without surgery. Consequently, small improvements in operativemortality have negligible impact on overall AAA mortality. In the short term early detectionof AAA by population screening and elective repair of aneurysms greater than 55 mmdiameter offer the best chance to reduce AAA mortality. In the long term current low rates oftobacco smoking among the higher socio-economic groups of North America and Europepresage the progressive disappearance of AAA as a major cause of premature death.

55

National statistical data

AAA is a disease of the elderly. Rupture of anAAA is uncommon in men under age 55 years orwomen younger than 60 years. It becomes increas-ingly common with advancing age. The incidenceof death from AAA as a percentage of all deathspeaks in men aged between 70 and 75 years. There

is, however, no peak in the incidence of deaths fromAAA per thousand at risk with increasing age. Theolder the cohort studied, the more deaths fromAAA are seen to occur per thousand at risk [1].

The relative risk of death from AAA is 10 timesgreater in men than in women at age of 60 years.Among those who survive into their late 80s, menare only three times more likely to die from AAA


56

than women of the same age. Since among the veryelderly, women outnumber men by more thanthree to one, the false perception has sometimesarisen that the disease is more common in elderlywomen than men. Throughout the developedworld the proportion of elderly men and womenin the population has been increasing since theagricultural revolution. In the United Kingdom,data from the 2001 census show that for the firsttime in history those over 65 years of age are morenumerous than those under 16 years. In additionto being old and male, in order to be at high riskof developing an AAA it is necessary to have smokeda substantial quantity of tobacco over a number ofyears. To be at high risk of AAA rupture, a patientwith a known AAA should be a current smoker withpoorly controlled hypertension [2]. In Europe, ciga-rette smoking became increasingly common in menduring and after the First World War of 1914 to1918. European women began to smoke in largenumbers from the Second World War (1939 to1945) onward. In Northern Europe and North Ame-rica, smoking rates among adult males have beenslowly declining for the last 30 years, particularly inthe higher socio-economic groups, but smokingrates among women have increased.

With all the above information in mind, it comesas no surprise to discover that over the last 20 yearsdeaths from AAA in the United Kingdom have con-tinued to increase [3]. Unless cigarette smoking sig-nificantly declines as a European addiction, there aresound reasons to predict that the number of patientspresenting with AAA will continue to increase.

Has electiveAAA surgery reduced

overall AAA mortality?

Data from the United Kingdom MulticentreAbdominal Aortic Aneurysm Screening Study(MASS) [4] have shown that for patients with AAAdiameters greater than 55 mm measured by ultra-sonography, the number needed to treat (NNT)with elective AAA repair to prevent one death fromAAA over the following four years is five. Forpatients with AAA diameters of 50 to 55 mm, theNNT is unknown but likely to be at best very sub-stantially larger. At worst it may be replaced by anumber needed to harm (NNH).

The United Kingdom Small Aneurysm Trial [5]showed that patients with AAA antero-posteriordiameters of 40 to 54 mm measured by ultrasono-graphy randomized to elective surgical treatmentwere more likely to die from an AAA-related causethan those randomized to best medical treatment.Not surprisingly, after elective surgery fewer deathsoccurred from AAA rupture but the number of rup-ture deaths prevented was exceeded by the num-ber of operative deaths from elective AAA repair. Itis clearly inadequate to use death rates from rup-tured AAA alone as the measure of successful man-agement of AAA. Scrutiny of death certification inthe MASS study revealed that for many patients whodied within 30 days of elective surgery, AAA was notmentioned as a cause of death and was not there-fore recorded in national statistics.

HAS MORTALITY RATE FOR RUPTURED AAA CHANGED OVER THE LAST 50 YEARS?

Present evidence supports the conclusion that forpatients with AAA diameter less than 55 mm, elec-tive AAA repair is likely to do more harm thangood. Until the publication of data from the SmallAneurysm Trial, it had become common to per-form elective repair on AAAs of modest size. Thecurrent fashion for transluminal graft insertion hasensured that many patients at low risk of AAA rup-ture continue to have surgical treatment for smallAAAs. The advocates for these internal fashionaccessories justify their enthusiasm by claims thatthe risks of insertion are low and that they protectthe wearer from subsequent AAA rupture. Neitherclaim currently withstands evidence-based analysis.

What treatment do patientswith ruptured AAA receive?

For practical purposes without surgical repair,rupture of an AAA has a mortality of 100%.Whether death occurs within minutes, hours, ordays is determined by the site of rupture and thestrength of the peri-aortic retroperitoneal connec-tive tissue. Anterior free rupture into the peritonealcavity results in exsanguination within minutes.Posterior or lateral contained rupture permitstransportation of the patient to a hospital. If thepatient is fortunate, the hospital will have a vascu-lar surgeon available who can perform emergencyAAA repair. If the patient is unfortunate, interhos-pital transfer will have to be arranged if judged tobe appropriate. Finally, both the patient and thevascular surgeon need to agree that an attempt torepair the AAA rupture is sensible and worthwhile.

Fewer than 50% of patients with AAA rupturehave sufficient initial containment of hemorrhageto survive long enough to reach the hospital alive.Those who do are further reduced in number bydelayed diagnosis, unnecessary diagnostic imaging,lack of a vascular surgeon, dilatory transfer arrange-ments, patient choice, and clinical selection basedon age, coexistent disease, and estimated proba-bility of operative survival. Overall, around onethird of patients who have AAA rupture currentlyundergo an operation for its attempted repair. Inindividual hospitals, operation rates on those admit-ted range from less than 50% to almost 100%.

Patel et al. [6] have shown that ruptured AAArepair is cost-effective provided the operative mor-

tality is less than 85%. It is likely therefore thatsome reduction in overall mortality from rupturedAAA could be achieved by better access to special-ist vascular surgical services.

Most published data on AAA mortality are diffi-cult to interpret. Clarity is obscured by misuse andinappropriate interchange of the distinctly differ-ent terms peri-operative, peroperative (intra-opera-tive), and postoperative. Additional fog is createdby often-deliberate confusion of emergency andeven urgent AAA surgery with repair of rupturedAAA. Bown et al. [7] have made a valiant attemptto penetrate this obfuscation with a recent meta-analysis of 171 articles covering 50 years of rup-tured AAA surgery. They have shown that afterallowance for publication bias, the intra-operativemortality for ruptured AAA surgery has remainedconstant at 20%. They deduce that when analysisof retrospective data from individual institutionsreveal a high intra-operative mortality rate, authorstend not to report it but instead disclose only theoverall 30-day operative or in-hospital mortality.

Operative mortality for urgent or emergencyoperations undertaken in the belief that an AAAhas ruptured or is about to rupture (acute AAA sur-gery) is around a third of that for ruptured AAAsurgery and three times that for elective AAA repair.Inclusion of acute AAA surgical data with that forruptured AAA has the remarkable property ofimproving the operative mortality figures for bothelective and ruptured AAA surgery.

In the author's experience, local audit of dataoften reveals large differences in intra-operative mor-tality rates between individual surgeons. Part of thedifference can be explained by the relative wil-lingness or reluctance of different surgeons to oper-ate on moribund patients with little or no chanceof survival. Operative technique and skill play anadditional part.

Surgery for ruptured AAA is difficult and unfor-giving of inexperience or carelessness. The mostimportant principle underlying success is to lose aslittle blood as possible during the operation addi-tional to that which has already and inevitably beenlost to the circulation by pre-operative bleeding.The common causes of unnecessary pre-operativeblood loss are listed in the Table. Most intra-oper-ative deaths tend to be attributed to a cardiac cause,which has the advantage of making the surgeonfeel better. The reality is different. In almost allcases, the proximate cause of the myocardialischemia and resultant arrhythmia, asystole, or

57


58

1 Failure to occlude the neck of the AAA beforeincising the posterior peritoneum.

2 Injury to renal, gonadal or adrenal veins byblind clamping of the AAA neck.

3 Injury to iliac veins by unnecessary dissectionbehind the common iliac arteries.

4 Delayed recognition of aorto-caval fistula.

5 Inadequate control of inferior mesenteric, lum-bar and median sacral arteries.

6 Heparin administration to a patient alreadyfully anticoagulated by massive blood loss andhypothermia.

7 Reperfusion back-bleeding through alreadyoversewn common iliac artery origins.

8 Closure of the abdomen before coagulationhas been restored by administration of freshfrozen plasma, platelets, cryoprecipitate andrewarming.

pump failure is blood loss and inadequate bloodreplacement.

The learning curve for successful repair of rup-tured AAA is long for this most difficult of vascularsurgical operations. In major tertiary referral cen-ters in the US, ruptured AAA may represent as lit-tle as 5% of all AAA operations performed [8,9].In the United Kingdom in some regional vascularcenters [10], they account for more than 50% ofall AAA operations. Most surgeons currently oper-ating on patients with ruptured AAA perform fewerthan five such operations per annum. Even in majorreferral centers, few individual surgeons operate onmore than 10 patients with ruptured AAA each year.In such circumstances it is no surprise that intra-operative mortality remains around 20% as it hasdone since the early days of the operation fifty yearsago. It is improbable that intra-operative mortalityrates will improve in the foreseeable future.

Postoperative mortalityafter ruptured AAA repair

In contrast to intra-operative surgical skill-basedmortality there is evidence that postoperative30-day mortality has progressively fallen by approx-imately 3.5% per decade [7]. This steady fall inpostoperative death rates is attributable to the de-velopment of the specialty of intensive care medi-cine and improvements in the management oforgan failure. Numerous authors have attemptedto devise predictive scoring systems for postopera-tive death based on both pre-operative and earlypostoperative evaluation of the function of differ-ent organ systems [11-13].

In order of relative importance, survival is deter-mined by control of cardiac, respiratory, renal, andhepatic failure. To date, most success has beenachieved by expert management of renal and car-diac failure and least impact has been made ondeaths from hepatic and respiratory failure. It isnow unusual for a patient to succumb from renalfailure alone without coexistent failure of at leastone 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 for30 days postoperatively who have little if anyprospect of independent survival. It is certainly thecase that beyond five days intensive care the ruleof diminishing returns begins to apply. Few pa-tients who are not fit for discharge from an inten-sive care unit five days after surgery will ultimatelyleave the hospital alive. With healthcare systemsaround the world in financial crisis, the cost effec-tiveness of long-term intensive care is increasinglybeing challenged.

Overall mortalityfor ruptured AAA

At present only a third of patients who rupturean AAA will have an operation. Thirty-day operativemortality rates are around 50%, with wide varia-tions in reported rates from different centers. Twofifths of all operative deaths occur during the op-eration and intra-operative mortality has remainedunchanged for decades. It is reassuring to learnthat 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 overallmortality from ruptured AAA remains stubbornlybetween 80% and 85%. The apparent 3.5% re-duction per decade in postoperative mortality attri-butable to the growth of the expensive and labor-intensive specialty of intensive care medicine hashad a negligible and undetectable effect on AAAmortality statistics.

Can AAAmortality be reduced?

Beyond any shadow of doubt, the most impor-tant factor underlying the current high incidenceof death from AAA was the 20th century pheno-menon of cigarette smoking by at its peak up to75% of the adult male population. Primary pre-vention of this disease is likely to be much moreeffective than any imaginable cure. Fashions inhuman habits and addictions change and the emo-tional props of one century are prone to disappearin the next as quickly as they appeared in the last.

The most hopeful sign that tobacco smoking inthe developed world may be in terminal decline isthat it has now been largely abandoned by thetrend-setting intellectual elite of Northern Europeand North America. Target growth areas for tobac-co sales are now largely third world countries.

Secondary prevention is directed at reducing therisk of AAA rupture in those who already have thedisease. The proven interventions are smoking ces-sation and control of hypertension. Specific thera-pies with drugs to reduce growth rates of AAA atpresent are unproven.

Recently the United Kingdom MASS study [4]established the value of a screening program forAAA detection in men aged 65 to 74 years. Elec-tive surgical repair of AAAs with a diameter greaterthan 55 mm reduces the incidence of death fromAAA-related causes, although all cause mortality isnot affected. It is probable that current AAA-spe-cific mortality could be reduced by restricting elec-tive AAA surgery to those patients with AAAantero-posterior diameters measured by ultra-sonography 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 inpatients kept under ultrasound surveillance. United King-dom 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. TheMulticentre Aneurysm Screening Study (MASS) into the effectof abdominal aortic aneurysm screening on mortality in men: arandomised controlled trial. Lancet m% 360:1531-1539.

5 Anonymous. The United Kingdom Small Aneurysm TrialParticipants. Mortality results for randomised controlled trial ofearly elective surgery or ultrasonographic surveillance for smallabdominal aortic aneurysms. Lancet 1998; 352:1649-1655.

6 Patel ST, Korn P, Haser PB et al. The cost-effectiveness ofrepairing ruptured abdominal aortic aneurysms. / Vase Surg2000:32;247-257.

7 Bown MJ, Sutton AJ, Bell PRF, Savers RD. A meta-analysis of

50 years of ruptured abdominal aortic aneurysm repair. Br JSurg 2002; 89: 71 4 -730.

8 Cooley DA, Carmichael MJ. Abdominal aortic aneurysm.

59

9 Lawrie GM, Morris GC Jr, Crawford ES et al. Improved results ofoperation for ruptured abdominal aortic aneurysms. Surgery1979: 85; 483 -488.

10 Collin J, Murie J, Morris PJ. Two year prospective analysis of theOxford experience with surgical treatment of abdominal aorticaneurysm. Surg Gymcol Obstet 1989: 169; 527-531.

11 Davies MJ, Murphy WG, Murie JA et al. Pre-operative coagu-lopathy in ruptured abdominal aortic aneurysm predicts pooroutcome, fir/ Swrg 1993; 80: 974-976.

12 Meesters RC, van der Graaf Y, Vos A, Eikelboom BC. Rupturedaortic aneurysm: early postoperative prediction of mortalityusing an organ system failure score. 5r/Swrgl994; 81: 512-516.

13 Brady AR, Fowkes FG, Greenhalgh RM et al. Risk factors forpostoperative death following elective surgical repair of abdo-minal aortic aneurysm: results from the United Kingdom SmallAneurysm Trial. On behalf of the United Kingdom SmallAneurysm Trial participants, fir/ Surg 2000; 87: 742-749.

7RUPTURED AAA:

SHOULD ENDOVASCULAR TREATMENTBE THE FIRST CHOICE?

JAAP BUTH, NOUD PEPPELENBOSCH, NEVAL YILMAZPHILIPPE CUYPERS, LUCIEN DUIJM, ALEXANDER TIELBEEK

Rupture of an abdominal aortic aneurysm (AAA) remains lethal despite rapid prehospitaltransport, early diagnosis and resuscitations, expeditious surgical repair and progress inanesthesia and intensive care. Mortality rates remain between 32% and 70% withsignificant associated morbidity [1-5]. Most centers quote rates near 50 % [6-8]. These highoperative mortality rates reflect the magnitude of the physiologic stress of patients followingrupture. Hemorrhage, prolonged hypotension, laparotomy and prolonged lower limb ischemiabecause of aortic clamping all contribute to the risk of cardiac complications, multiple organfailure and death. In addition, the patients are usually elderly and often have pre-existingcomorbidities.

Hypotension following rupture is often controlled at first by tamponade within theretroperitoneum, but the relaxation of the abdominal tone at induction of general anesthesiaoften precipitates cardiovascular collapse. Exposure of the neck of the aneurysm together withthe dissection through the hematoma causes disruption of retroperitoneal veins and smallarteries, resulting in further hemorrhage that is often difficult to control in coagulopathicpatients. In the presence of large retroperitoneal hematoma, the aorta is frequently clamped atthe supraceliac segment. This renders the viscera and lower extremities ischemic, whichcontributes to the establishment of a fibrinolytic state [9,10] and has a dramatic effect oncardiac afterload and lactic acid production. Subsequent reperfusion of the lower limbs addsfurther physiologic injury. Secondary bleeding episodes and other complications such as renalfailure, adult respiratory distress syndrome, and colonic and gallbladder ischemia areultimately responsible for most of the deaths.


The excessive operative mortality also has important resource implications since mostpatients will spend many days in the intensive care unit before finally succumbing to thecomplications of rupture and emergency surgery [11]. In general,, patients who undergo opensurgery represent a relatively favorable subset, as a considerable number are not operated atall because of significant comorbid factors. These patients inevitably will die without asurgical option [12].

62

Endovascular approach

Endovascular repair of ruptured AAA (rAAA)offers the possibility of a significant reduction inoperative mortality. This approach relies on theintravascular deployment of an aortic stent graft,introduced via the femoral arteries to exclude theaneurysm from the circulation [13,14]. Laparotomyis avoided and the procedure can be performedunder local anesthesia. It is likely that the risk ofturning a contained rupture into intraperitonealhemorrhage by the induction of general anesthe-sia would be significantly reduced. Additional bloodloss due to opening of the retroperitoneal hema-toma is avoided, while prolonged infra- or supra-renal aortic clamping is not necessary. Additionally,cardiac stress and duration of lower limb ischemiawill be minimized.

There is no ample evidence that endovascularaortic repair (EVAR) is technically feasible and safein patients scheduled for elective AAA repair [15-18]. In this chapter we will describe the results ofa consecutive cohort study, comparing the impactof a protocol of preferential management by EVAR.The study group includes patients who were mostly,but not all, treated by EVAR. The study group willbe compared with a historical control group con-sisting of patients treated routinely by open surgeryfor symptomatic or ruptured AAA (rAAA).

Methods

From May 2001 onward, patients with sympto-matic nonruptured AAA (snrAAA) and rAAA ofthe abdominal aorta presenting at the CatharinaHospital in Eindhoven were treated according to awell-defined management protocol involving intent-to-treat by emergency (e)-EVAR. Patients were con-sidered symptomatic nonruptured AAA if there were

no signs of hemorrhage outside the wall of theaneurysm on computed tomography (CT), but theyhad acute pain in the abdomen and an abdominalaneurysm that was painful at palpation. Aneurysmswere defined ruptured AAA if there was extravasa-tion of blood surrounding the aneurysm at CTexamination. In patients who did not undergo CTexamination, a retroperitoneal hematoma at opensurgery was the criterion for rupture of the aneur-ysm. Within the study period, all patients who werereferred to our hospital with a symptomatic aneur-ysm of the abdominal aorta were prospectively ana-lyzed and included in this study.

On arrival in the emergency ward, the intra-venous fluid infusion rate was minimized. The pro-tocol dictated that patients were taken to theradiology department for emergency CT examina-tion with intravenous contrast infusion to opacitythe aorta. An exception was made for patients inprofound shock or those who had a cardiac arrestduring transportation to the hospital. Diameter andlength of the infrarenal neck of the aneurysm weremeasured and the decision whether endovascularrepair was feasible was taken and communicatedwith the operating room staff. Exclusion criteria fore-EVAR were a short neck (less than 10 mm length),a wide neck (more than 30 mm in diameter), andinaccessible iliac arteries. Following CT examina-tion, patients were quickly transported to the oper-ating room for the selected emergency procedure,or taken to the intensive care unit (ICU) for fur-ther optimization (only in snrAAA). Patients withrupture of their aneurysm were preferentiallytreated with an aorto-uni-iliac (AUI) endograft(Fig. 1) combined with a crossover bypass.

The study group described above was comparedwith a control group of patients with symptomaticaneurysms, who were treated by open procedure,between January 1999 and May 2001. This histori-cal control group was retrospectively analyzed byhospital 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 ofproximal component of AUI device C - Intra-operative angiogram demonstrating bilateral iliac arteries D - PostoperativeCT examination demonstrating functioning AUI device with complete exclusion of the aneurysm.


were compared included: 30-day or in-hospitalmortality, morbidity, length of hospital and ICUstay, intra-operative blood loss, requirement ofblood products and overall fluid infusion duringoperation.

Statistical analysis was performed using SPSS® forWindows® version 9.0. Chi-square and Fisher testswere used for the comparison of discrete variablesand the Mann-Whitney test was used for continu-ous variables. Continuous variables are presentedas the mean range. A p value of smaller than 0.05was considered significant.

ResultsPATIENTS

From May 2001 until June 2002, 40 consecutive pa-tients in the study group were admitted and treatedin our hospital because of a ruptured or sympto-matic 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 conventionalopen surgery (COS [conventional open surgery]subgroup, Table II). While there was a trend that

a/ , //• ; Mean age SnrAAA/ Mean Systolic r ,. n ,Male/female , v A A A ^ . , ,, -.^ u Laraiac events Pulmonary events'J (range) rAAA 0 AAA <100mmHg N i%} N %}_ Years N (range) cm N (%) ^ ( / o ) ^ ( / c )

Group IStudy group(40 patients)

34/6 73.0 14/26 7.0 16 (40) 12 (30) 7 (18)(56.8-90.0) (3.6-10.0)

64

Group nControl group 22/6(28 patients)

73.2 6/22 7.5 14 (56) 9 (32) 6 (21)(58.1-86.7) (4.0-10.5)

Of IN I (40 PATMS)

Male/femaleN

Mean age(range)

Years

SnrAAA/rAAA

N

Mean0AAA

(range) cm

Systolic-JOOmrnHgN (%}

Cardiac events Pulmonary eventsN (%) N (%)

Subgroup withEVAR(26 patients)

23/3 74.1(56.8 - 90.0)

10/16 6.7(3.6-8.8)

(31) (31) 6 (23)

Subgroup withCOS(14 patients)

11/3 71.0(58.2 - 80.9)

4/10 7.7(5.0-0.0)

8 (57) 4 (29) 1 (7)

COS: conventional open surgeryEVAR: endovascular abdominal aortic aneurysm repairrAAA: ruptured abdominal aortic aneurysmSnrAAA: symptomatic nonruptured abdominal aortic aneurysm


patients in the conventional group were hemody-namically less stable and had larger aneurysms,these group differences in patient characteristicswere not significant (Table II). The control groupwith routine open repair consisted of 28 patientstreated between January 1999 and April 2001(Group II). Six patients in this group had ansnrAAA and 22 an rAAA (Table I). There were nosignificant differences with regard to patient char-acteristics, presence of pre-operative shock, or pre-vious cardiac and/or pulmonary events betweengroups I and II.

In the study group, 33 (83%) patients underwentemergency CT scanning. Seven patients did notundergo CT scanning, three in the EVAR and fourin the COS subgroup. Reasons for not performinga CT scan were profound hypovolemic shock (intwo patients) and logistical reasons in five patients.The mean neck length was significantly longer in

EVAR compared with COS, 18.0 (6 - 36) mm and7.5 (0-15) mm, respectively (p = 0.004). The neckdiameter in the two subgroups was not statisticallydifferent, at 23.8 (17-33) and 27.8 (20-34) mm inEVAR and COS, respectively.

APPLICABILITY OF E-EVAREVAR was performed in 26 of the 40 patients in

the study group. Reasons for COS were unavailableendovascular specialists in six patients and unsuit-able anatomical (dimensions of the infrarenalneck) or technical (profound hypovolemia) reasonsin eight patients. Thus, the feasibility of EVAR basedon an acceptable aortoiliac anatomy and hemody-namicswas80% (32/40).

PROCEDURAL DETAILSThe intra-operative and hospital aspects in groups

I and II are summarized in Table III. In the EVAR

Study group (40 patients)Total EVAR COS

(40 patients) (26 patients) (14 patients)

Mean operation time (range) - Minutes

Anesthesia - NumberLocalRegional

General

Technique performed - NumberTubeBifurcatedAUI + crossover

Mean blood loss (range) - Ml

Mean fluid infusion (range) - Ml

ICU stay (range) - Hours

Hospital stay (range) - Days

1550 - 270)

158

17

154(80 - 270)

15

155(90 - 240)

14

111019

1800(100-6000)*

6600(1 500 - 20 500)

81(0 - 408)

12.3(0 - 60)

2519

1100(100 - 2 500)

4700(1 500 - 12 500)

46(0 - 220)

7.2(0-21)

95-

2600(500 - 6 000)

104 000(3 400 - 20 500)*

154(12 - 408)

22.1(1-60)

Control group(28 patients)

176(100-240)

217

3900(300-12000)

9000(5 000 -13 700)

122(11-864)

13.0(0 - 59)

65

*p<0.01**p<0.004 number indicates patients unless stated otherwiseAUI: aorta-uni-iliac deviceCOS: conventional open surgeryEVAR: endovascular abdominal aortic aneurysm repair


subgroup, no conversions to open surgery wererequired. Most often an AUI device was used incombination with a femorofemoral cross-over bypass(19 patients). Two patients received a tube endo-graft and five received a bifurcated stent graft. Ofthe patients who received a bifurcated stent graft,two patients had an snrAAA. In 88% of the casesin the EVAR subgroup, either local (in 15 patients)or regional (in 8 patients) anesthesia was used. Twopatients with an snrAAA and one with an rAAAreceived general anesthesia. The patient with rup-tured aneurysm was in deep hypovolemic shock atarrival in the hospital. The responsible anesthesiol-ogists felt that in this patient a more rapid controlof the hemodynamic situation might be obtainedby general anesthesia. Mean operation time was 155(80 to 270) minutes in group I, and 176 (100 to240) in group II, which was not a significant dif-ference. Mean blood loss in group I was 1 800 (100to 6 000) mL, and in group II 3 900 (300 to 12 000).This difference was statistically significant (p = 0.01).In addition, there was a significant difference be-

tween groups I and II with regard to total fluid infu-sion (blood components, fresh frozen plasma, andcrystalloids combined; p = 0.0040). Administrationof blood components was comparable in the twogroups.

PERI-OPERATIVE MORBIDITYAND MORTALITY

The hospital and ICU stay in the study groupand control group was not statistically different(Table III). The peri-operative mortality rate in thestudy group with preferential EVAR was significantlylower than in group II: 20% and 43%, respectively(p = 0.043) (Table IV). If only patients with rup-ture of their aneurysms were considered, the mor-tality rate in group I was 31% and in group II 50%.This difference did not reach the level of statisti-cal significance (p = 0.10). Causes of death includedcontinued bleeding, cardiac failure, multiorgan fail-ure, respiratory insufficiency and bowel ischemia.The latter constituted 50% (two patients) of thecauses of death in the EVAR subgroup. The rate of

66 Study gn,«p (40 patients) Control groupTotal EVAR COS ? *

(40 patients) (26 patients) (14 patients) { Paiens)

Mortality (%)CardiacPulmonaryContinued bleedingMultiorgan failureBowel ischemia

8 (20)*

2-

2 12 12 2

12 (43)*2 2

11 21 4

3

Postoperative morbidity (% of survivors) 14 (44)**Cardiac 2 2Pulmonary 3 1Multiorgan failure 1Coagulation disorderCerebral vascular accident (CVA) 1 1Reoperation 3Wound infection/hematoma 4 4

4 (25)**

1

2

1

p = 0.04= 0.3


postoperative morbidity was higher in the studygroup than in the control group (35% versus 14%,respectively) (Table IV). However, this differencedid not reach statistical significance.

FOLLOW-UP OF PATIENTSIn the EVAR subgroup, three patients demon-

strated an endoleak during follow-up from 30 daysto 14 months: two patients had a type I endoleakand one patient a type II. The latter patient is stillunder survey and an intervention for coiling hasbeen planned. Both patients with type I endoleakrefused further intervention because of their agesof respectively 90 and 80 years. The 90-year-oldpatient has a follow-up time of 14 months and heremains without symptoms. The 80-year-old patientwas discharged from further follow-up at his ownrequest.

Follow-up was achieved in 90% of the patients inthe study group and 86% in the control group. Thepatients, with recorded follow-up data were fol-lowed in the hospitals from where they originallywere referred. The 6-month survival in group I was74% and in group II 52% (Fig. 2). The differenceof 22% already existed after the first postoperativemonth and there was no further change of this dif-ference in the subsequent follow-up period.

General considerations

Conventional open surgery has been the goldstandard for the treatment of acute symptomaticaneurysms for five decades. During this period, theperi-operative mortality and morbidity have im-proved only modestly [18]. After the successful in-troduction of elective stent graft repair of asympto-matic abdominal aneurysms [16-18], this techniquenow also becomes appealing for the treatment ofacute symptomatic aneurysms [13,14,19]. Mortalityrates in these studies range from 10% to 45%,which is promising considering the prohibitive mor-tality in open surgery. None of these studies, how-ever, was based on an intention to treat by EVARprotocol or on a consecutive patient group. Rather,patients were selected on the bases of availabilityof experienced staff and other practical aspects. Ina previous report from our group, Yilmaz et al. as-sessed the outcome in a consecutive series; howev-er patients with open procedures during the sameperiod were excluded from the analysis [20]. Thepresent study is the first in which all treated pa-tients were included, irrespective of whether themethod of aneurysm repair was by stent graft orby open technique.

FIG. 2 Life table graph of patients in the study group and in the control group. Initially existingdifference sustains during the first months of follow-up.

67


68

The present study group, consisting of patientswith EVAR and COS, understandably demonstratesless differences in pre-operative characteristics com-pared to controls undergoing surgical repair thanin our previous study. No differences in operatingtime and ICU admission time were noted betweengroups I and II. Patient selection criteria for EVARinvolve in the first place the presence of a suitableinfrarenal neck. This was apparent in the studygroup from a significantly shorter neck in the sub-group with COS compared to the subgroup withEVAR.

The use of local rather than general anesthesiamay be one of the important factors determiningthe outcome of treatment [21]. In our study group,58% received local or regional anesthesia. Thesetypes of anesthesia do not influence the tone of theabdominal wall. Relaxation of the abdominal mus-culature during general anesthesia may change acontained rupture into an intraperitoneal or freerupture, reducing the chance of survival signifi-cantly [3]. Local anesthesia has the additionaladvantage of leaving the sympathetic tone of thearterioles unchanged. Patients with rAAA usuallyare in a state of compensated shock with maximalvasoconstriction. Release of the sympathetic tone atinduction of general anesthesia may cause completecardiovascular collapse, as most of the surgeonsknow from practical experience. Reduction of bloodloss and fluid administered during operation in theEVAR subgroup are likely related to the avoidanceof general anesthesia as much as from avoidingopen surgery.

Pre-operative CT scanning on the one hand ap-pears quite useful for ascertaining whether endo-vascular treatment is feasible and for measuringanatomical dimensions. A drawback may be thetime delay until the treatment commences. In thepresent series, only two patients had blood pres-sures too low to allow an additional delay of 10 to15 minutes, which is the usual time an emergencyCT scan takes in our institution. During CT exam-ination, the operating room is prepared for theoperative procedure, making the actual time delayeven less.

The use of AUI rather than bifurcated endograftsis a matter of debate. During our institutional expe-rience, we have developed a strong preference forAUI endografts. The advantages of this device typeinclude a quick introduction and deployment,which rapidly lowers intra-aneurysmal blood pres-sure and provides control on the intra-abdominal

bleeding [22]. Only one groin needs to be exploredunder local anesthesia, which seems more easily tol-erated by the patient in emergency circumstancesthan bilateral groin exploitation. An additionaladvantage seems to be that patients with complexiliac artery anatomy can more be frequently treatedby AUI devices since only one suitable side isneeded. Nevertheless, Orend et al. and Lachat et al.used bifurcated stent grafts in their selected patientpopulation, with comparable operating times andexcellent results [21-23].

To demonstrate the impact of endograft treat-ment on the first-month mortality of acute AAArequires a carefully analysis. Simple assessment ofEVAR-treated patients will lead to skewed outcome,as patients with short necks or profound shock willhave the highest risk. It is of note that the presentstudy is also the first to demonstrate a significantdifference in first-month mortality in favor ofe-EVAR compared to conventional surgery in a com-bined group of patients with ruptured and symp-tomatic AAAs. The advantage of e-EVAR continuesduring the first postoperative months. Apparentlythere is no catch-up of mortality by delayed eventsand the favorable effect on survival seems durable.Admittedly, our present follow-up periods werestill rather short. It is of note that the incidence ofnonlethal postoperative complications in group Iwas somewhat higher than in group II. A plausibleexplanation may be that the occurrence of com-plications in the first group was assessed prospec-tively and in the latter retrospectively. Nevertheless,this finding signifies the fact that an rAAA remainsa serious condition irrespective of the type of treat-ment and, secondly, that open surgery may increasethe overall insult to a patient's condition, resultingin a higher mortality.

The present study has several flaws. First, a rela-tively small number of patients were included andthe follow-up period was short. Second, despite theintent to treat by EVAR protocol, six patients (15%)received conventional open repair because of anunavailable endovascular specialist at the time ofadmission. When these patients also would havebeen treated by EVAR, the difference in early mor-tality might have been even greater. Third and per-haps most importantly, the control group in thisstudy was retrospectively analyzed, which may influ-ence the comparability with the study group as wellas accuracy of recording of events. A large-scalemulticenter study is needed to confirm that emer-gency EVAR for acute symptomatic and ruptured


aneurysms is associated with improved survival.Once our findings are confirmed by such a study,additional evidence will be required from a ran-domized, controlled trial comparing EVAR andopen surgery for well-defined indications, distin-guishing patients with truly ruptured and sympto-matic nonruptured AAA. The importance of a trialmonitoring committee that terminates the study assoon as a statistical significant difference in ope-rative survival is obtained at regular interim analy-ses is obvious in such a randomized, controlled trial.

Late complications associated with e-EVAR in-cluded the occurrence of endoleaks. In the pres-ent study, three endoleaks (12%) of survivors werepresent after one month. Two patients had a type Iendoleak but refused further treatment; they remain

without symptoms so far. Nevertheless, in our opi-nion, these endoleaks should be treated either bythe use of a giant Palmaz stent, an aortic exten-sion endograft, or by laparoscopic banding of theaorta. The policy for type II endoleaks may be simi-lar to that for elective EVAR, and intervention shouldbe dependent of eventual increase in size of theaneurysm.

In conclusion, emergency endovascular repair ofruptured and acute symptomatic abdominal aorticaneurysms is justified when the patient has a suit-able anatomy, most importantly an adequate infra-renal neck. The first-month mortality, in the presentstudy, was significantly lower than in a control groupreceiving surgical repair. Further study of a largerstudy population to confirm our findings is needed.

R E F E R E N C E S

1 Johansson G, Swedenborg J. Ruptured abdominal aorticaneurysms: a study of incidence and mortality. BrJ Surg 1986;73: 101-103.

2 Johansen K, Kohler TR, Nicholls SC et al. Ruptured abdomi-nal aortic aneurysm: the Harborview experience. / Vase Surg1991;13:240-247.

3 Gloviczki P, Pairolero PC, Mucha P Jr et al. Ruptured abdom-inal aortic aneurysms: repair should not be denied. / Vase Surg1992; 15:851-859.

4 Kniemeyer HW, Kessler T, Reber PU et al. Treatment of rup-tured abdominal aortic aneurysm, a permanent challenge orwaste of resources? Prediction of outcome using a multi-organdysfunction score. EurJ Vase Endovasc Surg 2000; 19: 190-196.

5 Noel AA, Gloviczki P, Cherry KJ Jr et al. Ruptured abdominalaortic aneurysms: the excessive mortality rate of conventionalrepair. / Vase Surg 2001; 34: 41-46.

6 Katz DJ, Stanley JC, Zelenock GB. Operative mortality ratesfor intact and ruptured abdominal aortic aneurysms in Michi-gan : an eleven-year statewide experience. J Vase Surg 1994; 19:804-817.

7 Kantonen I, Lepantalo M, Brommels M et al. Mortality in rup-tured abdominal aortic aneurysms. The Finnvasc Study Group.EurJ Vase Endovasc Surg 1999; 17: 208-212.

8 Prance SE, Wilson YG, Cosgrove CM et al. Ruptured abdomi-nal aortic aneurysms: selecting patients for surgery. EurJ VaseEndovasc Surg 1999; 17: 129-132.

9 Green RM, Ricotta JJ, Ouriel K, DeWeese JA. Results ofsupraceliac clamping in the difficult elective resection ofinfrarenal aortic aneurysms. / Vase Surg 1989; 9: 124-134.

10 Illig KA, Green RM, Ouriel K et al. Primary fibrinolysis duringsupraceliac aortic clamping./ Vase Surg 1997; 25: 244-254.

11 van Ramshorst B, van der Griend R, Eikelboom BC. Survivaland life quality after surgery for ruptured abdominal aneurysm.In: Greenhalgh RM, Mannick JA (eds). The cause and manage-ment of aneurysms. London, W.B. Saunders, 1990: pp 433-440.

12 Bradbury AW, Makhdoomi KR, Adam DJ et al. Twelve-yearexperience of the management of ruptured abdominal aorticaneurysm. BrJSurglWl; 84: 1705-1707.

13 Ohki T, Veith FJ, Sanchez LA et al. Endovascular graft repairof ruptured aortoiliac aneurysms. J Am Coll Surg 1999; 189:102-113.

14 Greenberg RK, Srivastava SD, Ouriel K et al. An endoluminalmethod of hemorrhage control and repair of ruptured abdom-inal aortic aneurysms. / Endovasc 77zer2000; 7: 1-7.

15 Matsumura JS, Pearce WH. Early clinical results and studies ofaortic aneurysm morphology after endovascular repair. SurgClin North Am 1999; 79: 529-540.

16 Zarins CK, White RA, Schwarten D et al. AneuRx stent graftversus open surgical repair of abdominal aortic aneurysms:multicenter prospective clinical trial. J Vase Surg 1999; 29:292-308.

17 Becquemin JP, Lapie V, Favre JP, Rousseau H. Mid-term resultsof a second generation bifurcated endovascular graft for abdom-inal aortic aneurysm repair: the French Vanguard trial. / VaseSwr#1999;30: 209-218.

18 Cuypers P, Buth J, Harris PL et al. Realistic expectations forpatients with stent-graft treatment of abdominal aortic aneur-ysms. Results of a European multicenter registry. Em J VaseEndovasc Surg 1999; 17: 507-516.

19 Yusuf SW, Whitaker SC, Chuter TA et al. Emergency endovas-cular repair of leaking aortic aneurysm. Lancet 1994; 344:1645.

20 Yilmaz N, Peppelenbosch N, Cuypers PW et al. Emergencytreatment of symptomatic or ruptured abdominal aortic aneur-ysms : the role of endovascular repair. J Endovasc Ther 2002;9: 449-457.

21 Lachat ML, Pfammatter Th, Witzke HJ et al. Endovascular repairwith bifurcated stent-grafts under local anaesthesia to improveoutcome of ruptured aortoiliac aneurysms. EurJ Vase EndovascSurg 2002; 23: 528 -536.

22 Gawenda M, Heckenkamp J, Zaehringer M, Brunkwall J. Intra-aneurysm sac pressure. The holy grail of endoluminal graftingof AAA. EurJ Vase Endovasc Swig 2002; 24: 139-145.

23 Orend KH, Kotsis T, Scharrer-Pamler R et al. Endovascularrepair of aortic rupture due to trauma and aneurysm. Eur JVase Endovasc Surg 2002; 23: 61 - 67.

69

8URGENT OPEN SURGERY AFTERENDOVASCULAR AAA REPAIR

PIERGIORGIO CAO, FABIO VERZINIPAOLA DE RANGO, MASSIMO LENTI, GIANBATTISTA PARLANI

Urgent open surgery after endovascular aneurysm repair (EVAR) is infrequently requiredbut can carry a significant mortality in case of aneurysm rupture. Urgent treatment isusually indicated in cases ofischemic or hemorrhagic complications of EVAR and, rarely, forendograft infection. This repair may involve urgent conversion with graft removal at the timeof original operation (primary conversion) or at a later stage (secondary conversion), as well asadditional procedures with the endograft left in place (open surgery without conversion).Conversion to open repair after EVAR is usually more troublesome than a standard electiveoperation because it is usually subsequent to the endovascular procedure in patients who areoften excluded to open treatment due to severe comorbidities. The best method to avoid the highmorbidity and mortality of urgent open surgery after EVAR is prevention. Pre-operativeassessment with appropriate patient selection and infra-operative monitoring with possibilityof open conversion are essential. Strict surveillance for all patients undergoing EVAR iscrucial.

171

Indications

Rapidly evolving technology has resulted in a sub-stantial improvement in success rates of EVAR sincethe earliest published reports [1-4]. Nevertheless,although minimally invasive, EVAR can be associ-ated with an adverse early outcome. Recent studieshave addressed serious complication rates occur-ring in the mid and long term after EVAR, prima-

rily the risk of rupture [5-12]. For some of theseadverse events, an open repair can be urgentlyrequired.

This chapter addresses surgical indications, tech-niques and reported experiences on urgent opensurgery after EVAR.

Urgent open surgery after EVAR is usually indi-cated in cases of ischemic or hemorrhagic compli-cations and rarely for graft infection.


8_72

Surgical treatment may involve urgent conversionwith graft removal at the time of the original oper-ation (primary conversion) or at a later stage (second-ary conversion), as well as additional procedures withthe endograft left in place (open surgery without con-version).

PRIMARY CONVERSIONDespite adequate pre-operative imaging, correct

sizing of prostheses and appropriate case selection,EVAR may fail and require immediate conversionto open repair. Primary conversion usually occursfor vessel injury or endograft misplacement duringattempted EVAR in patients who have undergonehours of intervention and may have received a largequantity of contrast agent. Common causes of emer-gent conversion can be summarized as follows.1 - Rupture of the aorta or other vessels due to in-strumentation during the stent graft implantationprocedure. Although this is no longer an absoluteindication for immediate conversion, open repairprobably remains the safest treatment in thesecases.2 - Inability to deploy the graft because of inade-quate size of femoral or iliac arteries.3 - Graft deployment failure due to mechanical dys-function of the delivery system (e.g., catheter sheathrupture or elongation during retrieval, wire break-age with partially deployed endografts, impossibil-ity to retrieve the catheter after deployment).4 - Inaccurate deployment of the endograft (e.g.,irreversible twisting of the endograft leading toinability to complete deployment or to limb occlu-sion) .5 - Misplacement of the endograft that can lead toaortic, renal or iliac obstruction.6 - Inadequate exclusion of the abdominal aorticaneurysm (AAA) after apparent proper deployment(primary endoleak).7 - Graft occlusion.

Improvements in technology and interventionaltechniques, as well as increasing experience, haveresulted in a reduction in primary conversion rates.May et al. found that primary conversion rates re-duced from 20% to 2%, accurate case selectionbeing crucial to obtain success of deployment [13].Access problems can be largely overcome with ap-propriate case selection, the use of smaller diameterdevices, and planning preventive open techniqueas performing iliac conduits. The risk of aortic rup-ture can be minimized by limiting the oversizing ofballoons in balloon-expandable devices depending

on the severity of the atherosclerotic disease and byavoiding dilatation beyond the graft-covered vessel.

Immediate device migration can be avoided byproper aortic neck selection: the presence of muralthrombus, inverted funnel shape and heavy cir-cumferential calcification, in addition to a lengthof less than 15 mm and a diameter larger than30 mm, are relative contra-indications for the useof the endoluminal repair.

SECONDARY CONVERSIONOne of the main indications for urgent second-

ary conversion after EVAR is aneurysm rupture.Prevention of AAA rupture with its related mor-bidity and mortality is the primary driving forcebehind the concept of aneurysm repair, as the nat-ural history of an untreated AAA is to enlarge andrupture. In spite of the immediate successful exclu-sion of aortic aneurysm at the time of implantationof the endograft, reports on rupture of AAA afterEVAR continue to accumulate, showing a risk ashigh as 1% per year [14].

Migration, modular component disconnectionand other mechanical failures like fabric perfora-tion with acute onset of endoleak represent themost frequent causes of urgent secondary conver-sion after EVAR.

Another indication for urgent open repair afterEVAR is represented by graft infection, a rare com-plication reported in the literature. More prone tothis complication seem to be those grafts which arenot premounted into a delivery catheter at the timeof their insertion and therefore are more exposedto operator manipulations, and patients subjected tomultiple re-interventions for any cause [15]. Aorto-duodenal fistulae have been reported as rare seque-lae of EVAR secondary to stent graft disruption ina preexisting inflammatory process causing adhe-sions between the bowel and the aortic wall [16].

OPEN SURGERY WITHOUT CONVERSIONSome of the indications mentioned above can be

the cause of urgent open surgery with the graft leftin place, either immediately or after a primarily suc-cessful procedure. The more frequent causes of im-mediate urgent open surgery without conversionare hypogastric occlusion requiring revasculariza-tion and iliac artery rupture not amenable toendovascular repair. During follow-up the most fre-quent indication is represented by graft limb occlu-sion due to severe kinking of the graft limb.

URGENT OPEN SURGERY AFTER ENDOVASCULAR AAA REPAIR

Surgical techniques

PRIMARY AND SECONDARY CONVERSIONSeveral differences exist between conversion with-

out deployment, immediate explantation and lateexplantation. In the case of aortic rupture, the dif-ficulties encountered in obtaining vascular controland in dealing with an aorta that has lost much ofits integrity during the process of removing theendograft renders surgical repair much more dif-ficult than repairing a "de novo" ruptured AAA.On the other hand, it has been postulated that thepresence of an endograft may somehow limit thequantity and rate of blood loss outside the aneurys-mal sac, reducing the hemodynamic changes of theAAA rupture [7].

In conversions occurring during primary graftplacement, the possibility of using suprarenal aor-tic control through balloon inflation must be con-sidered. This technique may be applied quickly,particularly when a guide wire is already in placein the thoracic aorta. However, it may be difficultto maintain the inflated balloon in place becauseof the pulsatile pressure of the blood flow; balloonmigration can be prevented by advancing the bal-loon over an extra stiff guide wire and fixing bothto the field drapes with a hemostat. Alternatively,the balloon can be sustained with a long introducerfixed to the patient's skin.

Balloon control is not free from significant com-plications such as visceral vessel embolization andvisceral ischemia, and can render open surgeryeven more difficult in an operative field alreadycomplicated by the presence of the endograft. Forthis reason, it may be preferable to remove the bal-loon as early as possible after gaining access to theaortic neck with a standard cross-clamp.

Aortic and iliac cross-clamping technique mayvary on the basis of the position and degree ofdeployment of the endograft. A standard open AAAtechnique may be used in patients in whom theendoluminal approach has been abandoned due toaccess problems (primary conversion). In suchcases, infrarenal aortic clamping is usually possible[17,18].

In cases of secondary conversion for patients withan endograft with infrarenal fixation deployedimmediately below the renal arteries, clamps canbe gently applied to the aorta and common iliacarteries as in standard open AAA repair, includingthe underlying graft. After initial clamping and

opening of the aneurysm sac, the proximal end ofthe endograft may be removed by cautious traction,eventually after opening the aortic clamp and cross-clamping the main trunk of the endograft to reduceblood loss.

Following this, the iliac clamps will be openedand closed in sequence in a similar fashion to allowremoval of the underlying endograft within thejaws.

Supraceliac control of the aorta has been re-commended by many authors [5,10-11]. This ap-proach is usually required in the following cir-cumstances:

4 when the endograft has been incorrectly de-ployed over the renal arteries,

* in patients who experienced rupture at thelevel the proximal neck, e.g., for balloon inflationduring deployment of the endograft,

4- in patients with serious hemorrhage untilcontrol of the infrarenal neck is obtained,

* in cases of grafts with suprarenal fixation,* in cases of late conversion when the long stan-

ding endograft presence is associated with a peri-aortic inflammatory response with tissue fibrosis, andremoval of the endograft may result in a weak andthinned-out aortic neck for proximal anastomosis,

4 during removal of an infected endoprosthesis.The proximal anastomosis is performed in a stan-

dard fashion, usually including a dacron felt orpledgets in the suture line to reinforce the weak-ened aortic wall.

Although the procedure of choice in all instancesof explantation is complete removal of the endo-graft, in the case of endografts anchored by attach-ment systems at the level of the renal arteries orabove, it may be impossible to remove the com-plete graft, especially during a secondary conver-sion. In such cases the amputation of the infrarenalportion of the endoprosthesis, by cutting the metalframes of suprarenal attachment system, may beindicated.

When complete removal of the proximal portionof the covered graft is impossible, the techniqueused by Lawrence-Brown can be applied. The prox-imal transected endograft is incorporated in theproximal suture line, which anastomoses the newgraft to the neck of the aneurysm. This techniquemight be less traumatic than attempting to removethe entire prosthesis. However, some authors spec-ulate that the risk of pseudoaneurysm formationwould be increased with the inclusion technique,

8_73


74

particularly if there had been a proximal endoleak[18,19].

Distal anastomoses are usually carried out at thelevel of the iliac bifurcation in case of iliac aneurys-mal involvement. In the case of nonectatic iliacarteries, gentle removal of the iliac limbs of theendograft can prevent intimal damage and an aor-tic anastomosis can be performed (Fig. 1). In caseof firm adhesion of the endograft limbs in the iliacarteries, as in endografts with hooks for distal fix-ation system, the inclusion technique can beapplied also for the distal anastomosis. Alternatively,complete iliac artery transection below the iliacendograft ends should be performed.

OPEN SURGERY WITHOUT CONVERSIONAt the time of the initial EVAR operation, some

complications can lead to the subsequent need foradditional open surgery without the obligation toremove the total graft.

The most common indication for open surgerywithout conversion is bilateral hypogastric occlusiondue to incorrect graft planning with errors inlength measurement, low graft deployment, or dis-

FIG. 1 Gentle iliac limbs removed and clamped prior todistal aortic anastomosis durins secondary conversion foracute type III endoleak that occurred two years after EVAR.

tal migration of the graft. In such cases, risk ofintestinal ischemia is high and can be lowered byinternal iliac revascularization, at least at one side.The side to be revascularized must be chosen onthe basis of specific anatomical characteristics (e.g.,common trunk length, presence of an iliac aneur-ysm, calcium extent and possibility of mobilizingthe artery). In general, it may be preferable tochoose the left side over the right because of thelarger collateral pathways between the right inter-nal iliac and the mesenteric circulation.

Surgical approach to the iliac bifurcation is usu-ally best obtained through an eight centimeteroblique incision on the right or left lower quadrantwith a retroperitoneal approach. In some patientswith a prior vertical inguinal incision, it may bepreferable to extend the skin incision cranially withsubsequent oblique fascial incision. After mobilizingthe hypogastric artery, vascular clamps are appliedand the internal iliac is divided. A direct re-implan-tation of the distal segment over the external iliacis usually difficult because of the endograft insidethe proximal external iliac, so the best option is toperform an end-to-end anastomosis with a short seg-ment of PTFE or dacron graft and subsequentlysuture end-to-side to the distal external iliac.

Another possible immediate ischemic complica-tion after EVAR is inadvertent renal occlusion dur-ing deployment. An endovascular rescue treatmentby stent placement is usually successful in case ofpartial coverage of the renal ostium, whereas endo-graft removal is usually indicated in case of totalbilateral renal flow obstruction. In the rare eventof unilateral renal impairment, the endograft maybe left in place and an extra-anatomical renal revas-cularization can be performed: the hepatic, splenicor iliac arteries can be used as inflow arteries with-out the need for aortic clamping and graft removal(Fig. 2).

Limb ischemia is another complication usuallytreated by open surgery without endograft removal.Thrombolysis is usually indicated for late obstruc-tion and in cases of viable, nonthreatened ischemiclimbs. In our experience, most of the cases of limbischemia have occurred early after EVAR (withinthree months) and were related to undiagnosediliac dissection, graft kink, or compression. In suchcases, an open approach with thrombectomy, even-tually followed by balloon and stent angioplasty, isan option reserving the femorofemoral extra-anatomical bypass in case of failure of mechanicalclot removal.


FIG. 2 Left renal revascularization with splenic arterytransposition in a patient with renal occlusion due to endo-graft coverage of renal ostium: 6-month computed tomo-graphy reconstruction showing the proximal part of the aor-tic endograft, regular patency of the right renal artery andof the spleno-renal transposition.

Review of published casesand our experience

True incidence of AAA rupture after EVAR is dif-ficult to assess because many cases have beenreported as isolated anecdotes or from subgroupsof patients treated with specific endografts that areno longer in use. Bernhard et al. reported 5 rup-tures (4.9%) among 103 patients treated with a first-generation Endovascular Technologies (EVT) graft,but none in the subsequent 583 patients whoreceived a second-generation graft [12].

Zarins et al., reporting on 1067 patients treatedwith the AneuRx endograft (Medtronic AVE),found that the one-year risk of rupture by life tableanalysis was 0.4%, and the two-year risk of rupturewas 2.6% [10].

Vallabhaneni and Harris, reporting on patientsfrom EUROSTAR registry, calculated a rupture rateof about 1% per year that significantly increasedafter the fifth year up to 2.9% by life table analy-sis. They also identified type III endoleak (RR 7.47),migration (RR 5.35), and aneurysm diameter at lastmeasurement (RR 1.057) as three significant inde-pendent predictors of late rupture in the EURO-STAR population [20].

8_75

Colon ischemia is one of the most feared com-plications after EVAR. Fortunately, it occurs rarelyand most of the time the mild degree of a mucosalischemia can be treated medically without seque-lae. However, in the rare case of transmural colonicinfarction, an urgent bowel resection is needed.

Hemorrhagic complications of EVAR can rarelybe treated with endovascular methods. Iliac rupturescan seldom be repaired by endografting and urgentopen surgery is more often required, especiallywhen rupture occurs near the iliac bifurcation, usu-ally determined by too aggressive balloon dilatationoutside the stent graft distal ends. These maneuverscan actually tear off the hypogastric origin, and posi-tioning of a covered stent would not arrest back-bleeding from the internal iliac circulation. In suchcases, the same approach described for hypogastricrevascularization can be used to suture the dam-aged artery with the aid of balloon hemostatic con-trol inside the stent graft. Eventually, an iliacbending can be applied as shown in Figure 3.

FIG. 3 Left iliac artery repair with bending after rupturesecondary to iliac graft ballooning. A retroperitonealapproach with abdominal left lower quadrant incision wasperformed.


76

At least 47 cases of aortic aneurysm rupturesafter EVAR have been reported in referenced jour-nals and these were recently reviewed by Bernhardet al. [12]. Bifurcated configurations representedthe majority of the used grafts (30 patients). Dif-ferent models of endografts had been used, includ-ing 8 Medtronic-AneuRx, 5 EVT-EGS, 3 Guidant-Ancure, 10 homemade grafts, 5 MinTec Stentor,2 Medtronic/World Medical-Talent and 11 BostonScientific Vanguard. Four manufacturers were unre-ported. The time between implant and ruptureranged from 3 days to 85 months, with a mean of16.4 (±16.8) months (median 16 months). Berhardet al. found that among the causes of rupture, allbut one were associated with endoleaks, but only18 of them were evident before rupture. Withrespect to the type of endoleak, 12 were type I, 2were type II, and 4 were undetermined. Primarytype I endoleaks (i.e., recognized at implantation)had a tendency to rupture early (within one to sixmonths), which supports the recommendation totreat them without delay. The same authors foundthat an increase in aneurysm diameter was recordedin 13 of the 31 ruptured cases with available infor-mation (42%). The majority of patients had evi-dence of other abnormalities noted on preruptureimaging studies, some of which were recognizedonly in retrospection: besides aneurysm enlarge-ment, migration and loss of device integrity werethe most common underlying problems contribut-ing to the onset of an acute endoleak at the timeof rupture. Some of these problems appeared to be

related to early generation designs that are nolonger manufactured, whereas newer endograftshave been followed for too short a time to deter-mine their durability. Therefore, it is mandatory thatrigorous surveillance is applied to all patients untilsufficient long-term evidence exists to define themost reliable follow-up regimen for any given device.

In the Bernhard review of ruptured aneurysmafter EVAR, open surgical repair was performed in40 of 47 patients with an overall peri-operative mor-tality rate of 41% [12].

Personal experience

Between April 1997 and October 2002, 451 con-secutive patients underwent elective EVAR for AAAat our unit. Median follow-up was 25 months (range1 to 66 months). Early mortality rate in our cohortwas 1.1% (5/451), while immediate conversion ratewas 1.5% (7/451).

At a median follow-up of 24 months, overall latemortality occurred in 45 patients (10.2%). Causes oflate mortality included 3 AAA ruptures, 8 cardiacfailures, 1 bowel occlusion, 1 pulmonary embolism,10 myocardial infarctions, 11 cancers, 2 traumas, 1 re-nal failure, 1 suicide, 2 strokes, 3 respiratory insuffi-ciencies, 1 intracranial hemorrhage and 1 bleedingduodenal ulcer. Aneurysm-related death rate (i.e.,peri-operative mortality and late mortality due toaneurysm rupture or any aortic re-intervention) isshown in Table I and in Figure 4.

Fottow-up interval(month)

0 - 66-12

12-1818-2424-30

30-36

36-4242-4848-54

Numberat risk

45135029825322015011859

32

Number ofterminal events

5

0

01

1

0

0

0

0

% of patients free fromaneurysm-related death

98.75

98.7598.7598.2697.7197.7197.7197.7197.71

Cumulativestandard error

0.0056

0.00560.00560.0074

0.00920.00920.0092

0.0092

0.0092


FIG. 4 Freedom from aneurysm-related death in 451 patients after en-dovascular AAA repair (life table analysis).

Urgent open surgery during or immediately afterEVAR was required in 28 cases (6.2%) (see Table II).

Seven immediate urgent conversions were per-formed: six patients required immediate conversionbecause of impossibility to deploy the endograft as

planned, in all cases related to narrow, tortuous andcalcified vessels. In the remaining patient, aorticneck rupture occurred at the time of graft deploy-ment and required emergent conversion to openrepair; a supraceliac aortic control was necessary

Indication far urgent open surgery Peri-operative*N

LateN

Primary conversion 7

Impossibility to progress into diseased iliac arteries 6

Aortic rupture 1

Secondary conversion - 2

Symptomatic AAA expansion for acute type I endoleak secondary to migration 1

AAA rupture due to component disconnection 1

Open surgery without conversion 14 5

Iliac rupture 2

Graft limb or iliac occlusion 6 4

Unintentional bilateral hypogastric occlusion 3

Renal infarction and parenchymal hemorrhage secondary to renal angioplasty 2

Left colon infarction, without hypogastric occlusion 1

Renal ischemia due to renal artery occlusion 1

* Peri-operative: within 30 daysAAA: abdominal aortic aneurysm


8_78

and a tube graft was implanted. Unfortunately, thepatient died two days after surgery because of mul-tiple organ failure due to massive blood losses. Thiscase represents the only death related to urgentopen surgery after EVAR in our cohort of patients(5.2%).

Two patients underwent secondary urgent con-version (at 18 and 40 months after EVAR, respec-tively) for acute proximal type I endoleak due tograft migration and for AAA rupture due to prox-imal cuff-aortic body disconnection, respectively.Three other patients experienced rupture duringfollow-up to our knowledge; they were admitted toother hospitals and died without conversion toopen repair.

Urgent open surgery without conversion was per-formed in 19 patients: 14 early and 5 late.

Early open surgery included:•* two nephrectomies: one for intraparenchymal

hemorrhage after simultaneous EVAR and renalstenting for an AAA associated with renal stenosis,the other for renal infarction due to inadvertentleft renal artery coverage;

* one left colectomy for intestinal ischemia in a pa-tient with bilateral patency of internal iliac arteries;

* four femorofemoral bypass grafts and twothrombectomies for limb ischemia;

* two iliac artery repairs for intraprocedural rup-ture: one patient was treated with arterial sutureand bending and the other with external iliac-to-femoral bypass;

* three external-to-internal iliac bypasses in fourpatients after unintentional bilateral hypogastriccoverage. The fourth patient remained without

events although hypogastric revascularization hasnot been attempted because of the presence ofextensive iliac calcification.

Late open surgery included:* one spleno-renal bypass for rapidly evolving

renal insufficiency and hypertension secondary torenal artery occlusion;

* four femorofemoral bypass grafts for limbischemia due to graft occlusion.

Conclusion

We can conclude that urgent open surgery afterEVAR is required infrequently but, in the case ofAAA rupture, carries a significant mortality, similarto that expected for patients without prior endo-graft surgery.

The potential extremely dangerous consequencesof complications after EVAR impose a high level ofattention1 - pre-operatively, with appropriate patient selec-

tion,2 - in the operating room, with fully equipped

patient monitoring and possibility of open con-version,

3 - during follow-up.The best way to avoid the high morbidity and

mortality associated with urgent open surgery afterEVAR is prevention. All EVAR. patients should there-fore be indefinitely monitored at six-month inter-vals, and abnormalities should be identified andcarefully considered for elective endovascular oropen correction.

R E F E R E N C E S

1 ParodiJC, PalmazJC, Barone HD. Transfemoral intraluminalgraft implantation for abdominal aortic aneurysms. Ann VaseS«7gl991; 5: 491-499.

2 Coppi G, Moratto R, Silingardi R et al. The Italian trial ofendovascular AAA exclusion using the Parodi endograft.JEndovasc Surg 1997; 4: 299-306.

3 Moore WS. The EVT tube and bifurcated endograft systems:technical considerations and clinical summary. EVT investiga-tors. JEndovasc Surg 1997; 4: 182-194.

4 May], White GH, Waugh R et al. Comparison of first- and sec-ond- generation prostheses for endoluminal repair of abdom-inal aortic aneurysms: a six-year study with life table analysis.J Vase Surg 2000; 32: 124-129.

5 Lumsden AB, Allen RC, Chaikof EL et al. Delayed rupture ofaortic aneurysms following endovascular stent grafting. Am JSwrgl995; 170: 174-178.

6 Torsello GB, Klenk E, Kasprzak B, Umscheid T. Rupture ofabdominal aortic aneurysm previously treated by endovascularstentgraft. / Vase Surg 1998; 28: 184-187.

7 May J, White GH, Waugh R et al. Rupture of abdominal aor-tic aneurysms: a concurrent comparison of outcome of thoseoccurring after endoluminal repair versus those occurring denovo. EurJ Vase Endovasc Surg 1999; 18: 344-348.

8 Krohg-Sorensen K, Brekke M, Drolsum A, Kvernebo K. Peripros-thetic leak and rupture after endovascular repair of abdomi-nal aortic aneurysm: the significance of device design forlong-term results. / Vase Surg 1999; 29: 1152-1158.


9 Breek JC, Hamming JF, Lohle PN et al. Spontaneous perfora-tion of an aortic endoprosthesis. EurJ VascEndovasc Surg 1999;18: 174-175.

10 Zarins C, White RA, Fogarty TJ. Aneurysm rupture afterendovascular repair using the AneuRx stent graft. J Vase Surg2000; 31: 960-970.

11 Politz JK, Newman VS, Stewart MT. Late abdominal aorticaneurysm rupture after AneuRx repair: a report of three cases./Vase Surg 2000; 31: 599-606.

12 Bernhard VM, Mitchell SM, Matsumura JS et al. Rupturedabdominal aortic aneurysm after endovascular repair. / VaseSwrg2002;35: 1155-1162.

13 May J, White GH, Yu W et al. Endovascular grafting for abdom-inal aortic aneurysms: changing incidence and indication forconversion to open operation. Cardicrvasc Sing 1998; 6: 194-197.

14 Harris PL, Vallabhaneni SR, Desgranges P et al. Incidence andrisk factors of late rupture, conversion, and death after endovas-cular repair of infrarenal aortic aneurysms: the EUROSTARexperience. European Collaborators on Stent/graft Techniquesfor Aortic Aneurysm Repair. / Vase Surg 2000; 32: 739-749.

15 Matsumura JS, Katzen BT, Hollier LH, Dake MD. Update onthe bifurcated Excluder endoprosthesis: phase I results. J VaseSurg 2001; 33 (2 suppl): S150-153.

16 Norgren L, Jernby B, Engellau L. Aortoenteric fistula causedby a ruptured stent-graft: a case report. J Endovasc Surg 1998;5: 269-272.

17 Schlensak C, Doenst T, Hauer M et al. Serious complicationsthat require surgical interventions after endoluminal stent-graftplacement for the treatment of infrarenal aortic aneurysms./fcSwrg2001; 34:198-203.

18 May J, White GH, Harris JP. Techniques for surgical conver-sion of aortic endoprosthesis. EurJ Vase Endovasc Surg 1999; 18:284-289.

19 Jacobowitz GR, Lee AM, Riles TS. Immediate and late explan-tation of endovascular grafts: the endovascular technologiesexperience. / Vase Surg 1999; 29: 309-316.

20 Vallabhaneni R, Harris P. Overview of the complications fol-lowing endovascular AAA repair. In: Branchereau A, Jacobs M(eds). Complications in vascular and endovascular surgery (Part II).Armonk, Futura Publishing Co, 2002: pp 129-136.

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9ACUTE COMPLICATIONS FOLLOWING

LAPAROSCOPIC SURGERY

MARC COGGIA, ISABELLE DI CENTAISABELLE JAVERLIAT, OLIVIER GOEAU-BRISSONNIERE

Laparoscopy is now considered the technique of choice for many surgical procedures, _especially in general surgery, gynecology and urology. It offers the advantages of minimally Jinvasive surgery compared with conventional surgery: reduced surgical trauma, minimal 81postoperative pain, faster recovery and shortened postoperative hospital stay. With itsoverwhelming success, increasing numbers of patients are undergoing laparoscopy for avariety of procedures. Despite its popularity, a number of complications specifically related tothe laparoscopic approach have been described. Injuries to the great retroperitoneal vessels arethe most severe complications. These complications, which occur with Veress needles or trocars,are completely unknown in conventional surgery. More recently, aortic surgery has entered thefield of laparoscopic surgery. Even though no specific vascular complications have beenreported during totally laparoscopic or laparoscopic-assisted aortic procedures, suchcomplications are possible and will probably occur with the growing experience in these newapproaches.

Major vascular can be secondary to the surgical dissection requiredComplications in f°r sPec^lc laparoscopic procedures (23.5%) [1].

I " . The incidence of major vascular complicationslaparoscopic surgery during laparoscopic surgery is between 0.05% and

0.25% [1-6]. This incidence might seem insignifi-cant in view of the considerable number of lap-

Major vascular complications can occur during the aroscopic procedures, but it is probably underesti-set-up phase of laparoscopy (76.5%), related to the mated because many surgeons do not publish theirearly maneuvers to enter the peritoneal cavity, or experience [3].


82

THE SET-UP PHASE OF LAPAROSCOPYMajor vascular injuries. Major vascular injur-

ies occurring during laparoscopic surgery are de-pendent on the technique used to enter the peri-toneal cavity. The favored method of establishing apneumoperitoneum in laparoscopic surgery is theblind (or closed) technique. This involves insuffla-tion of the peritoneal cavity through a needle(Veress), which is blindly placed intraperitoneally.Subsequently, a trocar is inserted blindly to allowintroduction of a laparoscope. Predisposing factorsfor visceral and vascular injury due to perforationby the Veress needle or the first trocar are adhe-sion between viscera and the abdominal wall re-sulting from previous inflammation or surgery, pa-tients with a thin abdominal wall and poor techniqueor surgical inexperience. Using the blind techniqueto enter the peritoneal cavity, it is important to knowthe relationship of the umbilicus to the aortic bifur-cation. Kurd et al. [4] showed that the location ofthe umbilicus was more caudal in heavier women andnegatively correlated with body mass index (BMI).In nonobese women (BMI less than 25 kg/m2), themean location of the umbilicus was 0.4 cm caudalto the aortic bifurcation, and was at or cephalad tothe aortic bifurcation in 53%. In overweight women(25<BMI<30 kg/m2), the mean umbilical loca-tion was 2.4 cm caudal to the aortic bifurcation. Inobese women (BMI higher than 30 kg/m2), themean umbilical location was 2.9 cm caudal to theaortic bifurcation and was located at the level ofthe umbilicus in 30%. In all cases, the umbilicuswas located cephalad to where the common iliacvein crossed the midline.

The open technique is an alternative method ofcreating the pneumoperitoneum. In this techniquethe peritoneal cavity is opened under direct visionand a blunt-tipped trocar is introduced. Althoughthe open technique appears to be safer than theclosed technique, most surgeons prefer to use theclosed technique because it is faster, requires asmaller incision and is not associated with leakageof carbon dioxide. However, operative time of openlaparoscopy is significantly shorter than that ofclosed laparoscopy. Moreover, insufflation of theperitoneal cavity through the Veress needle is donewith a low-flow setting. In open laparoscopy, insuf-flation through the trocar can be done with highflow because of its diameter. Gas leakage can besolved by anchoring the trocar to the abdominalfascia and by replacing additional sutures aroundthe trocar.

Major vascular injuries related to the early ma-neuvers to enter the peritoneal cavity occur withthe blind insertion technique of the Veress needleand primary trocar [1-6]. In a review of the litera-ture, Bonjer et al. [6] collected six retrospectivestudies concerning 489 335 patients operated withthe closed technique. The total incidence of vas-cular injuries was 0.075%. Of the specified injuries,39.8% were caused by insertion of the Veress nee-dle. The location of vascular injury due to insertionof a trocar was reported as aorta (13/38), inferiorvena cava (5/38), iliac artery (12/38), iliac vein(7/38) and mesenteric artery (1/38). For Chapronet al. [1], major vascular injury occurred in the fol-lowing locations: vena cava (23.8%), external iliacvessels (23.8%), aorta (19%), common iliac vessels(19%), mesenteric vessels (9.6%) and unspecified(4.8%). In six other retrospective studies concern-ing 12 444 patients operated with the open tech-nique, vascular injuries were not reported [6],Prospective randomized studies of open versusclosed laparoscopy have not been performed. In-deed, since the incidence of vascular injuries dur-ing laparoscopy is low, a prospective study compar-ing open and closed technique would requireexcessive numbers of patients to allow statisticallysignificant statements to be made [3]. However, thecomparative study performed by Bonjer et al. [6] isin accordance with the literature review and showsthat the incidence of vascular injury associated withclosed laparoscopy is significantly greater than thatof open laparoscopy.

Vascular injuries secondary to Veress needle inser-tion usually result in small two to three millimeterspuncture lacerations, which can be repaired prima-rily with placement of a few interrupted vascular su-tures to obtain adequate hemostasis. The indicationsfor exploration include blood via Veress needle as-piration, hemodynamic instability, active intra-ab-dominal hemorrhage or expanding retroperitonealhematoma [2,3]. When there is a return of blood viathe Veress needle, the sheath must be left in placein order to tamponade the bleeding and help locatethe site of injury [3]. Usal et al. [3] underlined theimportance of inserting the insufflation needle ata 45 degree angle in order to prevent injuries.

Major vascular traumas secondary to the primarytrocar are caused by the same mechanism as theVeress needle. The indications for explorationinclude hemodynamic instability, active intra-abdom-inal hemorrhage or expanding retroperitoneal he-matoma [2,3]. Vascular injury is recognized imme-

ACUTE COMPLICATIONS FOLLOWING LAPAROSCOPIC SURGERY

diately in most cases and prompts emergency laparo-tomy to repair the lacerated vessel [1,6]. Regardlessof the mechanism of vascular injury, it is essentialthat the posterior wall of the injured vessel is ex-plored to assure that a through and through injuryhas not occurred [2],

To prevent perforation of viscera or blood ves-sels, disposable trocars with safety shields were de-veloped [6]. The safety shield is supposed to shootforward after the peritoneum has been penetrated.However, the shield can be held back for a con-siderable distance, particularly in cases of insuffi-cient pneumoperitoneum. This leaves the stylet ofthe trocar unprotected in the peritoneal cavity.Then, in thin patients or when the abdominal cav-ity is not sufficiently elevated, the unprotected styletcan easily cause vascular injury [6].

Mortality of major vascular injury is about 10%[1,3] and represents the second most commoncause of death for laparoscopic procedures afteranesthesia related causes. Delay in diagnosis is prob-ably the most significant contributor to associatedmorbidity and mortality [2].

Other vascular injuries. The use of multipletrocar sites increases the risk of injury to the epi-gastric vessels [3]. These injuries can be recognizedby the dripping of blood down the trocar sleeve intothe abdomen or by hematoma formation aroundthe trocar insertion site. It is important to avoidthese injuries by placing the trocar after lighting theabdominal wall videoscopically and identifying theepigastric vessels, especially in thin patients.

Gas embolism. Gas embolism is a rare but oftenfatal complication of laparoscopy. It is caused by di-rect insufflation of carbon dioxide into a blood ves-sel, especially vena cava or its branches. While theincidence of gas embolism is 0.001% in the closedtechnique, open laparoscopy is highly unlikely tocause gas embolism because the trocar is insertedunder direct vision. Delay in diagnosis can be dueto a number of factors, the most important beingthe absence of blood in the peritoneal cavity or thepresence of a small retroperitoneal hematomawhich can easily remain undetected,

THE LAPAROSCOPY PROCEDUREMajor vascular injury during the laparoscopy pro-

cedure is possible, as it can be observed during con-ventional surgery. The most common cause is theuse of monopolar electrode (iliac artery and vein)and sharp dissection (vena cava) [1]. It requiressurgical treatment, if possible by laparoscopy but it

depends on the severity of the hemorrhagic syn-drome and on the surgeon's experience.

Carbon dioxide pneumoperitoneum may cause asignificant decrease in splanchnic vessel blood flow[7,8]. Decrease in visceral blood flow results fromdrop in cardiac output (-30%), direct mechanicalcompression of intra-abdominal blood vessels or viahumoral mechanisms and mesenteric vasoconstric-tion due to hypercapnia (transperitoneal absorp-tion of carbon dioxide). Moreover, carbon dioxidepneumoperitoneum at a pressure above 15 mmHgmay cause visceral vasoconstriction as a result of in-tra-operative release of vasopressin, increasing por-tal vein pressure due to retained C02- Use of halo-thane may also contribute to the reduction invisceral vessel blood flow [8], Such a decrease insplanchnic vessel blood flow may be catastrophic inpatients with certain preexisting conditions (impair-ment of splanchnic vessels, hypercoagulable states).Then it is important that intra-abdominal pressurebe kept as low as possible throughout the procedureand should always be maintained below 15 mmHg.Minute volume insufflation should be maintainedat an adequate level to avoid hypercapnia (less than8 L/min).

Major vascular complicationsin laparoscopic aortic surgery

Vascular surgery recently entered the field oflaparoscopy, and specific vascular complications oflaparoscopic aortic surgery have not yet beenreported.

Since November 2000 we developed a new ap-proach for totally laparoscopic aortic procedures[9]. Initially we used this technique to treat severeaorto-iliac occlusive disease. Since January 2002 wehave used this totally laparoscopic approach for thesurgical treatment of infrarenal aortic aneurysms.Vascular injuries are possible during the laparoscopyprocedures or during the postoperative period.

LAPAROSCOPY PROCEDURESMajor vascular complications encountered dur-

ing laparoscopy procedures were hemorrhagic com-plications and clamping problems.

Hemorrhagic complications. Intraproceduralhemorrhagic complications were noted in two pa-tients and necessitated surgical conversions. One pa-tient operated for severe aorto-iliac occlusive disease

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84

had an acute bleeding from the left prosthetic limbafter completion of the aorto-prosthetic anastomo-sis. This was due to a leakage of the clamp that wasapplied on the prosthetic limb before tunneling.Actually, this complication is avoided by a bindingpreviously placed around the left prosthetic limb.The second patient was operated at the beginningof our experience in totally laparoscopic proce-dures for infrarenal aortic aneurysm. He had aback-bleeding from a lumbar artery after a laparo-scopic endo-aneurysmorrhaphy with aorto-bi-iliacbypass. Because of the poor visibility, it was not pos-sible to locate the origin of the bleeding and a sur-gical conversion was made. Actually, with the useof a stapler device designed for laparoscopic her-nia repair, an internal control of the lumbar arter-ies is always possible. Moreover, it is remarkable tonote that with the intraperitoneal pressure, theblack-bleeding from the lumbar arteries is less thanusually observed in conventional surgery.

Clamping problems. Aortic clamping is a chal-lenging problem during laparoscopic aortic surgery,especially when the infrarenal aorta is extensivelycalicified. Pre-operative computed tomography scanis then essential to assess the location and extentof aortic calcifications before a laparoscopic proce-dure is considered. Surgeons consider that aorticcalcifications are contra-indications for totally laparo-scopic aortic procedures [10-14]. However, with ourlaparoscopic approach of the abdominal aorta, asimple suprarenal aortic clamping is possible. Theapproach of the suprarenal aorta is obtained withthe use of a partial mediovisceral rotation. This tech-nical point is important regarding the technical dif-ficulties encountered with calcified vessels. Indeed,we performed, if necessary, grasping forceps endar-terectomies of the aortic wall and then moved theclamp distal to the renal arteries before perform-ing the aorto-prosthetic anastomosis. If back-bleed-ing is observed from the distal aorta, we performa rapid endarterectomy to reposition the aorticclamp and suture the aortic stump. A balloon occlu-sion of the distal aorta could also be used.

THE POSTOPERATIVE PERIODMajor vascular complications encountered in the

postoperative period were not specific but theirmechanisms were related to the aortic laparoscopictechnique.

Hemorrhagic complications. In our experi-ence, two patients had major hemorrhagic compli-cations. The third patient of our series was re-op-erated eight hours after the end of the laparoscopicprocedure for an aorto-prosthetic suture line bleed-ing. At re-operation, bleeding from large needleholes was observed on the posterior wall of the aorta.In one point, the suture had torn out of the aorta.We believe that these anastomotic problems weredue to needle size (3/0 poplypropylene sutures) andbrittleness of the aortic wall which was endarterec-tomized during the initial procedure. Actually, whenwe perform an aortic endarterectomy before theanastomosis, the suture line is carried out with athin polypropylene suture in order to reduce thesize of needle holes. Prosthetic pledgets are alsoused to reinforce some stitches.

Another patient had a retroperitoneal hematoma,which required a surgical exploration at day 21. Wedid not observe any anastomosis leakage or othercauses for this retroperitoneal hematoma. Fourother patients had retroperitoneal hematoma,which did not necessitate surgical exploration butrequired blood transfusions. We think that these he-matomas resulted from coagulopathy. This coa-gulopathy was induced by hemodilution and the useof heparinized saline for irrigation of the operativefield. Actually, these two factors have been correct-ed and, in the latest patients, we did not observesuch retroperitoneal hematomas. However, it is im-portant to know that with laparoscopy, tamponadeof the operative field is not as effective as in con-ventional aortic surgery. Therefore it is importantto control the surgical hemostasis, especially at thelevel of the suture line(s) and the dissection planes.

Thrombotic complications. Prosthetic limbthrombosis is a complication of aortic and periph-eral vascular surgery. However, it remains rare afteraorto-iliac or aortofemoral surgery. Two factors arepredisposing for such complications after aorticlaparoscopic procedures:1 - the aortic anastomosis time can be long andblood can then stagnate in the limbs of the pros-thesis,2 - twist of prosthetic limbs is possible because withlaparoscopy it is more difficult to position the limbduring the tunneling. If these technical problems arenot recognized during the procedure, they can leadto postoperative acute thrombosis of the prosthesis.

ACUTE COMPLICATIONS FOLLOWING LAPAROSCOPIC SURGERY

ConclusionLaparoscopic surgery is technically demanding,

especially in vascular surgery. Knowledge of surgi-cal anatomy is very important to avoid lesions. The

surgeon's experience is also an important and evencrucial factor for preventing vascular injuries. Webelieve that learning curve and laparo-training areessential and allow for a decrease in the numberof technical errors.

R E F E R E N C E S

1 Chapron CM, Pierre F, Lacroix S et al. Major vascular injuriesduring gynecologic laparoscopy. / Am Coll Surg 1997 ; 185 :461-465.

2 Saville LE, Woods MS, Laparoscopy and major retroperitonealvascular injuries. SurgEndosc 1995 ; 9 : 1096-1100,

3 Usal H, Sayad P, Hayek N et al. Major vascular injuries duringlaparoscopic cholecystectomy. An institutional review of expe-rience with 2589 procedures and literature review, Surg Endosc1998 ; 12 : 960-962,

4 Hurd WW, Bude RO, DeLancey JO, Pearl ML. The relation-ship of the umbilicus to the aortic bifurcation: implications forlaparoscopic technique. Ofetel Qjmcd 1992 ; 80 : 48-51.

5 Catarci M, Carlini M, Gentileschi P, Santoro E. Major and minorinjuries during the creation of pneumoperitoneum. A multi-center study on 12,919 cases. SurgEndosc 2001 ; 15 : 566-569.

6 Bonjer HJ, Hazebroek EJ, Kazemier G et al. Open versus closedestablishment of pneumoperitoneum in laparoscopic surgery,Br JSurg 1997; 84: 599 -602,

7 Sternberg A, Alfici R, Bronek S, Kimmel B. Laparoscopic sur-gery and splanchnic vessel thrombosis. / Laparoendosc Adv SurgTech 1998 ; 8 : 65-68.

8 Richmond BK, Lucente FC, Boland JP. Laparoscopy-associatedmesenteric vascular events: description of an evolving clinicalsyndrome. / Laparoendosc Adv Surg Tech 1997 ; 7 : 363-367.

9 Coggia M, Bourriez A, Javerliat I, Goeau-Brissonniere 0. Totallylaparoscopic aortobifemoral bypass: a new and simplifiedapproach. EurJ VascEndovasc Swrg2002 ; 24 : 274-275.

10 Dion YM, Gracia CR. A new technique for laparoscopic aorto-bifemoral grafting in occlusive aorto-iliac disease. J Vase Surg1997 ; 26 : 685-692,

11 Barbera L, Ludemann R, Grossefeid M et al. Newly designedretraction devices for intestine control during laparoscopic aor-tic surgery: a comparative study in an animal model, SurgEndosc2000 ; 14 : 63-66,

12 Said S, Mall J, Peter F, Muller J. Laparoscopic aortofemoralbypass grafting: human cadaveric and initial clinical experi-ences. / Vase Surg 1999 ; 29 : 639-648.

13 Alimi Y, Hartung 0, Orsoni P, Juhan C. Abdominal aortic laparo-scopic surgery: retroperitoneal or transperitoneal approach ?EurJ Vase Endovasc Surg 2000 ; 19 : 21-26.

14 Ahn SS, Hiyama DT, Rudkin GH et al. Laparoscopic aorto-bifemoral bypass. / Vase Surg 1997 ; 26 : 128-132.

85

10ACUTE TYPE B AORTIC DISSECTION:

SURGICAL INDICATIONS AND STRATEGY

MICHAEL JACOBS, TED ELENBAASGEERT WILLEM SCHURINK, BAS MOCHTAR

The clinical spectrum of acute type B aortic dissection is broad, varying from rupture with . _subsequent death to asymptomatic, uncomplicated presentation. Patient population also L(Jcomprises different ages and etiology, ranging from the young Marfan patient to the older 87hypertensive, atherosclerotic patient. This heterogenic etiology, symptomatology and patientpopulation obviously requires a differentiated approach.

The indications for emergency operation for acute type A aortic dissection are established,but the management of acute type B dissection remains controversial. In general it isadvocated that patients who have type B acute dissection without complications be treatedconservatively during the acute phase and surgical treatment be selected if the aortic diameterbecomes enlarged during the chronic phase. However, recent publications question thismedical treatment as the most optimal approach in acute type B dissections and propose amore surgical attitude.

This chapter summarizes the main issues determining the choice for surgical treatment inpatients with acute type B dissection, also addressing the outcome of conservative treatmentwith subsequent related indications for surgical intervention. Surgical strategies are describedwhereas endovascular techniques are discussed in another chapter of this book.

Non-surgical treatment patients are admitted to a critical care unit and EGGand blood pressure are closely monitored. During

Since most patients with acute type B dissection the acute phase of dissection, nitrate, calcium chan-suffer from (severe) hypertension, medical treat- nel antagonist and B-adrenergic receptor blockerment is focused on hypotensive therapy. In general, medications are administered intravenously. If no


10

complications occur, medical treatment is conti-nued until the blood pressure reaches acceptablelevels and can be managed by oral medication. Fol-lowing discharge from the hospital the intensive fol-low-up programme starts, including control ofblood pressure measurements and CT/MRA ima-ging. This conservative policy generally offersacceptable outcome in the majority of cases withlimited aortic enlargement during follow-up, assum-ing that antihypertensive treatment is successful [1].

According to a definition with a debatable peri-od of fourteen days, acute type B dissections be-come chronic type B dissections and retrospectiveanalysis of these patients might identify indicationsfor surgical treatment of acute patients in order toprevent serious complications in the chronic phase.Kato et al. [2] performed univariate and multivari-ate factor analyses in patients with type B dissectionwho had been treated medically during the acutephase to determine the predictors for chronic phaseenlargement (greater than 6 cm) of the dissectedaorta. The predominant predictors for aortic en-largement in the chronic phase were the existenceof a maximum aortic diameter of or greater than40 mm during the acute phase and a patent pri-mary entry site in the thoracic aorta. The values ofactuarial freedom from aortic enlargement forthese patients at 1, 3 and 5 years were 70%, 29%and 22%, respectively. No aortic enlargement wasobserved in the other patients throughout the en-tire follow-up period. The authors recommendedsurgical treatment during the acute phase in pa-tients with a large aortic diameter (superior or equalto 40 mm) and a patent primary entry site in thethorax. The clinical value of these recommenda-tions were completely confirmed by Kozai et al. [3]who described poor prognosis in these patients withopen false lumen and large aortic diameter.

Noteworthy is the analysis of Sueyoshi et al. [4]concerning type B aortic intramural hematoma(IMH). This IMH, initially described as dissectionwithout intimal tear, is believed to be rupture of thevasa vasorum and represents a continuum of aor-tic dissection in which progression of an IMH withrupture into the lumen may be one mechanism foraortic dissection. In the experience of Sueyoshi etal. [4] maximum aortic diameter and maximumaortic wall thickness on initial CT image were pre-dictive for progression of the affected aorta in pa-tients with type B IMH. They recommended carefulsurveillance studies in patients with a maximumaortic diameter of 40 mm or more or a maximum

aortic wall thickness of 10 mm or more becausethese patients are prone for complications directlyrelated to aortic rupture.

Marui et al. [5] also addressed the question whetheracute-phase factors could be identified, predictivefor chronic-phase aortic enlargement, by studyingchronic-phase enlargement of dissections in pa-tients without complications during the acute phase.In 101 patients with uncomplicated type B acutedissection, univariate and multivariate factor analy-ses were performed similar to the results of Katoet al. [2], a patent false lumen and a maximumaortic diameter greater than 40 mm were independ-ent predominant predictors for chronic phaseenlargement (larger than 60 mm). Actuarial free-dom from aortic enlargement for the patients witha maximum aortic diameter of 40 mm and a patentfalse lumen at 1.5 and 10 years were 43%, 33% and22% respectively, whereas in patients with a maxi-mum aortic diameter of less than 40 mm and aclosed false lumen, the values were 97%, 94% and84%, respectively. The authors suggest that patientswith a patent false lumen and a maximum aorticdiameter of larger than 40 mm should undergo sur-gery during the sub acute or early chronic phase,whereas patients with a closed false lumen and amaximum aortic diameter of less than 40 mmshould continue to receive hypotensive treatment.The main reason for this more aggressive approachis the fact that mortality rate of surgical treatmentfor patients with acute type B aortic dissection with-out complications has recently decreased. Otherarguments put forward by Marui et al. are that thesurgical results for late chronic phase cases ofenlarged aortas are not better than the results foracute phase surgery and the strength of the dis-sected aorta during the early chronic phase is sat-isfactory. The results of the above mentionedstudies clearly justify a more selective strategy forpatients with acute type B dissection. Before iden-tifying such a selective approach it would be impor-tant to analyze the complications of conservative,medical treatment.

Complications in acutetype B aortic dissection

Several retrospective studies have been performedto determine whether there are initial findings dur-ing the acute phase of type B dissection which can

TT

predict the long-term outcome of the disease.Genoni et al. [6] reviewed case records of 130 pa-tients treated for type B aortic dissection over a ten-year period. Thirty one percent of the patients wereoperated on in the acute phase (less than 14 days),29% were operated on in the chronic phase and45% were treated medically. The most frequent indi-cations for emergency surgery were malperfusion(34%), potential rupture (27%) and aortic rupture(19%). Indications for urgent surgery (before dis-charge from the first hospitalization) were malper-fusion, left pleural effusion, increasing aorticdiameter and persistent pain. Overall mortality ratein the acute phase was 10.8%, 5.6% of whom whohad until then only medical treatment and 22% ofpatients operated on in this phase. In-hospital mor-tality rate was 9% for the medically treated patientscompared with 9.1% for patients undergoing urgentsurgery and 27% for those undergoing emergencysurgery. Age, persistent pain and malperfusion weresignificant independent predictors of the need forsurgery. Paraplegia, leg ischemia, pleural effusionand aortic diameter larger than 4.5 cm were sig-nificant predictors of poor survival. Patients with-out malperfusion, pleural effusion, rupture orshock had a significantly better event-free survival.The actuarial survival rate for high-risk patients(malperfusion, rupture, shock) was 62% at one yearand 40% at 5 years. The corresponding values forlow-risk patients were 94% and 84%, respectively.Based on their experience the authors advocatemedical treatment in uncomplicated dissections,mainly consisting of long-term beta-blocker treat-ment. Emergency surgery should be performed formalperfusion such as leg ischemia and visceral/renal ischemia, potential rupture and rupture. Sur-gical mortality in the acutely operated patientsmainly occurs in patients with rupture and shock.It should be emphasized that surgical patients areat very high risk and can therefore not be com-pared with uncomplicated, medically treated pa-tients. Carrel et al. [7] assessed early and long-termoutcome of acute B aortic dissection after initial con-servative treatment. Seventeen per cent of 225 pa-tients underwent replacement of the descendingaorta within the first week after hospitalization, indi-cated by rupture, extensive dilatation, malperfusionor pseudocoarctation with uncontrollable hyper-tension. All other patients underwent primary con-servative treatment. Hospital mortality during andafter initial conservative treatment was 17.6%, dueto rupture, intestinal ischemia or cardiac failure.

Hospital mortality after early surgery was 21% forthe overall time period. After hospital dischargefrom the initial acute dissection, surgery for chronicdissection was performed in 47 patients because ofexpanding descending aortic aneurysm mainly (mor-tality 4/47). The authors recommend conservativetreatment in uncomplicated type B aortic dissec-tions and urgent surgery for rupturing disease, dis-tal malperfusion, uncontrollable hypertension orpain. Surgery should also be considered in youngerpatients or Marfan Syndrome with 5 cm diameterof the aorta at initial evaluation, in patients withlimited false aneurysm or retrograde dissection intothe aortic arch, and those with poor medical com-pliance or uncontrollable proximal hypertension.

Indications for surgery

Based on the above-mentioned clinical outcomeof conservative treatment and the complications inacute type B aortic dissections, indications for sur-gery can be distilled. Furthermore, this analysis alsosuggests that the timing of surgical interventionshould be differentiated, as summarized in Table I.Emergency surgery is indicated in patients presentingwith rupture, shock and hemodynamic instability.Malperfusion of visceral organs and kidneys, as wellas spinal cord and lower limbs, requires immediatetreatment. An uncomplicated type B dissection

Emergency surgery (open/endovascular)Rupture, shock, malperfusion, retrograde A

Urgent surgeryUnremitting pain, uncontrollablehypertension, rapid aortic expansion

Early chronic-phase surgeryPatent false lumen with initial aorticdiameter > 4 cm

Elective surgeryDiameter enlargement during chronic phase> 6 cm (Marfan > 5 cm)

89


w90

which extends retrogradely into the aortic archnecessitates emergency surgery via sternotomy.

Urgent surgery is indicated in case of unremittingpain, uncontrollable hypertension and rapid aorticexpansion. In the early chronic phase, patients witha patent false lumen and initial aortic diameterlarger than 4 cm should be considered for surgicalrepair in order to prevent long-term complications.Elective surgery during the chronic phase is limitedto patients who show enlargement greater than6 centimeters. In patients with Marfan or Ehlers-Danlos this threshold diameter is 5 centimeters.

It should be emphasized, however, that all theserecommendations are based on clinical experiencesand not on prospectively proven evidence. How-ever, the complex and inhomogeneous etiology andpopulation will never allow these kind of studies.

Selective and surgicalmanagement of acute type B

aortic dissection

In an attempt to describe a selective managementstrategy for acute type B aortic dissection, Schor et al.[8] retrospectively analyzed the outcome of theirmanagement of 68 consecutive patients. Medical ther-apy consisted of aggressive antihypertensive therapy.Patients with unremitting pain or uncontrollablehypertension despite antihypertensive treatmentunderwent early operation. Emergency operationwas also performed for rupture or significant aorticdilatation. Furthermore, if CT-scans showed increas-ing peri-aortic or intrapleural fluid extravasation,rapid aortic expansion or significant aortic dilata-tion, urgent operation was also recommended.

Three patients died soon after admission, 17 un-derwent operation and 48 were treated conserva-tively. In the surgical group, mortality did not occurand major complications were encountered in 59%of patients. In the conservative group, only one pa-tient (2%) died of rupture. However, 12 patients(25%) required aorta-related interventions. Actu-arial survival at one and five years were not dif-ferent between both groups (approximately 90%and 75%, respectively). When interpreting these re-sults it is important to emphasize that the author'shospital serves as a tertiary referral center, indi-cating that many of the patients are self selected,which means that those who died or were unfit forreferral, never reached the hospital. Importantly,

survival of both modalities improved significantlyduring the last decade. Rapid diagnosis, intensivemonitoring and aggressive modern pharmacolog-ic management increased survival rates of non-op-erative management. Taking all these issues intoaccount, the authors support a selective manage-ment of acute type B aortic dissection. It shouldbe emphasized, however, that the reader is left with-out a clear algorithm because no decision tree wasproposed.

Elefteriades et al. [9] supported a complication-specific approach: medical management for uncom-plicated acute descending dissections and surgicalintervention for complicated dissections. Nine of100 consecutive patients with acute dissection diedbefore any treatment was started. Sixty of the 91 sur-viving patients had a benign course and 31 patientshad a course complicated by rupture (8), vascularocclusion (17), early expansion or extension (12)and continued pain (4). Forty-two patients wereoperated (21 early, 21 late): direct aortic replace-ment (32), fenestration (6) and thrombo-exclusion(4). Six patients died after surgery and six devel-oped paraplegia. The authors conclude that thevast majority of patients will survive with medicalmanagement for acute type B dissection. Surgicalintervention is only indicated in complicated dis-section and includes direct aortic replacement forrupture, fenestration for vascular occlusion, andaortic replacement with thrombo-exclusion as anoption for patients with acute expansion.

Recently, the management and outcome of acuteaortic dissection (A and B) was evaluated in theexperience of 12 international referral centers [10].A total of 465 patients were treated: 62% type Aand 38% type B dissections. In type A patients, sur-gery was performed in 72%. In type B patients,20% underwent surgical therapy and 4% percuta-neous fenestration. Medically treated type B pa-tients had 10.7% in-hospital mortality, whereaspostoperative mortality was 31.4%.

This high surgical mortality rate could not be sup-ported by Lansman et al. [11]. They described theirresults of surgery (within 14 days) in 34 patientswith acute type B dissection. Indications for surgerywere pain, rupture, malperfusion or uncontrolledhypertension. Thirty patients underwent left tho-racotomy, 3 had thoraco-abdominal incisions, andone underwent thrombo-exclusion. Surgery wasperformed under hypothermic circulatory arrest(50%) or partial bypass (50%). There were no hos-pital mortalities, however, significant complications

ACUTE TYPE B AORTIC DISSECTION: SURGICAL INDICATIONS AND STRATEGY

occurred in 47% of patients including respiratoryproblems, renal failure, myocardial infarction andchylothorax. Neurologic deficit occurred in 6% ofcases.

Sasaki et al. [12] operated upon 22 patients withacute type B dissection and compared sub totalprosthetic replacement of the thoraco-abdominaldissected aorta (n = 7) with partial replacement ofthe descending aorta at the intimal tear (n = 15).All procedures were performed with femorofemoralpartial cardiopulmonary bypass. There was oneearly and one late death in the partial replacementgroup and no mortality in the other group, result-ing in an overall mortality rate of 9%.

Umana et al. [13] recently addressed the questionwhat the best treatment for acute type B dissectionis: medical, surgical or endovascular stentgrafting.Over a 36-year period they treated 189 patients withacute type B dissection. Sixty-seven patients receivedearly surgical treatment. The two main determinantsof death were shock (hazard ratio [HR] = 14.5) andvisceral ischemia (HR = 10.9). Arch involvement,rupture, stroke, previous sternotomy and coronaryor lung disease roughly doubled the hazard. Surgi-cal mortality decreased over the decades from 57%(1963 to 1969) to 27% (1990 to 1999). In general,their results of medical and surgical therapy werecomparable. With improving surgical outcome theydefend the tactic of early operation, especially inyounger individuals. Table II summarizes mortalityrates of emergency surgery in acute type B aorticdissection.

Surgical techniques

The surgical spectrum ranges from a limited fen-estration to a complete thoraco-abdominal aortic re-placement. This wide range obviously indicates thatthe results of different series in the literature can-not be compared since detailed information aboutthe applied techniques is most often lacking. A lim-ited left thoracotomy with aortic fenestration car-ries a significant lower mortality and morbidity ascompared to a thoraco-laparatomy with completeaortic replacement. The extend of the disease, aneur-ysmatic involvement and associated malperfusiondetermine the surgical strategy. Furthermore, sur-geon's preference and experience finally decidewhich approach and technique will be applied.

ADJUNCTIVE PROCEDURESOperations on the descending and thoraco-ab-

dominal aorta have been notorious for their detri-mental effects on organs supplied from theseportions. Paraplegia, renal failure and visceral in-farction are the most feared complications of ex-tensive aortic repair. Because of the fragile aorticquality with subsequent longer cross-clamp times andthe lack of collateral networks, these complicationsoccur even more frequently in acute dissections ascompared to degenerative aneurysmatic disease.

Spinal cord protection can be achieved by meansof retrograde aortic perfusion or profound hypo-thermia and circulatory arrest. The latter, however,

1091

First author[ref.]

Hagan [10]

Lansman [11]

Sasaki [12]

Umana [13] *

Surgical technique

Miscellaneous

Aortic replacement

Aortic replacement

Miscellaneous

Number of patients

35

34

22

67

Mortality%

31

0

9

57 (1963 - 1969)

Safi [14] Aortic replacement 22

27(1990-1999)

14

* Analysis of the entire experience over a 36-year period demonstrates a trend towards lower early surgical mortality riskover the decades from 57% to 27%.


1092

requires full heparinization carrying the disadvan-tage of bleeding complications. Especially in acute-ly dissected aortic tissue, hemostasis is an immenseburden. Therefore, we prefer left heart bypass withcannulation of the left atrium or pulmonary veinand the femoral artery, only requiring minimal he-parinization (0.5 mg/kg). The additional techniqueof cerebrospinal fluid drainage has extensively beenevaluated and recently proven to be an importantasset in the prevention of paraplegia [15].

Our surgical protocol in elective and emergencysurgery includes assessment of motor evoked po-tentials. This technique is an accurate method fordetecting cord ischemia, guiding surgical tactics toreduce neurologic deficit [16]. Unlike atheroscle-rotic aneurysmatic thoraco-abdominal aortas, acute-ly dissected aortas contain many patent intercostaland lumbar arteries. Monitoring motor evoked po-tentials helps to identify those arteries which arecrucial for spinal cord integrity, requiring reattach-ment or any technique to revascularize.

Distal aortic perfusion also has the advantages ofvisceral and renal perfusion during proximal cross-clamping. However, as soon as the abdominal partof the aorta is excluded by clamps, the visceral andrenal arteries are no longer perfused. In our ex-perience the technique of selective organ perfusionprevents visceral and renal ischemia, even in pa-tients with pre-existing renal insufficiency [17]. Fourperfusion catheters are connected to the left heartbypass-system and inserted in the origins of the celi-ac axis, superior mesenteric and both renal arter-ies. In patients with acute aortic dissection this tech-nique allows continuous organ perfusion, offeringthe surgeon the opportunity to perform an opti-mal vascular reconstruction of the visceral andrenal arteries. These arteries are almost always in-volved in the dissecting process and originate fromthe false or true lumen. Furthermore, side branch-es might be compressed or even contain extensionof the dissection, threatening distal outflow to thetarget organ. All these dramatic anatomic changesrequire optimal surgical repair, which is obviouslytime consuming. In addition, the fragility of the ar-terial and/or aortic wall often requires re-inforce-ment by means of teflon strips, adding even moretime to perform the reconstruction. Selective organperfusion allows these time consuming procedures.

Additional advantages of distal aortic perfusion in-clude unloading the heart, prevention of ischemia-induced metabolites and cooling/rewarming thepatient.

GENERAL CONSIDERATIONSSurgery for acute dissection has two primary ob-

jectives: replacement of the aortic segment at riskof imminent or manifest rupture and relief of dis-tal organ malperfusion. Because rupture is fre-quently located in the proximal half of the de-scending thoracic of infrarenal aorta, replacementcan be limited to these portions. It is rather uncom-mon that the entire thoraco-abdominal aorta hasto be replaced, however, pre-existing aneurysmaticdisease and extensive malperfusion might requiresuch an extensive procedure.

Several techniques have been described duringthe last decades, including thrombo-exclusion, tai-lored aortoplasty and local glue aortoplasty. Themost recent and frequently reported techniques areprosthetic replacement of the thoracic aorta andaortic fenestration [18].

In recent years improvements have been made insuture material, vascular clamps, impermeable grafts,tissue adhesives and antihemorrhagic agents. Acute-ly dissected aortas can preferably be anastomosedwith 4-0 polypropylene sutures. Cross-clamping afriable, dissected aorta should be performed withrubber-shod instruments because they are the leasttraumatic.

The use of biologic glue has greatly contributedto the performance of blood-tight anastomoses.These glues, however, are mainly used in type A aor-tic dissections. In acute type B dissections the prox-imal anastomosis can be re-inforced but distalapplication is not very popular because conjoiningthe aortic layers might induce exclusion of impor-tant side branches.

AORTIC REPLACEMENTThe intimal tear is most frequently located in the

proximal descending thoracic aorta and eventualrupture is most often situated in this segment. Thestandard approach, with the patient in the right lat-eral decubitus position and the left pelvis rotatedposteriorly for access to the left femoral vessels, isvia the fourth or fifth intercostal space. In dissec-tions affecting the thoraco-abdominal aorta the leftthoracotomy is performed in the sixth intercostalspace and extended with a laparotomy. We only tran-sect the anterior 5-10 cm of the diaphragm in orderto limit postoperative pulmonary complications.

The detailed surgical techniques are extensively de-scribed [18]. In summary, limited heparinization isadministered if distal aortic perfusion is performed.Following cross-clamping, a longitudinal aortotomy


visualizes the intimal tear, and false and true lumen.The dissected membrane is transversely removed atthe level of the targeted proximal anastomosis andthe complete aortic wall is then transected.

In a fragile aorta we perform a sandwich-technique,including a circular teflon-felt inside and outside theaortic layer with subsequent end-to-end anastomosisto this re-inforced circumference (Fig. 1).

The level of the distal anastomosis can vary con-siderably and depends on many parameters. Themost limited scenario comprises attachment a fewcentimeters distal to the proximal anastomosis. Inacute dissection this anastomosis is often performedto the true lumen, in chronic dissection to the outerlayer. Attachment to the true lumen, however, car-ries the potential risk of malperfusion of side bran-

ches originating from the false lumen. We thereforeprefer distal fenestration with a length of severalcentimeters and re-inforce the outer layer withinner- and outer circumferential teflon strips. Theelephant trunk principle might also be applied.

In case the total descending thoracic aorta isreplaced, the dissected membrane is completelyresected, leaving a longitudinal rim at the non-dis-sected edges. Three French (F) occlusion cathetersare inserted in the back bleeding intercostal arter-ies and based on our motor evoked potential infor-mation we reattach the important segmental vessels.Also this anastomosis is re-inforced with an exernalteflon strip (Fig. 2).

It is not uncommon that an acute type B dissec-tion with the tear in the proximal descending aorta

93

FIG. 1 Proximal anastomosis, just cephalad to the dissection tear. In fragile aortathe anastomosis can be re-inforced with a teflon layer outside, inside or both.


does not cause ischemic problems in the thoracicsegment (paraplegia) but leads to visceral or renalischemia, necessitating either fenestration or openrepair. The latter is performed through a laparo-tomy, extended with a limited, left anterior thora-cotomy via the eighth or ninth intercostal space,allowing adequate cross-clamping of the distal tho-racic aorta. Since adequate and safe reconstructiondemands time, we prefer to use selective perfusionin this situation as well. Obviously, the left heartcannot be reached via this low thoracotomy andpartial extracorporeal bypass is installed (femoro-femoral cannulation). Following cross-clamping,aortotomy and opening of the dissected membrane,the selective catheters are inserted in the visceraland renal arteries, and intercostal and lumbar arter-ies are temporarily occluded with 3F ballooncatheters. With a dry surgical field and continuousorgan perfusion the surgeon now has all the timeto analyze the damage.

At this point several surgical techniques are pos-sible depending on the extension of the dissection

into the side branches. Visceral or renal arterieswhich still have a conjoined connection with all lay-ers of the aorta and their origin offer the easiestreconstruction. In case the aortic wall is strongenough, resection of the dissected membrane withsubsequent closure of the aorta (teflon re-inforced)can solve the problem. This local fenestration isoften performed to relief a static obstruction of thevisceral arteries.

It often occurs, however, that the origin of the vis-ceral and/or renal arteries are disconnected fromthe inner aortic layer and compressed by the falselumen or even occluded if no re-entry exists. Also,the aortic dissection can extend into the visceraland/or renal arteries (Fig. 3). In all these circum-stances we prefer vascular repair by means of sepa-rate polyester grafts (Fig. 4). The affected artery isdissected as far as the dissection reaches and trans-versely transected. Depending on its diameter, a 6or 8 mm polyester graft is anastomosed in an end-to-end fashion with 5-0 or 6-0 prolene sutures, withor without a small, circumferential teflon strip. This

1094

FIG. 2 Reattachment of three intercostal arteries, temporarily occluded with 3F balloon catheters. A circular teflon stripre-inforces the anastomosis.


FIG. 3 Acute type B dissection with extension into the visceral (A) and renal (B) arteries.

10.95

FIG. 4 Diagram showing a dissected aorta with invol-vement of visceral and renal arteries. Selective organperfusion is continuously provided, allowing optimalvascular reconstruction of the affected arteries.

peripheral reconstruction is performed under con-tinuous perfusion. After all arteries are repairedthe proximal anastomoses of the aortic tube graftto the dissected distal thoracic aorta is performedaccording to the above described technique, fol-

lowed by the distal anastomosis and connection ofthe selective grafts to the tube graft.

Infrarenal fenestration is in most cases effectiveto relief a dynamic obstruction. The goal is to re-establish the same arterial pressures in the false and


1096

true lumen by creating a large re-entry in the in-frarenal aorta. It should be noted that primary clo-sure of the diseased aorta is not always feasible,requiring a small interposition graft with re-inforcedanastomoses.

Lower limb ischemia, in the absence of proximalischemic problems, is most often relieved by meansof catheter fenestration or extra-anatomic bypass(femoro-femoral bypass, axillo-femoral bypass).

CONNECTIVE TISSUE DISEASEAcute type B dissection in patients with Ehlers-

Danlos or Marfan disease who require emergencysurgery is a surgeon's nightmare. Acute dissectionin a pre-existing fragile aorta indeed diminishes suc-cessful outcome of open aortic repair, especially ifthe entire thoraco-abdominal aorta has to be replac-ed in case of a dissecting thoraco-abdominal aneur-ysm. The only advantage is that these patients aremost often young and have an adequate cardiopul-monary function. The same surgical principles areapplicable in these patients with even more empha-sis on re-inforcement and reconstruction with selec-tive grafts.

INTRA-OPERATIVE COMPLICATIONSIt is evident that emergency surgery in acutely

dissected aortas is associated with a high mortalityand morbidity. It is also clear that morbidity andmortality are depending on the extent of the sur-gical procedure. The main dilemma for the sur-geon is to perform a palliative, limited procedureto get the patient alive from the operating table orincrease the short-term risk by performing a moreextensive and curative procedure in order to im-prove long-term outcome.

It is not really possible to design an algorhythmbecause too many factors and parameters determinethe final outcome. However, it depends very muchon intra-operative complications which requireimmediate action.

The first problem which can arise after laparo-tomy is the appearance of (severely) ischemic bowel.In general, the vascular reconstruction is performedfirst, followed by judgement of the viability of thebowel. Most often bowel resection is required andit is not uncommon that the visceral ischemia isalready beyond repair, leaving minimal changes tosurvive.

Distal aortic perfusion by means of left heartbypass has the potential risk of aggravating malper-fusion of the visceral, renal or spinal cord arteries.

The structure and composition of the dissection isunpredictable and it can occur that reversal of flowexcludes side branches which were initially patent.Intra-operative monitoring of urine output andmotor evoked potentials can assist in the assessmentof acute malperfusion. Fortunately this is an uncom-mon complication, however we have observed thisphenomenon several times. Immediate arrest of theleft heart bypass is obviously necessary and the nextstrategy depends on the extend of the procedure.If replacement of the total abdominal or thoraco-abdominal aorta is planned we reverse the aorticreconstruction and start with implantation of abifurcation graft to both iliac of femoral arteries.The body of the graft is then clamped and a can-nula is inserted in the prosthesis, allowing extra-corporeal circulation and selective organ perfusion.Following, the reconstruction is performed fromthe distal into the proximal direction.

Intra-operative bleeding problems comprise amajor difficulty. Meticulous surgical techniques area prerequisite, but major bleedings also arise fromthe dissected layers and coagulation disorders.Intensive assessment of the complete coagulationspectrum and the administration of coagulationproducts are of imminent importance. It might benecessary to pack the complete surgical field andremove the gauzes one or two days later.

Conclusion

Acute type B dissection usually exists withoutacute complications and is generally treated conser-vatively. Emergency surgery is indicated in patientspresenting with rupture, shock and hemodynamicinstability. Immediate surgery is required in case ofmalperfusion of the visceral organs and kidneys,spinal cord and lower limbs. Urgent surgery is rec-ommended in patients with unremitting pain, un-controllable hypertension and rapid aortic expan-sion. In the early chronic phase, patients with apatent false lumen and initial aortic diameter larg-er than four centimeters should be considered forsurgical repair. Improved surgical techniques andthe application of adjunctive procedures have sub-stantially contributed to augmented surgical out-come. Future hope and ambition are focused onhybrid vascular procedures, in which minimal in-vasive techniques play a major role.


R E F E R E N C E S

1 Iguchi A, Tabayashi K Outcome of medically treated StanfordB aortic dissection. Jpn arc/1998; 62: 102-105.

2 Kato M, Bai H, Sato K et al. Determining surgical indicationsfor acute type B dissection based on enlargement of aorticdiameter during the chronic phase. Circulation 1995; 92(SupplII): 107-112.

3 Kozai Y, Watanabe S, Yonezawa M et al. Long-term prognosisof acute aortic dissection with medical treatment: a survey of263 unoperated patients./pn Qrr/2001; 65: 359-363.

4 Sueyoshi E, Imada T, Sakamoto I et al. Analysis of predictivefactors for progression of type B aortic intramural hematomawith computed tomography. / Vase Swrg2002; 35: 1179-1185.

5 Marui A, Mochizuki T, Mitsui N, et al. Towards the best treat-ment for uncomplicated patients with type B acute aortic dis-section. Circulation 1999; 100 (Suppl II): 275-280.

6 Genoni M, Paul M, Tavakoli R, et al. Predictors of complica-tions in acute type B dissection. Eur J Cardio Thor Surg 2002;22: 59-63.

7 Carrel T, Nguyen T, Gysi J, et al. Acute type B aortic dissec-tion: prognosis after initial conservative treatment and predic-tive factors for a complicated course. Schweiz Med Wochenschr1997; 127: 1467-1473.

8 Schor JS, Yerlioglu ME, Galla JD, et al. Selective managementof acute type B aortic dissection: long-term follow-up. Ann ThorSwrgl996; 61: 1339-1341.

9 Elefteriades JA, Lovoulos CJ, Coady MA, et al. Managementof descending aortic dissection. Ann Thorac Surg 1999; 67:2002-2005.

10 Hagan PG, Nienaber CA, Isselbacher EM, et al. The Interna-tional Registry of Acute Aortic Dissection (IRAD). New insightsinto an old disease. JAMA 2000; 283: 897-903.

11 Lansman SL, Hagl C, Fink D et al. Acute type B aortic dissec-tion: surgical therapy. Ann Thor Surg 2002; 74: SI833-1835.

12 Sasaki S, Yasuda K, Kunihara T et al. Surgical results of Stan-ford type B aortic dissection. Comparison between partial andsubtotal replacement of the dissected aorta. / Cardiovasc Surg2000; 41: 227-232.

13 UmanaJP, Miller DC, Mitchell RS. What is the best treatmentfor patients with acute type B aortic dissections. Medical sur-gical or endovascular stent-grafting? Ann Thor Surg 2002; 74:S1840-1843.

14 Safi HJ, Miller CC, Reardon MJ et al. Operation for acute andchronic aortic dissection: recent outcome with regard to neuro-logic deficit and early death. Ann Thor Surg 1998; 66: 402-411.

15 Coselli JS, Lemaire SA, Koksoy C et al. Cerebrospinal fluiddrainage reduces paraplegia after thoracoabdominal aorticaneurysm repair: results of a randomized clinical trial. / VaseSwig 2002; 35: 631-639.

16 Jacobs MJ, Elenbaas TW, Schurink GW et al. Assessment ofspinal cord integrity during thoracoabdominal aortic aneurysmrepair. Ann Thor Swrg2002; 74: S1864-1866.

17 Jacobs MJ, Eijsman L, Meylaerts SA et al. Reduced renal failurefollowing thoracoabdominal aortic aneurysm repair by selectiveperfusion. Eur] Cardiothorac Surg 1998; 14: 201-205.

18 Borst HG, Heinemann MK, Stone CD. Surgical treatment of aor-tic dissection. Churchill Livingstone Inc., 1996, 357 p.

1097

11ENDOVASCULAR TREATMENT

OF AORTIC TYPE B DISSECTION

RACHEL BELL, PETER TAYLOR

Acute aortic dissection is the most common aortic emergency,, with an incidence double thatof ruptured abdominal aortic aneurysms [I]. It affects 10 to 20 people per million populationper annum [2]. Without treatment, 36% to 72% of patients will die within 48 hours ofdiagnosis [3].

The Stanford classification is based on the presence or absence of involvement of theascending aorta. Type A dissection involves the ascending aorta. Type B dissection does notinvolve the ascending aorta and the primary intimal tear is usually just distal to the originof the left subclavian artery in the descending thoracic aorta. The distinction between acuteand chronic dissection is arbitrarily based on time since the onset of symptoms: less than14 days for acute dissection and greater than 14 days for chronic dissection.

1199

Treatment

The preferred treatment for acute type B aorticdissection is medical management with antihyper-tensive drugs and B-blockers. This is based on re-ports of survival rates of only 50% for open sur-gery compared with 80% for medical treatmentalone [4]. Emergency surgery or endovascular in-tervention is reserved for ongoing pain, refractoryhypertension, localized false aneurysm, end-organischemia, and rupture [5,6]. These complicationsoccur in 30% to 40% of patients. Recently, the Inter-national Registry for Acute Aortic Dissection (IRAD)

reported that mortality in patients with type B dis-section treated medically was 11% compared with31% in those who required surgery [7]. Pain usu-ally resolves with adequate treatment for hyperten-sion. The majority of patients have some fluid inthe left chest that is usually a transudate secondaryto the dissection, which must be differentiated fromrupture by the appearance of extravasated contrastmedium. Renal and mesenteric ischemia carry asurgical mortality of 50% and 88%, respectively [5].In the long term, those treated medically have a30% to 40% risk of aneurysm formation, which re-quires treatment if they are symptomatic or if the


diameter is more than 5.5 to 6 cm in diameter [8,9].Aneurysms related to previous dissection have ahigh risk of rupture and appear to rupture at asmaller diameter than degenerative aneurysms [8].Currendy there is no level I evidence regarding thediameter at which aneurysms related to previousdissection should be repaired.

Endovascular treatment of complicated type Bdissection includes covering the primary entry tearwith a stent graft, percutaneous fenestration of theintimal flap, and stenting of obstructed aortic sidebranches. Endovascular treatment has also beenrecommended for penetrating ulcers and intramu-ral hematomas of the descending aorta, which havebeen identified as precursors of dissection [7].

Technical advances have had an enormous im-pact on diagnosis and treatment of aortic dissection,and endoluminal repair is now considered the firstline treatment for complicated type B dissection.

Endovascular treatment

The endovascular techniques used to treat type Bdissection are:1 - placing a stent graft over the primary entry tear

to obliterate the flow into the false lumen,2 - percutaneous fenestration of the intimal flap,3 - stenting the aortic side branches.

Factors that influence the type and timing ofintervention are the type of dissection, the mech-anism of obstruction, and the aortic branchesinvolved. The endovascular techniques are compli-mentary and a combination of procedures may berequired depending on the clinical status of thepatient and the aortic branches affected.

The primary endovascular technique is place-ment of a stent graft across the primary entry tear,

n100

Mechanisms involvedin aortic dissection

Aortic dissection is thought to occur when thereis a tear in the aortic intima, allowing blood to trackbetween the intima and the media. The associationbetween intramural hematoma and aortic dissec-tion suggests that a dissection may also start as ableed from the vasa vasorum into the aortic media.A dissection can extend a variable distance, in aretrograde or antegrade fashion. The blood-filledspace between the intima and the media becomesthe false lumen. The dissection is commonly spiralin shape and often extends into the abdominalaorta. The right renal artery and the visceral arter-ies are usually perfused from the true lumen andthe left renal artery from the false lumen (Fig. 1).This, however, is not always the case and dependson the relationship of the intimal flap to the ori-gins of these vessels (Fig. 2). End-organ ischemiacan be caused by static obstruction resulting fromextension of the dissection into aortic side branches,or by dynamic obstruction due to distension of thefalse lumen causing the intimal flap to bow into thetrue lumen resulting in true lumen collapse (Fig. 3).Patency of the false lumen in the thorax correlatesclosely with the late complications of aortic dissec-tion such as aneurysmal dilatation and death fromrupture [10]. In chronic aortic dissection, a highflow rate in the false lumen is associated with anincreased risk of rupture [11].

FIG. 1 Arteriogram showing "floating viscera" with contrastfilling the celiac axis seemingly unconnected to the aorta.

ENDOVASCULAR TREATMENT OF AORTIC TYPE B DISSECTION

as this can relieve both static and dynamic obstruc-tion of aortic branches. Experiments have shownthat decreasing the false lumen inflow by placinga stent across the primary entry tear is the mosteffective treatment for true lumen collapse [12,13].Fenestration and aortic branch stenting are usuallylimited to those patients who have residual ischemiaafter redirection of inflow into the true lumen.However, fenestration can be used as a first line treat-ment for acute limb ischemia, which has becomethe major indication for this technique.

Imaging and devicesThe commercially manufactured devices cur-

rently available in Europe are the Talent thoracicstent (Medtronic AVE), which consists of a nitinolframe covered with polyethylene, and Endofit (En-domed, Inc), which is a nitinol frame with a poly-tetrafluoroethylene (PTFE) cover. The Thoracic Ex-cluder (W.L. Gore & Associates), manufactured fromnitinol and PTFE, was recently withdrawn volun-tarily from the market for redesigning following re-ports of fractures in the nitinol frame in 10% ofpatients in the United States. There are problemswith the rigid devices in this clinical setting, as theycan erode through the intimal flap, causing pres-

surization of the false lumen and subsequent rup-ture. It may be necessary to design a stent graftspecifically for the treatment of aortic dissection.Some authorities have recommended stenting allpatients presenting with acute type B dissection, toreduce the incidence of late aneurysm formation.However, this should be assessed against best med-ical treatment in a randomized controlled trial.

Computerized tomography (CT) and calibrationangiography are used to determine the dimensionsof the stent graft. The advent of multislice CT andmagnetic resonance angiography has supplantedthe need for conventional angiography. However,angiography may still be used to delineate the pri-mary tear and to show which arterial branchescome off the true and false lumens.

In cases of dissection it is difficult to know theoriginal diameter of the aorta, and the width of thenon-dissected aorta proximal to the entry tear isused to size the diameter of the stent. It is recom-mended that the devices be only oversized by 10%,as there is a risk of rupture with devices that aretoo big associated with perforation of the intimalflap.

Intravascular ultrasound (IVUS) can be used toidentify the location of the primary entry tear andto demonstrate the relation of the true and falselumens and the aortic branches. It is essential that

101

FIG. 2 CT scan showing an acute aortic dissection withthe left renal artery originating from the true lumen.

FIG. 3 CT scan showing "true lumen collapse" associatedwith partial thrombosis of the false lumen.


all patients have radiological follow-up with CTscan and plain chest X-ray at 3 months, 6 months,12 months, and annually thereafter. The ideal out-come is complete thrombosis of the false lumen.In patients with partial thrombosis of the falselumen, there is still a risk of aneurysmal dilatation.The long-term durability of stent grafts is unknownbut there is the potential for development of stentfractures, endoleaks, and migration.

PERCUTANEOUS FENESTRATIONThis technique can be used in cases of true lumen

collapse in order to direct blood flow into the truelumen, decrease the pressure in the false lumen,and allow reperfusion of aortic branches that havebeen isolated by the dissection. Arterial access isfrom the femoral artery and ideally biluminal

n102

Endovasculartechniques

COVERED STENTSThe procedures can be carried out in theater or

in the angiography suite. High-quality imaging isessential to ensure accurate graft placement. Theoperation can be performed under general, re-gional, or local anesthesia. Regional or local blocksare increasingly performed, as they allow assess-ment of distal neurologic function throughout theprocedure. Devices are usually inserted via the com-mon femoral artery and 5 000 units of unfraction-ated heparin are given intravenously prior to in-sertion of the introducer sheath. The stent graft isintroduced over a stiff guide wire into the truelumen and deployed to cover the primary entrytear. The proximal neck length must be at least twocentimeters to ensure adequate fixation (Figs. 4Aand 4B). It is possible to cover the left subclavianartery without pre-emptive revascularization. Occa-sionally the proximal neck requires balloon dila-tion after deployment to exclude a type I endoleak.However, it is not advisable to perform balloon di-lation in the area of dissection because of the riskof rupture and of tearing the fragile intimal flap.Deployment of stent grafts distally within the dis-section that do not cover the primary tear maycause retrograde dissection and turn a type B dis-section into a type A with disastrous consequences.Early devices required systemic hypotension for de-ployment to prevent migration, but with the newerstent grafts this is not necessary. Following deploy-ment, further angiography is performed to confirmthe position of the stent graft and exclusion of theprimary entry tear. The arteriotomy is repaired andthe wound is closed with dissolvable sutures. Thepatients are observed in recovery for several hoursafter which they return to the surgical ward. A CTscan is performed prior to discharge if there is anyconcern about the exclusion of the false lumen.

FIG. 4 A - Arch aortography showing the false lumenfilling from a primary entry tear just distal to the leftsubclavian artery. B - After deployment of a stent graftacross the primary entry tear resulting in exclusion of thefalse lumen.


manometry is performed before and after inter-vention. IVUS can be used to help direct balloonfenestration of the intimal flap. Single or multipletears are made in the intimal flap using a biopsyneedle, a guide wire is positioned at the puncturehole and a 12 to 14 mm angioplasty balloon is usedto complete the fenestration. Alternatively, fenes-trations can be created by dilating re-entry tearsidentified using IVUS. Fenestration should be per-formed in the abdominal aorta as more proximalfenestrations fail to provide adequate redirectionof blood flow in the distal aorta. Sometimes fenes-tration alone does not provide adequate reperfu-sion and adjunctive procedures may be required[14]. In acute dissection the intimal flap is fragile,tears easily and the fenestrations remain patent. Forchronic dissection the intimal flap is more rigid anddeployment of a bridging stent across the fenes-tration has been used to ensure adequate distalflow. In cases of true lumen collapse in the iliacarteries, placing guide wires in the true and falselumens and advancing a single introducer sheathover both wires causes a longitudinal tear in theintimal flap leading to reperfusion of the ischemiclimb. However, the technique is difficult and notwidely practiced. Fenestration is contraindicated inthe presence of partial or complete thrombosis ofeither lumen because of the associated risk of dis-tal embolization.

UNCOVERED STENTSResidual static obstruction of aortic branches

after stenting across the primary entry tear canoccur. In this circumstance, an uncovered stent canbe placed in the true lumen of the aortic branchto relieve the obstruction. Stents can also be placedfrom the false lumen of the aorta to restore flowto the true lumen of the branch vessel. Deploymentof an infrarenal stent graft in the true lumen ofthe abdominal aorta can be used to treat limbischemia.

Results

COVERED STENTSKato et al. showed experimentally that the false

lumen could be excluded by simply covering theprimary entry tear with a covered stent graft. Reduc-ing inflow into the false lumen promotes completethrombosis [15]. Covering only a short length ofdescending thoracic aorta reduces the risk of para-

plegia and this has been born out by the clinicalresults. Care must be taken with patients with Mar-fan syndrome, as there are often multiple tears inthe intima and just covering the primary tear maynot be effective. In these patients, the need toexclude the false lumen must be weighed againstthe increased risk of paraplegia.

The Stanford group was the first to report theirexperiences with custom-made grafts (Table I).They reported that revascularization of blocked aor-tic branches occurred in 76% of patients. Long-term follow-up has shown 79% (15/19) of patientshaving complete thrombosis of the false lumen[16]. Nienaber et al. reported zero mortality andmorbidity in a small series of 12 patients treated bystenting across the primary tear [17]. They havesince reported excellent results in an additional82 patients (Table I) [18]. However, it is difficultto interpret this data, as it does not specify the dis-tribution of acute and chronic cases or the num-ber with rupture or end-organ ischemia.

In comparison with open surgery, this endolu-minal technique has low morbidity and mortalityrates. Importantly, the risk of paraplegia appears tobe significantly lower than for conventional surgery.Endoluminal repair avoids thoracotomy, aortic cross-clamping, and cardiac bypass. As a consequence,blood loss is minimal and admission to intensivecare is rarely required. Endoluminal exclusion pro-motes thrombosis of the false lumen, which hasbeen shown to decrease the risk of aneurysm for-mation [10] (Figs. 5A and 5B).

PERCUTANEOUS FENESTRATIONAND AORTIC BRANCH STENTING

These adjunctive techniques can be technicallycomplex and time consuming, and are only requir-ed in a small number of patients. Slonim et al. re-ported successful revascularization in 93% (37/40)of patients treated with a combination of fenestra-tion and stenting. However, the 30-day mortalityrate for the group was 25% (10/40). The causes ofdeath were multiorgan failure, rupture of the falselumen, and right heart failure (Table II) [14].Williams et al. reported similar results with suc-cessful revascularization in 88% (21/24) and a mor-tality rate of 25% (6/24) [21]. The severity and du-ration of visceral ischemia prior to interventionhave an important impact on outcomes and patientsurvival. One of the disadvantages of endovascularrepair is that the degree of mesenteric ischemiaprior to revascularization cannot be visualized,

11103


, , Number Type1st author ,, , Jr,r , , Year of ofret 1r patients dissection

Dake [16] 1999 19 A 4B 15

Nienaber 1999 12 A 0[17] B 12

Rehders 2001 94*[18]

Lonn[19] 2002 16 A 2B 14

Lee [20] 2002 41

™ , . , ™, , . , Revascula- ,„ ,technical thrombosis of . . , ,, . . . 30-da}, , , J nzation of Complications /.

success false lumen , , ,,T , f , mortality,q}

J ,q. (Tranches (Number oj cases) /&\( /O) ( /OJ : (ff , ( /C)

100 C* 15/19 (79) 76 Colonic 3/19P** 4/19 (21) infarction(l) (16)

Limb ischemia (1)Pneumonia (1)Renal failure(l)

100 C 12/15 (80) - 0P 3/15 (20)

100 98 Stroke (1) 0TIA(l)Bleeding (3)

100 C 15/16(94) - Stroke (2) 0P 1/16 (6) Paraplegia(l)

Type 1 endoleak (1)

87.8 - Intimal tearsSaccular aneurysm

Follow-up(months)

4-28

12

12

12

1-91

11104

Complete thrombosis* Partial thrombosis

Contains the 12 patients from 1999 seriesTIA: transient ischemic attack

FIG. 5 A - CT scan showing an acute type B dissection associated with a small, contained leak into the left hemithorax.B - One-year follow-up CT scan showing thrombosis and shrinkage of the false lumen.


1st author[ref.]

NumberYear of

patients

Type ofdissection

SuccessfulFenestration revascularisation

(%)

Complications(Number of cases)

30-daymortality

(%)

Williams [21] 1997 24 13 Type A

8 TypeB

3 Atypical

6 fenestrations

2 fenestrations+ PTA

12 fenestrations+ stents

4 stents alone

21/24 Sepsis (1)

Slonim [14] 1999 40 10 Type A

30 TypeB

Gaxotte [22] 2002 41

2 fenestrations

0 fenestrations+ PTA

14 fenestrations+ stents

24 stents alone

37/40 Thrombosed(93) renal stent

(1)

Distalembolization

(1)

39/41(95)

Total: 6 (25)

3 multi-organfailure

1 ruptured falselumen

2 complicationsof surgery

Total: 10 (25)

5 multi-organ-failure

2 ruptured falselumen

1 right heartfailure

1 complicationof surgery

1 NA

Total: 7 (17)11105

NA: not availablePTA: percutaneus transluminal angioplasty

which can have catastrophic consequences. Unfor-tunately, exploratory surgery in these patients isoften delayed and, as a result, multiorgan failureand death are common. Cases of mesenteric andrenal ischemia require prompt diagnosis and rapidintervention to prevent complications and death.

Conclusion

The mid-term results for endoluminal treatmentof type B aortic dissection are encouraging but thismay be a highly selected group. These techniques

are relatively new compared with open surgery andare still under evaluation. It appears that stent graftplacement in the acute situation can prevent lateaneurysm formation by facilitating complete throm-bosis of the thoracic aortic false lumen. However,there are still problems with rigid stent grafts, whichcan erode through the intimal flap and cause pres-surization of the false lumen leading to rupture.There is a need for a stent graft that is specifical-ly designed for the treatment of aortic dissectionthat is blunt with a tapered end. Despite these prob-lems, endoluminal repair has a role in the treat-ment of acute and chronic type B dissection, pen-etrating ulcers, and intramural hematomas.


Future trials

Despite increasing experience in the endolumi-nal treatment of acute and chronic aortic dissec-tion, there are still areas that require furtherinvestigation. Ideally this research should take placeunder the auspices of randomized controlled trials.4> The role of endoluminal repair in the treatment

of uncomplicated type B dissection versus bestmedical treatment.

The role of endoluminal repair in the treatmentof complicated type B dissection versus surgicaltreatment.The indications for further procedures to ensurecomplete thrombosis of the thoracic and abdo-minal false lumens, such as the use of uncoveredstents distally.The precise diameter at which asymptomaticaneurysms related to chronic dissection shouldbe repaired.The long-term durability of the stent grafts.

R E F E R E N C E S

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2 Pate JW, Richardson RL, Eastridge CE. Acute aortic dissections.Ann Surg 1976; 42: 395 -404.

3 Anagnostopoulos CE, Prabhakar MJ, Kittle CF. Aorticdissections and dissecting aneurysms. Am J Cardiol 1972; 30:263-273.

4 Wheat MW Jr. Current status of medical therapy of acutedissecting aneurysms of the aorta. World J Surg 1980; 4: 563-569.

5 Cambria RP, Brewster DC, Gertler J et al. Vascular complicationsassociated with spontaneous aortic dissection./tocSwrgl988; 7:199-209.

-« -g 6 Fann JI, Sarris GE, Mitchell RS et al. Treatment of patients withj j aortic dissection presenting with peripheral vascular com-

.-*• *• plications. Ann Swrgl990; 212: 705-713.106 7 Ha§an PG' Nienaber CA, Isselbacher EM et al. The

International Registry of Acute Aortic Dissection (IRAD): newinsights into an old disease. JAMA 2000; 283: 897-903.

8 Griepp RB, Ergin MA, Galla JD et al. Natural history of des-cending thoracic and thoracoabdominal aneurysms. Ann ThoracSurg 1999; 67:1927-1930, discussion 1953-1958.

9 Juvonen T, Ergin MA, Galla JD et al. Risk factors for rupture ofchronic type B dissections./ Thorac Cardiovasc Surg 1999; 117:776-786.

10 Bernard Y, Zimmermann H, Chocron S et al. False lumenpatency as a predictor of late outcome in aortic dissection. Am]Cardiol 2001; 87:1378 -1382.

11 Erbel R, Oelert H, Meyer J et al. Effect of medical and surgicaltherapy on aortic dissection evaluated by transoesophagealechocardiography. Implications for prognosis and therapy. TheEuropean Cooperative Study Group on Echocardiography.Circulation 1993; 87: 1604-1615.

12 Chung JW, Elkins C, Sakai T et al. True-lumen collapse in aorticdissection: part I. Evaluation of causative factors in phantomswith pulsatile flow. Radiology 2000; 214: 87-98.

13 Chung JW, Elkins C, Sakai T et al. True-lumen collapse in aorticdissection: part II. Evaluation of treatment methods inphantoms with pulsatile flow. Radiology 2000; 214: 99-106.

14 Slonim SM, Miller DC, Mitchell RS et al. Percutaneous balloonfenestration and stenting for life-threatening ischemiccomplications in patients with acute aortic dissection. / ThoracCardiovasc Surg 1999; 117: 1118-1126.

15 Kato N, Hirano T, Takeda K et al. Treatment of aortic dissectionswith percutaneous intravascular endoprosthesis: comparison ofcovered and bare stents./ Vase Men Radiol 1994; 5: 805-812.

16 Dake MD, Kato N, Mitchell RS et al. Endovascular stent-graftplacement for the treatment of acute aortic dissection. NEngJMed 1999; 340: 1546-1552.

17 Nienaber CA, Fattori R, Lund G et al. Nonsurgical reconstruc-tion of thoracic aortic dissection by stent-graft placement. NEngJMed 1999; 340:1539-1545.

18 Rehders TC, Nienaber CA. Complications of stent graftplacement in the thoracic aorta. In: Branchereau A, Jacobs M(eds). Complications in vascular and endovascular surgery - Part I.Armonk, Futura Publishing Co 2001: pp 185-192.

19 Lonn L, Delle M, Lepore V et al. Endograft therapy of thethoracic aorta in aortic dissections. Cardiovasc Mervent Radiol2002;25(supp2):S158.

20 Lee DY, Choi DH, Shim WH et al. Elective endovasculartreatment of aortic dissections with stent grafts. CardiovascMervent Radiol 2002; 25 (supp 2): S158.

21 Williams DM, Lee DY, Hamilton BH et al. The dissected aorta:percutaneous treatment of ischemic complications - principlesand results. / Vase Men Radiol 1997; 8: 605 - 625.

22 Gaxotte VD, Haulon S, Willoteaux S et al. Endovasculartreatment in complications of aortic dissection: retrospectivestudy on 52 patients. Cardiovasc Mervent Radiol 2002; 25(supp2):S157.

12TRAUMATIC RUPTURE

OF THE THORACIC AORTA

ROBERTO CHIESA, RENATA CASTELLANO, CARLA LUCCIMARCELO R. LIBERATO DE MOURA, FEDERICO PAPPALARDOGERMANO MELISSANO, EFREM CIVILINI, YAMUME TSHOMBA

Aortic injury may be secondary to several mechanisms; the more frequent are penetrating,iatrogenic, and blunt trauma (Table I) [1-4]. In a recent large autopsy study, all penetratingtrauma victims died before reaching the hospital, whereas 5.5% of the blunt trauma victimswere admitted to the hospital alive [5], explaining why the surgeon will generally face bluntthoracic aortic trauma. Thus, in this chapter mainly blunt lesions will be discussed. Bluntaortic injury occurs as the result of motor vehicle accidents, falls, and crush injuries, and itmay account for 10% to 15% of deaths caused by motor vehicle accidents [6]. Thoracic aortainjuries have been implicated as the cause of death in as many as 17% of all motor vehiclecrash fatalities. It is estimated that between 70% and 90% of patients sustaining this injurydie at the scene from free aortic rupture. The 10% to 20% of patients with thoracic aortainjuries who survive long enough to reach the hospital have a dismal prognosis: it has beenestimated that approximately 30% of them will succumb within 6 hours, 40% to 50%within 24 hours, and 90 % within 4 months, unless expedient and proper diagnostic andtherapeutic measures are undertaken [7].

Pate et al. found that associated injuries were present in more than 90 % of patients withaortic transection, and 24% of them required a major operation before aortic repair [8]. Themajor complications of survivors diagnosed and treated have been related to associatedinjuries and spinal cord injury related to the surgical management.

The characteristics of thoracic aorta injuries have made it difficult for single centers toaccumulate large series of patients. Most studies have been performed on relatively smallpopulations [9-11], done over long time periods [12,13], or concentrated on one particularmethod of treatment [14-17]. Thus, many questions and controversies persist with regard tothe optimal methods of diagnosis and treatment of this pathology.


Penetrating latrogenic

Gunshot wounds

Stab wounds

Other: ice picks, shrapnel,spearing

Motor-related injuries: motor vehicular,motorcycle andauto-pedestrian accidents

Fall

Crush injury

Work/recreational-related: industrialaccidents, bull goring, equestrianaccidents

Central line insertion

Cardiac catheterization

Pacemaker insertion

Intra-aortic ballooncounterpulsation

Expandable stents(tracheal, bronchial or vascular)

12108

Pathogenesis

MECHANISMS OF TRAUMAMore than 90% of thoracic great vessel injuries

are caused by penetrating external or iatrogenictrauma [1]. Penetrating injuries include completeor partial transections and arteriovenous fistulae.Because the vessels involved are generally large, themechanism of muscular retraction usually fails tocontrol hemorrhage, which can result in rapidblood loss [18]. Most penetrating lesions are lo-cated at the ascending aorta and arch branches,with a very poor prognosis, which renders themrare in the clinical setting [5]. Although penetra-ting mechanisms predominate, the number of pa-tients with aortic disruption due to blunt traumahas continued to increase [19]. Aortic rupture inblunt trauma results most commonly from suddenhigh-speed deceleration or, less frequently fromchest compression. Other mechanisms involved inblunt aortic injuries might include compression ofthe vessels between bony structures such as ster-num and spine, and profound intraluminal hyper-tension during a severe traumatic event [20-22].There is much debate as to the type of motor vehi-cle collision that causes aortic disruption. Althoughmost authors agree that a direct frontal decelera-tion is the most common mechanism that can causetraumatic injury to the aorta (Fig. 1), recent stud-ies suggest that as many as 40% of the thoracic aor-tic injuries may be a consequence of side impactcollisions [23-26].

LESION TOPOGRAPHYThe typical point of injury is located in the most

proximal descending aorta, at the site of insertionof the ligamentum arteriosum, just distal to the ori-gin of the left subclavian artery. At this point, ahighly mobile region of the aorta is placed betweentwo fixed segments: the aortic arch is anchored withthe neck vessels including the left subclavian artery,and the descending thoracic aorta is fixed to thethorax by the ligamentum arteriosum and by the

FIG. 1 Common mechanism of aortic injury: a high-speedfrontal deceleration collision.

TRAUMATIC RUPTURE OF THE THORACIC AORTA

intercostal vessels. The mobile part of the aorta,the distal part of the arch and the most proximalpart of the descending are only loosely fixed to thechest wall by the parietal pleura. With abrupt tho-rax deceleration, the fixed portions decelerate withthe chest, but the loosely fixed parts continue tomove forward until they finally decelerate: aorticrupture occurs at the interface between these twoparts [27]. Figure 2 provides some informationregarding the site of thoracic aortic lesions in 144 pa-tients studied in a trauma registry [7].

To clarify the terminology, total rupture or tran-section applies to the full thickness separation ofthe aorta, which can be partial or circumferential(Fig. 3). On the other hand, injury or partial rup-ture refers to lesions without a complete wall dis-ruption. True traumatic dissection, which involvesa longitudinal separation of the media along thelength of the aorta, has rarely been reported [4].

Diagnosis

Each clinical situation, depending on the pa-tient's general status, must be individually judgedsearching for the best diagnostic tools.

MEDICAL HISTORYAlthough an accurate history and physical exam-

ination are necessary, clinical signs and symptoms

109FIG. 2 Principal location of thoracic aortic lesions.

FIG. 3 Types of aortic rupture: (A) partial, (B) circumferential, and (C) double.


110

are often lacking in these patients. A high index ofsuspicion is the cornerstone for timely diagnosisand repair of thoracic aorta injuries or rupture.Aortic injury must be suspected in any patient withhigh-energy trauma to the chest. The violence andmagnitude of the injury forces must be inferredfrom historical and clinical findings. Patients witha history of motor vehicle crash, with victims in thesame accident, or those having fallen from a greatheight, must be suspected of having an aortictrauma.

CLINICAL FINDINGSAortic trauma is often obscured by the presence

of other serious injuries [27]. Nevertheless, if thediagnosis is made, it can overshadow the presenceof other severe and more lethal lesions. Headtrauma, massive abdominal hemorrhage, extensiveburns and severe respiratory insufficiency can delaythe diagnosis and surgical repair of traumatic aor-tic injuries. The radiological finding of an expan-ding mediastinal area, increasing hemothorax and/or prolonged anuria conversely confers priority tothe treatment of a thoracic aortic lesion.

The clinical signs can be as unspecific as a deepor interscapular thoracic pain, which can happenwith aortic adventitia distension. However, patientscan rarely present more specific syndromes like anaortic pseudo-coarctation, coursing with upper limbhypertension and reduced or absent femoral pulses[28]. Intimal flaps or dissections can cause ischemiccomplications, and finally if a total rupture is pres-ent, bleeding to mediastinum and pleura will causehemodynamic instability, worsening pain and deathin the majority of cases.

IMAGING STUDIESThe diagnostic practice depends on the patient's

conditions on hospital admission. The kind of aor-tic and associated lesions influence the outcomeand diagnostic studies, according to the patient'shemodynamic stability and general status.

Chest X-ray. The first step is to obtain a frontchest X-ray, as initial radiological evaluation, inevery high-speed trauma patient with suspectedblunt traumatic aortic injury. There are several radio-logical findings in cases of traumatic aortic rupture.Many studies have shown that the widened media-stinum on chest X-ray is associated with more than90% of thoracic aortic injuries (Fig. 4) [29] . Witha 90% sensitivity, a 25% specificity and a 95% nega-

tive predictive value, the supine chest X-ray is avaluable screening tool for mediastinal hemor-rhage, but is worth little as far as definitive diag-nosis is concerned [30]. Other important signs areirregularity or blurring of the aortic knob contour,presence of a left apical cap and a tracheal dis-placement [31]. It is important to obtain serial fol-low-up chest films in patients with suspected mech-anism of injury, because radiographic abnormalitiesmay be absent on initial evaluation.

Spiral computed tomography (SCT). SCTis currently considered not only as a screeningmethod to select patients for thoracic aortography,but also as a definitive diagnostic procedure re-cognizing aortic injuries and rupture (Fig. 5). Com-pared to aortography, it is less invasive, faster toobtain, more readily available and less expensive[32]. Some direct signs of aortic lesions such as inti-mal flap, intramural hematoma or dissection, aor-tic wall or contour irregularity, pseudoaneurysm,and pseudo-coarctation are seen on SCT [33]. Thepresence of a hemomediastinum is well character-ized by a SCT and represents an important indirectsign of aortic trauma. The use of two- and three-dimensional reconstructions on SCT aortographycreates images very close to those obtained by con-

FIG. 4 Chest X-ray showing a widening mediastinum andleft lung contusion.


FIG. 5 SCT demonstrates: (A) descending aortic rupture at the isthmus level causing an intimal flap and lefthemothorax; (B) thoracic aortic injury at the descending part with vessel wall irregularity, left hemothorax, and lungcontusion.

ventional aortography [34], providing the surgeonwith important anatomical information. The nega-tive predictive value of 99.9% for aortic lesions hasbeen considered with a normal mediastinum anda regular aorta seen on SCT [35]. A total body studycan also provide important information regardingassociated lesions on stable patients with cranio-facial, thoracic and abdominal injuries.

Angiography. Aortography is traditionally con-sidered the gold standard imaging study to detectaortic injury, to define its location and extent(Fig. 6). It also provides important informationabout vascular anomalies and other factors thatinfluence operative strategy. The demonstration ofan irregular or discontinued contour of the aorticlumen represents the aortographic diagnosis ofblunt traumatic aortic injuries. Intimal flap, aorticdissection, post-traumatic coarctation or luminaloutpouching relating to a pseudoaneurysm are cur-rent aortographic patterns caused by blunt trau-matic aortic lesions. Thoracic aortography candetect blunt traumatic aortic injuries with a sensi-tivity and specificity of 95% to 99% and 94% to100%, respectively [36-38]. False-negative examina-tions relate to incomplete series, inadequate injec-tions or projections. False positives often relate toprominent ductus diverticulum or from ulceratedatheromas.

Transesophageal echocardiography (TEE).TEE combined with color doppler flow mappingcan accurately demonstrate blunt traumatic isth-mic aortic lesions [39,40] (Fig. 7). This diagnosticmethod can be rapidly and simultaneously realizedwith other procedures like mechanical ventilationor laparotomy. It is not indicated in patients witha difficult airway or suspected spinal cord injury.Moreover, atheromatous disease and pneumome-diastinum may interfere with the accuracy of TEE[36]. TEE may be very useful in unstable patients,as in such cases it is not possible to perform othertime-consuming studies.

Magnetic resonance angiography (MRA).MRA results are comparable to those of SCT andconventional aortography. Nevertheless MR has se-veral limitations such as the time spent completingthe exam and the inaccessibility of the patient dur-ing examination, which excludes its routine use inurgent cases [30].

Intravascular ultrasound. Intravascular ultra-sound imaging has been described as a complemen-tary method clarifying slight focal aortic abnor-malities not visible by thoracic aortography. Its useis still limited and it is mainly associated with en-dovascular procedures [41]. Diagnostic practice fortraumatic aortic injury is based on mechanism of

111


11112 FIG. 6 Distal thoracic aortic pseudoaneurysm evidenced by luminal

outpouchins durins aortosraphy in (A) frontal and (B) lateral views.

FIG. 7 TEE showins a postisthmic aortic pseudoaneurysm with a clear larseneck and hish-velocity flow inside (TL: true lumen; PA: pseudoaneurysm).


injury, chest X-ray and SCT scan or aortography;all of these modalities have limitations and thusmust be considered in concert.

Treatment

TIMINGThe treatment of patients who reach the hospi-

tal alive remains controversial. The original strat-egy of immediate aortic repair has been challeng-ed by recent reports of successful delayed repair[42,43] • Although traumatic rupture of the thoracicaorta has traditionally been considered a surgicalemergency, there exists a patient population forwhom nonoperative management may be appro-priate. Indications for urgent operative repairinclude hemodynamic instability, increasing hem-orrhage from the chest tubes and radiographic evi-dence of an expanding hematoma. Delayed repairmay be considered in selected hemodynamically sta-ble patients, who may not necessarily benefit fromimmediate repair, including patients with severehead injuries, risk factors for infections (majorburns, sepsis, heavily contaminated wounds) andsevere multisystem trauma with poor physiologicreserve.

A basis for nonoperative management is that main-taining the systolic blood pressure below 120 mmHgor mean arterial pressure less than 80 mmHg sig-nificantly reduces the risk of rupture. The risk offatal rupture of the peri-aortic hematoma in he-modynamically stable patients has been estimatedto be 4.5% within the first 72 hours, but it doesnot increase if conservative treatment is furthercontinued [43]. This might be related to the main-tenance of aortic adventitia continuity in patientswho survive. In those, hemorrhage is contained bythe surrounding mediastinal structures. In fact,some patients may develop chronic pseudoaneur-ysms. However, given that progression and rupturewere documented also in patients with small in-juries, the reason for delaying operation should notbe based solely on the size of the lesion, but alsoon high-risk physiologic criteria. Although a smallrisk of free rupture still remains, data support theconcept that nonoperative management of aorticlesions can be utilized safely in selected cases. Insome cases of smaller aortic tears, the lesion mayheal on its own. The downside of the delayed re-pair is that, due to the extensive scarring at the siteand around the injury, the surgical dissection of

the aorta is more difficult and tedious. Current in-dications for delaying the aortic repair in the hemo-dynamically stable patient include trauma to thecentral nervous system with coma, respiratory fail-ure from lung contusion, body surface burns, bluntcardiac injury, tears of solid organs that will un-dergo nonoperative management, retroperitonealhematoma, contaminated wounds, age 50 years orolder and medical comorbidities [4] (Fig. 8).

SURGICAL APPROACH (Fig. 9)As with any operative procedure, patient posi-

tioning and skin incision are important, as adequateexposure is mandatory for proximal and distal con-trol of the great vessels. General exposure and skinpreparation should include the anterior neck, tho-rax, abdomen and a lower extremity. When a sub-clavian injury is suspected, the ipsilateral armshould be prepared and draped in a fashion thatmaintains free mobility of the shoulder.

The posterolateral thoracotomy provides excellentexposure to virtually all portions of the hemitho-rax [44]. The incision extends from behind themedial border of the scapula, below its tip, andthen forward to the anterior axillary line. The chestcan be entered through the fourth to the seventhintercostal space, usually in the bed of the fifth rib.This incision generally offers an adequate accessfor replacing the upstream two thirds of thedescending aorta from the distal aortic arch downto the eighth intercostal space. If required, the fifthor sixth ribs may be removed. Particular care mustbe exercised when positioning hypotensive patientsfor this incision, because the right decubitus posi-tion interferes with venous return and can aggra-vate the condition. This approach may allow atransverse sternotomy in case of difficult control ofthe proximal aorta. Associated phreno-celiotomymay be performed to treat previously undiagnosedabdominal vascular and visceral injuries.

For hypotensive patients with undiagnosed injury,the mainstay of thoracic trauma surgery is the leftanterior thoracotomy through the fourth intercostalspace, with the patient in the supine position. Thisis also the incision of choice for rapid access to themediastinum for open cardiac massage. The inci-sion should start 2 cm lateral to the sternum toavoid injury to the internal mammary artery. It thenfollows a gentle curve laterally to the axilla. Whenadditional exposure is needed, an anterior thora-cotomy may be extended across the sternum in themidline, as previously described; it is also possible

113


114

FIG. 8 Schematic diasnosis and manasement flow chart of traumatic aortic lesions.

to extend the incision posteriorly in order to havea better control of proximal aorta.

A median sternotomy is preferred for injuries of theascending aorta and of the innominate and proxi-mal carotid arteries. Extension into the neck, alongthe anterior border of the right sternocleidomas-toid muscle, allows access to the proximal right sub-clavian artery and to the right vertebral artery.

A thoraco-sternotomy [45] associates the antero-lat-eral thoracotomy through the third intercostalspace to a median sternotomy; this access permitsa rapid access to the mediastinum, to have the con-trol of the proximal aorta and, if is necessary, toperform cardiopulmonary bypass.

TECHNIQUES OF ORGANPERFUSION/REPAIR

Discussion continues regarding the optimal man-agement of injury to the thoracic aorta after trau-ma, because of concerns about spinal cord ischemiaand subsequent neurologic deficit. Several methodsfor indirect assessment of perfusion are available

during thoracic and thoraco-abdominal aortic sur-gery. In emergency situations, however, the opera-tion must be performed as expeditiously as possiblewithout these techniques. The technique of choiceis indeed dictated by the urgency of the patient'scondition, availability of technical personnel andsurgeon preference at each hospital.

CLAMP-AND-SEWThe single clamp-and-sew method of repair has

many strong advocates, who point to the tech-nique's simplicity, the low paraplegia rate if cross-clamp times are short, and a low mortality rate ascompared with approaches that use heparin [17,29,46,47]. Sweeney et al. reported a mortality rate of12% and a permanent paraplegia rate of 1.3% witha mean cross- clamp time of 24 minutes [47]. How-ever, a cross-clamp time this brief cannot be guar-anteed [10] and most surgical groups do not meetthis mark [48,49]. Experimental data and clinicalseries have demonstrated that the occlusion of thedescending thoracic aorta longer than 30 minutes


FIG. 9 Most common approaches to the thoracic aorta:(A) postero-lateral thoracotomy, with possible abdominalextension; (B) anterior thoracotomy, with possiblecontralateral extension and/or sternotomy.

is associated with the development of postoperativeparaplegia [49-51]. The average international cross-clamp time, as reported by von Oppell et al., is41 minutes [51].

Even those who advocate the clamp-and-sew tech-nique have patients with paraplegia because ofunexpectedly long cross-clamp times. Most recently,groups using this technique reported paraplegiarates in the 2% to 24% range (Table II). This is incontrast to the 0% to 7% of those who use activedistal support [8,49,54].

Cross-clamping the thoracic aorta renders is-chemia of all organs distal to the clamp, includingthe liver, intestines, kidneys and skeletal muscle. VanNorman et al. demonstrated that aortic unclamp-ing after emergency surgery for traumatic thoracicaorta tears was associated with a decrease in P02,an elevated serum potassium level, and a markedmetabolic acidosis that persisted for up to six hoursafter declamping [55]. Roberts et al. demonstratedthat after release of the cross-clamp in unshuntedanimals, there was a reduction in renal function to50% to 85% of baseline values [56].

Occlusion of the descending thoracic aorta is alsoassociated with a multitude of physiologic derange-ments including the development of proximal hy-pertension, which increases the afterload and placesstrain on the left ventricle. A reduction of the car-diac index by 29% has been demonstrated togeth-er with an increase in left ventricular wall stress withthe application of a proximal thoracic cross-clamp[57]. This is extremely important, considering that

il115

1st author[ref.]

Schmidt [15]

Maggisano [43]

Sweeney [47]

Fabian [49]

Attar [52]

Jahromi [53]

Year

1992

1995

1997

1997

1999

2001

Numberof patients

3236

71

73

54

21

Mortality(%)

5

3

9

11

12

2

(16)

(8)(13)

(15)

(22)

(10)

Paraplegia/paraparesis* (%)

1

1

1

1210

3

(3.7)

(3)

(2)(16.4)

(24)

(16)

* Related to live patients


12116

many patients with blunt aortic injuries have an as-sociated cardiac contusion; this places the patientsat increased risk for peri-operative cardiac arrest,postoperative myocardial infarction and the devel-opment of adult respiratory distress syndrome aftersurgery [58]. Furthermore, the use of vasodilatorssuch as nitroprusside to control proximal hyper-tension after the application of the proximal cross-clamp reduces arterial perfusion pressure to thespinal cord, while the application of the cross-clampincreases cerebrospinal fluid pressure [59].

ACTIVE DISTAL CIRCULATORY SUPPORTActive distal circulatory support is very effective

in reducing the risk of paraplegia, particularly whenlong cross-clamp times are needed. Simple aorticclamping is known to raise cerebrospinal fluid pres-sures, which can exacerbate intracranial injuries.Unloading of the proximal aorta with an active dis-tal support system may minimize that rise. The ad-juncts for distal aortic perfusion reduce but do noteliminate the risk of neurological deficits [53]. Theorigin of the artery of Adamkiewicz arises betweenT5 and T8 in 12% to 15% of patients [8]. A lowplacement of a distal aortic clamp may result in ob-struction of the artery of Adamkiewicz [8]. Alter-natively, a clamp placed proximally to the leftsubclavian artery may transiently reduce the spinalcord blood flow through the vertebrobasilar system.Distal support has other theoretical advantages oversimple clamping: it provides proximal cardiac un-

loading, which may be helpful in elderly patientsand in those with myocardial contusions [60]. Themost common methods of distal circulatory sup-port are complete and partial cardiopulmonary by-pass via an external pump and left atrial to aorticor femoral bypass (left heart bypass, LHBP).

CARDIOPULMONARY BYPASSCardiopulmonary bypass has the ability to oxy-

genate, scavenge shed blood and heat and cool asdesired [8,48]. However, the use of full anticoagu-lation in a multiply injured patient may increase therisk of bleeding and death. For this reason com-plete cardiopulmonary bypass has largely fallen intodisfavor. Patients with thoracic aortic injuries at mul-tiple levels who require extensive repair are notableexceptions [18].

Partial cardiopulmonary bypass with heparin-bonded circuits has been validated as an attractiveoption in the setting of traumatic ruptured aorta asa means of avoiding the use of systemic hepariniza-tion. Cannulation of the right atrium via the femoralvein is simple and provides a clear and unobstructedworking field [61]. It can provide adequate distalcirculatory support and safely heat, cool, oxygenate,and transfuse as required as opposed to LHBP; withpartial cardiopulmonary bypass, improved oxy-genation may also be attained in the presence oflung contusions [8]. Some literature results are sum-marized in Table III.

ler author[ref.]

Soyer [54]

Pate [8]

Fabian [49]

Fabian (full) [49]

Gammie [48]

Attar [52]

Jamieson [62]

Year

1992

1995

1997

1997

1998

1999

2002

Numberof patients

43

88

39

22

10

43

42

Mortality

(%)

3

6

5

5

1

75

(7)

(7)(12.8)

(22.7)(10)(16)

(12)

Paraplegia/paraparesis * (%)

0

2

3

1

0

0

0

(2)(7.7)

(4.5)

* Related to live patients


FIG. 10 Illustration of LHBP7 anactive method of distal perfusion.

LEFT HEART BYPASSLHBP, which is connected between the left atrium

and distal aorta or a femoral artery (Fig. 10), canbe used with little or no heparin because an oxy-genator is not required. It also has some limita-tions; most LHBP systems do not incorporate a heatexchanger and are dependent on adequate pul-monary function for oxygenation. Cannulation ofthe left atrial appendage or pulmonary vein cansometimes be difficult in the presence of an exten-sive mediastinal hematoma. Additionally, becauseof the risk of air embolization in these closed sys-tems, physicians are reluctant to rapidly infuse vol-ume through them. Some authors also describedclamp-related embolic events due to heparinelesscircuit [63].

Injuries to the aortic arch, innominate artery orascending aorta, which represent a minority of aor-tic trauma cases, cannot be repaired with LHBP.Full cardiopulmonary bypass or even profoundhypothermic circulatory arrest may be necessary.Furthermore, in patients who present in extremis,necessitating immediate control of hemorrhage andrestoration of blood volume before repair, partialbypass may offer no advantage. However, the majo-rity of aortic transections occur at the isthmus; thepatients who survive to surgery are usually hemo-dynamically stable, with the peri-aortic hematomacontained in the mediastinum. These injuries maybe complex or close to the proximal cross-clamp,thus complicating and potentially prolonging therepair. The adjuvant use of LHBP may help inextending the critical window, so the aortic cross-clamp can be applied safely in such situations(Table IV).

11117

1st author[ref.]

Read [64]

Kipfer [65]

Contino [66]

Fabian [49]

Gammie [48]

Symbas [67]

Year

1993

1994

1994

1997

1998

2002

Numberof patients

16

10

24

69

14

19

Mortality(%)

2

0

5

10

1

5

(13)

(20.8)

(14.5)

(7)(26)

Paraplegia/paraparesis (%)

0

0

0

2

0

0

(2.9)


12118

SURGICAL TECHNIQUESInjury usually originates at the medial side of the

aorta, at the level of the ligamentum arteriosum.The goal of initial operative approach is to obtainproximal and distal control of the descending tho-racic aorta. Vascular clamps are applied to threelocations: proximal aorta, distal aorta and subcla-vian artery. The hematoma is entered and back-bleeding from intercostal arteries is controlled. Careis taken to avoid indiscriminate ligation of inter-costal vessels: only those required for adequate re-pair of the aorta should be ligated.

During aortic reconstruction clamps should bemoved as close as possible to the site of injury, inorder to reduce spinal cord ischemia, especiallywhen using the clamp-sew technique. Primarysuture and graft interposition (Fig. 11) are the mainstrategies of aortic repair after a traumatic lesion.The first is usually the preferred choice, being sim-ple and fast. This technique is adequate in cases ofpartial laceration, but also in disruptions when aor-tic stumps are not too distant and severely injured.Frequently in aortic trauma, adventitial layers areretracted and must be carefully included in the aor-tic suture. During this phase, the esophagus mustbe accurately separated from the posterior aorticwall. Teflon-felt pledgets can be useful to reinforcea friable suture line. Finally, the absence of a pros-

thetic graft decreases risk of infection. Graft inter-position has been used in more than 85% of thereported cases [11], and is advisable when morethan 2 cm of the vessel is injured. The aorta isgrafted with a straight polyester graft which is keptas short as possible.

COMPLICATIONSSignificant postoperative complications related to

the thoracic injury can develop in these patients.Cardiac, renal, pulmonary and neurologic morbidi-ties have been reported in the literature with ratesup to 50% [68]. Pate et al. registered significantpostoperative complications in 72.7% of the 44 pa-tients operated after 1984. The most common com-plications in their experience were adult respiratorydistress syndrome and pneumonia (29.5%), severesystemic hypertension (20.5%), coagulopathy, renalfailure, serious cardiac arrhythmias, late tensionpneumothorax and thoracic wound infection [8].There were additional problems stemming from or-thopedic, abdominal, cranial and burn injuries.

Paraplegia is the most devastating complicationafter repair of descending aortic transection sincemost of the patients who suffer blunt aortic injuryare young. The personal loss caused by paraplegiaand the economic impact on society are enormous.

FIG. 11 Methods of aortic repair: (A) simple suture, and (B) graft interposition.


The two central issues associated with preventionof paraplegia are duration of cross-clamp time anduse of distal aortic perfusion. Patients with acuteaortic rupture are at a greater risk for paraplegiaduring aortic repair than patients with chronicaneurysms or coarctation. This increased risk islikely due to the lack of preformed collaterals alongwith the additional complications unique to traumapatients including pulmonary and cardiac contu-sions, shock, hypoxia and hypo-osmolality fromfluid overload [8]. Late deaths, in fact, are mostoften due to multiple organ failure [69].

ENDOVASCULAR INTERVENTIONSDespite advances in surgical and peri-operative

care, conventional surgery for acute aortic rupturestill carries a significant morbidity and mortality.Thus, endovascular procedures may be an attrac-tive option for treating this kind of lesions. Theo-retical advantages of stent grafting are multiple; theabsence of aortic cross-clamping prevents rising ofintracranial pressure in some situations like severehead injury. Patients with pulmonary contusions donot need single-lung ventilation as used for con-ventional surgical repair. Critical statements havepronounced a high risk of spinal cord ischemia dueto the exclusion of intercostal arteries during

endovascular treatment. Nevertheless, the place-ment of vascular stent grafts has not yet been shownto increase the risk of paraplegia compared to con-ventional surgical intervention. The largest seriesof thoracic aortic diseases electively treated withendoluminal grafts reported a paraplegia rate of3.6% [70]. Up to 70% of traumatic aortic injuriesaffect the isthmus segment excluding only a fewbranches to the spinal cord if an endograft is placed(Fig. 12). The length of the covered aorta may belimited to a few centimeters near the diseased seg-ment, which could lessen the risk of medullarischemia.

Lachat et al. have reported significant lower ratesof morbidity and mortality for stent grafting ofacute aortic lesions demonstrating the benefits andadvantages offered by this minimally invasive tech-nique [71]. In this report patients were hemody-namically stable to undergo contrast enhanced CTand angiographic evaluation to determine the suit-ability for stent grafting. TEE and intravascularultrasound have been described as helpful associ-ated diagnostic studies [72]. Early endovasculartreatment was considered in the treatment of sta-ble nonbleeding lesions, after recovery of associ-ated life-threatening injuries. The rupture had tobe contained, with a proximal neck of normal

119

FIG. 12 A less invasive technique: endovascular exclusion of an isthmic injury.


12120

appearance and length greater than 5 mm and adiameter less than 36 mm. Depending on the asso-ciated lesions and the bleeding risk, no heparin atall or a maximum dose of 5000 IU was adminis-trated intravenously and completely reversed afterstent graft delivery. The immediate technical suc-cess rate was 100%, as the aortic lesion could beexcluded in all the cases; there was one early deathdue to hemorrhagic shock in a patient with a semi-circumferential rupture who probably had an unde-tected incomplete proximal sealing.

Because most injuries occur at the aortic isthmus,much concern has been raised regarding the place-ment of rigid devices in an angulated aortic arch.As previously described, this can cause an inade-quate seal of the thoracic aorta. However, this hasbeen largely overcome with newer and more flexi-ble devices. This new therapeutic strategy has fewdrawbacks worth describing. The delivery systemcalibers are actually of large diameter (18Fr to24Fr), being difficult to introduce through smalland spastic arteries of young people or tortuousand calcified arteries of older people. A furtherconcern is the stock inventory of devices, whichmust be available for emergency cases in differentsizes and lengths.

Another topic of concern is the relatively youngpopulation suffering from aortic trauma, whichcould be treated with this method. Stent grafts areactually produced mainly for treatment of chronicaortic pathologies, especially aneurysms, and do notcome in adequate diameters for the small vessels ofyoung people. Moreover, the mean age (38.7 years)of this population raises many questions about thelong-term follow-up after endoluminal treatment[49]. Additional study of the endovascular inter-vention role in aortic injury is required to obtaina stronger support for its use in this scenario.

Personal experience

Between January 1988 and September 2002,15 pa-tients with acute injury or rupture of the thoracicaorta were admitted to the emergency departmentof our institution. There were 11 (73%) males and4 (27%) females aged 19 through 68 years (meanage of 39.8 years). Ten patients had history of motorvehicle crash, two suffered from a motorcycle crashand three had lesions secondary to penetrating trau-mas. Seven patients died in the emergency depart-

ment, five of these arrived in extremely critical con-ditions. The other two died during urgent thora-cotomy dictated by hemodynamic deterioration,before the bleeding could be controlled. An earlychest X-ray was obtained in nine patients. SCTand/or aortography studies were performed inseven patients with stable hemodynamic conditions.Two patients also underwent TEE.

Associated lesions were found in every patient ofour series (Table V), and were present mainly inthose patients who died in the emergency depart-ment. The most common lesions were other tho-racic injuries in 12 patients and abdominal visceralinjuries in 7 patients. Table VI summarizes the clin-ical and surgical features of the patients. Hospitalmortality for patients undergoing surgical repair was3/8 (38%). One death occurred in a 56-year-oldwoman involved in a motor vehicle accident. Tho-racic aortic rupture repair was performed using theclamp-and-sew technique, and during wound clo-sure she suffered from an irreversible cardiac arrest.The second was a 43-year-old man who died ofuncontrolled bleeding during repair of a penetrat-ing lesion of median aortic arch. The third deathwas in a 48-year-old man who underwent repair ofan isthmic pseudoaneurysm using LHBP, and diedon the 12th postoperative day of multiple organ fail-ure. One patient developed paraplegia following a

InjuryNumber

of patients

Other thoracic traumas(including fracturesand great vessels)

Abdominal visceral

Closed-head injury

Peripheral fractures

Head fractures

Abdominal vascular

Neck fracture

12

7

6

6

4

2

1


Case

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

Sex

M

M

F

M

M

M

M

F

M

M

F

M

M

M

F

Age

28

19

56

31

43

26

34

63

48

38

22

56

31

68

35

Lesion characteristics

Isthmic rupture(MVC)

Descending thoracicaorta perforation(Gunshot)


Descending thoracicaortic dissectionand rupture (MVC)

Descending thoracicaortic perforation(Metallic bar forbuilding construction)

Descending thoracicaortic injury -pseudo-aneurysm (MC)

Isthmic injurypseudoaneurysm(MVC)

Ascending aortarupture (MVC)

Isthmic injury -pseudoaneurysm(MVC)

Ascending aortaperforation(Stab wound)

Isthmic anddiaphragmatic aorticrupture (MC)

Ascending rupture(MVC)



Isthmic rupture

Procedure

Urgent thoracotomy

Urgent thoracotomy

Graft interposition(clamp and sew)

Graft interposition(clamp and sew)

Urgent thoraco-phreno-laparotomy

Graft interposition(LHBP)


Graft interposition(CPB)


Sternotomy(simple suture)

Autopsy findings

Autopsy findings

Autopsy findings

Autopsy findings

Autopsy findings

In-hospital outcome

Death in emergency room(hemorrhagic shock)

Death in emergency room(hemorrhagic shock)

Death in immediatepostoperative period(cardiac arrest)

Discharged

Death in operating room(uncontrolled bleeding)

Discharged

Discharged

Discharged

Death in postoperativeperiod (MOF)

Discharged

Follow-up

Alive after 7 years

Alive after 1.5 year

Alive after 6 months

Alive and paraplegicafter 2 months

Alive after 5 years

121

(MVC)

CPB: cardiopulmonary bypassLHBP: left heart bypassMC: motorcycle crashMOF: multiple organ failureMVC: motor vehicle crash


graft interposition in the ascending aorta under car-diopulmonary bypass. The other four patients suf-fered no major complications and were dischargedin good condition.

Conclusion

The major difficulty in the evaluation of data con-cerning blunt aortic injury is that retrospective re-views often collect patients with all aortic injuriestogether, comparing outcomes for injuries in dif-

ferent locations of the aorta with different methodsof repair and different surgeons at different institu-tions. Concomitant severe lesions are usually pres-ent in patients suffering from aortic trauma, andthus diagnostic and therapeutic timing must be rap-idly established. The polytrauma patient should bemanaged under a multidisciplinary approach andtreated in a specialized center. Organizing traumacenters is a very important issue. In these places, pa-tients can be better treated, and prospective studieswill be helpful for creating guidelines and treatmentalgorithms.

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29 Hilgenberg AD, Logan DL, Akins CW et al. Blunt injuries of thethoracic aorta. Ann Thorac Surg1992; 53: 233-239.

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31 Tisnado J, Tsai FY, Als A, Roach JF. A new radiographic sign ofacute traumatic rupture of the thoracic aorta: displacement ofthe nasogastric tube to the right. Radiology 1977; 125: 603-608.


32 Novelline R, RheaJT, Rao PM, StukJL. Helical CT in emergencyradiology. Radiology 1999; 213: 321 - 339.

33 Gavant ML. Helical CT grading of traumatic aortic injuries.Impact on clinical guidelines for medical and surgical manage-ment. Radial Clin North Am 1999; 37: 553-574.

34 Reardon MJ, Hedrick TD, Letsou GV et al. CT reconstruction ofan unusual chronic posttraumatic aneurysm of the thoracicaorta. Ann Thome Surg 1997; 64: 1480-1482.

35 Wicky S, Wintermark M. Schnyder P et al. Imaging of bluntchest trauma. EurRadioimQ; 10:1524-1538.

36 Ben-Menachem Y. Assessment of blunt aortic-brachiocephalictrauma: should angiography be supplanted by transesophagealechocardiography?/Trauma 1997; 42: 969-972.

37 Gavant ML, Menke PG, Fabian T et al. Blunt traumatic aorticrupture: detection with helical CT of the chest. Radiology 1995;197:125-133.

38 Mirvis SE, Shanmuganathan K, Miller BH et al. Traumatic aor-tic injury: diagnosis with contrast-enhanced thoracic CT: fiveyear experience at a major trauma center. Radiology 1996; 200:413-422.

39 Brooks SW, Young JC, Cmolik B et al. The use of transesophagealechocardiography in the evaluation of chest trauma. / Trauma1992; 32: 761-768.

40 Buckmaster MJ, Kearney PA, Johnson SB et al. Further experi-ence with transesophageal echocardiography in the evaluationof thoracic aortic injury. J Trauma 1994; 37: 989-995.

41 Lobato AC, Quick RC, Phillips B et al. Immediate endovascularrepair for descending thoracic aortic transection secondary toblunt trauma. JEndovasc 77^2000; 7:16-20.

42 Parmley LF, Mattingly TW, Manion WC et al. Nonpenetratingtraumatic injury of the aorta. Circulation 1958; 17: 1086-1101.

43 Maggisano R, Nathens A, Alexandrova NA et al. Traumatic rup-ture of the thoracic aorta: should one always operate immedi-ately? Ann Vase Surg 1995; 9: 44-52.

44 Hurley EJ, Blaisdell FW. Aortic injuries. In: Blaisdell FW,Trunkey DD (eds). Cervicothoradc Trauma. New York, Thieme,1986: pp 223-245.

45 Villard J, Vial P, Dureau G et al. Thoraco-bisternotomy in car-diovascular surgery. Nouv Presse Med 1982; 11: 3647-3649.

46 Tatou E, Steinmetz E, Jazayeri S et al. Surgical outcome of trau-matic rupture of the thoracic aorta. Ann Thorac Surg 2000; 69:

^ 70-73. F S

47 Sweeney MS, Young DJ, Frazier OH et al. Traumatic aortic tran-sections: eight-year experience with the "clamp-sew" technique.Ann Thorac Surg 1997; 64: 384-389.

48 Gammie JS, Shah AS, Hattler BG et al. Traumatic aortic rup-ture: diagnosis and management. Ann Thorac Surg 1998; 66:1295-1300.

49 Fabian TC, Richardson JD, Croce MA et al. Prospective study ofblunt aortic injury: Multicenter Trial of the American Associationfor the Surgery of Trauma. / Trauma 1997; 42: 374-383.

50 Katz NM, Blackstone EH, Kirklin JW, Karp RB. Incremental riskfactors for spinal cord injury following operation for acute trau-matic aortic transection. J Thorac Cardiovascular Surg 1981; 81:669-674.

51 von Oppell UO, Dunne TT, De Groot MR, Zilla P. Traumaticaortic rupture: twenty-year metaanalysis of mortality and risk ofparaplegia. Ann Thorac Surg 1994; 58: 585-593.

52 Attar S, Cardarelli MG, Downing SW et al. Traumatic aortic rup-ture: recent outcome with regard to neurologic deficit. Ann77wracSwrgl999;67:959-965.

53 Jahromi AS, Kazemi K, Safar HA et al. Traumatic rupture of thethoracic aorta: cohort study and systematic review. J Vase Surg2001; 34:1029-1034.

54 Soyer R, Bessou JP, Bouchart F et al. Acute traumatic isthmic aor-tic rupture. Long-term results in 49 patients. EurJ CardiothoracSwrgl992;6:431-437.

55 van Norman GA, Pavlin EG, Eddy AC, Pavlin DJ. Hemodynamicand metabolic effects of aortic unclamping following emergencysurgery for traumatic thoracic aortic tear in shunted andunshunted patients./Trauma 1991; 31:1007-1016.

56 Roberts AJ, Nora JD, Hughes WA et al. Cardiac and renalresponses to cross-clamping of the descending thoracic aorta.J Thorac Cardiovasc Surg 1983; 86: 732 - 741.

57 Kouchoukos NT, Lell WA, Karp RB, Samuelson PN. Hemo-dynamic effects of aortic clamping and decompression with atemporary shunt for resection of the descending thoracic aorta.Surgery 19'79; 85: 25-30.

58 Kram HB, Appel PL, Shoemaker WC. Increased incidence ofcardiac contusion in patients with traumatic thoracic aortic rup-ture. Ann Surg 1988; 208: 615-618.

59 Szwerc MF, Benckart DH, Lin JC et al. Recent clinical experi-ence with left heart bypass using a centrifugal pump for repairof traumatic aortic transection. Ann Swrgl999; 230: 484-492.

60 Hug HR, Taber RE. Bypass flow requirements during thoracicaneurysmectomy with particular attention to the prevention ofleft heart failure. J Thorac Cardiovasc Surg-1969; 57: 203-213.

61 von Segesser LK, Weiss BM, Garcia E et al. Reduction and elim-ination of systemic heparinization during cardiopulmonarybypass. / Thorac Cardiovasc Surg 1992; 103: 790 - 799.

62 Jamieson WR, Janusz MT, Gudas VM et al. Traumatic rupture ofthe thoracic aorta: third decade of experience. Am J Surg 2002;183:571-575.

63 Duke BJ, Moore EE, Brega KE. Posterior circulation cerebralinfarcts associated with repair of thoracic aortic disruption usingpartial left heart bypass. / Trauma 1997; 42:1135-1139.

64 Read RA, Moore EE, Moore FA, Haenel JB. Partial left heartbypass for thoracic aorta repair. Survival without paraplegia.Arch Surg 1993; 128: 746 -752.

65 Kipfer B, Leupi F, Schuepbach P et al. Acute traumatic ruptureof the thoracic aorta: immediate or delayed surgical repair? EurJ Cardiothorac Surg 1994; 8: 30 - 33.

66 Contino JP, Follette DM, Berkoff HA et al. Use of Carmeda-coated femoral-femoral bypass during repair of traumatic aorticpseudoaneurysms. Arch Swrgl994; 129: 933-939.

67 Symbas PN, Sherman AJ, Silver JM et al. Traumatic rupture ofthe aorta: immediate or delayed repair? Ann Surg 2002; 235:796-802.

68 Butler KL, Moore EE, Harken AH. Traumatic rupture of thedescending thoracic aorta. AORV/1996; 63: 917-925.

69 Chiesa R, Lucci C, Castellano R et al. Multiple organ failure aftersurgical arterial reconstruction. In: Branchereau A, Jacobs M(eds). Complications in vascular and endovascular surgerj (Part II).Armonk, Futura Publishing Company, 2002: pp 23-32.

70 Mitchell RS, Miller DC, Dake MD et al. Thoracic aortic aneurysmrepair with an endovascular stent graft: the "first generation".Ann Thorac Surg 1999; 67:1971-1974, discussion 1979-1980.

71 Lachat M, Pfammatter T, Witzke H et al. Acute traumatic aorticrupture: early stent-graft repair. EurJ Cardiothorac Swig 2002; 21:959-963.

72 Thompson CS, Rodriguez JA, Ramaiah VG et al. Acute traumaticrupture of the thoracic aorta treated with endoluminal stentgrafts. J Trauma 2002; 52:1173-1177.

12.123

ACUTE OCCLUSION OFTHE RENAL ARTERIES

XAVIER BARRAL, PHILIPPE PACHECODANIEL GRANDMOUGIN, DIDIER BOURRAT, JEAN-PIERRE FAVRE

Acute renal ischemia rarely occurs. During the last ten years we have only encountered sometwenty publications in the literature addressing this issue. This limited scientific attention,associated with our personal data analysis, invites for three comments.

- Occlusion of atherosclerotic stenoses of the renal artery silently develops and is onlydiagnosed in the chronic stage, explaining the exceptional observation of acute failure despitethe high incidence of renal artery disease.

- Acute renal ischemia occurs in the setting of varying and uncommon pathologies withoutmutual causal relations. This multifactorial etiology delays the diagnostic process and doesnot allow a general treatment.

- In the literature, acute renal ischemia is evaluated in clinical cases which are pooled onthe basis of a specific etiology or treatment. Only one publication comprises more than30 patients thanks to a compilation of 20 years of experience [1]. Therefore, the treatment ofthis seldom acute ischemia is most often based on personal belief rather than scientific evidence.

11125

IncidenceThe exact incidence of acute renal ischemia is diffi-

cult to assess. Only few authors report on their per-sonal data. The publication of Hoxie and Coggin isoften referred to, describing 205 recent renal infarc-tions in 14 471 autopsies carried out in a nine-yearperiod, accounting for 1.4% renal infarctions in adeceased population [2]. This publication dates

from an era (1940) in which effective treatmentlike anticoagulation did not exist. A more recentand interesting study is described by Domanovitset al. [3] who, in a period of 45 months, found17 cases of renal infarction among 248 882 patientsadmitted to an emergency center (0.007%). In ourpersonal experience, excluding postoperative andearly post-transplantation occlusions, we haveencountered 18 cases of acute renal occlusion in


13126

a twenty-year period. These figures representapproximately 1.2% of our transplant and renalartery surgery and 0.13% of our overall peripheralvascular surgical procedures. The incidence of uni-lateral or bilateral acute occlusion in a single func-tioning kidney is even more exceptional and isfound in 5% to 20% of acute renal artery obstruc-tion [4]. Noteworthy is the fact that the majorityof acute infarctions occur in the left renal artery(more than 60%). The more oblique origin of theleft renal artery in relation to the aorta favors pref-erential passage of emboli as compared to the rightside [1,5].

Etiology

The causes of acute renal artery occlusion canbe distinguished in three main groups: emboli,thrombosis and trauma (Table I).

EMBOLIIn the literature only eight series included more

than ten patients and the rate of embolization was43.5%. These renal emboli correspond to 2.3% ofall embolic cases [11]. In 70% the source of emboliis the heart, either caused by arrhythmia, valve dis-ease or myocardial infarction [12]. Atheroscleroticemboli are more uncommon but can be dislodgedduring aortic cross-clamping, originating from

suprarenal ulcerating plaques. Finally, some casesof paradoxical embolism have been described [13].

ACUTE ARTERIAL THROMBOSISThe second important cause of acute renal is-

chemia is thrombosis, encountered in 32.6% of cases(Table I). The mechanisms of these thromboses areextremely variable. Progression of atherosclerotic ordysplastic stenosis, spontaneous or accelerated byangiotensin-converting enzyme inhibitors, can leadto complete occlusion. Furthermore, local throm-bosis can be associated with diseases like arteritis[14], Behcet's disease [15], oral contraceptives [16],marijuana [17] or cocaine abuse [18], coagulationdisorders [19,20], ergotamine intoxication [21],Chagas disease [22], umbilical artery catheterization[23] and heparin allergy (Fig. 1). Finally, acute renalischemia can be due to secondary thrombosis in anaortic dissection, extending to the renal arteries[24,25] or in an isolated, spontaneous renal arterydissection [26].

TRAUMATIC CAUSESThe third group of acute occlusions consists of

post-traumatic reasons and was identified in 23.8%of patients. Dorsolumbar or thoraco-abdominal trau-ma is most often the consequence of a car accidentor other acceleration/deceleration impact. Twomechanisms can cause a subintimal rupture andsubsequent thrombosis:

1st author[ref.]

Stables [6]

Ouriel [1]

Lacombe [7]

Blum [8]

Salam [9]

Bouttier [10]

Domanovitz [3]

Personal experience

Total

Year ofpublication

1976

1986

1992

1993

1993

1997

1999

2002

8 series

Numberof patients

21

35

20

14

10

12

17

18

147

EmboliN(%)

0

13

5

14

2

12

14

4

64 (43.5)

ThrombosisN(%)

0

16

15

0

4

0

3

10

48 (32.6)

TraumaN(%)

21

6

0

0

4

0

0

4

35 (23.8)

ACUTE OCCLUSION OF THE RENAL ARTERIES

FIG. 1 Acute occlusion of the left renal artery, discoveredthree days after heparine allersy. Medical treatment.

- crush injury of the artery against the spine,- tearing-off or overstretching the renal artery

pedicel.These traumatic lesions of the renal artery [27,28]

are observed in approximately 4% of abdominaltrauma. The injury can be the result of an iatro-genic trauma like selective renal artery arterio-graphy [29] or any endovascular procedure (angio-plasty, stenting, endograft). It should be noted thatthe latter causes decreased significantly because inthe majority of cases these complications can besolved immediately [30].

Diagnostics

Because of the low incidence and the extremelyvariable clinical features, acute renal artery occlu-sions often pass unnoticed. The clinical diagnosisis established in one of five patients [31], with asubstantial delay of additional investigations con-firming renal artery involvement.

Typically, the clinical picture is characterized byan intense pain in the flank with possible referredpain to the external genital organs, nausea, vomit-ing, paralytic ileus, and micro- or macroscopic hema-turia. Arterial hypertension might also be presentand light fever can develop after a few hours. Inpatients presenting with nephretic colic, previous

arrhythmia or emboligenic cardiopathy, the diag-nosis of acute renal occlusion should be kept inmind. The likelihood of a renal artery embolus canreach 80% [3] and only immediate diagnosis andtreatment offer a possibility for a functional recov-ery of the affected kidney. Therefore, emergencycontrast enhanced computed tomography (CT)scanning should be performed, especially if thegeneral and hemodynamic condition of the patientare acceptable. Again, any further time delay threat-ens the affected kidney (Fig. 2).

If the clinical situation is less urgent, assessmentof serum lactate dehydrogenase is useful. In caseof renal artery occlusion, this enzyme is generallyelevated [32]. Serum ureum and creatinine are rou-tinely investigated but they have limited diagnosticvalue. In case of oliguria secondary to renal arteryocclusion, it is worthwhile to assess the levels ofsodium in serum and urine, which are equivalentin most cases. The excreted sodium fraction is actu-ally 100% and the equivalent sodium levels inserum and urine should indicate immediate CTscanning [33].

CT angiography is currently the method of choiceto confirm the suspicion of renal artery occlusion.Performed before and after the injection, it allowsaccurate assessment of the renal artery and theparenchymatous damage [34]. Contrast enhancedCT allows for differentiation between recent acuteocclusions or pre-existing occlusions, the latterbeing characterized by renal atrophy, thin cortexand irregular capsule. Magnetic resonance angio-graphy could also be an useful method; however,its availability and accessibility are inferior to thoseof CT. Duplex scanning of the kidney is an easytechnique but it depends on the technician anddegree of meteorism and offers less information onthe renal parenchym [35]. At present it is a sec-ond-choice technique and is only applied in theabsence of CT. The goal should be not to dupli-cate diagnostic tests and not to lose important timeand start treatment as soon as possible.

Even though arteriography remains the gold stan-dard in the diagnosis of renal artery occlusions, thetechnique is currently replaced by the latest gen-eration CT scanners. Arteriography allows us toidentify the type of occlusion and the level of con-trast reinjection in the distal renal artery. If selec-tive angiography of the origin of the renal arterydoes not delineate the distal reinjection, selectiveangiography of renal artery side branches, lumbaror diaphragmatic arteries can be performed (Fig. 3).

_127


FIG. 2 A - Post-traumatic acute occlu-sion of the left renal artery. CT scan fourhours after the accident. B - Angio-graphy immediately performed after theCT scan. C - Completion angiographyshowing filiform intrarenal arteries andinhomogeneous parenchyma. No func-tional outcome.

FIG. 3 Catheterization of lumbar arteries, allowing vizualization of the right renal artery distal to the proximal occlusion.


Value of renal function

Before any treatment is started, renal functionshould be analyzed. In fact, all the costs and poten-tial iatrogenic complications cannot be justified ifan infarcted kidney is revascularized without a func-tional outcome. Analysis of the literature shows thatin many cases a successful anatomical reconstructionof an occluded renal artery leads to a poor func-tional outcome (Table II). In contrast, certain in-vestigations are required in order to assess whethera kidney is still functional. The associated time delaycan obviously progress the renal infarction and thisdilemma contributes to a blind treatment withoutadequate idea of prognosis in many patients. Thisprognosis depends on the distal perfusion pressure,the collateral network, and the level and durationof the renal artery occlusion. In 1956 Morris et al.[36] showed that with a distal perfusion pressureof 25 mmHg the kidney can survive two hours ofarterial occlusion. At this pressure level, the kidneyis anuric due to the insufficient filtration pressureat the level of the afferent glomerular arteries. Fol-lowing reconstruction, however, an adequate arte-rial pressure above 60 mmHg allows recovery of thekidney. In this way, as observed in ischemic myo-cardium, the hibernating glomeruli can regain theirfunction after revascularization. This also explainswhy severe hypertension discovered during acuterenal artery occlusion carries a good prognosis be-

cause it illustrates a functional juxtaglomerularfunction, secreting renin [1]. In contrast, the ab-sence of hypertension often indicates massive renalinfarction without hope for recovery.

This minimal residual pressure is related to thequality of the collateral network at the time of ar-terial occlusion. In case of acute thrombosis in apre-existing stenosis, the developed collateral ves-sels in the ureter, diaphragm, and lumbar and supra-renal areas can all contribute to a residual pressurewith which the kidney can be viable. Conversely, intraumatic or embolic cases, the collateral networkis not developed and the antegradely stasis-inducedthrombosis will rapidly reach the renal hilus, notallowing parenchymatous perfusion. This circulato-ry arrest immediately induces a massive, irreversibleinfarction. In these complete occlusions withoutcollaterals, the delay of intervention to achieve afunctional recovery can only be extremely short. Ina healthy animal kidney, a two-hour ischemia is tol-erated. Functional recovery occurs in two to threeweeks, indicating the time to regenerate the urothe-lium. Beyond four hours there will be no recoveryanymore [37]. In humans, renal survival beyondtwo hours of ischemia is very unlikely [8,38]. Thisfundamental role of the collateral network explainswhy the duration of occlusion prior to revascular-ization has no prognostic value [1]. It only explains,in general terms, that an acute thrombosis in a pre-existent stenotic renal artery carries a better prog-nosis than a post-traumatic or embolic occlusion.

11129

1st author[ref.]

Bouttier [10]

Ouriel [1]

Salam [9]

Blum [8]

Carey [13]

Year ofpublication

1987

1987

1992

1993

1999

Numberof patients

10

13

10

14

1

Treatment

Surgery

Surgery

UrokineseStreptokinese

Urokinese

Urokinese

Succesfullangiography

8

10

7

13

1

Functionalsucces

8

4

3

8

0

An angiographical success was obtained in 39 of 48 cases with only 23/48 functional successes


130

Strategy

In practice, the clinical context guides the thera-peutic strategy. In case of an embolus or traumaticocclusion and if the CT angiography or arterio-graphy show an arterial occlusion with absence ofdistal renal perfusion, the main decision criterionis the time interval between the occlusion and thediagnosis. If the interval exceeds three hours, asobserved in the majority of series (Fig. 4), revas-cularization is not justified. Additional to this inter-val, the time of desobstruction must be added: 2to 3 hours for surgery and 6 to 12 hours for throm-bolysis. In both circumstances, the changes of suc-cess are minimal. This abstention from therapy hasno major impact on the renal function if the con-tralateral is normal. The only exception for a des-perate salvage revascularization would be in case ofbilateral acute occlusion or occlusion of a singlekidney, even if the time interval seems to be exces-sive. Only few successes have been reported aftersix hours [39].

In some cases, the clinical and anatomical pic-ture is less clear. It can occur that distal to an arte-rial occlusion CT scanning shows a motley imagewith perfused and hypodense areas in the renalparenchyma. In this situation, active anticoagula-tion protects the kidney against further ischemia.Emergency arteriography (Fig. 5) will depict the

renal arterial tree and, according to the localiza-tion of the obstacle either in the common trunkor side branches, the decision is made to continuethe anticoagulation treatment or perform a desob-struction.

In case of acute thrombosis or even in emboliza-tion or trauma and if CT angiography or arteriogra-phy visualize kidney perfusion distal to the obstacle,the situation is completely different. Adequate anti-coagulation therapy should be started and revascu-larization can be postponed. Some authors [40]even recommend to prepare the patients during sev-eral days in order to reduce the surgical risks result-ing from pulmonary edema, hypertension or acuterenal failure with oligo-anuria, occurring in 15% ofpatients in the experience of Lacombe [7]. Dialysisor ultrafiltration is started and the cardiac conditionis optimized. This time period also allows assessmentof the actual and remaining renal function.

Isotope renography is the most accurate tech-nique, assessing the overall renal function andpercentage of function of the occluded kidney.Combined with the inuline clearance, it estimatesthe persistent glomerular filtration of the affectedkidney. This isotopic analysis should be combinedwith duplex scanning because the size and mor-phology of the occluded kidney are two parame-ters that will determine subsequent therapy. In caseof a small kidney with a lowered corticomedullarindex and increased arterial resistance, the success

FIG. 4 Delay between the assumed moment of occlusion and the diasnosis, before thestart of treatment ( personal experience and data from the literature). Only 7.3% ofpatients are diasnosed before the third hour, in the majority of cases after iatrosenicocclusion.


FIG. 5artery.

Example of distal embolization of the right renal

rate of a revascularization is minimal, especially ifthe individual function is less than 15% of the over-all function [41]. These patients benefit most fromanticoagulation therapy. In contrast, if the volumeof the kidney corresponds to the posture of thepatient and the corticomedullar structure is pre-served, a surgical or endovascular procedure shouldbe considered, depending on the aspect of theangiographic lesions.

Treatment

The desobstruction of acute renal artery occlu-sions has benefited from the progress in noninva-sive techniques: in-situ thrombolysis with or with-out angioplasty, angioplasty with or without a stent,percutaneous thrombosuction and fenestration.The choice of method depends on the clinical con-ditions, preference and experience of the team andthe type of lesion. In general, surgery should beperformed in cases in which recanalization mightinduce complications like progress of dissection,

false route or bleeding. Furthermore, extensive oc-clusions involving the hilus of the kidney as well asthe majority of noniatrogenic traumatic cases re-quire surgery.

SURGICAL TECHNIQUESEmbolectomy. Surgical access for renal artery

embolectomy is via a subcostal laparotomy or lum-botomy. The renal artery dissection should extendto the level of the bifurcating branches in order todirect the embolectomy catheters in each branch.A transverse arteriotomy distal to the aortic ostiumallows renal artery clamping once the inflow is re-stored. Distally, the handling of a N° 2 balloon cath-eter should be very cautious to prevent a intrarenalarterial rupture. Once the desobstruction has beenperformed, it is recommended to rinse the kidneyand eliminate all residual micro thrombi with500 cc of Ringer's lactate under a pressure of 150to 200 mmHg. A continuous flow of fluid at the endof this rinsing process is a good prognostic sign. Incontrast, a minimal drop-by-drop flow suggests in-traparenchymatous occlusions with subsequent sec-ondary failure. Following local heparinization, thearteriotomy is closed with a 7/0 monofilament su-ture. During renal embolectomy we prefer to avoidaortotomy because distal desobstruction and rins-ing is much more complicated. Furthermore, it re-quires suprarenal cross-clamping, compromising thecontralateral kidney.

Renal artery trauma. Kidney injury is oftenpart of a severe polytraumatic framework which pro-hibits any thrombolytic treatment. Especially if thecontralateral kidney is not affected, emergency sur-gical repair is not recommended in these multi-in-jured patients. Hemostatic difficulties after openingof the renal compartment as well as the incertain-ty of the result of the revascularization determinethe temporizing attitude of the majority of surgeons.However, if the patient becomes hypertensive dueto renal hypoperfusion by the collateral network,nephrectomy can be considered. In case of trau-matic injury of an anatomical and functional mono-kidney, the prognosis is obviously different, requir-ing emergency salvage surgery. In order to achieverealistic changes of success the procedure has to beperformed ex vivo [42] because of the three fol-lowing major reasons.1 - In case of renal artery subintimal rupture, ante-grade extension of the thrombus can involve the dif-ferent branches of the artery. Distal thrombectomy

131


11132

is very difficult to perform acurately in a contused,bleeding area.2 - Even if the scan does not reveal any transec-tions, a contusion or capsular fissure might inducesevere bleeding after reperfusion, carrying the riskof secondary nephrectomy.3 - Renal transections require repair by means ofgluing, which must be performed in a dry envi-ronment. Furthermore, the glue must be in freeair during ten minutes before any blood contact.

Following cooling and rinsing with Euro-Collins,the ruptured side branches are repaired with plad-get-reinforced sutures and the transections arefilled with glue. The kidney is then surrounded bya hemostatic gauze in order to limit the potentialbleeding after reperfusion. After the kidney hasbeen repaired, the arterial reconstruction is per-formed according to the ex vivo techniques. Dur-ing the whole procedure the renal area is tam-ponated. Finally, the kidney is autotransplanted inthe lower abdominal aorta and caval vein or com-mon iliac vessels.

Acute thrombosis. If the angiography shows re-injection in the renal trunk, revascularization canbe performed by means of thrombectomy, thrombo-endarterectomy or aortorenal bypass. The surgicalaccess is also via laparotomy or lumbotomy. Theapplied material is preferentially synthetic becauseof the frequently necessary long-term balloon dilata-tions of venous grafts. In children, the use of an ar-terial autograft is recommended because it will growwith time, offering a permanent reconstruction.

If the selective angiography shows a renogram witha poorly visible intrahilar re-injection [6], we andothers believe that ex vivo repair associated with au-totransplantation offers the best changes to save thekidney. The performance of several distal anasto-moses in small caliber arteries is delicate and impliesclamping of renal artery branches to avoid uncom-fortable back-bleeding, which even further deterio-rates renal ischemia in a poorly protected kidney. Exvivo repair avoids all these disadvantages [43] andallows high-quality completion angiography [44].

Endovascular techniques

The advantage of endovascular techniques is therapid availability as soon as the patient enters theradiology suite.

THROMBOLYSISSelective catheterization of an occluded renal

artery and local infusion of thrombolytic agents iscurrently the most frequently applied technique, ac-cording to numerous recently published case re-ports. The agents as well as the prescribed dosesvary considerably: Pilmore et al. [45] apply strep-tokinase at 30 000 units/hour (U/h), Sternberghet al. [46] use urokinase at 60 000 U/h, Salam etal. [9] follow a protocol with a loading dose of250 000 units urokinase and infusion at 60 000 U/hor loading dose of 90 000 units streptokinase withcontinuation at 5 000 U/h. We apply a local doseof 250 000 units urokinase and continue with2 000 U/h/kg. We perform a coagulation check-upevery four hours and temporarily stop the fibrinol-ysis if serum fibrinogen is less than one gramme.The average duration of treatment reported in theliterature differs considerably. It varies from 2 hoursin the shortest treatment of partial occlusion to anaverage of 23 hours with extremes of 50 hours. Ingeneral, there is no consensus on the type of agent,the doses and the duration after which the treat-ment becomes useless. Only one single animal studycompared the effect of thrombolytic agents in acuterenal artery occlusions: rt/PA was more effectivethan urokinase; streptokinase was not evaluated.

PERCUTANEOUS THROMBOSUCTIONPercutaneous thrombosuction techniques are ap-

plied mainly in peripheral and arteriovenous fistu-lae desobstructions [48], whereas renal artery oc-clusions treated by this method are rarely reported.Most often, the attempts were technical failures orpartial successes, necessitating completion by localthrombolysis. Different devices have been used.- Fogarty catheter, introduced in the renal arteryvia a guide wire,- thromboaspiration catheter based on the vortexeffects like the Amplatz Clotbuster catheter [49],- thromboaspiration catheter based on the venturieffect like the Rheolitic Angio-jet catheter [50].

ANGIOPLASTY AND STENTINGThe series in the literature addressing acute and

chronic renal artery occlusions do not always dif-ferentiate between angioplasty with or without astent. A recent publication reported on five emer-gency desobstructions for acute renal artery throm-bosis by means of angioplasty [51].

Angioplasty is obviously completed with stentplacement if the results of thrombolysis or throm-


bosuctionaire are only partially successful. Primarystenting is recommended in short thromboses withtruncal visualization and secondary occlusions afterprevious stenting. The latter indication is ratherdebatable for us because of the high incidence ofrecurrences. In general, the applied techniques arerather similar to the methods used in percutaneoustreatment of renal artery stenoses.

FENESTRATION OF AORTIC DISSECTIONSSome thoracic aortic dissections can cause acute

occlusion of one or both renal arteries by exten-sion of the false lumen, the mechanism of which isvariable. The intimal flap can behave as an obstruc-ting valve, occluding the renal artery. Otherwise,thrombosis of the false lumen might extend to theostium and obliterate the artery. In any cases, thegoal of treatment is to re-install communication be-tween the renal arterial trunk and the circulatinglumen. The most common applied technique con-sists of perforating the intimal flap by means of aballoon catheter and bursting the flap by inflatingthe balloon, re-establishing communication be-tween the true and false lumen and reperfusing thekidney (Fig. 6). If the reperfusion is inadequate, astent can be deployed in the renal artery. The prox-imal part of the stent is left unattached in the aor-tic circulating lumen. This technique generallyguarantees adequate revascularization [52]. Thesetechniques have recently been developed and long-term outcome of these stents positioned betweenthe aorta and renal artery is unknown.

For several reasons, the reported results in theliterature only have a limited value. The majorityof publications comprise one, two or three patientsand most often only report on therapeutic success,not indicating whether failures occurred as well.The smaller series report on different etiologieswith variable diagnostic and therapeutic measures.It is rather difficult to compare the outcome of aninjured kidney in a young adult with renal arteryembolization in an old person due to arrhythmia.The most extensive series date back to the 1980sand 1990s with a compilation of data spread over15 to 20 years. This implies that several patientshave been treated in the 1970s with limited means,before arrival of CT scanning, duplex, scintigraphy,and endovascular and thrombolytic therapies.

Finally, it would be interesting to compare the tech-niques of desobstruction as a function of the delayof treatment between the moment of obstructionand the end of the revascularization. In practice,the published data are too vague. Most often theexact moment of occlusion is not known and thetime intervals vary considerably (from 24 hours to2 weeks), which is probably caused by the chronicischemic process. In an attempt to assess the results,we have collected the published cases and relatedthem with each technique, obviously being a debat-able methodology.

We have identified 149 renal artery emergencydesobstructions in the literature between 1972 and2002. Our personal experience comprises 18 cases,adding up to 167 kidneys in 155 patients, 12 ofwhom who suffered from bilateral occlusion. In 98kidneys the technique was a surgical procedure andin 69 kidneys an endovascular approach was cho-sen. In the surgical series, 51 of 98 kidneys wereclassified as functional [52], which was similar tothe endovascular results (36/69; 52%). Mortalitywas 9.2% in the surgical group and 1.4% in theendovascular one. Our personal experience depictscomparable results with a functional kidney in 47%of patients.

If the surgical outcome is assessed as a functionof etiology, the emboli seem to carry the best prog-nosis (68% of salvaged kidneys), followed by acutethrombosis (63%). Traumatic occlusions have a poorprognosis (10%). Our personal experience slightlydiffers, showing a better prognosis in cases withacute thrombosis (Table I).

Thrombolysis followed by angioplasty with stent-ing offers the best endovascular results, with a suc-cess rate of 55%. Thrombolysis as a monotherapyis effective in 50% of cases; this is similar to theresults of angioplasty. Thrombosuction has onlybeen described in six cases: three failures, two par-tial successes, one complete success.

Conclusion

Acute renal artery occlusions have a worse prog-nosis than chronic occlusions. Improvement of theprognosis is only possible if the delay between themoment of occlusion and the final diagnosis is re-duced to a minimum. If feasible, the endovasculartechniques show similar results as compared to sur-gery, with a distinctly lower morbidity and mortality.

133


II134

FIG. 6 A - Type B dissection with extension in the abdominal aorta, with occlusion of the right renal artery. B - Cathe-terization of the right renal artery (via femoral access). Note that the catheter is not in the true lumen. C - Restored patencyof the right renal artery after fenestration and placing a stent in the right renal arterial trunc and the true lumen.


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16 Saint F, Quintela R, Salomon L et al. Acute renal arteryocclusion in a 15-year-old girl taking oral contraceptives. BJUInt2002; 89: 787-788.

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18 Goodman PE, Rennie WP. Renal infarction secondary to nasalinsufflation of cocaine. AmJEmergMed 1995; 13: 421 -423.

19 Peddi VR, Kant KS. Catastrophic secondary antiphospholipidsyndrome with concomitant antithrombin III deficiency. J AmSoc Nephrol 1995; 5: 1882 -1887.

20 Mysiak A, Kobusiak-Prokopowicz M, Kaiser T, Lipinska M.Thrombophilia complicated by multiple thrombo-emboliclesions in the arterial system - case report. Kardiol Pol 1997;47:492-495.

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23 Greenberg R, Waldman D, Brooks C et al. Endovascular treat-ment of renal artery thrombosis caused by umbilical arterycatheterization. / Vase Surg 1998; 28: 949 - 953.

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40 Higgins RM, Goldsmith DJ, Charlesworth D et al. Elective ratherthan emergency intervention for acute renal artery occlusionwith anuria. Nephron 1994; 68: 265-267.

41 Barral X, Gournier JP, Favre JP. Resultats tardifs de la revascu-larisation des occlusions chroniques de 1'artere renale. In:Cormier JM, Cormier F, FichelleJM, MarzelleJ (eds). Techniqueset strategies en chirurgie vasculaire. Paris, Pharmapost, 1995:pp 265-272.

42 Barral X, Lorin S, Grandmougin D, Favre JP. Chirurgie de1'artere renale. Encyl Med Chir (Editions Scientifiques etMedicales Elsevier SAS, Paris) Techniques chirurgicales -Chirurgie vasculaire, 43.110.C, 2002:18 p.

43 Barral X, Gournier JP, Favre JP. Chirurgie ex-vivo des arteresrenales. In: Kieffer E (ed). Chirurgie des arteres renales. Paris,AERCV, 1993: pp 205-214.

44 Barral X, Favre JP, Gournier JP. Le controle arteriographiqueperoperatoire des arteres renales. In: Branchereau A, MagnanPE. Methodes de controle peroperatoire des restaurations vasculaires.Marseille, CVN, 1994: pp 33-38.

45 Pilmore HL, Walker RJ, Solomon C et al. Acute bilateral renalartery occlusion: successful revascularization with streptokinase.AmJ Nephrol IMS; 15: 90-91.

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47 Haberstroh J, Wagner G, Kiefer T et al. Renal artery occlusionmodel in dogs for the evaluation of thrombolytic agents. J InvestSurg 1997; 10:183-188.

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versus a thrombectomy balloon in an animal model./ Vase Interv'

51 Dwyer KM, Vrazas JI, Lodge RS et al. Treatment of acute renalfailure caused by renal artery occlusion with renal artery angio-plasty. Am J Kidney Dis 2002; 40: 189-194.

52 Beregi JP, Cocheteux B, Koussa M et al. Traitement endovascu-laire des malperfusions au cours des dissections aortiques. In:Kieffer E, Fabiani JN. Chirurgie des dissections aortiques. Paris,AERCV, 2002: pp 231 -239.

136

14ACUTE INTESTINAL ISCHEMIA

BRANDON KRIJGSMAN, GEORGE HAMILTON

Intestinal ischemia is an uncommon condition presenting particular problems of diagnosisand management. The prevalence of the disease is difficult to establish. In the UnitedKingdom, approximately 2000 deaths a year are attributable to intestinal vascular insuf-ficiency, with 1883 deaths in 2000 [1]. At least 833 (44%) were classified as acute (834being unspecified as either acute or chronic). Women are more often affected than men by aratio of 2:1. The elderly are more commonly affected, the incidence being rare below fourty fiveyears of age, and with the majority of deaths occurring after seventy five years of age.

Most cases are caused by emboli (64%), followed by arterial thrombosis (27%), venousthrombosis (3.5%), and nonocclusive mesenteric ischemia (4.8%) [2]. Mortality is high andhas changed little since the 1970s, despite interventional advances (Table I).

11137

Pathophysiology

The arterial circulation to the gut has extensivecollaterals and arcades providing multiple sourcesof blood inflow (Fig. 1). This explains why vascularocclusion is well tolerated as evidenced by the re-lative lack of clinical intestinal ischemia despite thehigh prevalence of atherosclerotic disease of theaorta and visceral arteries. Certain collateral pat-terns are recognized, depending on which arteryis blocked. When either the celiac or superior me-senteric artery (SMA) is compromised, the maincollateral circulation is by the gastroduodenal andpancreaticoduodenal arteries. The main collateralchannels between the SMA and inferior mesenteric

artery (IMA) occur in the region of the splenic flex-ure between the middle and left colic arteries. Inthe presence of either SMA or IMA occlusion, themarginal artery of Drummond and the arch ofRiolan (an ascending branch of the left colic arteryanastomosing with branches of the SMA) enlargesignificantly. In the presence of an IMA occlusion,another important collateral circulation is betweenthe internal iliac artery and the left colic artery viathe superior hemorrhoidal arteries.

The SMA is the critically important vessel in main-taining visceral perfusion, as demonstrated byincreased blood flow after eating. This is not seenin the celiac artery. In chronic ischemia, all patientshave SMA stenosis or occlusion, in addition to celiacartery and/or IMA involvement (Table II) [27-29].


14138

1st author[ref.]

Czerny [2]

Cho [3]

Park [4]

Endean [5]

Foley [6]

Mamode [7]

Newman [8]

Urayama [9]

Duron [10]

Klempnauer [11]

Bronner [12]

Voltolini [13]

Konturek [14]

Ward [15]

Deehan [16]

Inderbitzi [17]

Levy [18]

Batellier [19]

Bapat [20]

Finucaine [21]

Sitges-Serra [22]

Wilson [23]

Lazaro [24]

Andersson [25]

Sachs [26]

Total

Year

1997

2002

2002

2001

2000

1999

1998

1998

1998

1997

1997

1996

1996

1995

1995

1992

1990

1990

1990

1989

1988

1987

1986

1984

1982

Numberof

patients

145

48

58

170

21

57

98

34

492

90

20

47

28

34

43

100

62

65

20

32

83

102

23

60

30

1962

Mortalityrate%

26

52

32

48

24

81

60

35

59

66

80

72

96

45

70

68

40

51

40

69

71

92

27

82

77

58

Arteries

SMA, CA, IMA

SMA, CA

SMA, IMA

SMA only

SMA occlusion

% of patientsinvolved

57

25

14

4

43

CA: celiac arteryIMA: inferior mesenteric arterySMA: superior mesenteric artery

About 10% to 20% of the cardiac output flowsthrough the visceral circulation (500 to 1200 mL/min.). Although intestinal mucosa forms one halfof the intestinal tissue mass, it receives a dispro-portionately large 75% of resting blood flow.

All causes of acute intestinal ischemia result inprolonged hypoxia with persistent severe pain outof proportion to the clinical findings. This is asso-ciated with early development of acidosis, hyper-amylasemia and leucocytosis. The ischemic damageto the mucosa results in the loss of the mucosal bar-rier. This allows translocation of bacteria, endotox-ins and cytokines with major systemic effects suchas septicemia and multiorgan failure. Successfulreperfusion releases free radicals causing an inflam-matory response with release of many cytokines,activated leucocytes and inflammatory mediators.This results in local mucosal and hepatic inflam-mation and systemic effects leading to multiorganfailure [27].

Etiology

OCCLUSIVE DISEASEEmboli. The SMA is the most common site of

embolic occlusion although the celiac artery can beaffected. There is classically an underlying cardiacproblem giving rise to the organized thrombus that

ACUTE INTESTINAL ISCHEMIA

B

If139

FIG. 1 A - Schematic representation of the collateral circulation of theintestine. B - Angiosraphic appearance of arch of Riolan from superiormesenteric artery (stented at its origin). C - Angiographic appearance ofmarginal artery of Drummond. D - Initial angiogram demonstrates occlu-ded IMA. The delayed film shows the colonic supply.


14140

embolizes. This is usually atrial fibrillation or lesscommonly a mural thrombus from an acute myocar-dial infarction. A history of previous embolic eventsis not uncommon. Other causes of emboli includeiatrogenic intra-aortic manipulations, paradoxicalemboli through a septal defect, atrial myxoma orprimary aortic tumors [30].

The history is of constant severe epigastric or peri-umbilical pain of sudden onset. It is frequently fol-lowed by copious vomiting and explosive diarrhea.Typically the patient has been previously well andasymptomatic. The abdominal signs are often lack-ing or nonspecific, with distension in associationwith absent or normal bowel sounds without anysigns of peritonism. This combination of severe ab-dominal pain out of proportion to the clinical find-ings is typical. Peritonism or blood in the stool orvomitus indicates severe advanced intestinal is-chemia with likely infarction and is generally a lateclinical feature.

The presence of proximal SMA pulsation and thedistribution of intestinal ischemia are intra-opera-tive clues for an embolus. The occlusion in em-bolism is usually distal to the origin of the pan-creaticoduodenal and middle colic branches, whichallows some blood flow to the small intestine to bemaintained. The stomach, duodenum, and proxi-mal jejunum are normal with ischemia extendingto the mid transverse colon.

Thrombosis. Superior mesenteric arterial thrombo-sis may occur as the result of progression of SMAstenosis that had not previously been diagnosed ortreated. There is often a history of intestinal orfood fear with severe weight loss, the hallmark ofchronic intestinal ischemia in about 65% of patients[4]. The typical patient is female and a heavy smok-er, often with evidence of widespread arterial dis-ease including previous myocardial infarction ordaudication. As with embolic occlusion, the com-bination of severe abdominal pain out of propor-tion to the clinical findings is typical. The throm-bosis of the SMA occurs at the origin of the artery.In contrast to embolic disease, the proximal SMApulse is absent and the distribution of intestinal is-chemia is more extensive. Only the stomach, duo-denum and distal colon are spared.

In the young patients, fibromuscular dysplasia cancause mesenteric arterial thrombosis with equallydevastating results [31]. Intravenous cocaine abuseis another increasing problem accounting for intes-tinal ischemia in the young patients. The extent ofintestinal ischemia and infarction tends to be focal

and less than that seen with atherosclerotic throm-bosis [32]. The mechanism of ischemia appears tobe occlusive rather than due to vasospasm. Mesen-teric ischemia should be considered in the differ-ential diagnosis when evaluating a young patientwith a history of cocaine abuse presenting with anacute abdomen.

Some prothrombotic states such as hyperhomo-cysteinemia or the 20210 A prothrombin gene mu-tation have resulted in primary arterial thrombosis[33,34].

Mesenteric venous thrombosis (MVT) is rare and ac-counts for 5% to 15% of all acute mesenteric is-chemia. It is classified as primary (where no causeis recognized) or secondary. Secondary MVT mayfollow hypercoagulable states, portal venous stasisand hypertension, intra-abdominal infection and in-flammation or malignancy, use of oral contracep-tives and splenectomy (see Table III). Long-termanticoagulation is required for MVT, because of thehigh recurrence rates. The clinical presentation isusually less acute than that of arterial occlusion.Severe but vague abdominal pain that tends to becolicky and slowly progressive is usually present. Fewabdominal signs are present except tenderness, dis-tension and decreased bowel sounds. The pain isout of proportion to the physical findings. Fecal oc-cult blood is present in the majority of patients.There is a pyrexia of greater than 38 °C in 25% to50% of patients, and 20% have a tachycardia [35,36]. Leucocytosis ranges from 12000 to 29000 [37].Frank peritonitis is seen only when transmural in-farction or perforation has occurred.

Surgical findings include blood-stained free peri-toneal fluid at laparotomy. The affected bowel iscyanotic and edematous with a rubbery texture.Mesenteric arterial pulsations are present but theveins contain fresh thrombus that extrude when theveins are cut. Infarction is most common in themid small bowel.

Other occlusive causes. Other causes formesenteric occlusion include aortic dissection orisolated SMA dissection [38]. Vascular toxicity fol-lowing chemotherapy with 5-FU, cisplatin and vin-cristine has been reported [39], as has been oc-clusion by Schistosoma mansoni infection [40].

NONOCCLUSIVE MESENTERIC ISCHEMIAMesenteric ischemia can occur without arterial oc-

clusion. It can develop in severe systemic illness inassociation with cardiorespiratory shock and multi-organ failure. Typically these patients are on critical


care units. Shock, either cardiogenic or secondaryto septicemia, is often present. The physiologic re-sponse of mesenteric vasoconstriction in response toboth normovolemic and hypovolemic shock appearsto be mediated by the renin-angiotensin axis [41].It is usually aggravated by the use of inotropic agents.It is a distinct complication of open heart surgerywith an incidence of 0.2% to 0.4 % although its mor-tality rate is 70% to 100% [42].

Long-term dialysis patients are another group ofsusceptible patients who may suffer from nonocclu-sive mesenteric ischemia (NOMI). A major charac-

Hypercoagulable states

Neoplasms

Deep venous thrombosis

Pregnancy

Factor V Leiden

Protein C deficiency

Protein S deficiency

Homocysteine

Antithrombin III deficiency

Anticardiolipin antibodies

20210 A prothrombin gene mutation

Hyperfibrinogenemia

Myeloproliferative disorders

Sickle cell disease

Abdominal pathology

Malignancy

Splenectomy

Splenomegaly

Estrogen containing oral contraceptives

Inflammation/infection

Pancreatitis

Inflammatory bowel disease

Intra-abdominal abscess

Mechanical venous occlusion

Portal hypertension

Vohoilus

Intussusception

MVT: mesenteric venous thrombosis

teristic finding is an episode of severe hypotensionor hypovolemia immediately before the onset ofabdominal symptoms [43,44].

Abdominal pain is the most common symptom,although in the unconscious patient abdominal dis-tension, gastrointestinal bleeding, leucocytosis orfever may be the presenting features. The morta-lity rate is approximately 65% [45].

IATROGENIC INTESTINAL ISCHEMIAIntra-aortic manipulations such as interventional

radiological procedures or intra-aortic balloon pumpspost cardiac surgery can result in this condition.Embolization can occur following pulsatile cardio-pulmonary bypass [46]. Embolization is usuallywidespread involving the kidneys, pelvis and lowerlimbs, as well as the viscera, and carries a very highmortality. The correct treatment is not known butshould probably include full intravenous anticoa-gulation, appropriate resuscitation and infusion ofprostacyclin or its analogues. Embolization due tocholesterol may be suspected by an eosinophilia inthe blood film. This may occur in patients under-going systemic thrombolysis or anticoagulation withaortic manipulation. Anticoagulation is relativelycontraindicated and the use of statins would seembeneficial.

Left colonic ischemia can occur following aorticreconstruction after interruption of the direct orcollateral blood supply. It is more common follow-ing aneurysm repair after ligation of a patent IMA.The accepted incidence is 2% (ranging from 0.2%to 10%). Mortality in this condition is 40% to 50%,and approaching 90% if there is full bowel wallthickness ischemia [47]. Diagnosis can be difficultin the postoperative period and depends on raisedclinical awareness. Watery diarrhea, bloody or not,should prompt urgent bedside colonoscopy. A leu-cocytosis greater them 20000, fever and shock, andsevere metabolic acidosis should alert the surgeonto the possibility of severe colonic ischemia.

Diagnosis

Acute intestinal ischemia is a life-threatening sur-gical emergency, yet can be a difficult diagnosis tomake, with delay contributing directly to infarction.The majority of cases are diagnosed more than12 hours after the onset of symptoms [16]. Delayeddiagnosis accounts for the majority of malpracticeclaims involving acute mesenteric ischemia in the

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United States [48]. Diagnosis depends on a highindex of suspicion. The main presenting feature isthe combination of severe abdominal pain out ofproportion to the clinical findings, as discussedabove.

Serum levels of lactate and leucocytes are ele-vated in the majority (65% to 90%) of patients togreater than 50 U/L and 15000/mL, respectively[2,49-51].

Hyperamylasemia is seen in just under half thepatients with acute mesenteric ischemia [50].

Elevation of serum inorganic phosphate levelshave been proposed as a marker of mesenteric is-chemia, as it is extensively found in gut, but thisonly occurs in 15% to 33% of such patients [50,51].However, in those patients who did have elevatedphosphate levels, it predicted extensive injury andpoor prognosis [52].

The fibrinolytic marker D-dimer is elevated inthrombo-embolic occlusion of the SMA, althoughlevels are also raised in other conditions of acutebowel ischemia such as strangulation or rupturedaortic aneurysm [53].

Animal studies have suggested intestinal fatty acidbinding protein (I-FABP) as a serum marker reflect-ing bowel ischemia. Early human studies showpromise, as patients with ischemic bowel diseasedemonstrate significantly higher I-FABP levels thaneither healthy subjects or patients with acute ab-dominal pain. Patients with mesenteric infarctionhad the highest serum I-FABP levels [54].

Plain radiographs of the abdomen may reveal non-specific bowel dilatation or, in MVT, wall edema(thumbprinting); or gas in the bowel wall or portalvein. Unfortunately they are not helpful in most cases.

Mesenteric angiography will confirm the diagno-sis of arterial occlusion but at the cost of delay intreatment. If there are clear abdominal signs of peri-tonitism, urgent laparotomy without angiography isthe best course of action. In the remainder of pa-tients suspected of acute intestinal ischemia with-out abdominal signs, angiography is indicated withlateral views of the visceral aorta and its branches.In acute SMA thrombosis, there is usually no visu-alization of the entire artery because of the ostialnature of the disease, although delayed views mayshow slow filling of the distal SMA. SMA emboliza-tion usually allows visualization of the proximal ar-tery to just beyond the level of the middle colicartery.

Although noninvasive imaging modalities such ascomputed tomography (CT), magnetic resonance

imaging (MRI) and ultrasound can evaluate theaorta and the origins of splanchnic arteries, selec-tive angiography of mesenteric arteries is still thegold standard in diagnosing peripheral splanchnicvessel disease in NOMI [55]. Angiography will showintestinal arterial vasospasm and, most importantly,exclude a significant arterial lesion.

Abdominal CT scanning has led to the correctdiagnosis in 80% of patients presenting with acuteintestinal ischemia in some centers [2]. Findingssupporting acute mesenteric ischemia include arte-rial or venous thrombosis, intramural gas, portalvenous gas, a focal lack of bowel wall enhancementand liver or splenic infarcts. The newer generationof multislice CT scanners allow a more detailedstudy of the small bowel and mesenteric vesselswhich has, in some authors' experience, eliminatedthe need for additional imaging studies such asangiography [56].

MVT can be diagnosed on contrast enhanced CTscanning by demonstration of thrombus within thesuperior mesenteric vein [57]. Venous infarctedbowel is clearly demonstrated by CT when othersigns for MTV such as ascites, bowel wall thicken-ing, bowel dilatation and pneumatosis intestinalisare present. It would seem that this is the imagingmodality of choice in MVT, as it seems to be a moresensitive test than angiography [58].

While it has good results in the hands of its advo-cates [59], duplex scanning is impaired by theincreased intestinal gas that is frequently presentin this condition.

Magnetic resonance angiography will reliablydemonstrate the proximal mesenteric vessels, butpresently imaging of the more distal branches andocclusions is not good.

Treatment

NONSURGICALIn all cases, the patient should be initially resus-

citated, given broad-spectrum intravenous antibi-otics and fully heparinized. As yet, the twin goals ofmesenteric revascularization and resection of non-viable bowel can only be achieved by surgical means.Surgery is indicated in all patients with peritonitis.Angiography in patients without peritonitis maydemonstrate NOMI or MVT. In NOMI, treatment isnonoperative and depends on optimizing cardiacoutput and treating underlying conditions such assepsis. Intramesenteric arterial infusion of papaver-


ine at a dose of 30 to 60 mglr1 may be beneficial.Up to 65% of patients who have undergone cardiacsurgery have had symptomatic improvement withinhours when diagnosed early [60].

If MVT is diagnosed at angiography, intra-arterialthrombolytic therapy has been given successfully[61]. Nonoperative management by full anticoagu-lation for acute MVT is feasible when the initialdiagnosis is certain and when the bowel infarctionhas not led to transmural necrosis and bowel per-foration. The morbidity, mortality, and survival ratesare similar in cases of surgical and nonoperativemanagement [62].

Other reported endovascular procedures foracute intestinal ischemia include fenestration andstent placement in aortic dissection [63,64], angio-plasty and stenting in an acute occlusion in a pa-tient with chronic mesenteric insufficiency [65,66],and angioplasty alone [67]. This contrasts with anincreasing use of angioplasty for chronic mesentericischemia [28].

SURGICALLaparotomy is indicated in patients with peri-

tonitis after rapid resuscitation. The first step is toassess the degree and extent of bowel viability. Free,foul smelling peritoneal fluid is a sign of advancednecrosis even if perforation has not occurred. Is-chemic bowel has a characteristic appearance withloss of its normal sheen. It is dull, gray in colorand flabby in tone without any peristalsis. Infarctedbowel is purplish black in color, often friable andperforated. In many cases the bowel ischemia willbe so extensive and advanced that no further sur-gical treatment is undertaken and palliative caregiven. Where there is hope of sufficient bowel via-bility, revascularization should be performed beforeany bowel resection is considered. After successfulrevascularization, previously precarious segments ofintestine may recover and resection of clearly is-chemic bowel can then take place.

SMA embolectomy. The proximal portion ofthe SMA is dissected free from the surrounding fatand lymphatic tissue just as it emerges from the pan-creatic neck into the base of the mesentery. Approx-imately 3 to 4 centimeters of artery is cleared, withcare taken not to damage the branches. Heparin(5000 units) is given intravenously. A transverse arte-riotomy is made and a 3F or 4F embolectomycatheter is passed proximally and distally to clear theembolus and reestablish vigorous pulsatile flow. If

proximal flow cannot be established, SMA thrombo-sis is likely and reconstructive surgery will be required.

SMA reconstruction. Revascularization can beperformed either using bypass grafting from theaorta to the patent SMA or by re-implantation ofthe healthy portion of the SMA into the aorta. Inthe presence of perforated bowel or infarctionrequiring bowel resection, prosthetic grafts must notbe used. Reversed saphenous vein aortomesentericgrafting or direct SMA re-implantation is the pro-cedure of choice in this situation (Fig. 2). Bypasswith vein or prosthesis is prone to kinking due toits configuration, and great care must be taken toalign the grafts to avoid this complication. Singlevessel revascularization is usually adequate in theemergency [6] and probably also in the nonemer-gency situation [4,68].

Assessment of intestinal viability. Determi-nation of which portions of bowel are nonviable canbe difficult especially when there is extensive infarc-tion. The decision about how much to resect canbe crucial to the long-term outcome. Clinical assess-ment by detecting pulsation in the arcades, colorof the bowel, peristalsis and bleeding from cut edgesis most commonly used. This is often complementedby the use of the doppler probe to detect flow inthe intestinal wall in addition to flow in the arcadevessels. Other techniques include the use of fluo-rescein and inspection under Wood's lamp, pulseoximetry and laser doppler flowmetry.

Ischemic bowel is resected with the aim of pre-serving as much bowel as possible, particularlywhere a short gut syndrome may be created. Thus,several segmental resections with multiple anasto-moses may be necessary. Contemporary practice isto leave all marginally viable intestine after revas-cularization, providing there is re-inspection of thebowel after 24 to 48 hours.

In cases of MVT, resection of infracted bowel withliberal margins should be performed with a primaryanastomosis if perfusion is adequate. Venous throm-bectomy has poor results with a high recurrencerate and is rarely indicated.

Post aneurysm repair colon ischemia requiringsurgery usually necessitates a Hartmann's procedure,a primary anastomosis being contraindicated. Con-sideration must be made to protect the aortic graftand its limbs from infection or contamination byusing antiseptic soaked swabs. Exposed grafts at theend of the procedure should be covered by a well-perfused omental pedicle flap.

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144

FIG. 2 A - Schematic representation of revascularization of the SMA with: bypass taking care to avoid kinking and obs-truction B - Or re-implantation of SMA into the aorta. C - Angiographic appearance of aorto-SMA bypass with vein graft.There is co-existing left common iliac occlusion. D - Angiographic appearance of re-implanted SMA into aorta, which hasa small saccular aneurysm at the site of occluded vein graft (aortoceliac bypass).


Postoperative management. This is especiallyimportant in those patients who have undergoneextensive bowel resection. Fluid losses (especiallypotassium and magnesium) must be carefully mon-itored and replaced. Total parenteral nutrition maybe started early in the postoperative period, andmay need to be continued for months in cases withshort gut syndromes.

Abdominal compartment syndrome has beenreported following revascularization of chronicmesenteric ischemia [69] and should be consideredin acute revascularization, especially if there hasbeen limited or no resection.

A second look laparotomy 24 to 48 hours afterthe initial procedure is mandatory to assess the via-bility of the marginally perfused parts of the boweland to check the intestinal anastomoses. Furtherlaparotomies are indicated until the viability of thebowel is established. In cases where major intestinalresection with primary anastomosis has taken place,there is an increasing vogue to performing a sec-ond look laparoscopy under local anesthesia. Thisis estimated to reduce the number of unnecessarylaparotomies by two thirds [70].

Continued intensive care is required with opti-mization of cardiac and respiratory status. This isin part a response to intestinal reperfusion and maylead to multiorgan failure, and patients undergo-ing endovascular revascularization should be caredfor similarly. There is an associated deteriorationin hepatic function with transaminases rising 90- to100-fold [27]. The hepatic impairment and associ-ated coagulopathy is usually transient, returning tobaseline within seven to ten days.

In cases of MVT, long-term anticoagulation is re-quired because of the high recurrence rates. Com-plications such as ascites and portal hypertensionmay require specific treatment [37].

Prognosis

Regardless of etiology, prognosis depends cruciallyon rapid diagnosis and institution of treatment toprevent or at least minimize bowel infarction. Inone study, mortality was 86% if the diagnosis wasmade more than 24 hours after onset of symptomscompared to 50% if diagnosis was within 24 hours[71]. The presence of peritoneal signs results in aworse mortality of 82% compared to 33% when

abdominal signs are absent. Extensive intestinalinfarction in this series had a 100% mortality ratewhereas early revascularization in limited bowelinfarction to less than one meter only had a mor-tality of 18%. Circulatory collapse was another prog-nostic indicator with a 100% mortality comparedwith 50% in patients with a systolic blood pressuregreater than 100 mmHg [71].

Studies, generally retrospective, demonstrate theworse prognosis of acute compared to chronicmesenteric ischemia. Thirty-day postoperative mor-tality is approximately 52% to 70% (compared toless than 5%), the majority due to bowel infarction[3,16]. Long-term patency and symptom-free sur-vival can be expected after successful mesenteric ar-terial reconstruction for acute mesenteric ischemia.Late survival rates have been reported as 54% to73% at 5 years and 20% at 10 years. Excluding peri-operative deaths, the probability of long-term sur-vival does not appear to differ between acute andchronic mesenteric ischemia [2,3,5]. A significantdecrease in the overall mortality rate, from 77% to59%, has been observed in France over the pastdecade [10]. This was a retrospective multicenterstudy by the French associations of surgical researchcomparing the periods from 1980 to 1985 and 1990to 1995. The main improvement was seen in thepatients' pre-operative condition. Mortality rates de-creased from 83% to 63% in thrombotic acute me-senteric ischemia and from 51% to 19% in MVT.There were no significant increases in frequenciesof angiography, vascular or second look procedures.

Long-term follow-up of patients with chronic me-senteric ischemia has shown that recurrent symp-toms at three years were more common if revascu-larized by endovascular means compared withsurgery (34%, 95% CI 14%-54% versus 13%, 95%CI 6%-21%) [72] (Fig. 3). Most of these symptomsoccurred in the first year (28% recurrence at 1 yearand 34% at 3 years). Mortality was similar with bothtreatments in this group of patients with chronicsymptoms. The literature suggests that there is amean technical success rate of 91% (±8%) with animmediate pain relief rate of 79% (±9%). This isassociated with a complication rate of 18% (±15%)and a mortality rate of 4%. There is no reason tobelieve that endovascular methods would confer anysymptom or survival advantage in patients with acutesymptoms unless there has been no progression tointestinal gangrene.

if145


FIG. 3 Cumulative freedom from recurrent symptoms in chronic mesenteric ischemia. At 3 years, recur-rent symptoms were more common in the sroup treated by endovascular means (34%) compared toopen sursery (13%)[72], Reproduced with permission from the Journal of Vascular Surgery, Mosby, Inc.

14146

Conclusion

Acute intestinal ischemia remains a surgical emer-gency with a high mortality and the key to its man-agement is prompt diagnosis. Current treatment isby laparotomy, revascularization and excision ofdead bowel. Some acute occlusions can be treatedendovascularly with assessment of bowel viability byminimally invasive means.

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64 Slonim SM, Miller DC, Mitchell RS et al. Percutaneous balloonfenestration and stenting for life-threatening ischemic compli-cations in patients with acute aortic dissection. / Thorae Car-diowMcSurg 1999; 117: 1118-1126.

65 Brountzos EN, Critselis A, Magoulas D et al. Emergency endo-vascular treatment of a superior mesenteric artery occlusion.Cardiovase Intervent Radiol 2001; 24: 57 - 60.

66 Loomer DC, Johnson SP, Diffin DC, DeMaioribus CA. Super-ior mesenteric artery stent placement in a patient with acutemesenteric ischemia. / Vase Interv Radiol 1999; 10 : 29-32.

67 Rundback JH, Rozenblat GN, Poplausky M et al. Re: jejunalartery angioplasty and coronary stent placement for acute mesen-teric ischemia. Cardiovase Intervent Radiol 2000; 23: 410-412.

68 Bjorck M, Acosta S, Lindberg F et al. Revascularization of thesuperior mesenteric artery after acute thrombo-embolic occlu-sion. BrJ Surg m% 89: 923-927.

69 Sullivan KM, Battey PM, Miller JS et al. Abdominal compart-ment syndrome after mesenteric revascularization. / Vase Surg2001; 34: 559-561.

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70 Seshadri PA, Poulin EC, Mamazza J, Schlachta CM. Simplified nosis in acute intestinal ischemia. Int Angiol 1987; 6: 415-420.laparoscopic approach to "second-look" laparotomy: a review. 73 Kasirajan K, O'Hara PJ, Gray BH et al. Chronic mesentericSurg Laparosc Endosc Percutan Tech 1999; 9: 286-289. ischemia: open surgery versus percutaneous angioplasty and

71 Giulini S, Bonardelli S, Cangiotti L et al. Factors affecting prog- stenting. / Vase Surg 2001; 33: 63-71.

14148

IF.)RUPTURE OF SPLANCHNIC

ARTERY ANEURYSMS

JOAQUIM BARBOSA, MARIA-JOSE FERREIRA

Splanchnic artery aneurysms represent an uncommon but important form of mesentericvascular disease since nearly 22 % present as clinical emergencies, including 8.5% that resultin death [1]. In routine autopsies, they appear in 0.01% to 0.2%, being diagnosed moreoften in the aged population [2]. Two necropsy studies in the elderly found a 10% prevalenceof visceral aneurysm, supporting that its incidence is dependent on the age of the studiedpopulation [3]. All visceral arteries can be affected by aneurysms. However, the most frequentlyaffected are the splenic, hepatic, superior mesenteric and celiac arteries being responsible foralmost 90% of the visceral aneurysms.

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History

The first report of a visceral artery aneurysm(VAA) dates from 1770 by Beaussier, who describeda splenic artery aneurysm in an anatomic demon-stration. In 1881, the American president James A.Garfield died from rupture of a splenic artery aneur-ysm, two months after a gunshot in the abdomen.DeBakey and Cooley reported, in 1953, the first suc-cessful resection of a superior mesenteric arteryaneurysm. Before 1960 only a few reports of VAAwere published with high mortality rates. In 1970,Stanley et al. reviewed the reports in the literatureconcerning 1098 cases, but since then the numberof cases increased dramatically [1].

Because splanchnic artery aneurysms are rare,the reports in the literature mainly comprise smallseries or particular forms of presentation. Account-ing to the small number there is a trend to enclosein the series different etiologies as well as true andfalse aneurysms. All these factors contribute to theincomplete knowledge and poor description of itsnatural history.

At present, advances in imaging technology andendovascular procedures are modifying the diag-nostic and therapeutic strategies and partly explainthe growing number of reported aneurysms. But de-spite all these advances, a significant number ofthese lesions are not discovered until rupture, whichoften results in the death of the patient. Therefore,


15150

an aggressive approach to the diagnosis and ma-nagement of these aneurysms is required. However,if there is no doubt about the surgical managementof ruptured visceral aneurysms, controversy remainsregarding the optimal management of the asymp-tomatic cases because the risk-benefit is difficult toaccess in the absence of a comprehensive natural his-tory. New therapeutic and less aggressive techniquesoffer new options for some patients, but there isstill no sufficient long-term follow-up for evaluationof the results.

Incidence

The introduction of more sophisticated imagingtechniques, like high-resolution computed tomogra-phy, high-resolution ultrasound and magnetic reso-nance angiography permitted to discover asympto-matic aneurysms. More than 3 000 splanchnic arteryaneurysms have been published in the internationalliterature.

Traditionally, the reported incidence of the aneur-ysms related to their anatomic location is: splenicartery 60%, hepatic artery 20%, superior mesen-teric artery 5.5%, celiac artery 4%, gastroduodenaland gastro-epiploic artery 4%, jejunal and ileal-colicartery 3%, pancreatoduodenal and pancreatic 2%,gastroduodenal 1.5% and mesenteric inferior arteryless than 1% [4].

However, in the last decade the most commonvisceral aneurysm reported in the literature oc-curred in the hepatic artery. This fact can be associ-ated with the increased use of percutaneous diag-nostic and therapeutic biliary procedures, as well asthe non-operative management of blunt hepatictrauma and the increased use of CT scan for diag-nosis. As a result, there is an increased detection ofpost-traumatic false aneurysms of the hepatic arte-rial branches, particularly intrahepatic aneurysms.More than 80% of hepatic artery aneurysms weretraditionally extra hepatic but now, these representonly 66%. The great majority of the hepatic arteryaneurysms are solitary (91%) and most commonlylocated in the common hepatic or the right hepaticartery. They occur mainly in males (66%), with anaverage age of 56 years (range 18-86 years).

The true incidence of splenic artery aneurysmsis unknown, but has been reported to be between0.02% and 10.4% in the general population and8.8% to 50% in cirrhotic patients. The mean ageof presentation is 52 years (range 2-93 years) and

78.8% of the splenic artery aneurysms occur inwomen. Most of them are small (smaller than 2 cm),saccular and almost 80% are located in the mid-ordistal splenic artery [5]. Aneurysms of the splenicartery occur in association with fibrodisplasia of therenal arteries. About 4% of patients with renal fi-brodisplasia present with concomitant splenic arteryaneurysms. Both intracranial and splenic aneurysmsare found in patients with medial displasia [6].

Aneurysms of the celiac artery constitute 4% ofthe visceral artery aneurysms and are characteristi-cally associated with aneurysms at other locations: ab-dominal aortic aneurysms are present in 20% of pa-tients and other visceral artery aneurysm in 40% [6].

Aneurysms of the superior mesenteric artery maybe saccular or fusiform and are almost always locatedin the proximal 5 centimeters of the artery. In thepast, most of these aneurysms were discovered inwomen, but now the incidence in men is 66%.

Etiology

Most aneurysms are caused by atherosclerosis ormedial degeneration, however, some authors defendthat the atherosclerotic changes are a secondaryprocess to the appearance of the aneurysm. Other,less common causes include trauma, infection andiatrogenic injury.

The etiology of splenic artery aneurysms remainsunclear, although several conditions have been asso-ciated like fibrodisplasia, pancreatitis, portal hyper-tension, hemodynamic and endocrine changes inpregnancy, atherosclerosis, inflammatory and infec-tious disorders, arteritis and collagen vascular dis-eases. The most common pathologic findings aredefects of the media characterized by fragmenta-tion of elastic fibers and loss of smooth muscle.

The first responsible factor for splenic arteryaneurysms is the presence of systemic arterial fibro-displasia. Patients with arterial fibrodisplasia exhibitsplenic artery aneurysms with a frequency six timesgreater than the normal population. They are morecommon in women with multiple pregnancies,probably due to the presence of estrogens and pro-gesterone receptors in the arterial wall. Hormonalshifts during pregnancy and relaxin (a gestationalhormone responsible for the dilatation) can inducedegenerative changes in the splenic artery like dis-ruption of the internal elastic lamina, fragmenta-tion of elastic fibers and fibrodisplasia of the media.

RUPTURE OF SPLANCHNIC ARTERY ANEURYSMS

The development of splenic artery aneurysms inpatients with portal hypertension and splenomegalycan be due to a hyperkinetic state in the spleen.These hemodynamic factors also explain the samesituation in patients after liver transplantation andrepresent an additional risk factor in pregnancy.

Another mechanism described is infection sec-ondary to sub acute bacterial endocarditis in intra-venous drug abusers.

Enzymatic injury to pancreatic and peripancreaticarteries (splenic, pancreatoduodenal and gastro-duodenal) or from erosion of a pseudocyst into adja-cent visceral arteries explain aneurysm formation inthe course of a pancreatic inflammatory process.These aneurysms are closely related to the intensityand duration of the disease and the incidence variesbetween 10% to 17% in chronic pancreatitis.

In celiac artery aneurysms, the most commonpathologic finding is medial degeneration and ath-erosclerosis. Other findings include poststenoticdilatation and re-entry from aortic dissection. Themajority of cases are true aneurysms (55%) but falseaneurysm secondary to penetrating trauma andinfection have also been reported.

Historically, mycotic aneurysms of the hepaticartery had the highest incidence but nowadays theyaccount for only 3% and usually occur in intra-venous drug abusers. False aneurysms now accountfor nearly 50% of reported hepatic aneurysms, dueto iatrogenic maneuvers during percutaneous bil-iary procedures or trauma.

The etiology of superior mesenteric aneurysms isdiverse, but a significant number is caused by infec-tion secondary to subacute bacterial endocarditisby nonhemolytic streptococcus. The incidence ofinfected aneurysms was 58% to 63%, but duringthe last decade it decreased to 33%. This was ac-companied by the increase of true atheroscleroticaneurysms (25%) as well as those related to inflam-matory processes like pancreatitis (12%). Nonethe-less, the superior mesenteric artery remains themost common site of infection of a peripheral mus-cular artery. Dissection also affects this artery morethan any other visceral artery.

Clinical presentationand diagnosis

Nowadays, with the increased use of abdominalimaging techniques a great number of splanchnic

artery aneurysms is discovered in the asymptomaticstate. However, in the study of Carr et al., 63% ofthe VAA were symptomatic at the time of presenta-tion and 23.9% presented with rupture [7]. A clas-sic presentation of an asymptomatic aneurysm is theappearance of a circular calcification on an abdomi-nal radiography (Fig. 1). Today they are depictedby ultrasound or CT scan.

If aneurysms are symptomatic, the most commonsymptom is abdominal pain. At physical examina-tion a palpable mass or abdominal bruit can befound.

Rupture of an aneurysm causes severe abdominalpain and hypovolemic shock. In case of a rupturedsplenic artery aneurysm, the hemorrhage is initiallyconfined to the lesser sac, resulting in a period ofhemodynamic stability. Following, the hemorrhageruptures into the peritoneal cavity, which is the socalled double-rupture phenomenon first describedby Brockman, in 1930 [6].

Splenic artery aneurysm rupture into the retro-peritoneum (11%), stomach (16%), colon (8%),pancreas (6%) and 13% develop gastro-intestinalbleeding secondary to erosion of the aneurysm intoadjacent viscera.

In splenic artery aneurysms, particularly thoseassociated with inflammatory lesions, bleeding isusually brisk but varies from short, repeated andself-limited episodes to massive hemorrhage. In

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FIG. 1 Plain X-ray of the abdomen showing the calcifica-tions of an aneurysm of the splenic artery.


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patients with pancreatitis, the presence of a falseaneurysm can be suspected by persisting or abruptincreasing abdominal pain or hemodynamic insta-bility and/or gastro-intestinal bleeding with noother obvious cause.

In up to 80% of patients with a hepatic arteryaneurysm, rupture can occur in equal frequencyinto the peritoneal cavity and biliary tract or duode-num, gallbladder, portal vein or stomach. Abdomi-nal pain is present in 55% of patients and gastro-intestinal bleeding or hemobilia occurs in 46% ofpatients. Jaundice can be present up to 10% of pa-tients due to extrinsic compression of the bile ductby the aneurysm.

Aneurysms of the celiac and superior mesentericartery are most often symptomatic at presentationand are suspected because of intermittent abdom-inal pain. This can result from repetitive emboliza-tion of mural thrombus with subsequent mesentericischemia. Between 38% and 50% of mesenteric ar-tery aneurysms and 13% of celiac aneurysms pres-ent with rupture, manifested by acute abdominalpain, hypotension or sudden death.

Aneurysms of the gastric and gastro-epiploicartery most often present with rupture (90%), twothirds manifested by gastro-intestinal bleeding andone third with intraperitoneal bleeding.

Aneurysms of the inferior mesenteric artery arevery rare and presentation is characterized by abdo-minal pain, gastro-intestinal bleeding or shock. Themajority is discovered during exploratory laparo-tomy for gastro-intestinal hemorrhage.

Despite advances in endoscopic diagnosis, thesource of gastro-intestinal bleeding is not found in5% of patients [8]. This is complicated by the factthat 70% to 80% of such bleeding stops sponta-neously. Although rare, splanchnic artery aneurysmscan cause recurrent gastro-intestinal bleeding dueto erosion into adjacent organs. The rarity of thispathology contributes to the delay in the diagnosisand higher mortality. Early angiography is recom-mended in most cases of gastro-intestinal bleedingin patients with no endoscopic diagnosis. CT-scancan also demonstrate an aneurysm and is very use-ful, particularly in elderly patients because it offersa lesser risk. It's also useful in defining the dimen-sions of the aneurysm and to delineate its relationswith the surrounding organs [8] (Fig. 2).

Clinical assessment of visceral aneurysms is verydifficult but selective angiography is the most valu-able exam for the diagnosis and therapeutic plan-ning (Fig. 3).

A selective biplanar arteriography is mandatoryfor the study of the celiac and superior mesentericarterial aneurysms. Spiral CT angiography withthree-dimensional reconstructions can give detailedanatomic information and may identify the vesselorigins. CT scanning is also useful in the diagnosisof ruptured aneurysm, identifying a contained hema-toma within the lesser sac or retroperitoneum [9].

FIG. 2 Giant aneurysm of the splenic artery. Note the cal-cifications within the splenic parenchyma due to previousinfarctions secondary to embolism from the splenic artery.

FIG. 3 Selective ansiosram of the celiac trunk showins ananeurysm located at the second third of the splenic artery.


Risk of rupture

The risk of rupture of visceral aneurysms is over-estimated by collective reviews because there is abias due to including symptomatic cases as well.Furthermore, the true incidence of visceral arteryaneurysms is unknown.

The reported risk of rupture of splenic arteryaneurysms varies from 3.0% to 9.6%. In the studyof the Mayo Clinic the rate of rupture was 2.9% forwomen and 10.9% for the male population with anoverall risk of 4.6% [10].

There appears to be a bimodal age distributionwith the majority of aneurysm rupture presentingeither in young adults or in the elderly. For in-stance, in splenic artery aneurysms the increasedincidence of rupture in young adults is associatedwith pregnancy or portal hypertension and carriesa poor prognosis. On the other hand, the risk ofrupture for aneurysms in elderly patients is proba-bly less than 2% with a much lower mortality risk.

The risk of rupture of a splenic artery aneurysmis also linked to the size of the aneurysm (morethan 2 centimeters of diameter), pregnancy, cir-rhosis and liver transplantation. In these two lastgroups the risk is particularly high in patients withoc-1-antitripsin deficiency due to the excessive pro-teolitic activity. Calcification of the aneurysm wasclassically associated to higher risk of rupture butthis fact has never been proven. B-blockade may beprotective against rupture. Growth rates are slowand growth is infrequent. Stanley suggests that thetrue risk of rupture of splenic artery aneurysm isless than 2%. Data of a single series suggests a riskof rupture between 3% to 10% [4].

The mortality after rupture remains high and wasrecently reported to be 36% [11]. Rupture of splenicartery aneurysms in pregnant women carries a highmaternal and fetal mortality (70% and 95% respec-tively). This rupture is more common in the thirdtrimester, labor or post-partum and in multipares.

On the other hand, mortality related to aneurysmsassociated with pancreatitis varies between 15% and43%, depending on the patient clinical state, siteand nature of the bleeding, lesion and the type ofmanagement. The exact risk of rupture of hepaticaneurysm is not known, but nearly 2/3 of the recentreports present with rupture into either the peri-toneal cavity or an adjacent viscera, most likely thebiliary tract. The mortality of these selected patientswas 21% [5] but it can be assumed that the mor-

tality of free rupture is much higher and an aggres-sive approach is clearly indicated.

Blumenberg et al., in 1974, consider the risk ofrupture of mesenteric artery aneurysms to be quitesmall [12], but Stone et al., in 2002, reported a rup-ture rate of 38% [13]. Probably, this variability ofthe reported risk of rupture can be related to theevolution of referred etiologies for this pathology.In this serie, male patients were particularly pronefor rupture with a risk of 50%. The mortality rateof ruptured superior mesenteric aneurysms is 30%.

The natural history of celiac artery aneurysmsappears to be one of expansion and rupture, withsome authors reporting a risk of rupture of approx-imately 13% [11]. The mortality rate with ruptureis very high, near 100%, and is often complicatedwith intestinal infarction.

The global mortality rate after rupture of a vis-ceral artery aneurysm ranges between 35% and100% as a result of the catastrophic hemorrhagethat may ensue, where as mortality of elective treat-ment is less than 10% [14]. Therefore aggressivesurgical policy of all aneurysms is recommended,especially because rupture cannot be predicted.

Indicationsfor the surgery

At present there is a trend towards observationof most small aneurysms in asymptomatic, high risk,elderly patients. Indications for surgery remaincontroversial in some groups of patients. Repair ismandatory for splenic artery aneurysms in the fol-lowing situations: symptomatic aneurysms, preg-nancy or women in childbearing age, liver transplantpatients, and diameter larger than two centimeters.Furthermore, patients should have a reasonableoperative risk and life expectancy of more than twoyears.

Operative intervention should be considered inall but the most high-risk patients with hepatic, celiacartery and superior mesenteric artery aneurysms,considering the high mortality with rupture. Aggres-sive surgical management of pancreatic and pancre-aticduodenal artery aneurysms is also mandatory,because of the very high risk of rupture at the timeof clinical presentation (56% for the gastroduode-nal and 38% for the pancreaticduodenal artery).

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Treatment

The current options for management of a VAAinclude endovascular and conventional surgery. Dueto the high morbidity associated with major opera-tions, various minimally invasive techniques havebeen developed. Transcatheter embolization hasbeen used successfully in the treatment of splenicand hepatic artery aneurysms, although end-organischemia, painful splenic infarction and late vesselrecanalization are potential problems [15]. Variouslaparoscopic techniques have also been applied tothe treatment of this pathology as well as the useof endovascular techniques with the use of stentgrafts. The option for each treatment modality de-pends on the presentation, location of the aneur-ysm, size, and general condition of the patient aswell as the experience of the vascular center.

Conventional surgical treatment of the visceralartery aneurysms usually involves ligation or resec-tion of the aneurysm with or without vascular recon-struction. Surgical strategies differ somewhat foreach type of aneurysm.

SURGERYRupture of visceral artery aneurysms requires ur-

gent surgical repair. In this emergency setting, liga-tion of the aneurysm without reconstruction can bethe best alternative whenever there is adequate col-lateral circulation, particularly in unstable or highsurgical risk patients. Ligation of the hepatic arteryproximal to the gastroduodenal, right gastric artery,gastro-epiploic and pancreatoduodenal is possiblewithout major ischemic complications. Ligation ofthe splenic artery is not always followed by spleennecrosis and ligation of the superior mesenteric ar-tery can be performed, followed by segmental bowelresection in a setting of emergency.

In large aneurysms or for those involved in inflam-matory tissue, the best option is to ligate the prox-imal and distal artery from inside the aneurysm.

Celiac or hepatic artery aneurysms involving thegastroduodenal artery and superior mesenteric ar-tery require resection of the aneurysm and revascu-larization by interposition or bypass graft.

For splenic artery aneurysms, we propose a goldenrule, that consists of dividing the artery in threemain segments. For the proximal aneurysms weadvise ligation of the splenic artery, normally with-out splenectomy. Those who are located to themedian third of the artery (Fig. 3), an intra-aneurys-

matic ligation with splenectomy, seems to be thebest solution.

Considering the distal segment, ligation of thesplenic artery and splenectomy is the preferentialtherapeutic option, in our opinion. It is mandatoryto perform the drainage of the pancreatic area, inall suspected pancreatic injury, to avoid the com-plications of a pancreatic fistula.

Surgical options for repair of celiac artery aneur-ysms include aneurysmectomy with or without revas-cularization, aneurysmorraphy, reimplantation andligation. The latter option is not always accompa-nied by hepatic necrosis, but this complication ismore frequent in the presence of liver disease.

Superior mesenteric aneurysms pose unique chal-lenges for surgical repair. They extend well beyondthe region usually encountered with atheroscleroticprocess. In addition, inflammation and infectionare common features of these aneurysms, makingthe dissection difficult. Therefore one of the mostattractive techniques for the treatment of suchaneurysms is ligation. There is no assurance thatthe collateral flow is sufficient to prevent ischemia,thus a careful assessment of adequate mesentericblood flow is necessary. Stone et al. described theirexperience with ruptured aneurysms and ligationwas the most used technique employed in 75% ofthe patients [13]. However, 38% of the patients withrupture needed concomitant bowel resection. No pa-tient that underwent elective intervention requiredbowel resection. Revascularization was recommend-ed only if bowel ischemia was present in patientsundergoing operation for rupture or if pre-opera-tive symptoms or evaluation, mainly angiography,suggested mesenteric ischemia. Most series have alsofound that adequate collateral blood flow exists andligation without revascularization is the procedureof choice.

Other techniques for repair of the superior me-senteric artery aneurysm comprise aneurysmectomyused in 35% of the reported cases and aneurysmor-raphy in 21%.

The first technique is used after proximal anddistal ligation and to resect the infected aneurysm.Aneurysmorraphy is used when the aneurysm issaccular and a portion of the arterial wall is free ofdisease. In only a minority of cases the revascular-ization was undertaken, accounting for less than15% in the literature [11]. Revascularization can bemade either by interposition or, in larger or moredistal lesions, by aorto-mesenteric bypass. When theaneurysm is not infected and there is no intestinal


ischemia, a synthetic graft can be used. In the othercases it is necessary to use vein.

Intrahepatic large and proximal aneurysms mayrequire partial liver resection. Alternatively, proxi-mal and distal ligation can be undertaken, accept-ing the risk of liver necrosis. Currently, approxi-mately 37% of hepatic artery aneurysms are treatedwith percutaneous embolization. [5].

MINIMAL INVASIVE TECHNIQUESLaparoscopic ligation, resection or clipping of the

aneurysm constitute other therapeutic alternatives.These approaches can be difficult in patients withprevious abdominal operations, obese patients orfor aneurysms located in pancreatic parenchyma ordeep in the splenic hilus.

During the past ten years, percutaneously directedembolization became the most employed techniquefor the treatment of intrahepatic aneurysms and si-tuations like those associated with pancreatitis. Withrespect to treatment of intrahepatic aneurysms, goodimmediate outcome with success rates between 67%-100% have been described [16,17]. Complicationsof this technique include hepatic necrosis, abscessformation or sepsis. Early failure was related to theinability to catheterize selectively the vessel due toarterial spasm, rupture of the aneurysm during theprocedure or arterial perforation by the catheter[16]. Embolization is a very attractive therapeuticmodality in high-risk patients or for lesions difficultto access surgically, like the aneurysms associatedwith pancreatitis. For some authors, embolization isconsidered a temporary process until definite sur-gery is performed. Surgery is reserved for instablepatients, failed embolization or for complicationslike infection or extrinsic compression. As these com-plications are most likely to occur in large aneur-ysms, excision or drainage should be consideredafter successful embolization.

Several reports of patients treated with emboliza-tion as a sole therapy described a high technical suc-cess rates (75%-100%), low morbidity (14%-25%)and low death rates (048%). However, most reportsinclude a small number of patients and short follow-up [8,17]. Carr et al. conclude that embolizationalone is not adequate because of the high primaryfailure rate with necessity to convert to open surgery[18]. All patients should be followed by CT-scan afterembolization because there is a risk of recurrenthemorrhage (12%) and recanalization (37%).

There are some reports describing ultrasoundguided thrombin occlusion of visceral aneurysms at

the time of the surgery [19]. The use of thrombininjection, was initially used in the treatment offemoral artery pseudoaneuryms.

Endovascular treatment by means of stent graftsis another option, with the advantage of the lowerprocedural risk and because it excludes the aneur-ysm while preserving end-organ perfusion [15]. Thearterial anatomy and the location of the aneurysmhave a large impact on the technical ability to placea stent graft. Normal caliber artery on either sideof the aneurysm is required to allow safe sealing.The introduction of more flexible stent grafts andsmaller introducer systems, also allow treatment intortuous vessels. The risk of vessel rupture or throm-bosis is also of major concern.

In conclusion, despite advances in the diagnosisand therapy, the heterogeneity of the VAA indicatesthat management should be individualized and tai-lored. Prognosis of this disorder depends on theanatomic location of the aneurysm, primary pathol-ogy and general condition of the patient.

Summary

The splanchnic artery aneurysms are an uncom-mon pathology with a high morbidity and mortal-ity rate. Rupture is the most frequent and danger-ous complication. The incomplete knowledge ofthe natural history of the disease contributes to thecomplexity of these situations.

The etiology of the process seems to be very dif-ferent according the involved vessel.

Age, general condition of the patient, size andlocation of the aneurysm play an important role inthe therapeutic decision. In case of rupture, all elec-tive conventional surgical techniques can be ap-plied, including simple ligation of the vessel.

The main objective is to stop the bleeding andsave the patients life and preserve the viability ofthe organ. Endovascular procedures are a goodalternative, especially in high-risk patients.

However, long-term follow-up is required to assessdurability and safety of these techniques.

R E F E R E N C E S

1 Stanley JC, Thompson NW, Fry WJ. Splanchnic arteryaneurysms. Arch Surg 1970; 101: 689-697.

2 Carr SC, Mahvi DM, Hoch JR et al. Visceral artery aneurysmrupture. / Vase Surg 2001; 33: 806-811.

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3 Busuttil RW, Brin BJ. The diagnosis and management of vis-ceral artery aneurysms. Surgery 1980; 88: 619-624.

4 Zelenock GB, Stanley JC. Splanchnic artery aneurysms. In:Rutherford RB (ed). Vascular surgery, 5th ed. Philadelphia, W.B. Saunders Co., 2000: pp 1369-1382.

5 Shanley CJ, Shah NL, Messina LM. Common splanchnic arteryaneurysms: splenic, hepatic, and celiac. Ann Vase Surg 19%; 10:315-322.

6 Carr SC, Pearce WH. Management of visceral artery aneurysm.In: Yao JST, Pearce WH (eds). Practical vascular surgery. Stam-ford, Appleton & Lange, 1999: pp 241-258.

7 Carr SC, Pearce WH, Vogelzang RL et al. Current managementof visceral artery aneurysms. Surgery 1996; 120: 627-634.

8 Wagner WH, Cossman DV, Treiman RLV et al. Hemosuccuspancreaticus from intraductal rupture of a primary splenic ar-tery aneurysm. / Vase Surg 1994; 19: 158-164.

9 Brunei WG, Greenberg HM. CT demonstration of a rupturedsplenic artery aneurysm. J Comput Assist TomogrlQQl; 15: 177-178.

10 Abbas MA, Stone WM, Fowl RJ et al. Splenic artery aneurysms:two decades experience at Mayo clinic. Ann Vase Swrg-2002; 16:442-449.

11 Messina LM, Shanley CJ. Visceral artery aneurysms. Surg ClinNorth Am 1997; 77:425-442.

12 Blumenberg RM, David D, Slovak]. Abdominal apoplexy dueto rupture of a superior mesenteric artery aneurysm: clipaneurysmorrhaphy with survival. Arch Surg 1974; 108: 223-226.

13 Stone WM, Abbas M, Cherry Kf et al. Superior mesenteric ar-tery aneurysms: is presence an indication for intervention?/ Vase Surg 2002; 36: 234-237.

14 Settembrini PG, Jausseran JM, Roveri S et al. Aneurysms ofanomalous splenomesenteric trunk: clinical features andsurgical management in two cases. / Vase Surg 1996; 24:687-692.

15 Larson RA, Solomon J, Carpenter JP. Stent graft repair of vis-ceral artery aneurysms. / Vase Surg 2002; 36: 1260-1263.

16 De Perrot M, Berney T, Buhler L et al. Management of bleed-ing pseudoaneurysms in patients with pancreatitis. Br J Surg1999; 86: 29-32.

17 Gambiez LP, Ernst OJ, Merlier OA et al. Arterial embolizationfor bleeding pseudocysts complicating chronic pancreatitis. ArchSurg 1997; 132: 1016-1021.

18 Carr JA, Cho JS, Shepard AD et al. Visceral pseudoaneurysmsdue to pancreatic pseudocysts: rare but lethal complications ofpancreatitis. / Vase Surg 2000; 32: 722-730.

19 Mclntyre TP, Simone ST, Stahlfeld KR. Intraoperative throm-bin occlusion of a visceral artery aneurysm. J Vase Surg 2002;36: 393-395.

16THE ABDOMINAL

COMPARTMENT SYNDROME

MICHAEL YAPANIS, JOHN WOLFE

Intra-abdominal pressure (IAP) has been studied since the late 19th century. Indeed, theeffects of raised IAP in cats were documented by Heinricius, who found that they could be fataldue to inhibition of respiration. Later, seminal studies by Emerson, Coombs, and Overholtlooked at IAP, its variation, and factors that could influence it. Although the clinicalconsequences of raised IAP have been known for many decades, the "abdominal compartmentsyndrome" (ACS) was only popularized as a concept in the early 1980s [1], when multi-organdysfunction was identified, in conjunction with a distended abdomen and intra-abdominalhypertension (IAH).

157

Definition

Broadly, compartment syndrome can be definedas a rise in pressure in a body compartment, caus-ing reduction in tissue perfusion thereby jeopar-dizing tissue function and viability. While thisconcept has been applied to ACS, there is no widelyaccepted definition. It is thought to occur whenthere is a sustained rise in IAP in conjunction witha distended abdomen, increased airway pressures,hypoxia, hypercarbia, a fall in cardiac output, andoliguria despite adequate fluid resuscitation. Char-

acteristically, the abnormal parameters show markedimprovement on abdominal decompression.

NORMAL IAP AND IAHThe normal range for LAP is thought to be mar-

ginally above atmospheric pressure (0 to 5 mmHg)[2]. However, marked variation has been foundwith diaphragmatic, abdominal wall, and pelvicmuscular contraction, body position, sex, and bodymass index [3]. The exact point at which this raisedIAP becomes significant is to some extent arbitrary,and definitions may quote values ranging from


16158

more than 10 mmHg to more than 25 mmHg. Mostauthors suggest a pressure of higher than 20 mmHg,as indicating IAH [4].

Epidemiology

The majority of studies are based in trauma cen-ter intensive care units [5] on a select group ofhigh-risk patients. Furthermore, they are frequent-ly retrospective or small prospective series with vari-able definitions of IAH or ACS, and subjects mayhave undergone prophylactic decompression priorto LAP measurement. Therefore, the true incidenceof ACS is difficult to ascertain. Ivatury et al. [6]showed that 32.9% of 70 patients admitted to sur-gical intensive care with life-threatening penetrat-ing abdominal trauma developed IAH (IAP supe-rior to 25 cmHsO). In a prospective series byMeldrum et al. [5], 14% of 145 acutely injured pa-tients, with an injury severity score higher than 15,requiring emergent laparotomy, developed ACS.Recently, Hong et al. [7] prospectively studied706 patients of all risks, with or without prior la-parotomy, admitted to a trauma intensive care unit.Only 2% of the patients developed IAH (IAP>20 mmHg), while only 1 % went on to develop full-blown ACS. This study implies that the true inci-dence of ACS is very low. Nevertheless, in a surveyof the current opinions of American trauma sur-geons, 85% had experienced ACS at least once inthe previous year, suggesting that it is a conditionof which every surgeon exposed to vascular traumashould be aware [8].

Etiology (Table I)

Essentially, any condition associated with visceralexpansion or which gives rise to an increase in intra-or retroperitoneal fluid, usually blood, can causeACS. Causes are divided into acute or chronic. Ofthe acute causes, abdominal trauma is the mostcommonly reported. Probable risk factors includesevere trauma, massive fluid resuscitation, a highinjury severity score, and the requirement of adamage control laparotomy. In a study by Ertel etal. [9], 17 of 311 patients with severe abdominal orpelvic injury, requiring damage control laparotomy,and admitted to the intensive care unit, developedACS. As many as 47% of these patients requiredpacking. Where primary fascial as opposed to pro-

phylactic mesh closure has been undertaken, theincidence of ACS has been higher.

Ruptured aortic aneurysm can result in ACSthrough massive intra- and retroperitoneal hemor-rhage and the large volume of fluid used duringresuscitation. In the experience of Fietsam et al.[10], 4 of 104 patients operated on for rupturedaortic aneurysm developed ACS. All received morethan 25 L of fluid resuscitation.

Maxwell et al. [11] studied the role of fluid resus-citation in the development of secondary ACS. Onehalf percent of 1216 trauma admissions (in theabsence of abdominal injury) underwent abdomi-nal decompressions for visceral edema. Fluid resus-citation averaged 19 ± 5 L of crystalloid and 29 ±10 units of blood before laparotomy. Consequently,they recommended that IAP should be monitoredwhen resuscitation volumes approached 10 L ofcrystalloid or 10 units of packed red cells.

Retroperitoneal hemorrhageRuptured aneurysmAcute pancreatitisSpontaneous

Mesenteric ischemia

Intestinal obstruction

Colonic pseudo-obstruction

Pneumoperitoneum

Ileus

Acute gastric dilatation

Severe abdominal

rogemc

Postoperative

Trauma

Burns

Massivefluid

Resuscitation

Chronic

Obesity

Ascites

Ovarian tumor

THE ABDOMINAL COMPARTMENT SYNDROME

Pathophysiology

The elucidation of the mechanisms of pathogen-esis in IAH has relied to a large extent on animalmodels. The advent of laparoscopy, especially in thelast decade, has demonstrated that some of theorgan changes seen in laparoscopy can mirror thosewith increased IAP as IAH begins to develop. Therise in IAP seen in ACS is often caused by the accu-mulation of large volumes of intra- and extraperi-toneal blood and fluid. This may relate partly tothe underlying pathology, but also to a bleedingdiathesis induced by consumption of coagulationfactors. Intra-abdominal packing and massive tissueedema from the liberal use of crystalloids and theexudation of fluid due to enhanced capillary per-meability can precipitate the development of ACS.

Organ dysfunction in ACS is usually multifactor-ial. Damage not only occurs as a result of the pres-sure effects of IAH, but also because of ischemicdamage from hypovolemic shock and then reper-fusion from resuscitation (ischemia-reperfusioninjury). It has been shown that hemorrhage follow-ed by resuscitation produces greater cardiorespira-tory damage at a lower IAP than IAH alone [12].More recently, in an animal study by Oda et al. [13],sequential hemorrhagic shock, resuscitation, andACS were associated with significantly increased por-tal and central venous cytokine levels and moresevere lung injury than hemorrhagic shock or ACSalone. In addition, there is often associated comor-bidity in an elderly population, which enhances anypressure induced damage. This includes ischemicheart, respiratory, and renovascular disease. How-ever, the importance of raised IAP is demonstratedby the often rapid reversal of organ dysfunction fol-lowing abdominal decompression [6].

The response of the systems to a raised IAP isgraded. At pressures of up to 10 mmHg, there areno effects. As the IAP exceeds 15 mmHg, cardio-vascular changes take place, which become moreprofound as the IAP exceeds 20 mmHg. Oliguriacan arise at lower pressures, but it becomes moreevident when they exceed 20 mmHg. As IAP ap-proaches 40 mmHg, anuria ensues.

THE CARDIOVASCULAR SYSTEMA rise in LAP leads to a reduction in venous return

[14]. This is due to functional obstruction of theinferior vena cava (IVC) as it moves from an areaof high pressure (intra-abdominal) to an area of

lower pressure (intrathoracic), the anatomicalobstruction of the IVC by diaphragmatic distortioncaused by IAH, and a drop in flow from the IVCand retroperitoneal veins. In turn, this leads to areduction in preload.

Peripheral vascular resistance increases due tocompression of vascular beds, resulting in an ele-vated afterload. Owing to a rise in intrathoracicpressure, cardiac compliance falls, increasing ven-tricular filling pressures. The combination of thechanges in preload, afterload, and cardiac compli-ance cause a fall in cardiac output. Consequently,in order to maintain blood pressure, there is a reflextachycardia. Mean arterial pressure does not changesignificantly.

The presence of underlying ischemic heart dis-ease renders the myocardium susceptible to theeffects of an increased afterload and tachycardia,and to the development of cardiac failure due tovolume overload.

THE KIDNEYSIn 1923, Thorington and Schmidt documented

the effects of raised IAP on urine output. Totalanuria was found to occur with an IAP of 30 mmHg.Sugrue studied the changes in renal function inIAH after laparotomy and found that the odds ratiofor developing renal impairment with increased IAPwas 12.4 [4]. The mechanism for this relates to arise in retroperitoneal pressure causing renal veincompression, and an increase in renal vascular re-sistance. These changes manifest in a fall in renalblood flow and glomerular filtration rate. Varioushumoral factors may play a role in oliguria, includ-ing rises in renin, aldosterone, and antidiuretic hor-mone production with increased IAP. Uretericobstruction is not thought to occur.

THE RESPIRATORY SYSTEMIAH forces the diaphragm upward thereby reduc-

ing chest wall and lung compliance. This necessi-tates a rise in peak airway pressure to maintainventilation. Since movement of the diaphragm isimpaired, the upper zones of the lungs, which nor-mally have a higher ventilation-perfusion ratio, areventilated even more [15]. This enhances any ven-tilation-perfusion mismatch. Hypoxia and hyper-carbia ensue.

INTRACRANIAL PRESSURE (ICP)An increase in ICP is caused by restriction in lum-

bar venous return. In addition, a raised ICP and a


16160

reduced cerebral perfusion pressure have beenshown to be caused by rises in intrathoracic andpleural pressures causing functional venous outflowobstruction to the cerebral veins via the jugularvenous system [16].

GASTROINTESTINAL SYSTEMEffects of increased IAP have been identified in

hepatic, gastric, and intestinal perfusion. Hepaticblood flow may become significantly reduced witheven mild IAH, and this is independent of cardiacoutput. A fall in gastric mucosal pH with IAH mayprecede the development of ACS. In an animalmodel, Diebel et al. [17] demonstrated a reductionin ileal mucosal blood flow and evidence of bacte-rial translocation with a raised LAP. They proposedthat this might explain septic complications andorgan failure in ACS. However, the part that bac-terial translocation plays in ACS is not proven.

Friedlander et al. [18] demonstrated a reductionin superior mesenteric arterial (SMA) flow follow-ing hemorrhage and resuscitation before increasingIAP. The reduction in SMA flow appeared greaterthan would be expected from the fall in cardiac out-put. It was concluded that optimization of hemo-dynamic status was not sufficient to maintain SMAflow but that early abdominal decompression wasimportant.

ABDOMINAL WALLThe abdominal cavity can accommodate small vol-

umes with relatively little increase in IAP. However,the pressure-volume curve for the abdominal wallis exponential, and as IAH ensues, relatively smallvolume changes create large rises in IAP.

IAH has been shown to reduce abdominal wallmuscle perfusion, which increases the likelihood ofwound healing problems including dehiscence orlater herniation. Furthermore, abdominal wall is-chemia may predispose to wound infection.

Diagnosis

This relies on the accurate measurement of IAP,having established that clinical findings are consis-tent with ACS. The difficulty arises where IAP isnot very high, since organ dysfunction is frequentlymultifactorial. In Hong's cohort of patients, thosewith IAH that did not require decompressive laparo-tomy for ACS had a mean IAP of 26 mmHg, whilethose that went on to develop ACS had a mean of

42 mmHg [7]. Meldrum (see below) devised a grad-ing system for management, based on the value ofIAP [5].

CLINICAL FEATURESThe clinical features of a distended and tense

abdomen, the requirement of high atrial pressuresto maintain cardiac output, increasing peak airwaypressures with increasing hypoxia and hypercarbia,and oliguria are consistent with ACS.

MEASUREMENT OF IAP (TABLE II)In a recent prospective blinded study, the sensi-

tivity and accuracy of abdominal examination in as-sessing IAP were evaluated. When IAP was 15 mmHg,sensitivity and accuracy were 56% and 84%, respec-tively [19]. This implies that clinical examination isinsufficient on its own at determining whether LAPis increased to such levels. However, it is not clearwhether the accuracy would be sufficient at the levelof pressure normally encountered in ACS.

The methods of measurement of IAP can bedivided into direct and indirect techniques. Directtechniques have usually been employed in animalexperiments, although laparoscopy has permittedthe direct assessment of IAP via a pressure trans-ducer connected to the laparoscope.

Indirect methods have largely been used to meas-ure IAP by assuming that visceral luminal pressurereflects the IAP generally. The most popular tech-nique involves utilizing a bladder catheter. It wasfirst described by Kron et al. [1] in 1984 and waslater validated.

It is thought that the bladder acts as a passivediaphragm when 50 to 100 mL is instilled into an

Direct Metal cannula

Intra-peritoneal catheter

Laparoscopy

Indirect Inferior vena cava

Nasogastric

Urinary Catheter


empty bladder. When the volume of sterile salinehas been introduced into the bladder via the Foleycatheter, the sterile tubing of a catheter bag is cross-clamped just distal to the culture aspiration port.The end of the tubing is connected to the catheterand the clamp partly released such that fluid fromthe bladder can fill the tube proximal to the clamp.After reclamping the tube, a 16-guage needle isplaced through the culture aspiration port and con-nected to a pressure transducer. The top of thesymphisis pubis is used as the zero point with thepatient supine. The technique may be unreliablewhere the bladder is small and contracted or wherethere is a large compressive pelvic hematoma. Oncemeasurements have begun, they should be repeatedapproximately every four to six hours to detectadverse changes in IAP.

OTHER INVESTIGATIONSSince ACS is a clinical diagnosis, computed

tomography scanning should not be used routinelyas an investigation. Recently, Pickhard et al. [20]identified findings common to four patients withproven ACS. These included tense infiltration of the

retroperitoneum, extrinsic IVC compression by hema-toma or exudates, and an increase of antero-poste-rior to transverse diameter (positive round bellysign).

Gastric tonometry has been shown to identifypatients with IAH likely to go on to ACS, althoughit is not widely used.

Management (Figure)

SUPPORTIVE TREATMENTThe aim of supportive treatment should be to

maximize cardiac filling pressure by fluid resusci-tation, and inotropic support as necessary. An accu-rate assessment will be required by the use of acentral line and Swann-Ganz catheter to determinepulmonary artery wedge pressures and cardiac out-put. In addition, attempts should be made to treatcoagulopathy using clotting factors, and hypother-mia by warming.

Cheatham et al. [21] have recently described theuse of abdominal perfusion pressure. The abdominalperfusion pressure is to equal the difference between

ii161

FIGURE Treatment diasram for abdominal compartment syndrome related to intra-abdominal pressures.


16162

the mean arterial pressure and the ZAP and wasfound to be a better predictor of survival and a bet-ter target for resuscitation.

A grading system has been proposed for the man-agement of IAH (Table III). The authors of thisstudy felt that purely volume resuscitation may beappropriate for an LAP of up to 25 mmHg. As thepressure exceeded 25 mm Hg, tissue perfusion pres-sure was thought to be impaired, requiring decom-pression. When greater than 35 mmHg, the causewas felt to be an arterial bleed and it was believedthat decompression followed by a further reexplo-ration was necessary [5].

ABDOMINAL DECOMPRESSION AND CLOSUREThe mainstay of treatment of ACS is abdominal

decompression. It may be undertaken prophylacti-cally, following a laparotomy where the woundwould otherwise have to be closed under extremetension or where the risks of ACS are thought tobe high, such as massive hemorrhage and fluidresuscitation and the use of abdominal packs.

Despite the use of pre-emptive measures, ACS canstill occur, although with a lower incidence [9]. Ina 10-year case control study at the Mayo Clinic,patients who underwent primary mesh closure werecompared with those who underwent standard clo-sure but then required a mesh for IAH. The twogroups of patients had similar demographic andclinical profiles, but multi-organ failure scores, endo-scopically detected colonic ischemia rates, and mor-tality from multi-organ failure were lower in theprophylactic mesh group. Various pre-operative andintra-operative risk factors were identified in thoserequiring a mesh postoperatively who would bene-fit in a prophylactic mesh. These included pre-op-erative anemia, prolonged shock and cardiac arrest,intra-operative massive resuscitation, profound hypo-thermia, and severe acidosis [22].

The type of closure can be either temporary ordefinitive (Table IV). Temporary closure may beachieved with a variety of methods. For example, alarge fluid bag or polypropylene mesh can be su-tured in a tension-free manner to the abdominalwound. It is also important that any closure keepfluid and viscera reasonably contained. After severaldays, when the edema has subsided, an attempt canbe made at closure. Where this is not possible, themesh can be reduced in size as the edema improvesor the abdomen can be closed in stages, where tem-porary bag or mesh can be removed and replacedwith a skin graft. The large ventral hernia can be

repaired several months later. A rectus sheath my-ocutaneous advancement flap or an absorbable meshand skin graft can be used for definitive closure.

An alternative to decompressive laparotomy hasbeen described in an animal model, where conti-nuous external negative abdominal pressure wasevaluated for the reversal of some of the effects ofIAH. Continuous external negative abdominal pres-sure appeared to reduce IAP, central venous pres-sure, and intracranial pressure significantly, andthere was a trend for a lower peak inspiratory pres-

Table ffl GRADING OF THE ABDOMINALCOMPARTMENT SYNDROME [5]

^ , Bladder pressureGrade \TmmHg

Recommendation

III

IV

10-15

16-25

26-35

>35

Maintainnormovolemia

Hypervolemicresuscitation

Decompression

Decompressionand re-exploration

Table IVMETHODS OF ABDOMINALWALL CLOSURE

Temporary Skin clips

PTFE

Polypropylene mesh

Fluid bag, e.g., "Bagota"

Zipper

Definitive Myocutaneousadvancement flap

Skin grafting ofan absorbable mesh


sure [23]. It is suggested that such a device couldbe used in humans when IAH occurs but where adecompressive laparotomy is not required.

Despite the immediate improvements noted, themortality of this subgroup of patients remains highand in excess of 50% [7,15].

Outcome of treatment Conclusion

Abdominal decompression has been shown toimprove cardiorespiratory and renal function. A sud-den reduction in IAP leads to a fall in blood pres-sure as a result of the sudden reduction in peripheralvascular resistance. Patients must therefore be vol-ume resuscitated and inotropes may be required.

Although ACS is relatively rare, it remains com-mon enough for any vascular surgeon to recognizeits existence. Prophylactic measures such as abdom-inal wall mesh closure or prompt decompressivelaparotomy can reduce mortality of this otherwiseuniversally fatal condition.

R E F E R E N C E S

1 Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure a criterion for abdominal re-exploration.Ann Surg 1984; 199: 28 -30.

2 Sugrue M. Intra-abdominal pressure. Clinical Intensive Care 1995;6:76-79.

3 Sanchez NC, Tenofsky PL, Dort JM et al. What is normal intra-abdominal pressure? Am Surg mi; 67: 243-248.

4 Sugrue M, Buist MD, Hourihan F et al. Prospective study ofintra-abdominal hypertension and renal function afterlaparotomy. BrJSurgWb; 82: 235-238.

5 Meldrum DR, Moore FA, Moore EE et al. Prospective character-ization and selective management of the abdominal compart-ment syndrome. AmJSurglWT, 174: 667-673.

6 Ivatury PvR, Porter JM, Simon RJ et al. Intra-abdominal hyper-tension after life-threatening penetrating abdominal trauma:prophylaxis, incidence and clinical relevance to gastric mucosalpH and abdominal compartment syndrome. / Trauma 1998; 44:1016-1023.

7 Hong JJ, Cohn SM, Perez JM et al. Prospective study of the inci-dence and outcome of intra-abdominal hypertension and theabdominal compartment syndrome. 5r/Surg 2002; 89: 591-596.

8 Mayberry JC, Goldman RK, Mullins RJ et al. Surveyed opinionof American trauma surgeons on the prevention of the abdomi-nal compartment syndrome. JTrauma 1999; 47: 509-514,

9 Ertel W, Oberholzer A, Platz A et al. Incidence and clinical pat-tern of the abdominal compartment syndrome after "damage-control" laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000; 28:1747-1753.

10 Fietsam RJr.( Villalba M, Glover JL, Clark K. Intra-abdominalcompartment syndrome as a complication of ruptured abdomi-nal aortic aneurysm repair. Am Swrgl989; 55: 396-402.

11 Maxwell RA, Fabian TC, Croce MA, Davis KA. Secondary abdom-inal compartment syndrome: an underappreciated manifesta-tion of severe hemorrhagic shock. J Trauma 1999; 47: 995-999.

12 Simon RJ, Friedlander MH, Ivatury RR et al. Hemorrhage lowersthe threshold for intra-abdominal hypertension-induced pul-monary dysfunction./Trauma 1997; 42: 398-405.

13 OdaJ, Ivatury RR, Blocher CR et al. Amplified cytokine response

and lung injury by sequential hemorrhagic shock and abdomi-nal compartment syndrome in a laboratory model of ischaemia-reperfusion./Trauma 2002; 52: 625-632.

14 Schein M, Wittman DH, Aprahamian CC, Condon RE. Theabdominal compartment syndrome: the physiological and clini-cal consequences of elevated intra-abdominal pressure. / AmColl Surg 1995; 180: 745 -753.

15 Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular,pulmonary and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med 1989;17:118-121.

16 Bloomfield GL, Ridings PC, Blocher CR et al. A proposed rela-tionship between increased intra-abdominal, intrathoracic andintracranial pressure. Crit Care Med 1997; 25: 496-503.

17 Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia andbacterial translocation in the abdominal compartment syn-drome. J Trauma 1997; 43: 852 - 855.

18 Friedlander MH, Simon RJ, Ivatury R et al. Effect of hemor-rhage on superior mesenteric artery flow during increased intra-abdominal pressures. J Trauma 1998; 45: 433-439.

19 Kirkpatrick AW, Brenneman FD, McLean RF et al. Is clinicalexamination an accurate indicator of raised intra-abdominalpressure in critically injured patients? Can J Surg 2000; 43:207-211

20 Pickhardt PJ, ShimonyJS, Heiken JP et al. The abdominal com-partment syndrome: CT findings. AJRAmJRoentgenol 1999; 173:575-579.

21 Cheatham ML, White MW, Sagraves SG et al. Abdominal perfu-sion pressure: a superior parameter in the assessment of intra-abdominal hypertension. / Trauma 2000; 49: 621-627.

22 Rasmussen TE, Hallett JW Jr., Noel AA et al. Early abdominalclosure with mesh reduces multiple organ failure after rupturedabdominal aortic aneurysm repair: guidelines from a 10-yearcase control study./ Vase SMrg2002; 35: 246-253.

23 Bloomfield G, Saggi B, Blocher C, Sugerman H. Physiologiceffects of externally applied continuous negative abdominalpressure for intra-abdominal hypertension. J Trauma 1999; 46:1009-1016.

163

17ACUTE THROMBOSISOF ILIOCAVAL VEINS

GUNNAR PLATE, LARS NORGREN

Pulmonary embolism and post-thrombotic sequelae were earlier common and frequentlydeleterious complications of deep venous thrombosis (DVT). An important landmark in thetreatment of DVT was the development ofheparin and coumarin derivatives during the 1930sand 1940s. Systemic thrombolysis was attempted during the 1960s, and has recently beenfollowed by catheter-directed thrombolysis. Although surgical removal of DVT was initiallyattempted during the early 20th century [1], it was not until the late 1970s that venousthrombectomy gained a more widespread use.

At present, DVT of the infrapopliteal, popliteal, and femoral veins is usually treated withheparin, unfractionated heparin or low molecular weight heparin, oral anticoagulation, andcompression. A more invasive treatment may be considered for more proximal thrombi in theiliofemoral or iliocaval segment.

17165

Pathophysiology

Proximal DVT, iliofemoral, or iliocaval throm-boses may have the same etiology as any DVT, e.g.,thrombophilia, malignancy, trauma, and surgery, ormay be of idiopathic origin. There are some spe-cific features with pelvic vein obstruction, however.Compression of the left iliac vein by an overridingiliac artery, the May-Thurner syndrome [2] is acommon cause of iliofemoral thromboses and acaval vein thrombosis is sometimes due to malfor-mations of the venous anatomy. Blue phlegmasia

(phlegmasia cerulea dokns) induced by a rapid occlu-sion of proximal veins is frequently associated withmalignant disease [3].

The major hazards associated with proximal DVTare occurrence of pulmonary embolism and laterdevelopment of post-thrombotic sequelae. Scinti-graphic evidence of pulmonary embolism is pres-ent in 40% to 50% of patients with iliofemoralthrombosis [4]. The most severe consequence ofthe post-thrombotic syndrome, leg ulceration, iscaused mainly by destruction of the femoropop-liteal vein valves [5] sometimes in combination with


17166

venous outflow obstruction. An impaired outflowmay also cause venous claudication.


Although some proximal thromboses may developslowly and give rise to limited symptoms, the mostfrequent presentation is a rapid swelling of the legwith pain in the leg or groin. The pain may be causedby an inflammatory process in the veins, phlebitis,but can also be caused by an increased compart-mental pressure, giving rise to an impaired tissueperfusion, which is the underlying mechanism inphkgmasia ceruka dolens. Clinical examination usual-ly reveals a swelling of the entire limb with discol-oration and dilated superficial veins. An inferiorvena cava thrombosis may cause symptoms from bothlegs simultaneously. Not infrequently, patients expe-rience symptoms of pulmonary embolism even be-fore leg swelling is evident.

Diagnosis

A carefully obtained history is crucial for theselection of therapy. Previous episodes of DVT andthe duration and extent of the current episodeinfluence the choice of treatment. Diagnostic prin-ciples also depend on which treatment could bereasonable. It is therefore important to determinethe etiology of the thrombosis, especially whethera neoplasm may have caused the present situation.It is also important to check for bleeding disorders.

Duplex ultrasonography is most useful in theinvestigation of DVT of the leg veins, although thepelvic veins may be difficult to demonstrate. Com-puted tomography scanning may assist in the eva-luation of the iliocaval veins and could furtherreveal malignancies in this region. The same maybe true for magnetic resonance imaging. There isalso a place for venography. In order to delineatethe proximal extension of an iliofemoral or ilio-caval thrombosis, puncture of both femoral veinsand catheterization of an arm vein to reach the up-per extension of a thrombus in the inferior venacava is sometimes required. This kind of extensiveinvestigation is only performed in those cases wherean interventional treatment is planned. When acatheter-directed thrombolytic treatment is con-templated (see below), puncture of the ipsilateralpopliteal vein is the preferred approach.

Treatment

CONSERVATIVE TREATMENTPatients of old age and/or with extensive malig-

nancy and without signs of quickly developing bluephlegmasia should be treated with anticoagulationonly. Infusion of unfractionated heparin or subcu-taneous low molecular weight heparin injectionsfollowed by oral anticoagulation combined withcompression treatment of the leg should be initi-ated. Such treatment alone is always acceptable andother treatment modalities are always combinedwith anticoagulation.

VENOUS THROMBECTOMYDuring the early experience with venous throm-

bectomy, it was learned that, while pulmonary em-bolism was prevented [6], the risk of post-thromboticsequelae and vein valve incompetence was not abol-ished [7]. Since the late 1970s, there has been a newinterest in venous thrombectomy [8].

The main objectives of venous thrombectomy areto re-establish and preserve venous patency and topreserve vein valve function, thereby avoiding ma-jor complications like venous gangrene, pulmonaryembolism, and late post-thrombotic sequelae. Theoperative mortality has been extremely low in sev-eral series [8]. Since thrombectomy is usually aneffective method to remove thrombi from the deepvenous system, development of venous gangrene isusually prevented. In addition, venous thrombec-tomy is often successful in restoring iliac vein pa-tency even when systemic thrombolysis has failed[9]. Early results have been excellent [8] (TableI).The long-term benefit with surgery has not beenconvincingly proven, however (Table II). At 5- and10-year re-examinations in the only prospective ran-domized study for iliofemoral thrombosis, the clini-cal and physiologic results were slightly betterfollowing venous thrombectomy combined with anarteriovenous fistula compared to anticoagulationtreatment alone [13]. Iliofemoral venous patencyand venous outflow were better following surgicalthan medical treatment, but valvular competencewas not clearly preserved by this surgical procedure.The long-term results suffer because of several miss-ing follow-up examinations, which might obscure apossibly beneficial effect. Still, venous hypertensionwas significantly less prevalent following surgerythan with anticoagulation treatment alone [13]. Aswith thrombolytic treatment, the question still re-

ACUTE THROMBOSIS OF ILIOCAVAL VEINS

mains whether the post-thrombotic sequelae in-cluding leg ulceration are prevented by this surgi-cal procedure.

Indication for surgery

Both our and other's experience show that a care-ful patient selection is of utmost importance inachieving good results. The main indications forvenous thrombectomy are phlegmasia cerulea dolensand other iliofemoral thrombosis if the thrombusis fresh (less than five to seven days) and the pa-tient is young and healthy. The success of surgerydepends greatly on the age of the thrombus. Afterfive to seven days, organization of the thrombosis

and vein valve destruction makes complete venousclearance impossible, and rethrombosis and valvularincompetence are likely to develop after thrombec-tomy. A careful analysis of the presenting symptomsand the history are therefore crucial, since no bet-ter means of establishing the age of the thrombusare available. Occasionally, venography may demon-strate recanalized veins without valves indicating pre-vious thrombosis, but other signs, e.g., the appear-ance of the thrombus and presence of collaterals,are less reliable indicators of thrombus age.

The extension of the thrombosis has implicationson the operative technique but not as much on se-lection of treatment. Thromboses limited to theiliac veins are usually easy to remove surgically withgood long-term results, but these patients also do

Table I POSTOPERATIVE RESULTS OF ILIOCAVAL VENOUS THROMBECTOMY

[ref.]Year of

publication PeriodNumber of

thrombectomiesMortality

Pulmonaryembolism

Primarypatency

Secondarypatency

Capdevilla [10] 1993 1974-1991 177

Juhan [11] 1997 NP 77

3.3

0

3.9

0

NA

87

II167

NA: not available

, ., Ar , f No Moderate Severet author Number of r „ , , , ,r f l ., i . • bollow-up sequelae sequelae sequelae[rej.J thrombectomies ' v V ot

Patency Patencyat 5 years at 10 years

% %

Capdevilla [10]

Juhan [11]

177

77

71 ± 22 months

8.5 years

63.2

80

30.9

13.7

5.9

6.3

79

84

71

84

(5-13 years)

Plate [12] 13 10 years 54 NA 42*

* Occlusion 17%, stenosis 41%, normal patency 42%NA: not available


11168

fairly well with conservative treatment alone. Com-plete clearance of the deep venous system is possi-ble in more than a third of patients with a throm-bosis involving the entire extremity, with excellentlong-term outcome. Even if the late results follow-ing thrombectomy of extensive thrombosis are notas good as with proximal thrombosis, these patientsalso do worse following conservative treatment[14]. Therefore, the extension of the thrombus perse does not affect the decision for or against sur-gery. There are no comparative therapeutic resultsof vena cava thromboses. Deep venous thromboseslimited to the femoropopliteal segment have occa-sionally been operated upon, but the usefulness ofsurgery has not been established in these cases.

Iliofemoral thromboses developing during preg-nancy must be managed in close cooperation withan obstetrician. Venographic examination should beminimized to avoid undue radiation, but venogramsnecessary to decide the proper treatment and toperform a safe procedure must be obtained. Dur-ing early pregnancy, thrombectomy combined withan arteriovenous fistula may be performed safely. Inthese cases, the fistula is not closed until severalweeks after delivery. During late pregnancy, venousthrombectomy may be combined with simultaneouscaesarean section. Since these patients are usuallyyoung, they are likely to develop late sequelae if avenous outflow obstruction persists and if the peri-pheral vein valves are destroyed. Pregnant womenand women taking contraceptives are presently thetwo groups most commonly subject to venousthrombectomy [15].

Operative technique

Routine laboratory tests including anticoagula-tion studies, blood typing, and cross-matching shouldbe administered at admission. Full dose intravenousanticoagulation treatment should be initiated incooperation with the radiologist and the anesthetistto decrease the risk of thrombus propagation orembolization during any time required for diag-nostic procedures and preparation for surgery. Pro-phylactic antibiotics are administered to reduce therisk of wound infection, which is otherwise com-mon in this edematous tissue in proximity to thegroin. It must be remembered that these patientshave accumulated a significant amount of fluid in

their swollen leg and are often hypovolemic. Thisvolume deficit must be adjusted by intravenousadministration of crystalloid and/or colloid solu-tions prior to surgery.

The operation may be performed under local orepidural anesthesia, but general intubation anes-thesia is preferred. This allows application of a pos-itive end-expiratory pressure of 10 to 15 cm waterduring manipulation of the thrombus in the iliacor caval veins, which probably reduces the risk forpulmonary embolism. Arrangements for autotrans-fusion are optimal, since these patients may lose asignificant amount of blood during clearance ofthrombus material from the deep veins.

The long saphenous vein, the common femoralvein, and the superficial femoral artery are exposedusing a vertical or transverse groin incision withminimal perivascular dissection and meticuloushemostasis. A transverse venotomy is performed inthe common femoral vein, controlling bleeding withdigital compression or application of soft Fogartyclamps. A venous balloon catheter (Fogarty, n°8-10)is introduced into the vena cava, the balloon isinflated with contrast material and intra-operativefluoroscopy is utilized to verify the position of thecatheter in the vena cava. Repeated thrombectomyis performed until no further thrombus material isretrieved from the iliac veins. Occasionally, the cath-eter may pass into the ascending lumbar vein, whichmay rupture if the balloon is inflated. There is alsoa risk that thrombus material at the caval bifurca-tion may become dislodged into the vena cava dur-ing return of an inflated balloon from the ascendinglumbar vein. Occasionally, it may be difficult to passthe catheter from the left iliac vein into the venacava due to compression from the overlying arteryand intraluminal fibrosis (venous spur). Sometimesthis problem can be overcome by bending the tipof the catheter. A guide wire may also be helpful.

The peripheral veins are cleared with simultane-ous obstruction of the proximal common femoralvein to prevent embolization. If the thrombosis isfairly fresh, the peripheral thrombi are easily milkedout of the deep venous system by vigorous manualcompression from the foot toward the groin. Thismust be repeated several times and may cause sig-nificant blood loss, which must be noted and com-pensated. Some distal thrombus material may beretrieved by careful retrograde introduction of aballoon catheter into the deep and superficialfemoral veins. Competent vein valves sometimescompromise this. Passage of these valves may be

ACUTE THROMBOSIS OF ILIOCAVAL VEINS

accomplished after careful inflation of the balloonto dilate the valvular region.

When clearance of the peripheral veins has beencompleted, patency of the iliac vein is secured byadditional thrombectomy to remove thrombi thatmay have become dislodged from the internal iliacvein or the peripheral veins. Clearance of the iliacsegment is checked by intra-operative venographyor angioscopy. The venotomy is closed with inter-rupted or continuous 6/0 polypropylene sutures. Anarteriovenous fistula is constructed by performingan end-to-side anastomosis between the dividedlong saphenous vein and the superficial femoral ar-tery. An infant-feeding catheter may be introducedthrough a (long) tributary of the saphenous veinand left in place for postoperative venographic con-trol. A suction drainage is brought out through aseparate stab incision and the wound is closed inlayers avoiding kinking of the fistula.

Technical problems

In the presence of thrombosis in the inferior venacava, there is an increased risk of creating pul-monary emboli. Some surgeons have used addi-tional balloon catheters introduced into the samevenotomy or through the contralateral groin veinswith the balloon inflated cephalad of the thrombusas protection against embolism during the proce-dure. This has been proven unnecessary if thethrombus is confined to the iliofemoral veins. Amore secure control of the vena cava itself is prefer-able if this vein is also involved.

In elderly patients with proven pulmonary em-bolism, it is often sufficient to insert a permanentfilter into the inferior vena cava cephalad of thethrombus. This is easily performed percutaneous-ly or by surgical exposure of the right internaljugular vein. Various devices are currently availablefor intraluminal control of the vena cava [16]. TheGreenfield filter is the most widely used filter, andhas proven effective and safe. In most young pa-tients, it is better to remove the caval thrombus inorder to preserve venous outflow from both lowerlimbs. The inferior vena cava is exposed using aright-sided transverse infracostal incision with extra-peritoneal dissection. The vein is controlled by ap-plication of soft Fogarty clamps. A longitudinalvenotomy is performed and the vein edges are sep-arated with stay stitches during careful removal of

the thrombus by milking, suction and use of venousFogarty catheters. The venotomy is closed with con-tinuous or interrupted 5/0 polypropylene stitches.It is advantageous to perform exploration of thevena cava simultaneously with thrombus removalfrom the groin in order to secure venous patencybefore the cavotomy is closed. With minimal pro-trusion of the thrombus into the vena cava, it is notalways necessary to perform a cavotomy.

Left-sided iliofemoral thromboses are often causedby compression from the overlying right commoniliac artery with secondary intraluminal fibrosis, aso-called venous spur [2]. In these cases, the risk forrethrombosis is greatly increased and the long-termresults are more dubious. Some surgeons use angio-scopy and ring catheters to overcome such venousspurs [17]. Others suggest direct exposure and re-construction of the caval inflow. The value of suchaggressive measures has not been proven. Therefore,we have previously relied solely upon iliofemoralthrombectomy in combination with an arteriove-nous fistula to keep as much as possible of the veinpatent and to promote development of collateralflow. Recently, we have utilized intra-operative orpostoperative balloon angioplasty with stent appli-cation with some success.

In ascending thrombosis where the peripheralthrombus is of an older age, clearance of the peri-pheral veins may be difficult. Gruss [18] has sug-gested exploration of the popliteal and/or tibialveins with construction of a peripheral fistula toallow clearance and maintenance of venous patencyin such cases. Intra-operative administration of localstreptokinase has also been used. The benefit ofthese additional procedures is not obvious, since itis likely that the valvular function has already beendestroyed in cases with old thrombosis. Hence, li-gation of the superficial femoral vein has been pro-posed to prevent pulmonary embolism and latevalvular incompetence. Although still controversial,it seems that this procedure is fairly well toleratedif the deep femoral vein is patent and competent.

In severe cases of phlegmasia ceruka dolens, in-creased pressures are often present in all musclecompartments of the calf. It is of utmost importanceto achieve a rapid decompression of these compart-ments. Except for immediate and successful throm-bectomy, this is best accomplished by fasciotomy ofall muscle compartments of the calf. In less severecases, the need for fasciotomy may be assessed bymeasurement of intracompartmental pressures, thecritical level being around 30 mmHg [19].

17169


17170

Postoperative management

Repeated thrombectomy combined with a venousreconstruction may be considered in cases of earlyrethrombosis with massive leg swelling, although thelong-term patency of such procedures has not beenconvincing [20]. The preferential procedure wouldbe a cross-femoral or iliocaval bypass using a largeautogenous vein or ringed polytetrafluoroethyleneprosthesis with a protective arteriovenous fistula. Per-cutaneous transluminal balloon dilation combinedwith stent implantation has occasionally been suc-cessful in treating residual stenoses of the iliac veinin combination with repeated thrombectomy.

Full anticoagulation should be resumed as soonas possible (meticulous operative hemostasis is there-fore crucial). Oral anticoagulation is started on thefirst postoperative day and continued for at leastsix months. The patient is allowed to ambulate onthe first postoperative day. Compressive stockingsupport should be used for several months and aslong as leg swelling persists. In most cases thepatient may be discharged from the hospital oneweek after the operation.

The arteriovenous fistula can be closed after sixto eight weeks, when healing of the venous endo-thelium has occurred. With a superficially placedfistula, this is easily accomplished using local anes-thesia and a short skin incision over the maximumthrill created by the fistula. An intra-operative ve-nogram may be obtained to check iliofemoral ve-nous patency. The fistula is then divided and lig-ated. This procedure is performed as an outpatientprocedure. Other techniques using interventionalradiology have also been used.

INDUCED THROMBOLYSISSystemic thrombolysis with either streptokinase

or urokinase may dissolve thrombotic material andrestore venous patency. In a pooled analysis f:~omsix randomized studies evaluating streptokinasetreatment versus heparin, it was noted that throm-bolysis occurred almost four times more often afterstreptokinase treatment. However, bleeding com-plications are common and recurrent thrombosisgiving rise to post-thrombotic sequelae has beenseen frequently. In three studies that allowed com-parison of bleeding complications, thrombolysis in-duced a three times greater rate of bleeding thanafter heparin treatment [21]. In addition, variousreports have shown that only 7% to 20% of patients

with DVT did not present centra-indications to sys-temic thrombolytic treatment. In a recent meta-analy-sis [22], it was again stressed that despite early veinpatency after systemic thrombolysis, there is noproven reduction in the incidence of post-throm-botic sequelae. One investigation showed that, outof 35 patients treated with streptokinase, only 2 pa-tients were free from symptoms and had normalvenous function after a mean of 29 months follow-up [23].

CATHETER-DIRECTED THROMBOLYSISTo reduce the risk of bleeding during systemic

thrombolysis, the thrombolytic agent may be in-fused directly into the thrombus using intravenouscatheters. This catheter-directed thrombolysis mayalso ameliorate the lysis and decrease the time re-quired. The presently preferred approach has beenthrough the ipsilateral popliteal vein using ultra-sound guidance to avoid additional venous or ar-terial punctures. An alternative approach would bevia the internal jugular vein. The lytic agents mostoften used in this setting have been urokinase andrecombinant tissue plasminogen activator adminis-tered using pulse-spray technique or a slow infusion.The effect of the thrombolysis checked frequentlywith venography and the position of the catheter iscorrected accordingly. Initially, most centers applieda temporary vena cava filter to prevent pulmonaryembolism during the thrombolysis. This has nowbeen abandoned at most places. Following com-pleted thrombolysis, an underlying stenotic process,e.g., the May-Thurner syndrome, may be dealt with.Balloon dilation of such lesions usually combinedwith placement of venous stents increases thechance of restoring patency thereby reducing therisk for recurrent thrombosis [24].

A few larger short-term studies of catheter-di-rected thrombolysis have been published. An excel-lent technical success rate was demonstrated in aprospective study from 1997 [25]. A national multi-center registry report was presented in 1999 claim-ing that the treatment is safe and effective [26].Major bleeding complications in 11% and a pri-mary iliofemoral patency rate of 60% at one yearwere reported. In these centers, urokinase was usedas the thrombolytic agent and 71% of the throm-boses treated were confined to the iliofemoral seg-ment; the remaining thrombi were localized moredistally. Recently, a randomized controlled trial com-paring catheter-directed thrombolysis with anticoa-

ACUTE THROMBOSIS OF I LI oc AVAL VEINS

gulation treatment of iliofemoral venous thrombosiswas presented [27]. In this study, the iliofemoralpatency rate at 6 months was 72% following throm-bolytic treatment compared to 12% with anticoagu-lation. In one series of 10 patients, catheter-directedthrombolysis and stent placement were used for treat-ment of the May-Thurner syndrome [28]. After amean of 15 months, 9 of 12 patients were asympto-matic. It has also been shown that this mode of treat-ment improves health-related quality of life [29].

Neither of the series presented specifically studiedpatients with iliocaval thrombosis. With thromboticengagement of the vena cava, one has to considerwhether the risk of pulmonary embolism due tofragmentation of the thrombus during thromboly-sis requires caval protection. In such cases, applica-tions of a permanent filter as the sole solution orplacement of a temporary filter during thrombolytictreatment are probably safer solutions.

Choice of treatment

The choice between anticoagulation treatment,thrombolysis and surgical thrombectomy dependson many factors, the most important of which are

the age of the patient, extension of the thrombo-sis and the etiology (cancer, obesity, trauma, May-Turner syndrome).

Anticoagulation combined with elastic stocking isa generally accepted treatment especially in olderpatients or patients with cancer (Figure). A moreaggressive attitude is justified in younger patientsin order to avoid the late post-thrombotic seque-lae. Non-randomized studies show the beneficialeffects of thrombolysis or surgical thrombectomycompared to anticoagulation treatment (Table III),but there are no studies comparing the results ofthrombolysis and thrombectomy. Thrombolysis hasgained a predominant role in the treatment of ilio-caval thromboses. Some authors consider all deepvenous thromboses an indication for fibrinolyticteratment, irrespective location or delay. Mewissenet al. [26] are more conservative and do not applyfibrinolysis for recurrent thromboses or femoro-popliteal thromboses older than 10 days. Obviously,the centra-indications for thrombolysis are directlydetermined by the potential complications of thetreatment. At present, iliocaval surgical thrombec-tomy should be considered for recent iliocavalthromboses in young patients inwhom a contra-indi-cation or failure of thrombolytic treatment can beexpected. 17

171

60 - 70 years > 60 - 70 years

(Or impending gangrene)

Centra-indication for thrombolysis?

(Or disseminated malignancy, or contra-indications)

Anticoagulation

NO YES

Catheter-directed thrombolysis(or anticoagulation)

Surgical thrombectomy(or anticoagulation)

FIGURE. Treatment algorhythm for iliofemoral and iliocaval thrombosis. Our conclusion is that anticoagulation is usually anaccepted method, althoush a more agsressive approach should be attempted in young patients to avoid late sequelae.


1st author[ref.]

Year ofpublication

Treatment Patency No sequelae

Plate [12]

AbuRahma [24]

Elsharawy [27]

1997

2001

2002

Anticoagulation (n=l7)

Thrombectomy (n=13)

Anticoagulation (n=33)

Endovascular (n=18)

Anticoagulation

Thrombolysis(n=17)(n=18)

10 years

5 years

6 months

2942

1869

1272

2442

7830

Endovascular: thrombolysis ± angioplasty ± stent

R E F E R E N C E S

17172

1 Leriche R. Traitement chirurgical des suites eloignees desphlebites et des grands cedemes non medicaux des membresinferieurs. Bull Mem Soc Nat Chir 1927; 53: 187-195.

2 May R, Turner]. The cause of the predominantly sinistral occur-rence of thrombosis of pelvic veins. Angeiology 1957; 8: 419-425.

3 Perkins JM, Magee TR, Galland RB. Phlegraasia caerulea dolensand venous gangrene. BrJ Surg 1996; 83: 19-23.

4 Plate G, Ohlin P, Eklof B. Pulmonary embolism in acuteiliofemoral venous thrombosis. BrJ Surg 1985; 72: 912-915.

5 Shull KG, Nicolaides AN, Fernandes e Fernandes J et al. Sig-nificance of popliteal reflux in relation to ambulatory venouspressure and ulceration. Arch Surg 1979; 114: 1304-1306.

6 Fontaine R, Tuchmann L. The role of thrombectomy in deepvenous thromboses./ Cardiovasc Surg 1964; 5: 298-312.

7 Lansing AM, Davis WM. Five-year follow-up study of iliofemoralvenous thrombectomy. Ann Surg 1968; 168: 620-628.

8 Plate G, Einarsson E, Ohlin P et al. Thrombectomy with tem-porary arteriovenous fistula: the treatment of choice in acuteiliofemoral venous thrombosis. / Vase Surg 1984; 1: 867-876.

9 Stiegler H, Hiller E, Arbogast H et al. Thrombectomy afterunsuccessful thrombolytic therapy of deep leg vein thromboses:an effective procedure? Vasa 1992; 21: 280-288.

10 Capdevilla JM, Estallo L, Ballon H, RancanoJ. Resultats de lathrombectomie veineuse. In: Branchereau A, Jausseran JM.Chirurgie des veines profondes. Marseille, CVN, 1993 : pp 32-36.

11 Juhan CM, Alimi YS, Barthelemy PJ et al. Late results of ilio-femoral venous thrombectomy. / Vase Surg 1997; 25: 417-422.

12 Plate G, Eklof B, Norgren L et al. Venous thrombectomy foriliofemoral vein thrombosis. Ten-year results of a prospectiverandomised study. EurJ VaseEndovasc Surg 1997; 14: 367-374.

13 Plate G, Akesson H, Einarsson E et al. Long-term results ofvenous thrombectomy combined with a temporary arteriove-nous fistula. EurJ Vase Surg 1990; 4: 483-489.

14 Browse NL, Clemenson G, Thomas ML. Is the postphlebitic legalways postphlebitic? Relation between phlebographic appear-ances of deep-vein thrombosis and late sequelae. BrMedJIQSO;281: 1167-1170.

15 Torngren S, Bremme K, Hjertberg R, SwedenborgJ. Late resultsof thrombectomy for ilio-femoral venous thrombosis. Phlebology1991; 6: 249-254.

16 Greenfield LJ, DeLucia A 3rd. Endovascular therapy of venousthromboembolic disease. Surg Clin North Am 1992; 72: 964-989.

17 Jakob H, Maass D, Schmiedt W et al. Treatment of major venous

obstruction with an expandable endoluminal spiral prosthesis.J Cardiovasc Surg 1989; 30: 112-117.

18 Gruss JD. Venous reconstruction. Part 1. Phlebology 1988; 3:7-18.

19 Qyarfordt P, Eklof B, Ohlin P. Intramuscular pressure in thelower leg in deep vein thrombosis and phlegmasia ceruleadolens. Ann Surg 1983; 197: 450-453.

20 Plate G, Einarsson E, Eklof B et al. Iliac vein obstruction asso-ciated with acute iliofemoral venous thrombosis. Results of earlyreconstruction using polytetrafluoroethylene grafts. Ada ChirStand 1985; 151:607-611.

21 Goldhaber SZ, Buring JE, Lipnick RJ, Hennekens CH. Pooledanalyses of randomized trials of streptokinase and heparin inphlebographically documented acute deep venous thrombosis.An JMed 1984; 76: 393 -397.

22 Wells PS, Forster AJ. Thrombolysis in deep vein thrombosis: isthere still an indication? Thromb Haemost 2001; 86: 499-508.

23 Albrechtsson U, Anderson J, Einarsson E et al. Streptokinasetreatment of deep venous thrombosis and the post-thromboticsyndrome. Follow-up evaluation of venous function. Arch Surg1981; 116:33-37.

24 AbuRahma AF, Perkins SE, Wulu JT, Ng HK. Iliofemoral deepvein thrombosis: conventional therapy versus lysis and percu-taneous transluminal angioplasty and stenting. Ann Surg 2001;233: 752-760.

25 Bjarnason H, Kruse JR, Asinger DA et al. Iliofemoral deepvenous thrombosis: safety and efficacy outcome during fiveyears of catheter-directed thrombolytic therapy. / Vase IntervRadial 1997; 8: 405 -418.

26 Mewissen MW, Seabrook GR, Meissner MH et al. Catheter-directed thrombolysis for lower extremity deep venous throm-bosis: report of a national multicenter registry. Radiology 1999;211: 39-49.

27 Elsharawy M, Elzayat E. Early results of thrombolysis vs antico-agulation in iliofemoral venous thrombosis. A randomised clin-ical trial. EurJ Vase Endovasc Surg 2002; 24: 209-214.

28 Patel NH, Stookey KR, Ketcham DB, Cragg AH. Endovascularmanagement of acute extensive iliofemoral deep venous throm-bosis caused by May Turner syndrome. J Vase Interv Radial 2000;11: 1297-1302.

29 Comerota AJ, Throm RC, Mathias SD et al. Catheter-directedthrombolysis for iliofemoral deep venous thrombosis improveshealth-related quality of life. / Vase Surg 2000; 32: 130-137.

18ACUTE SUBCLAVIAN-AXILLARY

VEIN THROMBOSIS

RAMON BOFILL, JOSEP ROYO,JOSE MARIA FUENTES, JOSE MARIA ESCRIBANO, MANUEL MATAS

Acute subclavian-axillary vein thrombosis (SAVT) is uncommon compared to deep veinthromboses in other vascular territories. While the risk of developing fatal pulmonary thrombo-embolism in this condition is relatively small, it can occur even with anticoagulant treatment.Furthermore, clinical manifestations of pain, cyanosis, swelling and functional limitationscan be disabling. The development of secondary SAVT can be a consequence of generaldiseases, a state of hypercoagulation, or tumors, but the main cause is the increasing use ofintravenous devices for diagnostic or therapeutic purposes. The primary form of SAVT, firstdescribed more than a century ago and known as Paget-Schroetter syndrome, is usually theresult of repeated effort by the upper extremity and scapular girdle. This condition presentsmost frequently in young, otherwise healthy individuals performing strenuous occupationalor recreational activities.

The literature shows particular interest in this type of primary venous thrombosis, withreference to diagnostic and therapeutic methods directed toward recuperating patency of theaffected venous vasculature and maintaining good long-term clinical and hemodynamicresults. The main points of controversy regarding treatment reside in the following: timing ofinitiation of fibrinolytic therapy and anticoagulation; assessment of the need, ideal timingand choice of approach for surgical decompression of the thoracic outlet; and the suitability ofother interventional techniques aimed toward recovering venous patency or correctingresidual occlusive lesions after surgery. Nevertheless, experience documented in the literatureregarding this condition shows relative agreement on some aspects. Since primary SAVTgenerally occurs in young patients at the height of physical activity, rehabilitation should beas quick and effective as possible. Thus, the process is considered to require other measures in


addition to anticoagulant therapy. The current use of thrombolytic agents together withsurgical or endovascular procedures, applied after careful assessment of each individual case,has resulted in a notable improvement in the outcome ofSAVT.

18174

Etiology

SAVT can be divided into primary and second-ary forms and each form requires a different typeof therapeutic management. Primary SAVT wasdescribed 1875 and published in 1884 by J. Pagetand Von Schroetter, respectively. In 1949 Hughesconducted a study involving more than 300 patientswith acute spontaneous venous thrombosis of theupper extremities, and first used the term Paget-Schroetter syndrome to refer to this condition.

The causes of primary SAVT are mainly relatedto strenuous upper body activity, venous compres-sion at the thoracic outlet, and upper limb immo-bility or anatomical abnormality causing intimaldamage to the vein at the thoracic outlet. The ante-rior scalene muscle, the subclavian muscle and theclavicle against the first rib are three key points ofnarrowing of the superior thoracic outlet at whichthe axillary and subclavian veins can be compressed,particularly with movements of abduction. Anatom-ical anomalies can produce other susceptible points[1,2]. Repeated compression has a traumatic effecton the vein wall that leads to thickening, fibrosis andintimal proliferation. Thrombosis develops whenheightened physical activity of the upper limb in-creases this traumatic effect.

Secondary SAVT can be related to systemic dis-eases such as cardiac failure, an hypercoagulationstate often associated with neoplasm, amyloidosis, sar-coidosis, or oral contraception, or as a consequenceof a local aggression in the venous territory due toradiotherapy, instrumentation, indwelling catheters,pacemaker wires, parenteral nutrition, dialysis fis-tulae, intravenous drug abuse, shoulder trauma ortumor mass compression.

Incidence

The primary form of SAVT accounts for less than2% of all cases of deep venous thrombosis. The se-condary form is becoming notably more prevalentdue to the increasing use of central venous system

devices and catheters. It has been estimated thatmore than 18% of patients with central venouscatheters develop partial or total thrombosis. Cer-tain factors, such as the duration of catheter implan-tation and the type of material used in their manu-facture, can influence the development of venousocclusion [3]. The possibility of presenting venousthrombosis is almost null before the sixth day aftercatheter placement and is relatively remote beforethe fifthteenth. The new materials used in cathetermanufacture such as polyurethane, silicone and sili-cone elastomer, offer better results regarding main-tenance of catheter patency and a smaller risk ofpulmonary thrombo-embolism, as compared to poly-vinyl or polyethylene [4].


Swelling, pain or discomfort, venous engorgementand mild cyanosis are the classic symptoms of SAVT.These symptoms become enhanced with increasedactivity of the affected extremity. Swelling of thehand and fingers is especially disabling and less tol-erable than the swelling of the foot that occurs inpost-thrombotic syndrome in the lower extremity,which is usually mild. The great majority of patients(more than 80%) develop these symptoms in thefirst 24 hours. Nonetheless, a delay in their presen-tation is not infrequent and may extend to monthsif the patient has had episodes of similar symptomspreviously as a result of intermittent extrinsic ve-nous compression without actual thrombosis [5].SAVT occurs in both sexes and at all ages, but thecharacteristic patient with this condition is a youngor middle-aged male, often presenting a history ofvigorous use of the affected upper limb. Immobil-ization or forced positioning can be the cause ofSAVT in an elderly person. The upper right limbis affected significantly more often, a fact explainedby the preponderance of right-sided dominance inthe general population.

Secondary SAVT usually has a more benign ex-pression, probably owing to the anatomical charac-teristics of the affected location and a more limited

ACUTE SUBCLAVIAN-AXILLARY VEIN THROMBOSIS

extension of the thrombotic lesion. For this reasonthe secondary form of SAVT is usually more sus-ceptible to the favorable effect of collateral circu-lation. From the hemodynamic standpoint, it is verydemonstrative that dialysis patients with a throm-bosed temporary venous access in the subclavianterritory manifest symptoms of proximal venousocclusion only after establishment of an arteriove-nous fistula at the level of the elbow. This is becausethe clinical effects of the thrombosis associated withthe initial venous access are expressed only whenthe collateral circulation becomes overloaded andcannot absorb the increase in venous supply. Therehave been cases of SAVT secondary to paraneo-plastic origin in which significant extension of thethrombus has produced symptoms of ischemiaresulting from the difficulty in providing arterialsupply due to compromised venous return.

Diagnostic methods

After recording the clinical history and per-forming a complete physical examination, dopplerultrasound is the initial technique used for estab-lishing the diagnosis of SAVT. This noninvasivemethod is limited by bony structures that can pro-duce acoustic shadowing and the occasional pres-ence of highly developed collateral vessels that mayinduce diagnostic errors. The diagnostic reliabilityof doppler ultrasound is highest when results arepositive in patients with clinical symptoms clearlysuggestive of SAVT. Being a noninvasive, reliabletechnique that is comfortable for the patient, dop-pler ultrasound is also especially useful for repeat-ed follow-up studies of any treatment applied.Nonetheless, the gold standard for the diagnosis ofSAVT is still contrast enhanced venography, prefer-ably through the basilica vein (Fig. 1). Despite itsmore invasive nature, it allows proper static and dy-namic evaluation of the deep venous system andthe collateral circulation, and visualization of ex-trinsic compression. Venography is also excellentfor the application and control of thrombolytictreatment and any associated surgical or endovas-cular technique. The basic examination of any pa-tient with suspected SAVT should also include gen-eral laboratory analyses with special attention tocoagulation alterations, as well as radiography andcomputed tomography scanning directed towardthe detection of thoracic outlet anomalies.

Therapeutic management

The important etiological and clinical differencesbetween the primary and secondary forms of SAVTare reflected in the therapy used for their manage-ment. Treatment for primary SAVT has changedconsiderably since Paget and Schroetter's descrip-tion of this condition more than a century ago, butit is still controversial. Moreover the developmentof thrombolytic and endovascular treatment hasprovided a new arsenal to sustain this controversy.Treatment for secondary SAVT is mainly limited topostural measures directed toward favoring venousreturn, elastic contention and anticoagulant ther-apy, when there are no centra-indications. Surgicalresection of tumors responsible for SAVT often pro-vides good results [6].

ANTICOAGULANT THERAPYIn the current therapeutic management of pri-

mary SAVT, anticoagulation has a co-adjuvant func-tion with other treatments. Administration of he-parin-Coumadin was advocated in the past becauseof its favorable effect on the stabilization and re-canalization of primary thrombi and the preven-tion of pulmonary embolism [7,8]. Nowadays thismonotherapy has lost favor because of its deficientlong-term control of the disabling consequences ofprimary SAVT. The same can be said regarding elas-tic contention and postural measures. Moreover, inthe use of anticoagulant treatment, as well as in the

175

FIG. 1 Thrombosis of right subclavian-axillary vein.


18176

other therapeutic measure described below, thereis still relevant controversy regarding factors relat-ed to timing [7-9].

In contrast, anticoagulation has a fundamentalrole in the treatment of secondary SAVT, evenwhen the thrombosis is more extensive than is usu-ally seen in these cases and the symptoms moreintense. In general the behavior and course of thesecondary form is similar to that of deep venousthrombosis in other locations. For this reason theuse of anticoagulant treatment in secondary SAVTadheres to more standardized criteria, and the man-agement of contra-indications and complicationsassociated with heparin-Coumadin administrationfollows the same pattern as in other thromboses.Thus, the indication for vena cava filters for theprevention of pulmonary thrombo-embolism is thesame in secondary SAVT as in cases where thesources of the emboli are the lower extremities.

THROMBECTOMYThrombectomy, initially introduced as an isolated

surgical technique and later associated with tho-racic oudet decompression, showed notably goodoutcome in some of the published series, thoughthe number of patients included was not extensive.In at least one of these reports there was evidencethat the results were favorable in the long term.Nevertheless, this is an aggressive approach that re-quires extensive dissection of the subclavian vein toinsure proper control of lumen repair. Since theadvent of thrombolytic therapy, thrombectomy hasbeen displaced from its prominent position as thetechnique of choice for the treatment of SAVT [10].

THROMBOLYTIC THERAPY (Fig. 2)Catheter-directed thrombolysis is, in the opinion

of many experts, the first therapeutic option to beused in well-selected cases of primary SAVT [11].This variant of thrombolytic treatment presents sev-eral advantages over systemic thrombolysis. One ofthe main features is the possibility for real-timeangiographic control of the results obtained in lysisof the thrombus. Moreover, the presence of extrin-sic compression can be detected in functional exam-inations and corrected later. The maximum recom-mended interval between the initiation of thethrombotic episode and application of effectivetreatment is notably longer for thrombolysis than forthrombectomy, with delays of 5 to 10 days consid-ered acceptable. Naturally, thrombolytic treatmentis contra-indicated in patients at risk for hemorrhage

FIG. 2 Venogram with acute thrombosis recanalized withlytic therapy.

and its application should be performed under pro-tocolized analytic control. When angiography dem-onstrates no significant changes at 24 hours afterthe initiation of thrombolytic treatment, interrup-tion of the treatment is recommended.

At this time, there is no established protocol fordosage of thrombolytic agents. Table I shows anexample of a possible therapeutic model from thevarious regimens used in the published experienceof several authors. Most groups applying thrombo-lytic therapy use urokinase rather than streptoki-nase or RPT because of its relative safety and effi-cacy. Nonetheless, the major drawback to all theseagents is still a risk of hemorrhage.

THORACIC OUTLET DECOMPRESSIONAfter restoring venous patency with thrombolytic

treatment, persistence of the musculoskeletal mech-anisms producing thoracic outlet compression in theaxillary-subclavian venous territory will, of course,continue to act unfavorably (Fig. 3). This circum-stance is clearly reflected in post-thrombolysis ve-nography controls, which show filling defects whenthe patient is at rest or in positions that exacerbatethe problem. Most authors agree that definitive cor-rection of this factor is essential to avoid newepisodes of thrombosis and to obtain long-term pa-tency. Surgery, rather than endovascular therapy,proposed more than a decade ago, is generally re-


Thrombolytic agent

Urokinase>

Initial bolus

First variable infusion rate

Second variable infusion rate

Under monitored surgical intensive care

Heparin Na administered concomitanly (•)

Heparin Na infusion concomitanly (*) (••)

200 000 U

150 000 - 250 000 U/h for 6 hours

60 000 -100 000 U/h for no more than 72 hours

5 000 U intravenous bolus

(•) Not in all groups(**) Infusion rate must be adapted to maintain PTT ratio at 2.0 - 2.5 times normal

commended as the best method for eliminatingthese compression mechanisms [5,12-15]. The pooroutcome recorded with the use of endovasculartreatment, specifically stent placement, is attributedto the compressive force of the musculoskeletalstructures, which in these circumstances is superiorto the capacity of the stent to maintain the lumen

FIG. 3 Residual compressive abnormality at costoclavicu-lar space after successful thrombolytic therapy duringupper extremity abduccion.

of the vessel or the caliber of the vein sufficientlyopen. Deformity or breakage of the stent has oc-curred in some cases. Table II lists the various sur-gical techniques used for thoracic outlet decom-pression and the timing criteria applied by eachauthor.

ENDOVASCULAR THERAPYAfter successful thrombolytic treatment and pro-

per thoracic outlet decompression, angiographicexamination may still demonstrate vessel lumen ir-regularities due to residual thrombotic material orinflammatory alterations of the venous intima. Sev-eral opinions regarding therapy for these cases havebeen voiced in the literature, depending on the ex-tension of the lesion and the patient's symptoms.In these circumstances endovascular therapy wouldseem to be a reasonable option.

It is interesting to note that the introduction ofendovascular thrombolysis has led to changes in theconcept of conventional surgery for this condition,making it much less aggressive. The classic transclav-icular approach with clavicle resection and direct re-pair of the subclavian vein has been substituted bythe current use of the transaxillary, supraclavicularor infraclavicular approaches plus complementaryendovascular therapy, particularly the use of stents[12,16,19]. In cases of contralateral stenoses detect-ed during bilateral venography in patients withsymptoms in only one upper limb, the benefit ofprophylactic correction has not been demonstrated.

177


18178

1st author[ref.]

Year Number ofpatients

Immediatethrombolysis

Surgicaldecompression

Surgicalapproach

Averagefollow-up

Machleder [11] 1993

Azakie [12] 1998

50

33

43 12 PTA pre-operatively9 PTA postoperatively

6 first rib resection

Heron [8] 1999

Lee [15] 2000

Angle [16] 2000

Arko [17] 2001

Feugier [14] 2001

Kreienberg [18] 2001

Lokanathan [13] 2001

54 0 thrombolysis 3 first rib resection48 anticoagulation

alone

22

18

12

10

18 13 scalenectomy1 first rib resection

18 9 early surgicaldecompression

9 staged surgicaldecompression

12 8 first rib resection+ venolysis

7 10 first rib resection9 scalenectomy3 bypass

23 16 first rib resection23 scalenectomy

2 exostosis resection14 stent

25 1 claviculectomy12 PTA

12 transaxillary 3.1 years1 transclavicular

2 transaxillary 31 months32 supraclavicular21 plus infraclavicular

5 years

13 supraclavicular 22.3 months

18 transaxillary 3 months

3.9 months

45 months

4 years

1 transaxillary 2.9 years

PTA: percutaneous transluminal angioplasty

MANAGEMENT OF IMPOSSIBLEOR INADEQUATE THROMBOLYSIS

In certain cases, thrombolysis may not be possi-ble, it may be contra-indicated, or it may be com-pletely or partially ineffective. In these situations,the therapeutic alternatives are directed toward cor-recting symptomatic residual obstruction. Opinionson the suitability of using one or another of these

techniques depends on the assessment of severalparameters including length of the lesion [20],severity of the symptoms and the age and activityrequirements of the patient at work or in sports[14,17]. In general terms, it is accepted that surgi-cal treatment has a favorable outcome in carefullyselected patients with relatively short obstructivelesions and certain disability in their daily activities.


Jugular vein turndown seems to be favored overclaviculectomy [2], bypass or venous interposition.

Possible scenariosin the near future

In a comprehensive review of the literature car-ried out by Rutherford in 1998 and published inSeminars in Vascular Surgery, the term possible scenarioswas used to refer to the sequence in which exist-ing therapeutic options are applied after the ap-pearance of a new treatment such as, for example,thrombolysis [10]. The conclusion formulated after

an overview of the most recent publications onSAVT is that the configuration of these therapeu-tic scenarios is beginning to coincide, but alwayswithin the context of the experience of individualgroups. The series may be more or less extensive,but the situation is far from a collective effort inwhich consensus is achieved after obtaining datafrom large prospective, multicenter studies. Such acollective effort is needed to resolve doubts aroundthe use of low molecular weight heparin in secondarySAVT, for example, and to establish specific criteriaon the use of thrombolytic, surgical and endo-vascular treatment at the best time and in the bestway possible for patients with either form of thiscondition.

R E F E R E N C E S

1 Palerme LP, Chan AM, Hsiang YN. Axillary vein thrombosissecondary to congenital stricture in a left-sided superior venacava. Ann Vase Surg 2000; 14: 648-651.

2 Hurlbert SN, Rutherford RB. Primary subclavian-axillary veinthrombosis. Ann Vase Surg 1995; 9: 217-223.

3 Martin C, Viviand X, Saux P, Gouin F. Upper-extremity deepvein thrombosis after central venous catheterization via the axi-lary vein. Crit Care Med 1999; 27: 2626-2629.

4 Monreal M, Raventos A, Lerma R et al. Pulmonary embolismin patients with upper extremity DVT associated to venouscentral lines. A prospective study. Thromb Haemost 1994; 72:548-550.

5 Hicken GJ, Ameli FM. Management of subclavian-axillary veinthrombosis: a review. Can J Surg 1998; 41: 13-25.

6 Branchereau P, Alric P, Berthet JP et al. Surgical exposure ofsuperior sulcus lung tumors with vascular involvement. AnnVase Surg mi; 15: 206-211.

7 Tilney ML, Griffiths HJ, Edwards EA. Natural history of majorvenous thrombosis of the upper extremity. Arch Surg 1970; 101:792-796.

8 Heron E, Lozinguez 0, Emmerich J et al. Long-term sequelaeof spontaneous axillary-subclavian venous thrombosis. AnnIntern Med 1999; 131: 510-513.

9 Donayre CE, White GH, Mehringer SM, Wilson SE. Pathogen-esis determines late morbidity of axillosubdavian vein throm-bosis. AmJSurgim; 152: 179-184.

10 Rutherford RB. Primary subclavian-axillary vein thrombosis: therelative roles of thrombolysis, percutaneous angioplasty, stents,and surgery. Semin Vase Surg 1998; 11: 91-95.

11 Machleder HI. Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vase Surg 1993; 17: 305-317.

12 Azakie A, McElhinney DB, Thompson RW et al. Surgical man-agement of subclavian-vein effort thrombosis as a result of tho-racic outlet compression./ Vase Surg 1998; 28: 777-786.

13 Lokanathan R, Salvian AJ, Chen JC et al. Outcome after throm-bolysis and selective thoracic outlet decompression for primaryaxillary vein thrombosis. / Vase Surg 2001; 33: 783-788.

14 Feugier P, Aleksic I, Salari R et al. Long-term results of venousrevascularization for Paget-Schroetter syndrome in athletes.Ann Vase Sing 2001; 15: 212-218.

15 Lee WA, Hill BB, Harris EJ Jr et al. Surgical intervention is notrequired for all patients with subdavian vein thrombosis. J VaseSwrg2000; 32: 57-67.

16 Angle N, Gelabert HA, Farooq MM et al. Safety and efficacyof early surgical decompression of the thoracic outlet for Paget-Schroetter syndrome. Ann Vase Swrg2001; 15 : 37-42.

17 Arko FR, Harris EJ, Zarins CK, Olcott C 4th. Vascular com-plications in high-performance athletes. / Vase Surg 2001; 33:935-942.

18 Kreienberg PB, Chang BB, Darling RC 3rd et al. Long-termresults in patients treated with thrombolysis, thoracic inlet de-compression, and subclavian vein stenting for Paget-Schroettersyndrome. / Vase Surg 2001; 33 (2 Suppl): S100-105.

19 Kunkel JM, Machleder HI. Treatment of Paget-Schroetter syn-drome. A staged, multidisciplinary approach. Arch Surg 1989;124: 1153-1158.

20 Molina JE. Need for emergency treatment in subclavian veineffort thrombosis. J Am Coll Surg 1995; 181: 414-420.

19AORTOCAVAL FISTULA

DOMINIQUE MAIZA, JEAN ADER JULES

Spontaneous rupture of an abdominal aortic aneurysm (AAA) into the inferior vena cava(IVC) system is the most common cause of an aortocaval fistula (ACF). It is a seldom but

formidable complication because the symptoms are protean and can mislead the diagnosis.If not treated, it can lead to right heart failure resistant to medical treatment and finallyending in the patient's death. Discovery during the surgical cure of such an aneurysm isassociated with significant blood loss and a high peri-operative mortality. The pre-operativediagnosis can improve the prognosis by allowing the surgical team to anticipate and adapt thetreatment. In the aim to clarify the symptomatology and the results of surgical treatment, theAssociation Universitaire de Recherche en Chirurgie (AURCFrance) performed a survey which ledto a retrospective study concerning 39 cases of active ACFs operated between 1973 and 1989.

19.181

Retrospective studyof the AURC

Retrospective review identified a total of 39 pa-tients who underwent operation in 11 of the 28AURC centers for a documented arteriovenous fis-tula (AW) between a ruptured abdominal aortic oriliac aneurysm into the IVC or iliac vein (Table I).Patients with another cause of ACF were not in-cluded in the study group. The patients (36 men,3 women) were aged between 42 years and 87 years(mean 69 years). The records of these patients were

reviewed in detail to specify the etiology and thelocation of the fistula, the clinical symptoms at thetime of the initial presentation, the management andthe results of the surgical treatment. All 39 aneur-ysms were of atherosclerotic origin. In 37 of these,aneurysm involved the infrarenal aorta, extendinginto the iliac vessels in 30 cases, whereas two patientshad isolated common iliac artery aneurysms. Theaverage length of the fistula was 30 ± 21 mm (3 to80 mm). In 34 patients, the fistula was eroded intothe vena cava, in 4 patients into the right commoniliac vein and in 1 patient into the left medial iliacvein. In 4 patients, a concomitant retroperitonealaneurysm rupture was present.


19182

n , c NumberCenter burgeon t, .. .6 of patients

Angers CHU JM Chevallier 4

Bordeaux CHU JM Serise 2

Caen CHU D Maiza 7

Clermont-Ferrand JP Ribal 4CHU

Creteil CHU JP Becquemin 1

Grenoble CHU H Guidicelli 1JL Magne

Lille CHU C Stankowiak (Y) 10

Nancy CHU G Fieve 2

Paris, Hopital F Bacourt 1Ambroise Pare

Rouen CHU J Testart 5J Watelet

Toulouse A Barret 2CHU Purpan

The clinical manifestations are summarized inTable II. The continuous abdominal bruit with sys-tolic intensification observed 27 times, was lookedfor only in 29 patients. The pathognomonic triadassociating abdominal pain, abdominal bruit andabdominal mass was present in 13 cases. The diag-nosis of an ACF was recognized before surgery in29 patients (74.4%) and in 23 patients based onlyon the physical findings. The observation of anabdominal bruit or abdominal bruit associated withabdominal pain and an abdominal mass allowedthe diagnosis in most of the cases (Table III) . Themean interval between the fistula formation, deter-mined by the appearance of symptoms and the diag-nosis, was 7 ± 12 days (some hours to 60 days). The7 / \ j /

angiographic or echographic examinations wererealized only in a fickle way. A pre-operative aorto-graphy was performed in 16 patients. The 13 aorto-graphies performed by arterial way always allowedto assert or to confirm the diagnosis, and in

Clinical manifestations N %

Abdominal

Pain 31 79

Bruit 27 69

Mass 21 54

Thrill 13 33

Cardiac

Tachycardia 24 61.5

Dyspnea 15 38.5

Global heart failure 10 25.6

Right heart failure 3 7.7

Shock 9 23.1

Angina 1 2.6

Renal

Oliguria 12 30.8

Anuria 12 30.8

Venous engorgement

Lower limb edema 19 48.7

Lower limb cyanosis 12 30.8

Abdominal cyanosis 3 7.7

Lower limb pulsatile varicose veins 3 7.7

Lower limb subacute ischemia 2 5.1

Priapism 2 5.1

Rectal bleeding 1 2.6

Abdominal pulsatile varicose veins 1 2.6•k T 1 •Neurologic

Paraplegia 1 2.6

Hemiplegia 1 2.6

rr • , Aortocaval fistulat /7777/Y7/ J

•t . ,. Number recognized before surgerymanifestations ° „ /o/\1\ ( /o)

Abdominal bruit 27 22 (81)

Abdominal bruit+ abdominal pain+ abdominal mass 13 11 (85)

AORTOCAVAL FlSTULA

Number

Aortic control

Upstream to the fistula

Suprarenal aortic clamping

Infrarenal aortic clamping

Downstream to the fistula

Aortic or iliac clamping

Endovascular occlusion

Not clarified

Venous control

Upstream to the fistula

Clamping


Downstream to the fistula

Clamping


Digital compression throughopened aneurysm

Not clarified

5

34

30

72

613

11

11

10

Techniques

Arterial repair

Aorto-aortic bypass

Aorto-bi-iliac bypass

Aortobifemoral bypass

Aorto-iliac bypass

Ilio-iliac bypass

Venous repair

Lateral suture

Patch

Ligation

7

18

8

2

2

19492255

761113

12 patients to clarify the location of the fistula. Onthe other hand, three aortographies performed byvenous way allowed only one time to assert the diag-nosis. A computed tomography (CT) scanning withcontrast performed in five patients allowed to assertor to confirm the diagnosis in three patients, twiceto clarify the origin of the fistula and twice toobserve an associated retroperitoneal hematoma.An abdominal echography, performed in 11 pa-tients, always confirmed the diagnosis of an AAAbut suspected the presence of the fistula only inone patient because of the existence of a lowerextension of the vena cava.

Treatment

The surgical approach to the vessels has been byway of laparotomy in 38 patients (32 xyphoid-to-pubis midline incisions and 6 supra-umbilical trans-verse incisions). Because of the history of abdomi-nal surgery, a retroperitoneal abdominal route waschosen in one patient. In four patients, a circula-tory arrest occurred at the time of aortic clamping.Three patients could be resuscitated by closed-chestheart massage. The modalities of arterial and ve-nous control are summarized in Table IV. Thechronology of the venous control with regard tothe aortotomy is clarified only in 35 patients: in30 patients the venous control was realized only afterthe aortotomy. The techniques of restoring arterialand venous flow are summarized in Table V. Theyconcern only 37 patients because two patients diedbefore the repair: one of a cardiac arrest at the timeof the aortic clamping; the other one, to whom thediagnosis of ACF was not established before surgery,died of an uncontrolled venous bleeding during theaortotomy. Mean blood loss was 4 600 ± 3 500 mL(1 000 to 15 000 mL). An auto transfusion systemwas used in only two patients.

Operative mortality, defined as death occurringduring the hospitalization, was 28.2% (11 patients).There were three intraoperative deaths (7.7%): onepatient died of cardiac arrest at the time of aorticclamping, the two others of hemorrhage. Therewere eight postoperative deaths (20.5%) occurringbetween 0 and 39 days (mean 10±14 days). Thecauses and incidence of peri-operative deaths aresummarized in Table VI. Pulmonary and cardiaccomplications are responsible for 54.5% of deaths.Twelve patients (30.7%) had one or several non-lethal complications as summarized in Table VII.

19.183


Number Patients Deathsofdeaths % %

Pulmonarycomplications

Cardiac failure

Coronary disease

Hemorrhage

Renal failure

Biliary peritonitis

Staphylococcusaureus septicemia

3

2

1

2

1

1

1

7.7

5.1

2.6

5.1

2.6

2.6

2.6

27.2

18.2

9.1

18.2

9.1

9.1

9.1

chronic renal failures) within 6 ± 5 days (1 to15 days). Thirteen patients presented a pre-opera-tive congestive cardiac failure. Four of them diedduring the hospitalization. Among the survivors, thetime of recovery could only be assessed in seven pa-tients: in six cases, the cardiac function normalizedin 3 ± 3 days; one patient kept signs of left cardiacfailure during two months. Two patients presentedwith pre-operative neurologic signs. A right hemi-plegia due to the shock in a patient who had a leftcarotid stenosis recovered quickly without afteref-fects in the postoperative period. One pre-opera-tive paraplegia has only partially declined and im-proved to a partial paraparesis allowing walking. Inseven patients, the vena cava patency was assessedby a cavography realized at distance of the repair:twice the vena cava was thrombosed and in five pa-tients it was patent.

19184

Complications

Deep venous thrombosis

Digestive hemorrhage

Wound infection

Chronic renal failure

Colorectal ischemia

Paraplegia

Serratia septicemia

Number

6

2

2

1

1

1

1

Pulmonary embolism due to deep venous throm-bosis was not encountered. No gastrointestinalcomplications required surgery. The postoperativeparaplegia observed in one patient recovered spon-taneously within a few days. Nine of 21 patientswho had a pre-operative creatinine greater than150 pmol/L died during the hospitalization. Onepatient suffered from chronic renal failure. Elevenpatients regained a normal renal function (n = 9)or identical to the previous state (two pre-existent


Spontaneous rupture into the adjacent venoussystem is an unusual complication of rupturedAAAs. According to the literature, the incidence ofthis event is quite low, occurring between 1% and7% of all ruptured aneurysms [1-8] (Table VIII).Only two patients (1.4%) suffered from such a rup-ture in the AAA prospective study realized by theAURC from January until December 1989 [4].Ruptured arteriosclerotic aneurysms are the mostcommon cause of ACF [6,9-12]. This etiology rep-resents 92.8% of the ACF observed during the sameperiod by the AURC members having participatedin our study.

UNUSUAL CASES OF ACFVery rare cases of ACF in association with inflam-

matory ruptured AAA have been reported [13,14].ACF resulting from rupture of syphilitic or mycoticaneurysms, as well as aneurysmal lesions seen inMarfan's syndrome, Ehlers-Danlos syndrome [15]or Takayasu's arteritis [16] are exceptional. Veryrarely, neoplasms may also cause a major AVF byerosion of adjacent arterial and venous structures[17]. Traumatic ACF due to a simultaneous pene-trating injury of the aorta or iliac artery and theIVC or one of the iliac veins represent 10% to 20%of current cases. The most frequently reported trau-matic lesions are those caused by gunshot abdom-inal wounds and iatrogenic complications of lumbarspine surgery [11,18-20]. Davidovic et al. reported

AORTOCAVAL FISTULA

1st author[ref.]

Year ofpublication Type of study

NumberPeriod of operated

AAA

Numberof operated

ruptured AAA

Aortovenousfistulas

(%)

Ghilardi [5]

Koskas [4]

Bednarkiewicz [6

Tsolakis [7]

Alonso Perez [8]

1994

1997

1997

1999

2000

Retrospective

Single-centerretrospective

Multicenterretrospective

Single-centerretrospective

Single-centerprospective

1965 -1992

1989

1980 -1994

1990 -1997

1996 -1997

2152

1034

580

112

NP

373 26 (6.9)

146 2 (1.4)

111

52

144

7 (6.3)

4 (7.7)

3 (2)

AAA: abdominal aortic aneurysm

one case of ACF caused by blunt abdominal traumaafter a traffic accident and one fistula developedafter cardiac catheterization [21]. Although ACFsresulting from penetrating wounds frequently havea dramatic presentation, iatrogenic fistula producesless acute symptoms than traumatic and sponta-neous aortic or iliac fistula. Pagni et al. reportedin 1996 a case of ACF secondary to a retro-aorto-caval false aneurysm which had ruptured into theIVC, in an 81-year-old woman, 7 years after primaryinfrarenal aortic aneurysm repair [22]. In 2002,Tuma et al. reported a case of contained ruptureof an AAA and tear of the IVC 15 months afterplacement of an aortic endograft [23]. The aorticrupture was probably caused by poor proximal fix-ation of the graft, and an angulated right iliac limbof the stent graft penetrated into the IVC just abovethe common iliac junction and caused sealed per-foration. Erosion of the aneurysm into the venoussystem occurs most often in the infrarenal IVC. Morerarely, it occurs in an iliac vein [3,11] or in left renalvein [3,24,25]. In a review, Mansour et al. reported16 cases of spontaneous aorto-left renal vein fistula,and 94% had a retro-aortic left renal vein [24].

CLINICAL ASPECTSThe fistulization of the aneurysm may be asymp-

tomatic and discovered at operation. In general,total or partial obstruction of the fistula by the intra-aneurysmal mural thrombus exists [3,11]. In themajority of the cases, the clinical symptomatologyis highly variable associating, in different degrees,local symptoms due to the aneurysmal rupture andregional and general signs due to the high-flow AW.These protean clinical manifestations and the rar-ity of such lesions may lead to delay in the diag-nosis (Table IX). When the diagnosis of aneurysmis overlooked, the untoward hemodynamic conse-quences of the AW may lead to misdiagnosis suchas phlegmasia cerulea, sciatic pain with motor defi-cits and congestive heart failure [10]. Conversely,the palpation of an aneurysm associated with ab-dominal pain and shock can lead to the diagnosisof retroperitoneal rupture.

PATHOPHYSIOLOGYHemodynamic consequences of the fistula are

responsible for the protean clinical picture whichincludes cardiac, renal, venous or even neurologic

185

VA

SC

UL

AR

E

ME

RG

EN

CIE

S

19

AORTOCAVAL FISTULA

findings. Cardiac manifestations are secondary tothe shunting of blood through the fistula into thelow-resistance and low-pressure venous system,increasing venous return, and consequently cardiacoutput and blood volume [28]. Systolic blood pres-sure decreases transiently and then returns to thenormal level while diastolic pressure remains low.The flow rate through the fistula and the myocar-dial reserve determine whether the arteriovenouscommunication is tolerated. Usually, tolerance isinitially good. Gradually, however, right and thenoverall heart failure develops and does not respondto medical treatment. Of traumatic fistulas only30% of the patients present with signs of cardiacfailure because these generally have a small size andarise in young people having a good cardiac reserve[9-11].

Several pathologic mechanisms explain renal fail-ure [29-31]. Hypertension of the renal veins is ahemodynamic obstacle, initiating a drop in renalblood flow and thereby in glomerular filtration[31]. The decreased mean arterial pressure and theheart failure add to the renal low-flow state. Reac-tional hypersecretion of aldosterone by the juxta-glomerular apparatus induces water and salt re-tention, which then leads to water overload. Theclinical manifestations of renal failure are oliguriaor anuria and azotemia. Regional venous hyper-tension is a constant finding and involves mainlythe lower limbs. Symptoms are generally bilateralbut they can be unilateral when the fistula is locat-ed in one iliac vein [10]. Heart failure and venouscompression secondary to the aneurysmal mass in-crease venous hypertension. Clinically edema andcyanosis are frequent. Superficial veins may be dis-tended or pulsatile at palpation. The arterial inflowto the leg reduced by the fistula explains the fre-quent low-grade ischemia observed distally. Thesefindings, especially in the one-sided forms, may leadto the incorrect diagnosis of phlegmasia cerulea[10,11]. Venous hypertension in the pelvic veins maylead to hematuria [32-34], rectal hemorrhage [6,10,11] or priapism [12,33], which may cause diagnosticconfusion. Neurologic manifestations have occa-sionally been reported in the literature. Brain dis-orders, ranging from obtundation to syncope, resultfrom the low cerebral blood flow [9,10]. Full-scaleparaplegia is rare and can result from functionalarterial insufficiency due to the increased spinal ve-nous stasis induced by venous hypertension in theepidural space associated with arterial lesions in ath-erosclerotic patients [10,35].

DIAGNOSISThe diagnosis of an aortocaval or iliac AVF is

dependent on recognition of its clinical features.Whatever the mode of clinical expression, a simplecomplete clinical examination should lead to thediagnosis: a continuous bruit with systolic accentu-ation is considered pathognomonic for AW. In thepresence of a painful abdominal mass or signs ofpelvic or lower limb venous hypertension or pro-gressive cardiac failure, the diagnosis becomes moreobvious. Common features in patients with aortoto left renal vein fistula include abdominal pain,hematuria, impaired renal function and nonvisual-ization of the left kidney. Less common but alsopresent in the majority of cases are a left-sided bruit,pulsatile abdominal mass and proteinuria. Overtsigns of high-output cardiac failure are less likelybecause of the smaller size of the renal vein com-pared with the IVC and iliac vein [3,24].

If the clinical presentation is not acute, there istime to perform pre-operative imaging studies.Various diagnostic techniques like B-mode ultra-sonography, doppler ultrasonography, aortography,CT scan and magnetic resonance (MR) angiogra-phy will confirm the diagnosis in most patients,unless the fistula is occluded by a thrombus. Ultra-sonography associated with doppler analysis caneasily confirm the diagnosis [36]. Because of its reli-ability and noninvasiveness, this method can besuperior to aortography. Although angiographyremains the best method to document the presenceof ACF for many authors [3,11], the diagnosis maynot be apparent if thrombus material occludes thefistula. Aortography is not really mandatory, mostlyconfirms only what is clinically evident and shouldnot delay surgical treatment in emergent situations.In contrast, arteriography can be very valuable ifthe clinical findings are unclear, and delineation ofanatomy may be particularly important in the man-agement of traumatic fistulas.

The role of CT scan during the AURC study isprobably underestimated due to the time period ofthe survey (1973-1989). CT scan has been demon-strated to be similarly useful in establishing the diag-nosis of ACF with its characteristic findings of cavaleffacement, loss of fat plain between the aorta andIVC, and rapid flow of contrast from the aorta intoa dilated IVC [37,38]. In case of retro-aortic leftrenal vein fistula, CT scan can demonstrate not onlythe anomalous location of the left renal vein butalso the AAA and poor enhancement of the left kid-ney. Early and intense enhancement of the FVC is

187


19188

underlined with gadolinium-enhanced MR angio-graphy. The exact location of the fistula and a com-plete pre-operative assessment of AAA can be per-formed with this noninvasive imaging technique[39,40]. Moreover, the absence of iodinated con-trast media makes it particularly suitable for patientswith renal insufficiency, but the long time for im-aging acquisition requires the patient to be stable.

SURGICAL STRATEGYIf the diagnosis is not established before surgery,

the surgeon may still recognize the entity at oper-ation before opening the aneurysm, by palpating athrill over the major vascular structures and observ-ing engorgement of the vena cava and adjacentretroperitoneal or pelvic veins. Classic surgical re-pair consisting of suture of the fistula from withinthe sac in patients with aneurysm or lateral veno-graphy in traumatic injuries, must be performed assoon as possible. No attempts to improve pre-oper-ative cardiac or renal failure are worthwhile becausemedical therapy is unavailing. All nonoperatedpatients will die in some days or some weeks afterthe appearance of symptoms [12].

Treatment is currently well established. Intraop-erative hemodynamic monitoring requires place-ment of at least one arterial and one right atrialpressure line. If there is a history of heart failureor coronary artery disease, intraoperative monitor-ing of left ventricular filling pressure using a Swann-Ganz catheter is recommended [10]. Continuoushemodynamic monitoring is necessary to preventfluid overload at the beginning of surgery, whichmay worsen congestive cardiac failure. At cross-clamping, an increase in peripheral resistance andreduction in venous return may cause ventricularfibrillation and cardiac arrest. Furthermore, hypo-volemic shock caused by bleeding during fistula re-pair or by sudden peripheral resistance decreaseafter aortic clamp removal, should be avoided [41].As intraoperative blood loss is often significant, au-totransfusion equipment is helpful to decrease theheterologous blood transfusion [11,42]. It was onlyused twice during the AURC study, which is ex-plained by the time period of the survey. Minimalaneurysm manipulation is important to prevent par-adoxical embolization of intraluminal debris [43].The aortic control is similar to standard aorticaneurysm surgery without AVF, even if supraceliaccontrol is necessary in the presence of large aneur-ysms. The proximal aortic clamping must be per-formed before the distal arterial clamping to avoid

a sudden increase of the arteriovenous shunt [11].The IVC control is determined by specific anatom-ical conditions [10]. When the reno-caval junctioncan be approached easily, the vena cava may beclamped distal to the renal vein before opening theaneurysm. When venous clamping or compressionis performed in this manner, blood loss is limitedand the risk of air or atheromatous embolism is re-duced. The strategy of compression to control mas-sive venous hemorrhage from the fistula should bechosen before the aneurysm is opened. In case ofan aorto-renal vein fistula, proximal and distal con-trol of a retro-aortic left renal vein is difficult anddangerous and should not be attempted. The dis-section of the infrarenal aorta should be performedunder direct vision to avoid injury to a retro-aorticleft renal vein. In this situation, direct compressionof the left renal vein from inside the aneurysmlumen should be carried out. After aortotomy, thefistula defect should be oversewn inside the aneur-ysm cavity after all thrombus and debris are re-moved. Venous bleeding from the fistula can becontrolled by direct finger compression or spongestick if the fistula is small or, in others cases, by bal-loon occlusion catheters inflated in the vena cavaon both sides of the fistula [1,11,27]. Transvenouspositioning of balloon catheters in the vena cavabefore aortic opening was found to be helpful inreducing hemorrhage by Ingoldby et al. [44] andNaito et al. [45]. Closure of the venous tear shouldbe rapid and done from inside the aneurysm by arunning suture, taking wide bites on the edges ofthe fistula. A patch is rarely necessary and it in-creases operative time and blood loss but can beuseful in some cases of traumatic ACF. In case ofinadequate venous bleeding control, large fistulaor iliac fistula, it is possible to ligate the vein atboth sides of the fistula [10,11]. Although IVC lig-ation is generally well tolerated, many complica-tions (recurrent deep vein thrombosis, leg edema,varicose veins) may occur [7]. In case of friablevena cava wall, the replacement of the destroyedpart of the IVC with graft interposition has beenproposed but with an increased postoperativethrombosis and pulmonary embolization risk [5,46]. Woolley et al. described an aortic exclusionwith proximal and distal ligation of the aorta andbypass grafting in one patient [47]. In this situa-tion, the fistula remains undisturbed but only com-municates with the excluded aneurysm sac. Thisoperation could cause deep venous thrombosis andcontinued aneurysm growth. Routine use of IVC

AORTOCAVAL FISTULA

interruption by clips should not be performed,since embolization can occur after technical failure[11,27]. Aortic repair is performed according tostandard prosthetic graft implantation.

SURGICAL RESULTSDuring the postoperative period, cardiovascular

and renal symptoms induced by the high-flow AVFgenerally decrease rapidly in surviving patients.Postoperative complications are due to the generalconsequences of the blood transfusion, pre-existingcomorbidities or general infectious problems. Theyare explained by the necessity of an urgent surgi-cal treatment, without wasting the time necessaryfor an adequate pre-operative evaluation in olderarteriosclerotic patients with coronary artery dis-ease and severe physiologic disturbances. Reportedoperative mortality after surgical repair of ACFcaused by aneurysmal rupture is high, ranging from6% to 36% (Table X). In the studies of Brewsteret al. and Davidovic et al., all deaths occurred inpatients in whom the correct diagnosis was not

established before surgery [11,21]. In a review of184 aortovenous fistulas (159 aorto-caval, 8 aorto-iliac, 17 aorto-renal), Calligaro et al. reported a sur-vival of 72% of patients with ACFs and 88% ofpatients with aortorenal vein fistulas after surgery[3]. The lower mortality rate found with aortore-nal vein fistulas was explained by an associatedlower incidence of ruptured aneurysms, becauseonly 12% of patients with an aortorenal vein fistulahad a separate retroperitoneal rupture comparedwith 22% of patients with an ACE In the experi-ence of Brewster et al., iliac AW had a better prog-nosis than ACF because most of these patients wereless hemodynamically compromised [11]. Resultsare much better in cases of traumatic or iatrogenicACFs, because of younger age, absence of heart dis-ease and better hemodynamic status of patients[11,20,21].

ENDOVASCULAR TREATMENTEndovascular stent graft repair may offer an at-

tractive and minimally invasive treatment alternative

1st author[ref.]

Harrington [26]

Calligaro [3]

Salo [32]

Brewster [11]

Ghilardi [5]

Davis [27]

Davidovic [21]

AURC

Year ofpublication

1989

1990

1990

1991

1994

1998

2002

2002

Time period

1975 - 1989

Review

1976 - 1988

30 years

1965 - 1992

1970 - 1997

NA

1973 - 1989

Number of AWin ruptured AAA

10

159 ACF8AIF

17ARF

11

14

22

16

14

39

Number oftraumatic AW

0

000

0

6

0

2

2

0

Overallpostoperativemortality %

20

282912

36

10

36.4

6

25

28.2

Postoperativemortality

traumatic AW

-

---

-

0

-

0

0

.

189

ACF: aortocaval fistulaAIF: aorto-iliac fistulaARF: aorto-renal fistulaAW: arteriovenous fistulaNA: not available


19190

to open repair management especially in cases inwhich a pre-operative diagnosis can be made. It of-fers the theoretical advantage of reduced intraop-erative blood loss and can subsequently reduce themortality and the morbidity rates. Boudghene etal. [48] reported successful treatment of ACF withpercutaneous stent grafts in an experimental studyin which the ACF was created percutaneously ineight sheep. The use of an endovascular stent graftin the repair of a spontaneous aortovenous fistulahas only been reported four times for rupturedAAA (three ACF and one aorto-left renal vein fis-tula) , one time for an ACF that recurred after con-ventional AAA repair and one time for an ACF dueto retroperitoneal sarcoma [17,49-53]. Such appli-cation was not without technical problems duringintroduction and deployment of the stent graft. Intheir case, Beveridge et al. [49] described the tech-nical problems during introduction and deploy-ment of the contralateral limb of the bifurcatedstent graft because of the displacement of the com-mon iliac artery by the aneurysm. Umscheid andStelter [50] used a bifurcated stent graft in theircase because the distal aortic neck was very shortand the iliac vessels had a normal caliber. However,postoperative CT showed that one of the iliac limbsof the bifurcated graft was compressed by the nar-row distal cuff of the aneurysm, potentially leadingto limb occlusion or claudication in the future. Lauet al. [51] used an aorto-uni-iliac device with afemorofemoral cross-over graft from the right toleft side, and the left common iliac artery was em-bolized with metallic coils after successful deploy-ment of the stent grafts to excluded inflow into

the aneurysm sac. The intraoperative angiogramshowed complete exclusion of the aneurysm withabsence of endoleak and closure of the ACF, buta repeat spiral CT showed a persistent fistula witha small inflow from the left common iliac artery.The coils had clearly not occluded the left com-mon iliac artery. Two weeks later, the patient wasreadmitted with acute ischemia of both legs due toocclusion of the aortic stent graft. Post-thromboly-sis arteriography showed a patent graft with goodrun off and no evidence of any endoleaks or per-sistence of ACF, but with a persistent stenosis at thejunction between the aorto-uni-iliac graft and theiliac extension. Sultan et al. [52] reported a caseof a contained rupture of the aorta communicat-ing with the left renal vein. An aorto-aortic stentgraft was used and the postoperative CT showedno evidence of an endoleak. The left renal vein,however, continued to fill the saccular para-aorticstructure. The endovascular repair was only par-tially successful, as the defect in the left renal veinhad to be repaired at open laparotomy few dayslater. Duxbury et al. [17] treated a right commoniliac AW resulting from a retroperitoneal sarcomawith a straight stent graft, but ten days after stent-ing the patient had clinical deterioration and an-giography showed partial prolapse of the proximalend of the stent graft into the IVC, enlarging thefistula. A bifurcated stent graft was placed withoutcomplication. Unlike a rupture or contained rup-ture of an AAA, spontaneous ACF may not alwaysrequire emergency treatment, and time may beavailable for obtaining the suitable endovascularstent graft.

R E F E R E N C E S

1 Baker WH, Sharzer LA, Ehrenhaft JL. Aortocaval fistula as acomplication of abdominal aortic aneurysms. Surgery 1972; 72:933-938.

2 Duppler DW, Herbert WE, Dillihunt RC, Ray FS. Primary arte-riovenous fistulas of the abdomen. Their occurrence second-ary to aneurysmal disease of the aorta and iliac arteries. ArchSuigim-, 120: 786-790.

3 Calligaro KD, Savarese RP, DeLaurentis DA. Unusual aspects ofaortovenous fistulas associated with ruptured abdominal aorticaneurysms. / Vase Surg 1990; 12: 586-590.

4 Koskas F, Kieffer E. Surgery for ruptured abdominal aorticaneurysm: early and late results of a prospective study by theAURC in 1989. Ann Vase Surg 1997; 11: 90-99.

5 Ghilardi G, Scorza R, Bortolani E et al. Primary aortocaval fis-tula. Cardiovasc Surg 1994; 2: 495-497.

6 Bednarkiewicz M, Pretre R, Kalangos A et al. Aortocaval fistulaassociated with abdominal aortic aneurysm: a diagnostic chal-lenge. Ann Vase Surg 1997; 11: 464-466.

7 Tsolakis JA, Papadoulas S, Kakkos SK et al. Aortocaval fistulain ruptured aneurysms. Eur J Vase Endovasc Surg 1999; 17:390-393.

8 Alonso-Perez M, Segura RJ. Surgical risks of emergency AAArepair. In: Branchereau A, Jacobs M (eds). Surgical and endo-vascular treatment of aortic aneurysms. Armonk, Futura PublishingCo, 2000 :pp 271-280.

9 Reckless JP, McColl I, Taylor GW. Aortocaval fistulae: an uncom-mon complication of abdominal aortic aneurysms. Br J Surg1972;59:461-462.

10 Petetin L, Pelouze GA, Mercier V et al. Rupture of abdominalaortic aneurysm into the inferior vena cava: a study of sevencases. Ann Vase Surg 1987; 1: 572-577.

AORTOCAVAL FISTULA

11 Brewster DC, Cambria RP, Moncure AC et al. Aortocaval andiliac arteriovenous fistulas: recognition and treatment. J VaseSwig 1991; 13: 253-265.

12 Gilling-Smith GL, Mansfield AO. Spontaneous abdominal arte-riovenous fistulae: report of eight cases and review of the lit-erature. BrJSurgim; 78: 421-425.

13 Ferrari M, Bonanomi G, Fossati N et al. Surgical managementof inflammatory abdominal aortic aneurysm associated withoccult aortocaval fistula. Surgery 2000; 127: 234-236.

14 Farid A, Sullivan TM. Aortocaval fistula in ruptured inflam-matory abdominal aortic aneurysm. A report of two cases andliterature review. / Cardiovasc Surg 1996; 37: 561-565.

15 Taniyasu N, Tokunaga H. Multiple aortocaval fistulas associatedwith a ruptured abdominal aneurysm in a patient with Ehlers-Danlos syndrome. Jpn CircJ 1999; 63: 564-566.

16 Gronemeyer PS, deMello DE. Takayasu's disease with aneurysmof right common iliac artery and iliocaval fistula in a younginfant: case report and review of the literature. Pediatrics 1982;69: 626-631.

17 Duxbury MS, Wells IP, Roobottom C et al. Endovascular repairof spontaneous non-aneurysmal aortocaval fistula. Eur J VaseEndovasc Swrg2002; 24: 276-278.

18 Krishnasastry KV, Friedman SG, Deckoff SL, Doscher W.Traumatic juxtarenal aortocaval fistula and pseudoaneurysm.Ann Vase Surg 1990; 4: 378-380.

19 Pincu M. Traumatic aortocaval fistulas of late diagnosis. / VaseSwgl994; 19: 1097-1098.

20 Papadoulas S, Konstantinou D, Kourea HP et al. Vascular injurycomplicating lumbar disc surgery. A systematic review7. Eur JVase Endovasc 5wrg2002; 24: 189 -'195.

21 Davidovic LB, Kostic DM, Cvetkovic SD et al. Aorto-caval fistu-las. Cardiovasc Surg 2002; 10: 555-560.

22 Pagni S, Halene S, Kwass W, Khachane V. Ruptured aorticpseudoaneurysm: a rare presentation as aortocaval fistula.) Cardiovasc Surg 1997; 38: 165-168.

23 Tuma MA, Hans SS. Rupture of abdominal aortic aneurysmwith tear of inferior vena cava in a patient with prior endo-graft. / Vase Surg 2002; 35: 798-800.

24 Mansour MA, Rutherford RB, Metcalf RK, Pearce WH. Spon-taneous aorto-left renal vein fistula: the "abdominal pain, hema-turia, silent left kidney" syndrome. Surgery 1991; 109: 101-106.

25 Masood T, Naylor AR, Edge JM et al. Double aortovenous fis-tula: a unique presentation of a ruptured abdominal aorticaneurysm. Eur] Vase Surg 1994; 8: 107-109.

26 Harrington EB, Schwartz M, Haimov M et al. Aorto-caval fis-tula: a clinical spectrum. / Cardiovasc Surg 1989; 30: 579-583.

27 Davis PM, Gloviczki P, Cherry KJ Jr et al. Aorto-caval and ilio-iliac arteriovenous fistulae. Am J Surg 1998; 176: 115-118.

28 Houben PF, Bollen EC, Nuyens CM. "Asymptomatic" rupturedaneurysm: a report of two cases of aortocaval fistula present-ing with cardiac failure. Eur] Vase Surg 1993; 7: 352-354.

29 Albalate M, Gomez Octavio J, Llobregat R, Fuster JM. Acuterenal failure due to aortocaval fistula. Nephrol Dial Transplan.1998; 13: 1268-1270.

30 Gregoric ID, Jacobs MJ, Reul GJ, Rochelle DG. Spontaneouscommon iliac arteriovenous fistula manifested by acute renalfailure: a case report. J Vase Surg 1991; 14: 92-97.

31 Brunkwall J, Lanne T, Bergentz SE. Acute renal impairmentdue to a primary aortocaval fistula is normalised after a suc-cessful operation. Eur] Vase Endovasc Surg 1999; 17: 191-196.

32 Salo JA, Verkkala KA, Ala-Kulju KV et al. Hematuria is an indi-cation of rupture of an abdominal aortic aneurysm into thevena cava. / Vase Surg 1990; 12 : 41-44.

33 Saxon SR, Glover WM, Youkey JR. Aortocaval fistula and con-tained rupture of an abdominal aortic aneurysm presentingwith pelvic venous congestion. Ann Vase Surg 1990; 4: 381-383.

34 Steinke TM, Reber PU, Hakki H, Kniemeyer HW. Haematuriaand an abdominal aortic aneurysm- -warning of an aortocavalfistula. Eur] Vase Endovasc Surg 1999; 18: 530-531.

35 Jauslin PA, Muller AF, Myers P, Velebit V. Cauda equina syn-drome associated with an aortocaval fistula. Eur] Vase Surg 1991;5: 471-473.

36 Daxini BV, Desai AG, Sharma S. Echodoppler diagnosis of aor-tocaval fistula following blunt trauma to abdomen. Am Heart J1989; 118: 843-844.

37 Quiroga S, Alvarez-Castells A, Hidalgo A et al. Spontaneous aor-tocaval fistula: CT findings with pathologic correlation. AbdomImaging 1995; 20: 466-469.

38 Rosenthal D, Atkins CP, Jerrius HS et al. Diagnosis of aorto-caval fistula by computed tomography. Ann Vase Surg 1998; 12:86-87.

39 Walter F, Blum A, Quirin-Cosmidis I et al. An aortocaval fis-tula diagnosed with 1.5-T magnetic resonance angiography./ Cardiovasc Magn Reson 2000; 2: 213-216.

40 Gaa J, Bohm C, Richter A et al. Aortocaval fistula complicat-ing abdominal aortic aneurysm: diagnosis with gadolinium-enhanced three-dimensional MR angiography. Eur Radiol 1999;9: 1438-1440.

41 Miani S, Giorgetti PL, Arpesani A et al. Spontaneous aortocavalfistulas from ruptured abdominal aortic aneurysms. Eur] VaseSurg 1994; 8 : 36-40.

42 Doty DB, W'right CB, Lamberth WC et al. Aortocaval fistulaassociated with aneurysm of the abdominal aorta: current man-agement using autotransfusion techniques. Surgerj 1978; 84:250-252.

43 Cooperman M, Deal KF, Wooley CF, Evans WE. Spontaneousaortocaval fistula with paradoxical pulmonary embolization.Am JSurg 1977; 134: 647-649.

44 Ingoldby CJ, Case WG, Primrose JN. Aortocaval fistulas and theuse of transvenous balloon tamponade. Ann R Coll Surg Engl1990; 72: 335-339.

45 Naito K, Sakai M, Natsuaki M, Itoh T. A new approach for aor-tocaval fistula from ruptured abdominal aortic aneurysm.Balloon occlusion technique under echogram guidance. ThoracCardiovasc Surg 1994; 42: 55-57.

46 Kiskinis DA, Saratzis N, Megalopoulos A et al. Primary aorto-caval fistula in association with ruptured aneurysms. Ann VaseSurg 1994; 8: 496-499.

47 Woolley DS, Spence RK. Aortocaval fistula treated by aorticexclusion. / Vase Surg 1995; 22: 639-642.

48 Boudghene F, Sapoval M, Bonneau M, Bigot JM. Aortocaval fis-tulae: a percutaneous model and treatment with stent grafts insheep. Circulation 1996; 94: 108-112,

49 Beveridge CJ, Pleass HC, Chamberlain J et al. Aorto-iliac aneur-ysm with arteriocaval fistula treated by a bifurcated endovas-cular stent-graft. Cardiovasc Intervent Radiol 1998; 21: 244-246.

50 Umscheid T, Stelter WJ. Endovascular treatment of an aorticaneurysm ruptured into the inferior vena cava. J Endovasc Ther2000; 7: 31-35.

51 Lau LL, O'reilly MJ, Johnston LC, Lee B. Endovascular stent-graft repair of primary aortocaval fistula with an abdominalaorto-iliac aneurysm. / Vase Surg 2001; 33: 425-428.

52 Sultan S, Madhavan P, Colgan MP et al. Aorto-left renal veinfistula: is there a place for endovascular management? J EndovascS«rgl999;6:375-377.

53 Gandini R, Ippoliti A, Pampana E et al. Emergency endograftplacement for recurrent aortocaval fistula after conventionalAAA repair. J Endovasc Tfor 2002; 9: 208-211.

191

TRAUMATIC INJURY OF THEVENA CAVA AND ITS MAJOR BRANCHES

LAURENT CHICHE, EDOUARD KIEFFER

No vascular lesion is more appalling to manage than that affecting the caval veins andtheir branches. Once limited to cases from military conflicts, these traumas have become, sincenearly thirty years ago, the legacy of specialized trauma centers, particularly in North Americafrom which most of the publications originate.

The impact of the initial shock, the nearly always concomitant vascular or extravascularlesions, exposure difficulties and the control over and repair of damaged veins all explain thevery high mortality associated with these lesions, despite the use of modern techniques. Aftera short historic overview, this chapter will address the trauma mechanisms, the local conse-quences and the general therapeutic approach to these lesions. We will focus on the descriptionof damage to the inferior vena cava (IVC) because this occurs with the highest incidence, andwe will not discuss trauma to the suprahepatic veins (SHVs) because this is usually associatedwith parenchymal damage to the liver, which is beyond the scope of this chapter.

20_193

History

The modern era of vascular anastomoses startedin 1912 with the work of Alexis Carrel [1]. In 1894,this French physician was frustrated by the techni-cal impossibility to repair a lethal injury to the por-tal vein of President Sadi Carnot resulting from adagger stab. Nevertheless, Eck had described earli-er, in 1877, an anastomosis between the IVC andthe portal vein in the dog, and in 1882 Schedeclosed an injury of the femoral vein laterally in a

human being. The first experimental end-to-endanastomosis is ascribed to Clermont in 1901. Thefirst attempts of venous repair were reported dur-ing the Balkan war in 1911 and subsequently dur-ing the two World Wars. In 1916, Taylor [2] re-ported on the first patient to survive an IVC injury.Since the Korean conflict (1950 to 1953), the in-terest in venous repairs has been growing as illus-trated by the series of 37 IVC injuries reported byOchsner et al. in 1961 [3]. At that time, only 19 sur-vivors of this type of injury had been published.


20194

In 1981, the Vietnam Vascular Registry [4] report-ed 82 traumatic lesions of the caval vein, compris-ing 78 IVCs and four superior vena cavae (SVC).In 1978, the group in Houston had already report-ed a series of 301 cases, observed in 30 years of civilpractice [5].

It is estimated that 10% to 15% of the pene-trating traumas of the abdomen are accompaniedby major venous injury and that one in 50 shotwounds damages the IVC [6]. In 50% of the cases,the patients die from hemorrhage before reachingthe hospital. These data illustrate the place trau-matic lesions of the IVC currently occupy outsidethe battlefield.

Trauma mechanisms

In general, the superior thoracic, intrapericardialand retrohepatic segments of the caval vein may sus-tain either a penetrating or a closed trauma. TheIVC is usually involved in single penetrating injuries.

CLOSED TRAUMAClosed injuries usually result from a severe dece-

leration trauma in the horizontal direction such asin traffic accidents, or in the vertical direction, likein a fall from high altitude. The resulting shearforces cause a partial or total avulsion of the ve-nous segment, as can be observed at the atriocavalor hepatocaval junctions, or at the level of the azy-gos, renal, or superior mesenteric veins.

The common and internal iliac veins are dam-aged where they pass bony structures, especiallyafter pelvic fractures.

In the literature, 10 cases of post-traumatic throm-bosis of the IVC were found in 1999 [7], occurring3 days to 3 years after a high-energetic trauma. Thisthrombosis could have been secondary to organiza-tion of an initially localized thrombus, which allowedspontaneous hemostasis after an injury to the vesselwall.

As an anecdote, a laceration of the IVC was report-ed following a nonpenetrating trauma caused by thehigh-pressure water jet of an industrial cleaner [8].

PENETRATING TRAUMAThe most frequent penetrating traumas are those

from gunshots rather than stabbing weapons. Thestatistical preponderance of dexterity among theattackers explains why the caval vein, in its right

lateral position, is spared most of the time duringfrontal attacks on the left part of the body.

All kinds of trauma, varying between a localizedpuncture and injuries with substantial tissue loss,can occur. Bullet injuries are the most destructive.Except for the trauma to the caval vein, they areoften responsible for other serious lesions to neigh-boring structures that induce a risk of sepsis, whichin part influences the prognosis.

IATROGENIC TRAUMAThis may concern vessel wall perforations due to

the introduction of an endoluminal catheter orcaval filter, of which the prognosis is usually goodwhen untreated, or injuries occurring during sur-gery. Trauma occurring during thoracoscopy or la-paroscopy may either pass unnoticed or be revealedsecondarily, or may be diagnosed directly becauseof excessive blood loss during the procedure.

As this type of trauma is becoming more and morefrequent due to the increasing use of these tech-niques, it forms the topic of another chapter of thisbook. Finally, direct iatrogenic damage to the leftinnominate vein or the intrapericardial caval veincan complicate certain cardiac re-interventions.

CONCOMITANT LESIONSNearly all patients who have suffered a trauma of

the caval vein have at least one concomitant arte-rial or venous and/or neighboring visceral organinjury [9]. The most frequent arterial lesions con-cern the abdominal aorta. In several series [9-13],this association has significantly influenced the mor-tality risk. In rare cases, direct identification of anaortocaval fistula resulting from a penetrating trau-ma could protect the patient from a fatal hemor-rhage. Some chronic aortocaval fistulae have beendescribed [14], as have some cavorenal fistulae [15].The venous lesions most frequently associated in-volve the portal, hepatic, splenic and superior mes-enteric veins. Although all organs may be damaged,the most common ones are the liver, the kidneys,the duodenum, the small intestines and the colon.Recently, a traumatic cause of duodenum fistulaewas found in 9 out of 37 (24%) cases in the litera-ture [16]. The trauma was either related to a pene-trating trauma of the abdomen, ingestion of aforeign body or early or late migration (7 days to11 years) of a caval filter.

TRAUMATIC INJURY OF THE VENA CAVA AND ITS MAJOR BRANCHES

Local consequencesof caval vein trauma

Half of the patients who suffered from a cavalvein trauma, and particularly those with an arteriallesion, present with a severe hemorrhagic shock. Asopposed to the arteries, the veins show a poor vaso-constrictor response and cannot generate an effec-tive hemostasis through their own physiologicproperties.

Because of the absence of valves, IVC injuriesare not only characterized by bleeding from theiliac, but also by reflux from the atrial side. Theseveins, however, do have some features that can leadto a spontaneous hemostasis, at least temporarily.The circulation, including the caval veins, is main-tained at low pressure. In case of an IVC injury,the neighboring tissues can cause an effective plug-ging that limits the hemorrhage and sometimesleads to thrombus formation and healing of thevessel wall. The hemorrhage may thus be containedby the retroperitoneum, the pancreas, the duode-num or the posterior side of the liver. This phe-nomenon is particularly seen in simple lesionscaused by stabbing weapons or low-velocity shotwounds, but is exceptional in case of a perforatingtrauma of the IVC or damage secondary to high-velocity fire weapons.

Primaryreanimation measures

In case of a penetrating trauma, the localizationof one or more openings and the estimation of theroute of the damaging agent can help to suspect atrauma of the caval vein. Sudden profound hemo-dynamic shock just after induction of anesthesia orafter installation of mechanical ventilation is a verysuggestive sign. A rapid response to massive fluidsuppletion confirms this suspicion. If not, it indi-cates that the structures usually capable of internalcompression are damaged and cannot prevent thecaval bleeding, which is a poor sign. In order toensure a quick filling, the reanimation team shouldhave two large venous accesses at their disposal. Itis possible to use the saphenous vein at the ankle,even in patients with IVC lesions [17]. This hasbeen proven experimentally [18]. The rich venoussupplies, together with the internal plugging capac-ity of a caval vein that has regained approximatelyits normal size, explain this controversial fact.

The fluid suppletion, initially consisting of macro-molecules, also requires large quantities of bloodproducts, red blood cell concentrates, plasma con-centrates and platelets. Restoration of the bloodvolume is indispensable during this kind of surgery.In the majority of series, if specified, the mean num-ber of blood product units supplied varied between15 and 30, having a statistically significant impacton the mortality. It is important to prevent hypo-thermia using external warming devices and bywarming the administered products.

Generalintervention principles

Generally speaking, no additional investigationshould interfere with the initial reanimation of apatient with an injured abdomen or thorax. Notuntil the condition has been stabilized can a trans-thoracic cardiac or abdominal ultrasound exam beperformed. When the clinical suspicion of a majorvascular trauma has risen, a surgical exploration isjustified.

In several North American series, patients inwhom reanimation remained insufficient under-went an urgent clamping of the thoracic descend-ing aorta through a left anterolateral thoracotomy.Although meant to restore arterial pressure in thesedying patients, this heroic maneuver yielded dis-appointing results. In 2001 Carr et al. [9] reportedonly 14 survivors out of 151 cases in the literaturetreated in this manner. In another series [11] re-porting on the outcome of 302 abdominal vascularinjuries, thoracotomy was performed in 131 cases(43%), of which 43 times (14%) were in the shock-room and 88 times (29%) in the operating room.The survival rates in these two groups were only2% and 10%, respectively. In another recent serieson 136 IVC injuries, one single patient survived outof 25 who underwent a thoracotomy for clamping[12]. These results can be explained by the factthat the most severely injured patients would obvi-ously have died already on the site of the accident,were it not for the modern means of transport andprehospital reanimation.

COMMON PRINCIPLES OFMAJOR VENOUS INJURIES

Patients who make it to the operating room shouldbe treated by a surgical team of sufficient number.In order to respond to a possible decompensation

20195


20196

during anesthetic induction or surgical incision,they are usually anesthetized after preparation ofthe skin and operation field. In most cases the pa-tient is positioned in the dorsal decubitus position,and the operation field runs down from the tho-racic and abdominal areas to the knees. The unan-imously acknowledged surgical access in case of anabdominal venous injury is a median laparotomyfrom xyphoid to pubic area, to which a median ster-notomy is added. After the intestines are movedaside, the peritoneal cavity is emptied of a variableamount of blood by means of aspiration into a res-ervoir. A nonpulsating hematoma of black blood di-rectly identifies a venous injury. Continuous aspi-ration of it carries the risk of exsanguination andshould be prohibited. Preferably, gauzes should bepacked into all abdominal quadrants, as it is diffi-cult to localize the origin of the venous bleeding,which expands like a flat surface rather than a jet.This hemostasis enables to optimize the hemody-namic situation by correcting the volume. A tem-porary clampage of the infrarenal aorta only, per-formed without difficulty and visibly, or even simplecompression, can help to reach a stable situation.

In contrast with arterial injury, for which clamp-ing of the inflow to obtain adequate hemostasisusually suffices, hemostasis of a venous injury re-quires checking of both the inflow and the outflowtract. Use of conventional clamps is dissuaded, es-pecially when they have to be applied half blindly.Moreover, the posterior side of the IVC should bechecked even more carefully to avoid additionaldamage.

Whenever possible, hemostasis should be achievedthrough direct digital compression, fixed gauzes,covered atraumatic clamps placed under visual con-trol or by using tourniquets. Most of the traumaticlesions of the caval vein and its branches may thenbe treated by means of direct closure or simple lig-ature in certain localizations. The use of prostheticmaterial in the form of patches or tubular grafts israrely necessary. Autologous venous jugular orsaphenous grafts, sometimes composed and organ-ized in order to obtain sufficient material for thereconstruction (helical graft), are preferred.

Specific aspects for each area

When the hemorrhage is controlled by means ofpacking gauzes and the hemodynamics are cor-

rected, the search for venous lesions can begin. Thefirst maneuver to perform is to tilt the patient'shead down to minimize the risk of a massive airembolization. On the basis of the points of impact,the route of the damaging agent and the localiza-tion of the hematoma, it is often possible to pre-dict the traumatized vein. Schematically, the me-dian supramesocolic hematomas suggest a lesion ofthe superior mesenteric vein. Lateral, retroperi-toneal peri-renal hematomas point to an injury ofthe renal veins. Lateral pelvic hematomas indicatea lesion of the iliac vein. Finally, hematomas in theportal region, in the middle of the hepatic pedi-cle, designate a portal vein injury, and those in theretrohepatic area point toward a trauma of theretrohepatic IVC and/or SHV.

The decision to explore contained hematomas forwhich hemostasis could be achieved is controversialin view of the technical difficulties to be anticipat-ed after decompression of venous hematomas. Thisis not so much the case when an infrarenal IVC in-jury is suspected, because of the frequently associ-ated visceral or vascular lesions and the relativelysimple reconstruction techniques. In contrast, it ismore controversial in case of a retrohepatic IVC le-sion, which shows no spontaneous hemorrhagicproblems, but may lead to a fatal shock after mo-bilization of the liver [6]. A re-bleeding is indeedrare, whereas it is estimated that 10% to 40% ofthe patients die from a direct exposure during theattempt to repair the lesion [6].

TRAUMA OF THE IVCThe IVC is more frequently subjected to trauma

than the SVC. The abdominal vascular structuresare mostly injured, mainly through a penetratingtrauma [11], The problems of each segment aredescribed separately.

Infrarenal IVC. The infrarenal IVC is involvedin 25% to 50% of the injuries to the IVC [4,5,13,19-24]. Its exposure via a right mediovisceral approachis preferred over a median retroperitoneal ap-proach, which offers the right access to the abdomi-nal aorta and the left renal vein but less to the IVC.The coloparietal exposure is pursued while retain-ing the duodenal area and the head and body ofthe pancreas to the left (Fig. 1). This allows expo-sure of the right kidney and its ureter. After rota-tion of the viscera, the IVC can be exposed nicelyfrom the junction of the iliac veins to its juxta-hepatic segment.


A serious hemorrhage occurring during exposureof the IVC should be compressed by an assistant toallow the surgeon to continue the exposure. Sub-sequently, various procedures can be chosen for thehemostasis and reconstruction. The simplest one isto apply gauze over the lesion. However, maintain-ing sufficient compression during the whole dura-tion of the venous repair is difficult. Total clampingof the IVC at a distance from the lesion by meansof conventional clamps or tourniquets is risky dueto the vulnerability of the vessel wall and the pos-sibility of permanent reflux supplied by the collat-eral circulation from the azygos and lumbar veins.A smaller vessel wall trauma can be treated bymeans of bipolar endoluminal clamping usingocclusive balloon catheters (Fogarty), or urinarycatheters (Foley). Lesions of the anterior or lateralsides of the IVC can best be handled using a largeSatinsky clamp (Fig. 2), which has the advantagethat it partially clamps the lumen and thereby does

not induce venous hypertension. Direct closure isthe technique of choice to repair lesions of the in-frarenal IVC. In urgent cases, a quick closure usingthicker stitches (3/0 or 4/0) is preferable to tryingto do a more esthetical but more time-consumingreconstruction using thinner stitches. This is under-lined by the finding that there is no relation be-tween the outcome of the reconstruction and thedegree of residual stenosis [6]. Rarely, a secondaryenlargement of the sutured area is required. Le-sions of the posterior side can be closed, either viadirect exposure by rotating the IVC (Fig. 3) afterresection of one or more lumbar veins, or via atranscaval approach (Fig. 4) after having enlargedthe entry opening in the anterior side, which is tobe repaired afterward. In case of major destructionof the vessel wall, particularly in combination withshock and other vascular lesions, ligation of theinfrarenal IVC or iliocaval junction together withligation of all lumbar veins is generally advocated.

197

FIG. 1 Approach of the IVC, from its orisin to the subhepatic segment, bymediovisceral rotation after mobilizing the right colon, duodenum, and pancreas.


FIG. 2 Lateral clamping of the vena cava by means of a Satinsky clamp after digital control of the bleeding.

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FIG. 3 Exposure and closure of a lesionin the posterior side of the IVC after trans-ection of lumbar veins and axial rotation.


FIG. 4 Closure of a perforating lesion of the IVC. The posterior wall is sutured first via theinterior of the vein after having enlarged the lesion in the front. This is closed secondarily.

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Juxtarenal and juxtahepatic IVC. The jux-tarenal IVC extends two centimeters above andbelow the junction with the renal veins. It runsupward through a short juxtahepatic IVC, accessi-ble via the lower border of the liver. Involvementof these segments comprises 20% to 50% of thetraumatic lesions of the IVC [13,19,21-23].

Access to the Juxtarenal segment is obtained by aright mediovisceral rotation (see above). Exposureof the posterior side by means of an axial rotationrequires either a right retrorenal release, mobilizingthe kidney to the median line, or a complete re-section between two clamps of the right renal vein,which is to be reconstructed after repositioning theIVC. The juxtahepatic segment can be approachedsimilarly, by means of a complete right mediovis-ceral rotation, or more selectively by mobilizingonly the duodenum and pancreas. The narrow re-lation between the anterior side of the IVC and theposterior side of the portal vein should be kept inmind, to avoid any damage to the latter during thedissection.

The clamping techniques do not differ muchfrom those used for the infrarenal segment. Toobtain a dry operation field at the Juxtarenal levelrequires the simultaneous clampage of both renalveins, sometimes including the renal arteries.

Control over the inflow and outflow of the Jux-tarenal segment usually does not cause any prob-lems. However, the outflow of the juxtahepatic IVCmay be difficult because it is a short segment. Ex-erting anteroposterior pressure on the liver andthereby compressing the end of the juxtahepaticJVC leads to the same result. Reflux from the supra-renal vein, if any, is usually minimal. The recon-struction options for the Juxtarenal and juxtahep-atic segments of the IVC can be superposed onthose for the infrarenal segment in case of simplelesions. They basically consist of direct closure. Al-though a stenosis with a 75% caliber reduction dueto this suture may be acceptable [6], we find it im-portant to preserve a residual lumen of at least 30%of the initial diameter. Correction of remainingstenoses regarded excessive is the only indication


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for enlargement procedures by means of a venouspatch rather than prosthetic material. Complete re-placement of this caval segment using a venous orprosthetic graft is exceptional and restricted to caseswith extensive vessel wall damage in patients whosehemodynamic condition and hemostasis allow for acomplex reconstruction.

Retrohepatic IVC. Traumatic lesions of theretrohepatic IVC are the ones most feared. Theycomprise 10% to 40% of the IVC injuries and areassociated with the worst prognosis. They are fre-quently associated with severe damage to the liverparenchyma and/or SHV. They should be suspect-ed when single clampage of the hepatic pedicledoes not lead to a reduced hemorrhage. The retro-hepatic caval segment is the least surgically acces-sible. The risks of serious hemorrhage and massiveair embolization during its exposure are unpre-dictable and there are extremely high mortalityrates during the operation. Moreover, the most re-cent reports [6,12] advise to refrain from this pro-cedure, as far as the structures surrounding the IVCare intact and ensure sufficient hemostasis, eitherspontaneously or after field compression. Re-infor-cement of these structures is sometimes even bet-ter than exposing maneuvers, which may be fatal.In case of active hemorrhage despite tamponade,access to the retrohepatic segment may be obtainedby rotating the hepatic lobe to the right, after tran-section of the right triangular ligament, to reachthe lesions that appear from the right lateral side,or by rotating the left lobe, after transection of theleft triangular ligament, for those appearing fromthe left lateral side. These maneuvers greatly ben-efit from an extension of the median laparotomyby means of a right thoracophrenotomy and, evenbetter, by a vertical median sternotomy which of-fers an additional exposure of the intrapericardialIVC and the heart. The anterior side of the IVC,united with caudate lobe through multiple veins isinaccessible without dissecting the hepatic parenchy-ma. The context of these maneuvers limits the in-dications. In case of active bleeding from the an-terior side of the liver, it may be better to "fingerfraction" the liver parenchyma after clamping thehepatic pedicle (Pringle maneuver), which limitsthe bleeding. The nonviable tissues are removedprogressively to reach the IVC and to repair thelesion across the hepatic defect [25]. Numerousprocedures have been proposed in an attempt todry the operation field and to enable the repairof a lesion of the retrohepatic IVC. They all have

their pros and cons and deserve a more detaileddescription.

1) Vascular exclusion of the liver. Complete vascularexclusion of the liver, as proposed in traumatologyby Heaney et al. [26] in 1966, gives a dry operationfield. It consists of a quadruple clampage (Fig. 5),which comprises clamping of the vena cava, justabove the renal veins and at the intrapericardiallevel, after a previous total clamping of the aortawhere it emerges from the diaphragm, and follo-wed by clamping of the complete hepatic pedicle.Exclusion of the hepatic vasculature is limited bythe severity of the shock and the initial hypovole-mia. Without substantial filling beforehand, themain consequence of the quadruple clampage is anabolished venous return, which may cause arrhyth-mias and sudden cardiac arrest.

2) Atriocaval shunt. The blossoming of transplanta-tion techniques has facilitated the concept of shunt-ing in traumatic lesions of the retrohepatic IVC. In1968 Buckberg et al. [27] described the placementof a completely internal shunt. This shunt, placedbetween the juxtarenal IVC and the right atrium,was combined with selective perfusion of the he-patic pedicle. The flow was maintained by meansof a cannula inserted in the retrohepatic IVC iso-lated between two tourniquets. In the same year,Schrock et al. [28] reported on the use of a shunt,similar to the one of Buckberg, in a case with atrauma to the liver and SHV, introduced via a rightthoracoabdominal approach, from the right atriumto the juxtarenal IVC. The subsequent modifica-tion made by Fullen et al. [29] in 1974, is the sys-tematic approach of traumatic lesions of the retro-hepatic IVC through a median sternolaparotomy.This approach enables the easy introduction of theatriocaval shunt across a pocket made onto theright atrium, and facilitates hepatic mobilizationmaneuvers. The most frequently used shunt is a sim-ple thoracic drain with a large caliber (higher than32F) in which an additional lateral orifice shouldbe cut to allow for the blood to return to the rightatrium. Finally, the retrohepatic IVC is excluded byclosing the infrahepatic and intrapericardial tourni-quets. The upper end of the drain exteriorizedfrom the right atrium is of course clamped, but mayalso be used to administer substantial intracardialtransfusions. The use of a large-caliber endo-tracheal tube (superior to 9 mm), in which a lat-eral opening is cut, seems in our view to offer ad-ditional advantages (Fig. 6). Its curvature allows itsintroduction while pushing on the posterior side of


FIG. 5 Vascular exclusion of the liver through quadru-ple clamping. First the aorta is clamped, followed byclamping of the hepatic pedicle, the suprarenal venacava, and the intrapericardial vena cava.

the FVC without inserting it into a SHV or exteri-orizing it via the opening of the caval injury. In ad-dition, the distal balloon which ensures the water-tightness at the level of the juxtahepatic FVC,renders unnecessary the direct inspection of it. Inall cases the administration of heparin is not nec-essary. Despite its apparent simplicity, the atriocav-al shunt has not really brought the desired beneficein caval traumatology. In various series, very highmortality rates (80% to 100%) were found despitethe use of a shunt [30]. On the basis of the NorthAmerican literature between 1971 and 1996, Carret al. [9] showed a survival of only 29 patients outof 90 who were treated with a shunt, i.e., a mor-tality rate of 68%. The majority of these failures

20201

FIG. 6 The usage of an endotracheal balloon tube as atrio-caval shunt to treat traumatic lesions of the retrohepaticinferior vena cava.


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were due to massive bleeding when the shunt waspositioned. The other failures were mainly causedby a late decision to place a shunt in an alreadyexsanguinated patient, and the occurrence of amassive gas embolization, a perforation of the IVCor, more rarely, a thrombosis of the shunt.

3) Cavo-atrial balloon shunt. The disappointingresults of the atriocaval shunt have led to the intro-duction of balloon shunts, inserted via a saphe-nofemoral route, which has a number of lateralorifices that drain the blood from the juxtarenalIVC to a single distal axial opening [31] (Fig. 7).Inflation of a circumferential balloon, localized afew centimeters away from the distal end of theshunt, enables internal tamponade of the cavallesion. Placement of this shunt can be performedbefore the laparotomy, although the positioning ofthe balloon is rather uncertain. The main advan-tage is that it does not require a sternotomy. It isessential to fill the balloon with water to avoid anyrisk of embolization in case of rupture. The risk ofintrashunt thrombosis is not averted as hepariniza-tion is not usually done in this kind of injury.

4) Hypothermic circulatory arrest and active venove-nous shunting. The place of extracorporeal circula-tion (ECC) techniques in retrohepatic IVC injuriesis limited. Initially proposed in cases with major he-patic trauma, ECC allows for a hypothermic circu-latory arrest in order to obtain a completely clearoperation field [32,33]. High-dose heparinization,which is a prerequisite for this technique, is oftencontra-indicated in case of multiple other lesions.For this purpose the use of active venovenous shunt-ing has been proposed according to what was al-ready in use for certain hepatic transplantations[34]. Together with clamping of the caval vein onboth sides of the liver and clamping of the hepaticpedicle, this kind of shunting via a saphenofemoralapproach allows drainage of the caval territoryand, for some, the portal area distal the inferiormesenteric vein. Venous return to the heart is ac-complished via the internal jugular or axillary vein.

Powered by a pump, this shunt requires onlysmall dosages of heparin (50 lU/kg), but needssome installation time, like the conventional ECC,for access, placement of the cannulas and installa-tion of the circuit. These two techniques do notyield control over the initial bleeding and are rarelyused in the end. They do not make initial hemo-stasis redundant by means of compression. Theirapplication requires a stabilized hemodynamic sit-uation. The true aim is to enable a direct repair of

the retrohepatic IVC in a dryer operation field. Sim-ilar to the procedure for the infra or juxtarenalIVC, direct closure is preferred. Complex recon-structions at this level should remain an exception.The reconstruction of an IVC lesion at a juncturepoint of an SHV may require a venous or pericar-dial patch. In these cases downward retraction ofthe liver is often sufficient to expose the lesion,especially when it is located at the end of the leftSHV. It should be replaced by standard rotatorymaneuvers.

FIG. 7 Scheme of a cavo-atrial balloon shunt introducedvia the saphenofemoral route. The balloon, inflated atthe level of the retrohepatic caval lesion, ensures thehemostasis.


JUXTADIAPHRAGMATICAND INTRAPERICARDIAL IVC

The short juxtadiaphragmatic and intrapericar-dial segments of the IVC form the end of it. Itsanatomical situation makes it subject to penetratingtrauma and closed deceleration injuries. In the lat-ter, the heart is violently pushed forward and some-times undergoes a rotation around its venous axis,which induces an avulsion of the IVC at the dia-phragmatic orifice. The sudden occurrence of a car-diac tamponade due to a massive hemopericardiumrapidly leads to death and explains why these le-sions are so rarely seen in practice. A global reviewin 1990 [35] reported on 15 of these cases (7%)of 219 IVC traumas of which 8 (53%) were lethal.

Access to the terminal segment of the IVC is eas-ily made through a median sternolaparotomy. A lon-gitudinal median opening of the pericardium alongthe right atrium exposes the IVC at its cavo-atrialjunction. Digital control of the lesion is commonand may also be obtained by means of a Satinskyclamp. Vascular exclusion of the liver, an atriocavalshunt or ECC may be performed. Direct closure isthe ideal mode of venous repair. Interposition of ashort prosthetic tube or reconstruction by means ofvenous or prosthetic patch is rarely used. A com-plete transection of the IVC may be repaired via atransatrial route using ECC under the condition thatthe stump of the juxtadiaphragmatic IVC has a suf-ficient length and solidity. In one case [36] wherethe proximal stump was retracted into the hepaticparenchyma, the reconstruction was performed intwo sessions, consisting of a double ligation of theIVC, followed by an interposition of a re-inforcedprosthetic graft (22 mm) between the juxtarenalIVC and the right atrium. The 24-hour interval be-tween the sessions was used to stabilize the hemo-dynamic situation and correct the disturbed coagu-lation and hypothermia, while the abdomen wasonly partially closed by means of a mesh attachedto the borders of the laparotomy incision to mini-mize the intra-abdominal pressure while the juxta-diaphragmatic IVC was ligated. In another case [37]an avulsion of the IVC occurred after a cardiac re-intervention using ECC, which was treated by meansof a triangular pericardial tissue transplant stitchedat a distance from the borders of the lesion.

SVC INJURIESTraumatic lesions of the SVC are mainly caused

by penetrating trauma. The surviving patients,mainly described as case reports, are few [38]. latro-

genic perforation of the SVC caused by an endo-luminal procedure is usually less severe. A mediansternotomy is the preferred approach in these in-juries. The presence of a right hemothorax suggestsan avulsion of the azygos vein, which is better ex-posed via a right thoracotomy. The main difficultyin the exposure is related to the amount of bleed-ing from a low-pressure circulation with a very highflow. Lateral closure, performed under digital con-trol or after placing a lateral Satinsky clamp, is thetechnique of choice. The urgency of the situationdoes not justify the use of composed venous grafts.Replacement of an extremely damaged SVC mayrequire an autologous internal jugular vein or aguarded prosthetic graft.

INJURIES OF THE MAJOR BRANCHESIliac veins. Apart from the osseous trauma to

the pelvis, iatrogenic lesions from laparoscopic pro-cedures or maneuvers to obtain control at the com-mon iliac artery are the most common causes ofthis type of injury. Access to the iliocaval junctionand the distal ends of the iliac veins becomes dif-ficult due to the bleeding that quickly fills the pel-vic cavity. The best route is obtained via mobiliza-tion of the right colon, retaining it to the left ofthe aorta and the right common iliac artery, tran-sected between two clamps. The ureter is the onlycritical structure in this region. Hemostasis is obtain-ed by compressing the IVC with gauzes against thespine and the common iliac veins against the prom-ontory. Hemostasis of iliac vein injuries extendinginto the internal iliac veins is more difficult, becauseof their rich collateral circulation. Direct closure isstandard. A too extensive venous damage shouldbe treated with ligation of an iliac vein or iliocavaljunction. The large number of side branches be-tween the iliac veins and the reno-azygolumbar net-work explains why these ligations are usually welltolerated.

Renal veins. Injuries to the renal veins accountfor 8% to 12% of abdominal vascular injuries [5,23,39,40]. They occur in 6% to 13% of the IVCinjuries [10,23,38,41,42]. These veins are injured bypenetrating as well as by closed traumas. Iatrogenictrauma of the left retro-aortic renal vein duringabdominal aortic surgery, should be avoided bycareful analysis of the pre-operative computed tomo-graphy (CT) scan. Surgical exploration of retro-peritoneal peri-renal hematomas is not justified inthe case of a closed trauma, until an intravenous

203


204

pyelography, a renal angiogram or a CT scan in astable patient have shown a normal renal excretion.In contrast, surgical exploration of peri-renal pen-etrating injuries is standard.

The right renal vein is accessed by means of mo-bilization of the duodenum and colon. The leftrenal vein is approached via a median longitudinalincision of the retroperitoneum. To reduce thebleeding it may be useful to control and clamp therenal arteries. A lateral closure, performed underdigital control, either after clamping the injuredvein or after lateral clamping of the IVC at its os-tium, can most often be realized. If ligation of theright renal vein is necessary, one should choose be-tween a nephrectomy and a renal autotransplan-tation if the hemodynamics allow for it. Ligationof the left renal vein is well tolerated as long as thecapsular and genital veins are spared.

Azygos vein. The azygos vein can be injuredthrough penetrating and closed traumas. A massivehemothorax is common and indicates an approachvia a right thoracotomy. The bleeding can be en-hanced while spreading the ribs. There is a con-siderable risk of air embolization, which is why oneshould opt for an initial compression maneuverrather than excessive aspiration of the operationfield. Final treatment consists of ligation of the azy-gos vein with lateral closure of the SVC when it iscontrolled by a Satinsky clamp.

Venous brachiocephalic trunk. The right andleft venous brachiocephalic trunks join to form theSVC. A lesion at this level may extend into the SVC.In practice, the left trunk is the most affected be-cause of its length and its tract, which crosses themedian line and is exposed particularly during ster-notomies for cardiac procedures. Ligation is welltolerated without any sequelae.

Postoperative measures

Whether the lesion of the IVC is repaired, lig-ated or simply compressed, certain measures mustbe taken to prevent thrombo-embolic complicationsresulting from stasis of blood in the lower part ofthe body. These comprise elevation of the legs, elas-tic compression and antithrombotic drugs. Thereis no consensus on the anticoagulation regimen.Late sequelae, such as deep venous insufficiency,are rare regardless of the treatment chosen.

FOLLOW-UP ANDPROGNOSTIC FACTORS

In nearly 50% of cases, patients suffering from atraumatic lesion of the IVC die before any treat-ment is given. The results of 20 series in the liter-ature, comprising 2032 operated patients, are pre-sented in the Table [4,5,9-13,19-24,40-46], whichshows that the mortality rate for all the differentlocations is 44% on average, ranging from 21% to75%. No improvement is clear with time, despite asubstantial progression in treatment options. Nev-ertheless it is plausible that the improvement of col-lection and transport of the wounded has led tothe operation of more and more diseased patients.Death occurs mostly within 24 hours. In morethan 90% of the cases this is due to massive bleed-ing, mainly during attempts to explore and repairthe damage. During the early follow-up period, thebleeding induces an irreversible disseminated intra-vascular coagulopathy. Multi-organ failure or a sep-sis, often related to intestinal lesions, are the othermajor causes of death after this period. The pres-ence of shock on arrival, the existence of concomi-tant lesions, especially of the aorta, the closed char-acter of the trauma [19,20,38], absent spontaneoushemostasis of the lesion and the retrohepatic orjux-tadiaphragmatic localization are significantly asso-ciated with a poor outcome.

We observed a mean mortality rate of 69% (42%and 100%) in 17 series comprising a total of 344 pa-tients operated for a retrohepatic lesion of the IVC(Table). In comparison, the mean mortality rate incase of an infrarenal lesion of the IVC is estimatedat 24.5% [46]. The mortality rates of traumatic le-sions of the SVC and the azygos vein surpass 50%[47]. That of the iliac veins is estimated at a meanof 25%, ranging from 10% to more than 40%, de-pending on whether accompanying vascular lesionsare present. Finally, renal vein lesions are mortalin 12% to 30% of the cases and up to 50% whenother vascular lesions are present [11,40,46].

The most frequently reported complications,whichever localization of the trauma, are respirato-ry complications (pulmonary embolism, pneumo-nia, respiratory insufficiency), abdominal infectionsand collections (subphrenic and parietal abscesses,peritonitis, pancreatitis, etc.), thoracic infections(mediastinitis), renal complications (renal insuffi-ciency, venous thrombosis) and intestinal compli-cations (gastroduodenal ulcers, ileus). The long-term prognosis of the patients surviving the acuteperiod is, however, excellent.


1st author[ref.]

Turpin [24]

Graham [5] *

Byrne [43]

Wright [4]

Sirinek [41]

Millikan [44]

Berguer [22]

Stewart [23]

Wiencek [45]

Burch [10] *

Klein [21]

Leppaniemi [13]

Feliciano [46] *

Ombrellaro [20]

Rosengart [19]

Kuehne [12]

Hansen [42]

Asensio [11]

Carr [9]

Davies [40]

Total - Mean(range)

Year

1977

1978

1980

1981

1983

1983

1985

1986

1986

1988

1994

1994

1995

1997

1999

1999

2000

2001

2001

2001

OverallNumber Deaths

(%)

34

301

26

82

51

58

54

77

67

276

38

23

495

27

37

136

47

77

38

88

2032

53

37

38

23

65

38

59

30

57

37

21

39

29.5

48

51

52

55

75

28

43.5

44(21 - 75)

Retrohepatic IVCNumber Deaths

(%)

9

69

2

NS

NS

12

11

6

15

36

12

3

88

12

9

36

9

12

3

NS

344

77

60

100

NS

NS

83

73

67

60

64

42

66

42

67

78

83

66

100

43

NS

69(42 - 100)

* Series from the same centerIVC: inferior vena cavaNS: not specified

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38 Kudsk KA, Bongard F, Lim RC Jr. Determinants of survival aftervena caval injury. Analysis of a fourteen-year experience. ArchSwrg 1984; 119:1009-1012.

39 Jackson MR, Olson DW Beckett WC Jr et al. Abdominal vasculartrauma: a review of 106 injuries. Am Surg 1992; 58: 622-626.

40 Davis TP, Feliciano DV, Rozycki GS et al. Results with abdominalvascular trauma in the modern era. Am SurgWQl', 67: 565-571.

41 Sirinek KR, Gaskill HV 3rd, Root HD, Levine BA. Truncalvascular injury: factors influencing survival./ Trauma 1983; 23:372-377.

42 Hansen CJ, Bernadas C, West MA et al. Abdominal vena cavalinjuries: outcomes remain dismal. Surgery 2000; 128: 572-578.

43 Byrne DE, Pass HI, Crawford FA Jr. Traumatic vena cavalinjuries. Am}Surg 1980; 140: 600-602.

44 Millikan JS, Moore EE, Cogbill TH, KashukJL. Inferior vena cavainjuries: a continuing challenge. JTrauma 1983; 23: 207-212.

45 Wiencek RG Jr, Wilson RF. Inferior vena cava injuries: thechallenge continues. Am Surg 1988; 54: 423-428.

46 Feliciano DV. Truncal vascular trauma. In: Callow AD, Ernst CB(eds). Vascular surgery. Theory and practice. Stamford, Appleton &Lange, 1995: pp 1059-1085.

47 Mattox KL. Thoracic vascular trauma.} Vase Surg 1988; 7: 725-729.

ACUTE ISCHEMIA OF THE UPPER LIMB

JOSE GONZALEZ-FAJARDO, MIGUEL MARTIN-PEDROSALOURDES DEL RIO, CARLOS VAQUERO

Acute ischemia of the upper limb is seen infrequently compared with events in the leg. Ingeneral, occlusion of a major artery in the upper limb is better tolerated than in the lower limb,possibly because the potential for the development of an extensive collateral blood flow, but alsobecause the bulk and work rate of the muscles of the arm are considerably less than those of ZiLthe leg. Failure to recognize a critical arterial injury, however, can result in disabling ischemic 207symptoms including cold intolerance, claudication, and pain. Acute arm ischemia can becaused mainly by embolism, thrombosis, or trauma, although other vascular disorders (e.g.,drug abuse, arteritis, thoracic outlet syndrome, hypercoagulable states) may contribute to thedevelopment of upper extremity arterial insufficiency. Today, iatrogenic brachial arterialcatheter injury secondary to coronary and peripheral vascular procedures is the most commoncause of direct arterial injury requiring surgery. Although there is some controversy about howaggressively acute arm ischemia should be treated, particularly when the arm appears viable,current management is aimed at restoring arterial inflow to the limb. Functional integrity ofthe upper limb, and more specifically the hand, is essential for daily activity, and theconsequences of impaired function or amputation of an arm are disastrous, with loss ofindependence and/or livelihood.

This chapter reviews the evidence on acute upper limb ischemia in the literature, anddescribes the management strategies for the treatment of traumatic and atraumatic acuteocclusions of the upper limb extremity.

thrombosis, and trauma [1]. The incidence ac-counts for a mean of 16.6% (range 7% to 31.5%)

Acute ischemia of the upper limb may occur se- of cases of acute ischemia of the limbs [2]. Thesecondary to a variety of causes, including emboli, patients usually tend to be older than those with


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leg ischemia, and females present a slight prepon-derance in both observational and operative series.

EMBOLISMEmbolism is considered the most common cause

of acute arm ischemia (74%) [2]. The emboli areattributed to a variety of sources.

Cardiac embolism is the most frequently report-ed cause of acute arm ischemia (58% to 93%) [2-5] and atrial fibrillation is the usual etiology. Overthe years the incidence of atrial fibrillation has re-mained fairly constant although the cause of fib-rillation has changed from valvular heart disease asa result of rheumatic fever to ischemic heart dis-ease and myocardial infarction. Rare causes includeendocarditis, atrial myxoma, ventricular aneurysm,cardiac failure, and paradoxical embolism [2].

Non-cardiac embolism determines 1% to 32% ofthe acute arm emboli [2-5]. Proximal upper limbstenosis caused by atherosclerotic plaque or exter-nal compression (cervical ribs) can result in throm-bo-embolism or atheroembolism, which may causelarge vessel occlusion or acute digital ischemia.Other causes include atheroma in the aortic arch,primary subclavian aneurysm or aneurysm second-ary to extrinsic compression from thoracic outletsyndrome, old fracture, and chronic trauma suchas that from the use of crutches. Rarer sources arethe proximal end of an occluded axillofemoralgraft, arteritis, malignant emboli, and fibromuscu-lar dysplasias [2]. Despite a classic embolic presen-tation and operative findings, an embolic sourcemay not be found in at least 12% of patients.

THROMBOSISReports suggest that 5% of cases in population

studies and 9% to 35% in surgical series are due tothrombosis [2-5]. Jivegard et al. [6] estimated thatin patients who had embolectomy, the chance ofthrombosis being the true cause was 5.5% in thearm. Most of the proximal arterial lesions that cancause emboli can also result in thrombosis, includ-ing atherosclerotic plaques, aneurysm, acute aorticdissection, and arteritis (Takayasu's disease) [2].

Atherosclerosis in the upper extremity appears es-pecially prominent in older men. The disease maybe at the origin of the great vessels or distally in theaxillary or brachial arteries. Aneurysms of the sub-clavian or axillary arteries may also result in upperextremity ischemia through two mechanisms. Theymay directly cause ischemic symptoms by thrombo-

sis or by producing emboli that occlude the distalcirculation (Raynaud's phenomenon) [5].

Less common causes include arteritis from con-nective tissue disorders (scleroderma), radiation ar-teritis, hyperthrombotic conditions and thrombosisassociated with malignancy or steroid use [5].

TRAUMATrauma is responsible for 15% to 45% of cases of

acute arm ischemia [5,7], This ischemia may resultfrom blunt or penetrating injuries. In penetratinginjuries, especially from high-velocity missiles, theartery can be damaged either by direct penetrationor by shattering of bone. These injuries usually leadto complete transection of the artery with retrac-tion of the damaged ends of the vessel and subse-quent thrombosis, thus limiting blood loss but pro-ducing severe distal ischemia. Although penetratinginjuries can be caused by bullets and knives, cur-rent brachial artery injury secondary to cardiac orperipheral vascular catheterization is probably themost common cause of direct arterial injury re-quiring surgery.

In blunt trauma, vascular injury can be mediatedby joint dislocation or fracture. These injuries mayproduce severe longitudinal vessel traction by com-pression or laceration leading to intimal disruption,subintimal hematoma, and subsequent thrombosis.Because of the possibility of intimal damage caus-ing delayed arterial occlusion, arteriography maybe indicated in select instances of this type of injury.

latrogenic arterial trauma. With the increa-sing performance of percutaneous transluminal an-gioplasty and insertion of intravascular devices, therisk of acute upper ischemia has increased in re-cent years [8], occurring in less than 1% of all bra-chial catheterizations. The acute arterial occlusionis the result of intimal flap or dissection from wireor catheter manipulation. The risk of thrombosisis increased if the procedure is therapeutic or ifthe catheter is left in place for long time. Surgicaltreatment is frequently indicated, and unless theischemia is mild, observation for improvement inadults is inappropriate. Early repair under localanesthesia followed by simple thrombectomy andclosure is satisfactory in most cases. Occasionally,patch angioplasty or segmental resection and anas-tomosis can be necessary. On the other hand, can-nulation of the radial artery for pressure monito-ring causes occlusive thrombosis in 10% to 20% ofpatients, most of which do not result in distal is-


chemia because of the rich collateral network inthe hand [9].

Vascular trauma associated with fracturesand dislocations. Associated vascular injury inthe context of general orthopedic trauma is quiteinfrequent (3.8% to 6.5%). However, the incidencedoes vary remarkably with the type of orthopedicinjury encountered, being extremely rare in mid-shaft long-bone fractures but much more frequentwith joint dislocations [10]. Given that the closeran artery lies to a bone, the more likely it is to beinjured, the majority of vascular injuries associatedwith blunt trauma affect the brachial artery justabove and below the antecubital fossa in the upperextremity.

Blunt arterial injuries of the shoulder.Although vascular injury associated with blunt trau-ma about the shoulder is uncommon, it can be de-vastating. The mobility of the shoulder allows trac-tion and avulsion of the underlying vascular andneurological structures with sometimes relativelyminor bony injury. Typically, arterial injury in theshoulder area presents as a pulse or blood pres-sure deficit with associated shoulder or supraclavi-cular hematoma. The degree of ischemia is oftennot severe because of good collateral circulation,but there is often a distal neurological deficit caus-ed by brachial plexus injury (Fig. 1). Furthermore,when brachial plexus injury occurs, the incidenceof vascular injury is high (approximately 35%), andassociated arterial injury should be carefully inves-tigated [10].

Arteriography is important in these injuries todetermine the presence and, more importantly, thelevel of the injury. Often, proximal control can beobtained through a supraclavicular approach.

Blunt arterial injuries of the elbow. Supra-condylar fractures and elbow dislocations are themost common injuries associated with blunt traumain the upper limb. A review by Bunt et al. [11] sho-wed a 3% incidence of vascular injury with supra-condylar fractures and a 10% incidence with openelbow dislocations. Dislocation of the joint or directsupracondylar fracture essentially bow-strings theartery, and the resultant traction leads to intimaldisruption or even transection.

Clinical examination including documentation ofpulse by palpation and doppler will identify mostvascular injuries. However, because of extensive col-lateral flow around the elbow, up to 10% of patients

with upper limb arterial injuries have preserved dis-tal pulses [7,9,10].

When these fractures or dislocations present withobvious distal ischemia, emergent reduction is re-quired. If perfusion is immediately restored with fullpulses equal to the contralateral limb, the limb canbe observed. Occasionally, reduction will improveperfusion but a pulse will not return. In these cases,angiographic assessment should be performed.

The major morbidity with brachial artery injuriesis attributable to the associated nerve injuries thatoccur twice as frequently in the traumatized upperlimb as in the lower limb. Thus, although viabilityis maintained by vascular repair, functional out-come depends mainly on the nerve injury.

FIG. 1 Twenty-five-year-old man with blunt impact of theleft shoulder. The patient had a pulseless and cool left armwith brachial plexus deficit secondary to the joint disloca-tion. Angiogram shows occlusion of the proximal axillaryartery and reconstitution of the proximal brachial artery. Atoperation, the axillary artery was badly contused and wasrepaired with saphenous vein bypass graft.

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MISCELLANEOUS CAUSESlatrogenic intra-arterial injection. Acute

ischemia of the upper extremity after intra-arterialdrug injection is rare. Its treatment is frequentlyunsuccessful and its prognosis is usually poor, oftenleading to gangrene. This complication is rarelyseen iatrogenically [12] and is most frequently seenin intravenous drug abusers. Digital artery throm-bosis is the final common pathway in the genera-tion of critical ischemia and necrosis, which maybe immediate or delayed. Different mechanismshave been suggested for this, including vasocon-striction, crystal formation of the drug in small ves-sels, mechanical obstruction by constituents orimpurities, direct cytotoxicity, intimal damage, sta-sis, and thrombosis. Other factors that affect theamount of tissue damage are the dose and thenature of substances being injected.

Arterial injury secondary to drug abuse.Vascular injury associated with drug abuse is a chal-lenging problem of relatively recent origin. Its mani-festations in the acute setting are frequently catas-trophic [13]. The most common site of inadvertentarterial injection in drug abuse has been the ante-cubital fossa. Diagnostic studies should includecolor-flow duplex scanning. Arteriography is not ad-visable because it may exacerbate vasospasm and in-timal damage without changing the course of the-rapy. Because clotting and obstruction begin in thesmall arterioles and can progress to involve moreproximal vessels, systemic anticoagulation is indica-ted in an effort to retard the process and preventfurther tissue loss. Lytic therapy is not advisable be-cause this may exacerbate extravasation, which hasbeen well documented in experimental models,and contributes to the development of a compart-ment syndrome. Intravenous papaverine, prostaglan-din Eg, or iloprost may also be helpful. Prophylacticantibiotics are recommended to prevent infectionof compromised soft tissues.


The symptoms and signs of acute ischemia in theupper limb are the same as those for the lower limband are traditionally called the six P's: pain, pallor,paralysis, paresthesia, pulselessness, and perishing cold[I]. The patient usually complains that the limb hassuddenly become lifeless and numb with a variabledegree of pain. The severity of the symptoms de-

pends on both the acuteness of the episode and thelocalization of the occlusion. Subsequent develop-ment of ischemic changes depends on the efficiencyof the collateral circulation around the shoulderand the elbow. The most common sites of upperlimb occlusion are the axillary and brachial arter-ies, consistent with the likely sites for embolic oc-clusion. If acute changes are confined solely to thehand, it is likely that the distal vessels are affectedor that there is a microvascular phenomenon.

Diagnosis

A careful history and physical examination oftensuggests a diagnosis or at least eliminates a numberof disease categories [1]. A history of ischemic heartdisease or recent myocardial infarction is of para-mount importance. Thrombosis in an unusual sitesuch as the axillary artery is more likely to give riseto acute symptoms and in these cases an identifiablefactor may be present in the history, e.g., radiationfor breast cancer or a thoracic outlet syndrome.

The differential diagnosis with thrombosis is im-portant because treatment of the latter frequentlyrequires bypass surgery [3,4]. In general, the moreproximal the lesion, the more likely thrombosis isthe cause of the acute ischemia, especially if thereis evidence of previous Raynaud's-like symptomsdue to distal embolization [2].

This information allows for selection of the bestnon-invasive diagnostic work-up. Initial evaluationconsists of pulse palpation and segmental dopplerpressure measurement on the involved as well asthe uninvolved extremity. The most reliable physi-cal sign of acute ischemia is the absence of pulsesin the affected limb in the radial and ulnar arter-ies at the wrist or the brachial artery in the ante-cubital fossa [1]. The arterial pulse should be pal-pable in the vessels proximal to the occlusion andin the opposite unaffected limb. The distributionof pulses will provide information about the levelof the occlusion.

Arterial occlusion caused by blunt trauma, frac-tured bones, joint dislocations, or prolonged ex-trinsic pressure can be recognized by a reductionin arterial pressure distal to the site of the injury(Fig. 2). In these circumstances, it must be empha-sized that the presence of an audible doppler sig-nal or even a palpable pulse does not exclude aninjury, because collateral development may con-tinue to supply some blood flow to the peripheral


tissues [7,9,10]. Careful pressure measurements arenecessary to avoid overlooking a potentially disas-trous injury. A duplex scan should be obtainedwhenever there is doubt. Depending on the clini-cal presentation, the nature of the trauma, and theuncertain duplex diagnosis, arteriography can beconsidered.

Management strategies

Surgical intervention remains the most reliablemethod of restoring arterial inflow to the acuteischemic limb. Conservative treatment will leaveone third of patients with an unsatisfactory out-come, and even accounts for an amputation rate

FIG. 2 Supracondylar fractures and elbow dislocations arethe most common injuries associated with acute upper armischemia.

of 6% [1]. The only centra-indications to surgeryare inoperatibility (serious medical condition thatprecludes surgical intervention even under localanesthesia) and distal emboli extended to sidebranches that are inaccessible for balloon embolec-tomy or thrombectomy. These patients are bettertreated with anticoagulation and vasodilators. Thedanger of significant disability from an emboluslodging in the radial or ulnar artery is minimal andoperation is not warranted for an embolus in thisarea [1].

NON-TRAUMATIC ACUTE ISCHEMIAOF THE UPPER LIMB

Pre-operative evaluation. The difficulty in thetypical case of acute arterial ischemia relates to dis-tinguishing an embolic from a thrombotic occlu-sion. A pre-operative arteriogram is not indicatedin a clear-cut case of embolism but may be usefulin making the distinction between thrombosis andembolism and in planning an operative strategy. Aninappropriate embolectomy or thrombectomy isassociated with high morbidity and mortality rates[2]. However, the delay in getting to the operatingroom must be balanced against the possible bene-fit of this test.

Pre-operatively, the patient should be given ade-quate analgesia and 5 000 units heparin intrave-nously. Successful embolectomies can be performedeven after several days of symptoms; there is norigid time criterion for surgical intervention. Thetime of ischemia is not as critical as the status ofthe extremity. An arm that remains viable for sev-eral days after embolization usually has an intactdistal circulation, enabling restoration of flow byembolectomy at this later stage.

Embolectomy. The patient is placed supine onan operating table and the affected limb, axilla, andupper chest are prepared with antiseptic solutionand draped. Local anesthesia with an anesthesio-logist monitoring is the best and safest way to beginan embolectomy. Mild sedation can be used if ne-cessary. The brachial artery is exposed through anS-shaped incision over the antecubital fossa. Furtherdissection will expose the biceps tendon, the me-dian nerve, and the brachial artery. The arteryshould be dissected out to reveal its division intoradial and ulnar branches and all three vesselsshould be controlled with rubber slings or arterialclamps. This is supported by Beckingham et al.[14], who were able to cannulate only one artery

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of the forearm in 42% of occasions using a bra-chial arteriotomy and conventional embolectomycatheter. A transverse incision in the brachial arte-ry is preferred to prevent narrowing when the ar-teriotomy is repaired. A Fogarty catheter should bepassed proximally to restore inflow and then dis-tally down both the radial and ulnar arteries untilback-bleeding is obtained. Following this, the ves-sels should be flushed with heparinized saline so-lution and the arteriotomy closed with 6/0 prole-ne. After release of the clamps, the radial pulseshould be palpable at the wrist. Postoperatively thepatient should be fully heparinized. Long-term anti-coagulation should be routine after embolectomyunless there are medical contra-indications, parti-cularly when the heart is the source as there is ahigh risk of recurrent embolism. Anticoagulationnot only reduces the rate of recurrence, but alsoreduces postoperative mortality.

OPERATIVE ADJUNCTSFailure to restore the radial pulse is a string in-

dicator of poor outcome. In this situation, treat-ment options include repeat embolectomy, use ofintra-operative thrombolysis [15], or peri-operativeangiography to identify any residual occlusion or ar-terial lesion. When the source of emboli is a proxi-mal arterial lesion, definitive surgery or angioplastymay be required, either at the same time as embo-lectomy or later. If adequate inflow to the brachialartery is not achieved, we prefer to delay the op-eration to a second stage with general anesthesia,because the technical procedure should be tailoredto the particular cause. Acute ischemia resultingfrom thrombosis has a poor outcome if treated bysimple catheter thrombo-embolectomy and is morelikely to require reconstructive surgery [2-4].

Today, an atherosclerotic stenosis of the subcla-vian or axillary artery is managed by angioplasty,with or without stenting. Occasionally, surgical by-pass may be required if angioplasty is unsuccessful.Proximal lesions can be dealt with by anatomicalor extra-anatomical grafting, while saphenous veinbypass to distal arm arteries is effective for selecteddistal occlusions [2-4]. Vascular throracic outletcompression is a clear indication for relieving sur-gery, since the extrinsic compression can be thecause of occlusion or distal embolism [16]. In thesecases, poststenotic subclavian aneurysms require re-section and grafting to prevent recurrent embolism(Fig. 3).

MEDICAL THERAPYThere is no universally accepted treatment pro-

tocol. Rest, analgesia, and heparinization are re-commended. Some patients improve on heparinalone. The mainstays of treatment are aimed atimproving the microcirculation. Regional nerveblocks, stellate ganglion blocks, and sympathec-tomies have been performed in the past for painrelief but do not improve the eventual outcome.The use of thrombolytic agents in the treatment ofpatients with acute upper arm ischemia seems tobe an effective means of removing thrombus fromoccluded vessels. However, the potential value ofthis technique has been documented in small serieswith limited long-term follow-up data [17].

Heparinization and vasodilators have been widelyused to reverse the thrombotic process and maxi-mize the surviving circulation. Recently, iloprost(prostacycline, a prostaglandin inhibitor) and pros-taglandin Eg have shown be a useful adjunct medi-cal therapy [12].

TRAUMATIC ACUTEISCHEMIA OF THE UPPER LIMB

Pre-operative evaluation. Given that vascularinjuries associated with limb fractures and disloca-tions are usually caused by high-energy trauma, thesurgical dictum of life before limb prevails in the treat-ment of these injuries. When significant upperextremity ischemia coexists with a life-threateningcervical, thoracic, or abdominal injury, such lesionsmust be initially treated before initiating definitivetreatment for any extremity. These patients demanda well-organized multidisciplinary approach forappropriate care [18]. In this regard, we have foundthat it is best to have orthopedic and vascular sur-geons present in the room during the entire ope-ration. This frequently allows the orthopedic teamto choose their fixation devices in such a way thatthey will not hinder or complicate the subsequentvascular repair.

Precise and prompt diagnosis of arterial injury isparamount in order to ensure limb viability. In mostcases of penetrating or blunt arterial trauma, pre-operative diagnostic arteriography is not necessary.However, surgical exploration may not be sufficientfor precise location of the extension of the arterialdamage in all cases. An arteriogram, for example,is especially useful in defining shotgun blast injuriesin which there is a wide distribution of pellets orin patients with extensive hematoma or compart-


ment syndrome associated with fractures and dis-locations [7,10].

Operative preparation. The operative prepa-ration of the patient for combined and orthopedicrepairs is conducted in a standard fashion regard-less of whether arteriography has been perform-ed pre-operatively or will be performed during theoperation. In these cases of upper extremity inju-ries, at least one lower extremity is prepared anddraped to allow vein harvesting, if necessary.

Sequence of repair. Although the sequence ofvascular repair and fracture stabilization remains

FIG. 3 Severe acute ischemia of the upperlimb in a youns patient with a cervical rib.Angiography shows thrombosis of the axil-lary artery and reconstitution of the bra-chial artery through collateral flow (A).

unclear, orthopedic stabilization and immobiliza-tion should precede vascular repair in almost allpatients. This is desirable for two reasons [7]:1 - if orthopedic reduction and stabilization are per-formed after vascular repair, the necessary mani-pulation and traction may place the previously per-formed vascular repair under excessive tensionleading to disruption;2 - it allows the vascular surgeon to debride soft tis-sue that has been injured and route the bypass graftthrough uninvolved tissue planes without fear thatsubsequent orthopedic repair will expose or injurethe vascular repair.

Operative repair. After administration of intra-venous antibiotics, the injured vessel is approachedthrough a longitudinal incision. Proximal and dis-tal control is established away from the focus of thelesion, using vessel loops, and the traumatized seg-ment is then isolated and exposed. A survey of asso-ciated venous and nerve injuries as well as the extentof soft tissue injury is also undertaken. The vesselwall adjacent to the fracture site should be carefullyevaluated for any sign of contusion. Afterward, aballoon embolectomy catheter should be used rou-tinely for clearing all possible distal thromboticmaterial, and loco-regional anticoagulation withsaline heparinized solution should be administer-ed. There are no reports of systemic heparinizationhaving an effect on outcome [19]. Although directend-to-end anastomoses are preferred by some

2J_213

This patient was treated during several yearsfor Raynaud's-like symptoms and upper limbdigital ischemia. Repeated trauma contribu-tes to the intimal damage and subclavianartery aneurysm (B).


21214

authors, our experience has been that the ends ofthe brachial artery retract readily and, hence, thisanastomosis tends to be under tension. It is ourpreference to use an interposition autogenous veingraft. The preferred conduit for repair of most arte-rial injuries is autologous greater saphenous vein[3,4]. The greater saphenous vein has an adequatediameter for most repairs of injured upper extre-mity arteries.

Associated venous injuries. Management ofconcomitant venous injuries in the upper extremityis less controversial than in the lower limb, becauseacute or chronic edema is unusual after ligation ofvenous injuries in conjunction with arterial repair,as confirmed by the experience of Timberlake etal. [20]. All venous injuries were handled by liga-tion in conjunction with the appropriate arterialreconstruction, and neither fasciotomies nor sub-sequent amputations were reported. Based on thisexperience, we recommend repair of concomitantvenous injuries in the upper extremity when tech-nically simple and ligation of extensive injuries thatwould otherwise require interposition grafting.

Soft tissue coverage. Vascular repairs absolu-tely require viable soft tissue coverage [10]. Failureto do so leads to graft infection and potentially life-threatening hemorrhage. Many combined arterialand bone injuries have associated extensive soft tis-sue destruction that, following debridement, leavesextensive defects. It is not advisable to perform ar-terial or venous repairs in the depth of such defectsbecause many of these wounds will require frequentdaily debridement of devitalized and infected tis-sue. This debridement may result in exposed graftsin the depths of the wounds and place them at riskof infection and graft blow-outs. When such woundsare encountered, it is preferable to debride andligate the injured vessels and perform arterialreconstruction using a saphenous vein bypass graft

originating from an uninvolved artery proximal tothe injury, routing this bypass through intermus-cular or subcutaneous tissue planes remote fromthe injured area, and performing the distal anas-tomosis distal to the injured area. This approachfrequently precludes the repair of associated venousinjuries, which in such cases should be ligated.

Ligation. Arterial ligation is more likely to beconsidered when these injuries occur very distallyin the limb and are associated with good collateralcirculation. This may be the case in isolated injuriesof single arteries of the forearm. Studies focusingon small vessel trauma have shown that outcome islimited not by the ligation or repair of the injuredvessel but by the frequent concomitant nerve injury.Evaluation of patency rates after repair of single-vessel lacerations reveals that 50% to 68% of thesevessels remain open at a minimum follow-up of fivemonths. It has been demonstrated that the remain-ing vessel in a single vessel forearm injury experi-ences a compensatory flow volume increase of 46%to 65% [9].

Fasciotomy. Distal pulse palpation or dopplerregistry must be obtained to ensure that an ade-quate functional result has been achieved. Imme-diate postoperative follow-up consists of neuromo-tor, neurosensory, and vascular evaluations withspecial attention to the development of early signsof compartment syndrome. When any significantdegree of increased compartment pressure is de-tected on physical examination, full-length com-partment fasciotomy is performed immediately. Ad-herence to this policy may lead to an occasionalunnecessary fasciotomy, but delay in performanceof fasciotomy until the signs of compartmentalhypertension are clearly evident frequently leads toirreversible muscle necrosis, nerve damage, andsignificantly decreased function in an anatomicallysalvaged extremity.

R E F E R E N C E S

1 Williams N, Bell PR. Acute ischaemia of the upper limb. BrJ

2 Eyers P, EarnshawJJ. Acute non-traumatic arm ischaemia. BrJSurg 1998; 85: 1340- 1346.

3 Katz SG, Kohl RD. Direct revascularization for the treatment offorearm and hand ischemia. Am/Swrg-1993; 165: 312-316.

4 Pentti J, Salenius JP, Kuukasjarvi P, Tarkka M. Outcome ofsurgical treatment in acute upper limb ischaemia. Ann ChirGpa««>n995;84:25-28.

5 Edwards JM, Porter JM. Upper extremity arterial disease:etiologic considerations and differential diagnosis. Semin Vase5u^ 1998; 11: 60-66.


6 Jivegard L, Holm J, Schersten T. The outcome in arterialthrombosis misdiagnosed as arterial embolism. Ada Chir Scand1986; 152: 251-256.

7 Schuler JJ, Meyer JP. Arterial injuries associated with extensivesoft tissue trauma. In: Ernst CB, Stanley JC (eds). Current therapyin vascular surgery, 2d edition. Philadelphia, B.C. Decker Inc1991: pp 636-643.

8 Nehler MR, Taylor LM Jr, Porter JM. latrogenic vascular trauma.Semin Vase Surg 1998; 11: 283-293.

9 Hammond DC, Gould JS, Hanel DP. Management of acute andchronic vascular injuries to the arm and forearm. Indicationsand technique. Hand Clin 1992; 8: 453-463.

10 Winkelaar GB, Taylor DC. Vascular trauma associated withfractures and dislocations. Semin Vase Surg 1998; 11: 261-273.

11 Bunt TJ, Malone JM, Moody M et al. Frequency of vascularinjury with blunt trauma-induced extremity injury. Am J Surg1990-160:226-228.

12 Samuel I, Bishop CC, Jamieson CW. Accidental intra-arterialdrug injection successfully treated with Iloprost. EurJ Vase Surg1993; 7: 93-94.

13 Cooper JC, Griffiths AB, Jones RB, Raftery AT. Accidental intra-arterial injection in drug addicts. EurJ Vase Surg 1992; 6: 430-433.

14 Beckingham IJ, Roberts SN, Berridge DC et al. A simpletechnique for thrombo-embolectomy of the upper limb. EurJVflscSi«gl990;4:173-177.

15 Gonzalez-Fajardo JA, Perez-Burkhardt JL, Mateo AM. intraope-rative fibrinolytic therapy for salvage of limbs with acute arterialischemia: an adjunct to thrombo-embolectomy. Ann Vase Surg1995; 9: 179-186.

16 Gelabert HA, Machleder HI. Diagnosis and management ofarterial compression at the thoracic outlet. Ann Vase Surg 1997;11:359-366.

17 Widlus DM, Venbrux AC, Benenati JF et al. Fibrinolytic therapyfor upper extremity arterial occlusions. Radiology 1990; 175:393-399.

18 Katsamouris AN, Steriopoulos K, Katonis P et al. Limb arterialinjuries associated with limb fractures: clinical presentation,assessment and management. EurJ Vase Endovasc Surg 1995; 9:64-70.

19 Pillai L, Luchette FA, Romano KS, Ricotta JJ. Upper extremityarterial injury. Am Swrgl997; 63: 224-227.

20 Timberlake GA, O'Connell RC, Kerstein MD. Venous injury: torepair or ligate, the dilemma. / Vase Swrgl986; 4: 553-558.

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22ACUTE COMPLICATIONS

OF ARTERIOVENOUS FISTULAFOR HEMODIALYSIS

VOLKER MICKLEY

In the immunocompromised and multimorbid dialysis patient, access complications can ZiZ/rapidly become life- or at least limb threatening. Access thrombosis should be treated urgently 217to prevent implantation of a central venous catheter for hemodialysis. In autologous fistulae,pre-operative clinical examination and color-coded duplex-sonography help to identify thecausative stenosis, whereas in grafts on-table angiography immediately after surgical orinterventional declotting is mandatory. Correction of the stenosis is an integral part of anydeclotting procedure. The endovascular surgeon would be the ideal partner for patients withthrombosed access, because he is free to choose the best interventional or surgical treatmentoption depending on the site and the extent of the obstruction.

Access infection must be taken very seriously because it can result in major bleeding andseptic complications. Immediate hospitalization, adequate antibiotic treatment, andconsequent surgical intervention often resulting in access abandonment are the only meansto reduce the otherwise high mortality rate. In the majority of patients with (pseudo-)aneurysmor peripheral steal syndrome, adequate pre-operative imaging and careful planning of theprocedure together with skillful surgical technique will allow for correction of the vascularpathology and at the same time result in preservation of access function.

Renal failure prevalence of 200 000 patients in Europe and grow-ing at a rate of about 8% per year. Due to the limi-

End-stage renal failure (ESRF) is one of the major ted availability of donor kidneys and to logistic andproblems in public health care with an estimated medical limitations of peritoneal dialysis, life-long


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hemodialysis remains the only treatment option forthe majority of ESRF patients.

The native arteriovenous fistula (AVF) has beenshown to provide the most reliable and durable ac-cess to the patient's bloodstream. Complicationrates are lower than those of arteriovenous grafts(AVG) and central venous catheters (CVC), and pa-tient survival is significantly longer, even when cor-rected for comorbidity [1,2]. However, when hy-poplastic or exhausted peripheral veins or severelydiseased peripheral arteries make construction of anautologous access impossible, a graft or even a cath-eter will be needed for starting or maintaining renalreplacement therapy.

Complications associated with vascular access area major cause of morbidity and mortality in hemo-dialysis patients. In particular, those acute compli-cations leading to failure of the access site (throm-bosis, infection) represent a direct threat to thepatient's life. Peripheral circulatory disturbances(aneurysm, steal syndrome) will at least endangerthe afflicted extremity. Timely and effective treat-ment is necessary, aiming at restoration and preser-vation of access function whenever possible.

Thrombosis

The most common complication of arteriovenousaccess for hemodialysis is thrombosis. One mightargue that acute occlusion of the access site is nota life-threatening complication, because it can bebridged with a CVC for hemodialysis until a plannedintervention the next day or even some days later.However, one must not forget that implantation ofa CVC is associated with a high rate of acute andlate complications. Depending on the site of cath-eter insertion, arterial puncture, hemothorax, pneu-mothorax, cardiac tamponade, and retroperitonealhematoma have been reported to occur at fre-quencies varying between 1% and 10% [3]. Evenmore important is the 40% to 50% risk of centralvenous obstruction after multiple or prolongedcatheterization of mediastinal veins causing dis-abling arm swelling when located centrally to a func-tioning access and often requiring complex radio-logical or extensive surgical corrective measures[4,5]. And, of course, there is a significant risk ofcatheter-associated bacteremia with high rates ofmetastatic complications and death in the immuno-compromised ESRF patient [3]. The well-known dis-

advantages and potential dangers of CVC for hemo-dialysis should be the main motivation for imme-diate declotting of a thrombosed access with cor-rection of any underlying stenosis in such a waythat the access can be used again for the next plan-ned hemodialysis session. Pre-operative CVC im-plantation should only be considered in patientswith severe electrolyte disturbances or hyperhydra-tion, when immediate hemodialysis is necessary.

The various surgical and interventional alterna-tives for the treatment of stenosed and thrombosedAVF and AVG are discussed extensively in an ear-lier EVC textbook [6]. This chapter therefore ad-dresses only their application in acute thrombosis.

AVF THROMBOSISDiagnosis of fistula thrombosis is easily made from

clinical findings. There is no bruit or murmur onauscultation and the typical thrill will be missing onpalpation, although there may be pulsation of a veinsegment close to the anastomosis. Identification andtreatment of the underlying stenosis are integral ele-ments of any access declotting procedure. As onlysuperficial (or superficialized) veins are used forAVF construction, in most patients inspection andthorough palpation will reveal a fibrous and stenoticvein segment as the cause of thrombosis. Additionalcolor-coded duplex-ultrasound may be helpful inadipose patients or otherwise questionable cases toidentify the site of stenosis and the extent of throm-bosis. Due to their lack of side branches, cephalicor transposed basilic veins will thrombose up totheir junctions with the brachial or axillary vein,whereas forearm AW often thrombose only up tothe next patent side branch.

Treatment of AVF thrombosis must aim at preser-vation of the puncture site. Only then can CVCimplantation be avoided. Surgical and interven-tional methods are equally effective as far as clotremoval is concerned. Location and extent of theunderlying stenosis, however, must be taken intoaccount in every individual patient in order tochoose the best treatment modality. The followingclassification of AW stenosis is intended to help toidentify the adequate corrective procedure (Fig. 1).

Type I - stenosis (anastomotic venous steno-sis). About 80% of stenoses leading to occlusionof AW are found at or close to the arteriovenousanastomosis. Surgical dissection and mobilizationof the vein on the one hand, and the extremelyturbulent flow within a functioning arteriovenous

ACUTE COMPLICATIONS OF ARTERIOVENOUS FISTULA FOR HEMODIALYSIS

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T Y P E I I IFIG. 1 Classification of AVF stenoses.


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connection on the other, have been implicated asthe causes.

After interventional declotting, a guide wire canbe passed through the stenosis, and a percutaneoustransluminal angioplasty (PTA) can be attempted.In most cases, these fibrotic stenoses afford high-pressure balloons and prolonged dilatation times.Nevertheless, long-term results are so disappointingthat even dedicated interventionalists recommendsurgical revision [7]. After surgical dissection, theaccess vein is transversely opened proximal to thestenosis without affecting the puncture site. Centralclot can be removed with a Fogarty catheter, assistedby digital massage in tortuous or aneurysmatic veins.On-table completion phlebography is mandatory torule out residual clot and additional stenoses. Inperipheral radiocephalic AW, distal ligation of thestenotic vein segment and proximal re-anastomosisof the cephalic vein to the radial artery is the eas-iest and most durable method of reconstruction [8].Proximal re-anastomosis is often difficult in type I-stenoses of brachiocephalic fistulae, when the veinmust be extensively mobilized to bridge the greaterdistance to the artery. In these cases, a short inter-position graft substituting the stenosed segment isthe better alternative, because the needling segmentof the access vein remains untouched [9].

Type II - stenosis (stenosis of the needlingsegment). Short stenoses within the needling seg-ment or between two needling areas of the accessvein may be late consequences of venous cannula-tions before AW construction. Multiple or longstenoses may reflect fibrotic reactions of the veinwall to the repeat cannulations for hemodialysis.

PTA is the only means to treat a puncture sitestenosis and at the same time completely preservethe site for immediate hemodialysis access; itshould therefore be attempted first. As stent im-plantation is strictly contra-indicated in the need-ling segment, stenosis recoil, early failure, or repeat-ed failures within short time intervals are indicationsfor surgery [7].

In order to preserve as much of the access siteas possible, short stenoses should be patched. Intortuous veins, resection of the stenosis and end-to-end anastomosis of the vein may be possible. Theskin incision should be as short as possible to leavesome untouched access vein for the next hemodia-lysis sessions. When the wound is completely healed,the patched or re-anastomosed segment can bepunctured again. Unfortunately, there are no studies

comparing the patency rates of autologous and syn-thetic patches. The latter have at least the theo-retical advantage that the venous capital of theESRF patient is not further damaged by harvestinga segment of superficial arm or saphenous vein.

Multiple or long type II-stenoses should bebypassed. The author prefers a greater saphenousvein interposition graft when the caliber of the ac-cess vein upstream the stenosis is less than 5 mm,and ePTFE in larger veins. Comparative studies, how-ever, are lacking. Only the diseased vein segmentshould be replaced, because 1 or 2 cm of un-touched vein proximally or distally to the interpo-sition graft may be sufficient for immediate post-operative hemodialysis access.

Type III - stenosis (functional stenosis). Inbrachiocephalic AW, a stenosis of the vein at itsjunction with the axillary vein can cause thrombo-sis because the cephalic vein in most individualslacks sufficient collateral side branches. Followinginterventional declotting, PTA of the stenosis mustbe performed very carefully in order to avoid rup-ture. Once a rupture occurs, a stent must be im-planted reaching into the subclavian vein possiblycausing axillary vein thrombosis and thus makinglater access grafts to the brachial or axillary veinimpossible [7].

The surgical alternative is to dissect the centralpart of the cephalic vein distal to its stenosis andtranspose it to the central basilic or brachial vein.Of course, late stenosis of this anastomosis canoccur. Comparative studies of PTA versus surgeryfor this rather infrequent problem are lacking.

AVG THROMBOSISLike in AW, clinical diagnosis of AVG thrombo-

sis is based on absence of thrill and murmur. Pre-operative clinical detection of stenosis in a clottedAVG is not that easy. Arterial and venous graft anas-tomoses lie deeply under scar tissue, so that palpa-tion is unlikely to identify stenotic vessel segments.Once the graft is clotted, neither color-coded duplex-ultrasound nor arteriography or phlebography canhelp to detect anastomotic stenoses. Consequently,after surgical or interventional declotting, on-tableangiography of the AVG delineating both anasto-moses together with the feeding artery and thedraining vein is mandatory to define and immedi-ately treat the cause of thrombosis.

By definition, AVG patients are those with ex-hausted peripheral veins. Treatment of AVG ste-


nosis therefore must aim not only at preserving thegraft as the puncture site but also at preserving thepatient's already reduced venous capital. In con-trast to surgery, interventional procedures do notrequire (venous) graft material or more proximal(venous) anastomotic sites. These advantages make

them an intriguing alternative for the treatment ofthe majority of AVG stenoses. A simple classifica-tion of AVG stenosis based on clinical considera-tions is proposed to help identify the adequatesurgical or interventional procedure for every indi-vidual finding (Fig. 2).

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FIG. 2 Classification of AVG stenoses.


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Type I - stenosis (arterial anastomotic ste-nosis). The arterial anastomosis of an AVG is al-most always a side-to-end anastomosis. Arterial anas-tomotic stenosis resulting from intimal hyperplasiawill therefore have a complex three-dimensionalconfiguration involving the artery immediately up-stream and downstream from the anastomosis, andthe anastomotic graft segment. PTA of such a steno-sis can be very difficult. Depending on the accesschosen for interventional graft declotting and de-pending on the angle in which the graft was suturedto the artery, one of the three areas of stenosis willbe difficult or even impossible to traverse with aguide wire and balloon catheter.

Surgical revision with resection of the anastomo-sis, patch or graft reconstruction of the artery, andre-anastomosis of the AVG is also demanding insmall and diseased peripheral arm vessels but allowsfor complete correction of the stenosis.

Type II - stenosis (midgraft stenosis). Insome individuals with longstanding AVG access, mid-graft stenosis occurs due to excessive ingrowth offibrous tissue through multiple puncture holes.These stenoses can be dilated or curetted [10], thusleaving in place the cause of the problem. The morestraightforward therapeutic option is to bypass thestenosed graft segment with a new prosthesis. Ifonly a part of the access site must be replaced, theremaining old puncture site can be cannulated forhemodialysis. If the access site is completely stenot-ic, half should be curetted and the rest bypassed,just to avoid the need for CVC implantation. Whenrestenosis develops in the curetted graft segment,it can be bypassed at a later date, again without theneed for a dialysis catheter.

Type III - stenosis (venous anastomoticstenosis). The great majority of grafts occlude be-cause of progressive stenosis of the venous anasto-mosis. The combination of surgical trauma to veinwall and endothelium during graft implantation,compliance mismatch between graft and vein, andflow disturbances in the anastomotic area are con-sidered the main causes.

Although the graft-to-vein anastomosis is fre-quently sutured in an end-to-side fashion, hemo-dynamically it is an end-to-end anastomosis (pro-vided the vein valves distal to the anastomosis arecompetent). Therefore, PTA of the stenosis is sim-ple and should be attempted first, because it is themost vein-preserving treatment modality, althoughsurgical thrombectomy and graft revision has been

shown to be more effective in most controlled tri-als [11]. In short stenoses, the surgical alternativeis patch angioplasty. Stenoses longer than 5 cm orcomplete occlusions of the draining vein affordgraft extension to a more proximal vein segment[12,13]. Graft extension should also be consideredin early or repeat restenoses.

Infection

Hemodialysis patients are at permanent risk ofarteriovenous access infection. Uremia itself has astrong immunosuppressive effect. Again and againthe natural skin barrier is broken by repeated accesspunctures allowing for eventual bacterial invasion.Arm swelling caused by central venous obstructionor hematoma caused by a false puncture or com-pression technique are additional risk factors. Thesame is true for pyoderma induced by uremic pru-ritus and dermatitis. While the most frequentlygrown organism is Staphylococcus aureus, a wide spec-trum of gram-positive and gram-negative bacteriahas been isolated in access-related bacteremia.

In ESRF, bacteremia is always a serious and life-threatening problem. About 20% to 25% of bac-teremic episodes are followed by metastatic com-plications, and 5% to 7% of the patients die [14,15].Therefore, even localized puncture-induced accessinfections without signs and symptoms of bac-teremia must be treated consequently and ade-quately. Patients should be hospitalized, and sys-temic antibiotic therapy should be given, accordingto sensitivity testing. In cases accompanied by chillsand fever or positive blood cultures, early aban-donment of the access site must be considered.

AVF INFECTIONLife-threatening infections of native AVF are rare.

Postoperative deep wound infections are always anas-tomotic infections (Fig. 3A). If untreated they willresult in formation of a false aneurysm (Fig. 3B) orin anastomotic rupture and profuse bleeding. Imme-diate surgical revision is mandatory. In cases withsevere local inflammation, ligation of the fistula veinand reconstruction of the artery with a vein patchto the arteriotomy or a venous interposition graft(Fig. 3C) are necessary. Suturing a more proximalfistula through a clean operative field can provideearly use of the revised fistula. Only in selectedpatients with minor signs of local infection, repairof the disrupted suture line may be performed.


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FIG. 3 PATIENT 1. A - Purulent discharge from broken skin incision three weeks after surgical revision of a formerlystenosed brachiocephalic fistula anastomosis. B - Pre-operative angiogram showing false aneurysm in extensively infectedand partially necrotic access vein. C - Postoperative angiogram after complete resection of the infected access vein andarterial reconstruction with a short saphenous vein interposition graft. An end-to-end anastomosis of the cubital arterywas not possible because the wall of its elongated proximal portion was heavily inflamed and partially necrotic.


In largely dilated access veins, parietal thrombuswill develop, especially when there is a central(type II- or type III-) stenosis leading to a reductionin flow velocity (Figs. 4A, 4B). A parietal thrombus

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can cause sterile thrombophlebitis like in superfi-cial varicose veins in the leg. After eventual inocu-lation of bacteria, however, septic endophlebitis willdevelop, often complicated by endocarditis and sep-tic pulmonary metastases. Immediate extirpation ofthe whole access vein is mandatory together withlong-term antibiotic treatment.

AVG INFECTIONReported infection rates for prosthetic grafts

range from 11% to 35% [16]. The rate of infectionassociated with graft implantation may be as highas 15%. Needling-induced late infection can betreated with segmental graft resection and bypass[6], together with long-term antibiotics and closemonitoring for recurring infection. Early infectionfollowing graft implantation always involves thecomplete graft with both anastomoses. To preventor treat anastomotic rupture and bleeding, the graftmust be completely excised. At the arterial anasto-mosis a small cuff may be left for easier closure ofthe arteriotomy [17]. The draining vein can be lig-ated proximally and distally to the anastomosisunless it is the main draining vein of the extremity.

Aneurysm

Whereas a graft has a defined caliber and will not,or will only minimally, dilate over time, successiveenlargement of the vein lumen is a prerequisite ofsuccessful long-term AW function and efficient

FIG. 4 PATIENT 2. A - Aneurys-matic degeneration of the rightupper arm cephalic vein nine yearsafter creation of an elbow fistula.A proximal type Ill-stenosis of theaccess vein could be assumedfrom inspection of the right infra-clavicular region. Reddening of theskin with local pain, chills, andfever indicated bacterial endophle-bitis. Blood cultures were posi-tive for growth of Staphylococcusaureus. Immediate and completeextirpation of the access vein wasperformed. B - Pre-operative an-giogram showing aneurysmatic de-generation of the right cephalicvein due to type Ill-stenosis.


hemodialysis therapy. An arterial aneurysm hasbeen defined as a vessel segment having a maximaldiameter larger than 1.5 times that of the normalartery. This definition can easily be adapted to agraft with a known diameter, but it seems prob-lematic in an access vein, which can and will changeits "normal" diameter over time. A circumscript ve-

nous dilation should be called an aneurysm whenits diameter is more than 1.5 times larger than themaximal diameter of the "normal" access vein up-stream and downstream (Fig. 5). Excessive dilation/elongation of the access vein without obvious "nor-mal" segments should rather be called aneurysmaticdegeneration (Fig. 4).

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FIG. 5 PATIENT 3. A - A rapidly expandins anastomotic aneurysm 4.5 years after creation of a periphe-ral Brescia-Cimino-fistula on the left forearm. Pre-operative angiogram demonstrates additional posta-neurysmatic stenosis. B - Postoperative angiogram after resection of the aneurysm with end-to-endanastomosis of the radial artery and re-anastomosis of the cephalic vein to the proximal radial artery.


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AVF ANEURYSMAneurysm formation is a common phenomenon

in native AW and in general can be treated as rou-tine. A postaneurysmatic stenosis must be investi-gated as a possible causative factor in all cases(Figs. 4B, 5A). Needling of only a small area of thevein can also lead to aneurysmatic dilation due tothe permanently repeated impairment of the wallintegrity of a short vessel segment. An aneurysmshould be treated when the postaneurysmatic steno-sis causes low access flow with inefficient hemodia-lysis and the risk of thrombosis. Mural thrombidetected by color-coded duplex-ultrasound or clin-ically apparent thrombophlebitis are indicators forthe hemodynamic relevance of the stenosis and forimpending complete access thrombosis. Likewise,mural thrombi are a risk factor for septic compli-cations (Fig. 4A).

There are two indications for emergency surgeryin access vein aneurysms: septic phlebitis (see above)and rapid expansion with impending skin necrosisor active bleeding. Rapidly expanding aneurysmsare mainly located adjacent to the arterial anasto-mosis, and are associated with a postaneurysmaticstenosis (Fig. 5A). When the arteriovenous anasto-mosis is involved in the aneurysmatic dilation, re-section of the aneurysm (and the postaneurysmaticstenosis) must be combined with reconstruction ofthe artery. A simple end-to-end anastomosis is oftenpossible if the artery was sufficiently elongated dur-ing the time of aneurysm growth (Fig. 5B). Other-wise, a short interposition vein graft will be necess-ary to restore arterial continuity. The access veinis then re-anastomosed to the proximal artery,again if necessary with an interposition graft. Whenthe arterial anastomosis is not involved, and whenthere is a short segment of "normal" vein beforethe aneurysm, resection of the dilated vein seg-ment and reconstruction with a vein-to-vein graftwill suffice.

AVG PSEUDO-ANEURYSMIn grafts, aneurysms are always associated with

local destruction of the graft wall (Fig. 6). This willoccur some months after graft implantation, whenonly one or two areas are needled. By definition,these aneurysms represent pseudo-aneurysms, asthe normal graft wall is missing in a certain areaand the wall of the pseudo-aneurysm consists offibrous tissue. Resection and replacement of thedestroyed graft segment(s) is the treatment ofchoice. Percutaneous implantation of a stent graft

in contra-indicated, because this would compromisethe needling segment. Education of patient andnurses is necessary to avoid further area puncturein favor of the so-called rope ladder technique.

Steal syndrome

In arteriovenous access, the steal phenomenon isdefined as retrograde diastolic flow from the distalartery into the access. This is a normal finding infunctioning access, because resistance in the cen-tral venous system is significantly lower than inperipheral muscle arteries. Steal syndrome (i.e.,steal phenomenon with signs and symptoms ofperipheral ischemia) does not normally occur afterarteriovenous access construction, because relativeischemia will induce vasodilation. This results inenhanced net arterial inflow into the respectiveextremity and increased collateral flow to the hand.The sensitive balance between enhanced arterialinflow and arteriovenous blood drainage can be dis-turbed when access flow exceeds the compensatorycapacity of the arterial tree of the arm, when severemediosclerosis or arterial obstructions prohibit suf-ficient vasodilatation, or in a combination of bothmechanisms.

Like peripheral arterial obstructive disease in thelower extremities, steal syndrome can be classifiedaccording to the Fontaine classification. Stage I-stealsyndrome is synonymous with steal phenomenon, asthere is retrograde flow in the distal artery (demon-strated by color-coded duplex-sonography) but nosymptoms of ischemia. Stage II-steal syndrome con-notes forearm or hand pain during exertion/ele-vation or during hemodialysis, stage Ill-steal syn-drome is characterized by rest pain, and stage IV bynecrosis.

STAGE II - STEAL SYNDROMEAs a result of fistula maturation, blood flow tends

to rise in AVF over time. Once stage II-disease hasdeveloped, there is a significant risk of deteriora-tion. Patients with this condition must be moni-tored very carefully so that they are treated whensymptoms become disabling and before rest painor necrosis occur. In grafts, stage II-disease is likelyto disappear when venous anastomotic stenosis suc-cessively reduces access flow. After correction ofsuch a stenosis, there is a high risk of recurrenceand even deterioration of symptoms.


STAGE III - ANDSTAGE IV - STEAL SYNDROME

Once rest pain or acral necrosis has occurred,urgent diagnostic work-up and therapy are indi-cated. Color-coded duplex-ultrasound will demon-strate diastolic retrograde flow in the distal arteryand should be used to measure flow volume in theproximal brachial artery. Arteriography includingthe aortic arch and the proximal arm arteries ismandatory to exclude proximal stenosis. Visualiza-tion of the forearm and hand arteries will be pos-sible only after digital compression of the access.

With an estimated frequency of 0.2% to 2.0%, theincidence of severe ischemic complications in ra-diocephalic AW is rather low when compared to the2.7% to 7% in grafts and the 10% to 25% in bra-

chiocephalic or brachiobasilic basilic fistulae [18].Surgical ligation or interventional embolization ofthe radial artery distal to the anastomosis will blockretrograde inflow and, in most cases, cure stealsyndrome.

In elbow fistulae, steal is associated with high flowvolume in one third of the patients. Several band-ing procedures have been described for flow reduc-tion. They are only effective when they result in ahigh-grade stenosis, and therefore are associatedwith the risk of persisting or recurring steal syn-drome on the one hand and insufficient access flowor access thrombosis on the other. In the majorityof patients, in whom steal syndrome occurs due tosevere mediosclerosis and at low access flow(600 mL/min or less), sufficient banding would

FIG. 6 PATIENT 4. A - Rapidly expanding pseudo-aneurysm 1.5 year following implantation of an upper arm curved AVG.The punctured graft areas can easily be identified from the needle scars. B - Intraoperative angiogram demonstrates alarge graft pseudo-aneurysm with partially floating mural thrombus and a smaller one without thrombus beneath the distalpuncture site.

22227


possibly result in a reduction of flow below thequantity needed for efficient hemodialysis therapy.For this situation the distal revascularization-inter-val ligation (DRIL) procedure (Fig. 7) was devel-oped [19]: ligation of the cubital artery will blockretrograde arterial flow without significant reduc-tion of access flow. A bypass from the brachial arterymore than 5 cm proximal to the access anastomo-sis to the cubital artery distal to the ligation willfurther enhance hand perfusion without deterio-rating access function.

In AVG, the risk of thrombosis is inversely cor-related with flow volume. Efficient graft bandingwill therefore lead to reduced patency. DRIL islikely to be the better alternative because it has vir-tually no influence on graft flow.

Conclusion

The rapidly growing number of hemodialysispatients and the growing number of access-relatedcomplications demand increasing attention fromvascular surgeons and interventional radiologists.In particular, those potentially limb- (steal syn-

(J (J drome, aneurysm) and life-threatening (thrombo-j~j~ sis, infection) complications pose specific problems.228 A dedicated endovascular surgeon would be the

ideal partner for access patients because he is freeto choose or combine conventional surgical andendovascular procedures according to the natureand location of the access problem.

FIG. 7 DRIL technique (Distal Revascularization IntervalLigation) : ligation of the cubital artery will block retrogradearterial inflow without significant reduction of access flow.

R E F E R E N C E S

1 Dhingra RK, Young EW, Hulbert-Shearon TE et al. Type of vas-cular access and mortality in U.S. hemodialysis patients. KidneyInt 2001; 60: 1443 -1451.

2 Pastan S, Soucie JM, McClellan WM. Vascular access andincreased risk of death among hemodialysis patients. Kidney Int62; 2002: 620-626.

3 Mickley V. Central venous catheters: many questions, fewanswers. NephrolDial Transplant 2002; 17:1368-1373.

4 Mickley V, Gorich J, Rilinger N et al. Stenting of central venousstenoses in hemodialysis patients: long-term results. Kidney Int1997; 51: 277-280.

5 Mickley V. Subclavian artery to right atrium haemodialysisbridge graft for superior vena caval occlusion. Nephrol DialTransplant 1996; 11: 1361 -1362.

6 Tordoir JHM, van de Sande F, Leunissen KML. Complications ofvascular access for hemodialysis. In: Branchereau A, Jacobs M

(eds). Complications in vascular and endovascular surgery. Parti.Armonk, Futura Publishing Company 2001: pp 225-235.

7 Turmel-Rodrigues L, Raynaud A, Bourquelot P. Percutaneoustreatment of arteriovenous access dysfunction. In: Conlon PJ,Schwab SJ, Nicholson ML (eds). Hemodialysis vascular access.Practice and problems. New York, Oxford University Press 2000: pp183-202.

8 Oakes DD, SherckJP, Cobb LF. Surgical salvage of failed radio-cephalic arteriovenous fistulae: techniques and results in 29patients. Kidney Int 1998; 53: 480-487.

9 Polo JR, Vazquez R, Polo J et al. Brachiocephalic jump graft fis-tula: an alternative for dialysis use of elbow crease veins. Am JKidney Dis 1999; 33: 904-909.

10 Puckett JW, Lindsay SF. Midgraft curettage as a routine adjunctto salvage operations for thrombosed polytetrafluoroethylenehemodialysis access grafts. Am]Surg 1988; 156:139-143.


11 Green LD, Lee DS, Kucey DS. A metaanalysis comparing surgi-cal thrombectomy, mechanical thrombectomy, and pharmacomechanical thrombolysis for thrombosed dialysis grafts. J VaseSMrg2002;36:l-7.

12 Marston WA, Criado E, Jaques PF et al. Prospective randomizedcomparison of surgical versus endovascular management ofthrombosed dialysis access grafts. / Vase Surg 1997; 26: 373 - 381.

13 PolakJF, Berger MF, Pagan-Marin H et al. Comparative efficacyof pulse-spray thrombolysis and angioplasty versus surgicalsalvage procedures for treatment of recurrent occlusion ofPTFE dialysis access grafts. Cardiovasc Intervent Radiol 1998; 21:314-318.

14 Marr KA, Sexton DJ, Conlon PJ et al. Catheter-related bac-teriemia and outcome of attempted catheter salvage in patientsundergoing hemodialysis. Ann Intern Med 1997; 127: 275-280.

15 Nielsen J, Ladevoged SD, Kolmos HJ. Dialysis catheter-relatedsepticaemia - Focus on Staphylococcus aureus septicaemia.NephrolDial Transplant 1998; 13: 2847-2852.

16 Padberg FTJr, Lee BC, Curl GR. Hemoaccess site infection. SurgGynecol Obstet 1992; 174:103-108.

17 Deneuville M. Infection of PTFE grafts used to create arteriove-nous fistulas for hemodialysis access. Ann Vase Surg 2000; 14:473-479.

18 Morsy AH, Kulbaski M, Chen C et al. Incidence and characteris-tics of patients with hand ischemia after a hemodialysis accessprocedure. J Surg Res 1998; 74: 8-10.

19 Berman SS, Gentile AT, Glickman MH et al. Distal revascular-ization-interval ligation for limb salvage and maintenance ofdialysis access in ischemic steal syndrome. J Vase Surg 1997; 26:393-404.

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GUNSHOT AND EXPLOSIVE PROJECTILEVASCULAR INJURIES

TOMISLAV SOSA, IVANA TONKOVlC, LIDIJA ERDELEZANDRIJA SKOPLJANAC-MACINA, MARKO AJDUK, ANDREJA CRKVENAC

The number of military and civilian gunshot and explosive projectile vascular injuries hasincreased in the past decades. In most of the conflicts, non-Geneva weapons are in use, withthe majority of wounds made by high-velocity fragments and high-velocity soft-point bullets.The initial mine or mortar fragment velocity has reached 2000 m/s [1,2]. The doubling ofmissile velocity quadruples its kinetic energy, and also the increase in mass augments thekinetic energy. Quadrupling of the projectile mass can have an eightfold increase in kineticenergy at the same velocity. Acting this way, the missile disperses a high quantity of the kineticenergy in the tissues, provoking the grinding effect. In addition to its direct effect, the bullet candamage the blood vessels with the high-velocity cavitational effect, resulting in stretching,disrupting, or thrombosis. The formation of a temporary cavity, however, is not a newphenomenon associated with modern high-velocity weapons.

23_231

Missile passage

Some investigators maintain that a larger exitthan entry wound is evidence of the devastatingpotential of an increase in velocity. While exitwounds are larger than entry wounds in 60% ofcases, the difference in the size of these wounds isnot per se directly attributable to the velocity, sincethe velocity is greater at the smaller entry woundand lesser at the greater exit wound. The largerexit wound is caused by projectile yaw or by pro-

jectile fragmentation or is a result of multiple sec-ondary bone fragment projectiles.

The point to be born in mind is that while thehigh-velocity projectile has the potential for higherenergy transfer with subsequent greater tissue dis-ruption, this may not always be the case. Missilesthat penetrate the human body disrupt, destroy orcontuse tissue, invariably resulting in a contaminatedwound. The penetrating missile or fragment destroystissue by crushing it as it punches the hole throughthe tissue. This hole is the permanent cavity. After


23232

passage of the projectile, the walls of the perma-nent cavity are stretched radially outward. The max-imum lateral tissue displacement delineates thetemporary cavity. Any damage in this area is a resultof the tissue stretching. The sonic shock wave pre-cedes the projectile's passage through the tissue.Although the magnitude of the sonic wave mayrange up to pressures of 100 atm, its duration is sobrief, about 2 us, that it does not displace tissuesor have detectable harmful effect on tissues (Fig. 1).

FIG. 1 Sonic shock wave and temporary cavity made byoutward stretch of the permanent cavity (modified from [2]).

Types of projectiles

+ .45 Automatic. The full metal jacketed mil-itary bullet is one of few that do not yaw signifi-cantly in soft tissue. Lack of yaw results with deeppenetration. The crush tissue disruption remainsnearly constant throughout the bullet path, andthe temporary cavity is too small to show a stretchwounding effect, being maximal at the point ofentry and gradually diminishing with penetration(Fig. 2).+ .22 Long Rifle. The solid lead round-nosed

bullet yaws through 90 degrees and travels base-for-ward for the last half of tissue path. The crush effectreaches its maximum when the bullet is travelingsideways, but it is too small to add a detectablestretch wounding effect (Fig. 3).

+ .38 Special. This has a special lead, round-nosed bullet. Seventy percent of these bullets yaw

through 90 degrees and travel base-forward for thelatter part of their tissue path, while 30% after yaw-ing straighten and travel point-forward for theremainder of their paths. The temporary cavity is20% greater than that made by the Long Rifle.^ 9 mm Parabellum. This is widely used both

in pistols and submachine guns. It produces theprofile that resembles that of the .38 Special butthe maximum temporary cavity is about two cen-timeters larger in diameter and will show somestretch effects (radial splits) in less elastic, moresusceptible tissues such as those of the liver.

*• 7,62 Nato FMC-FMC. Full metal cased, itis still used in sniper's rifles and machine guns. Itshows the characteristic behavior in tissue observedin nondeforming pointed bullets. It yaws through90 degrees and, after reaching the base-forwardposition, continues the rest of its path with little orno yaw. However, the rotation impaired to the bul-let by the rifled gun barrel is sufficient to causepoint-forward travel in the air but not in tissue,where such bullet shape and location of center ofmass outweigh rotation effects. The tissue disrup-tion in the first 15 to 18 cm of bullet penetrationis minimal. At 20 to 35 cm, a large temporary cav-ity is produced, after marked bullet yaw. If this tem-porary cavity occurs in the liver, the amount oftissue disruption is likely to make survival improb-able (Fig. 4).

+ AK-74. This smaller caliber Russian assaultrifle uses the full metal cased bullet with the cop-per-plated steel jacket as its predecessor, the AK-47.A unique design feature of AK-74 is an air spaceinside the jacket at the bullet's tip. The air spaceserves to shift the bullet's center of mass towardthe rear. This bullet yaws after only 7 cm of tissuepenetration, assuring an increased temporary cavi-ty stretch disruption, even in extremity hits. Thetypical exit thigh wound is stellate, with skin splitmeasuring 9 to 13 cm across. The underlying mus-cle split is about half that size. The bilobed yaw pat-tern results from initial bullet yaw returning to zeroyaw (first lobe), but then yawing a second time(second lobe) to 180 degrees, where the center ofmass stabilizes the projectile in base-forward travel(Figs. 5 and 6).4 .357 Magnum JSP. The jacketed pistol soft-

point bullet and the jacketed hollow-point bulletflatten their tips on impact. This expansion or mush-rooming results in doubling of effective bullet diam-eter in tissue, enabling the bullet to crush four timesas much tissue. This conversion of the bullet to a

GUNSHOT AND EXPLOSIVE PROJECTILE VASCULAR INJURIES

FIG. 2 .45 AUTOMATIC. The short, round-nosed, full metal cased bullet penetrates deeply but doesnot deform or yaw significantly (modified from [2]).

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FIG. 3 LONG RIFLE. This solid bullet yaws through 90 degrees, similarto the .38 Special bullet (modified from [2]).

FIG. 4 7,62 NATO CARTRIDGE. After about 16 cm of penetration, the bullet yaws through 90degrees, forming a large temporary cavity at the point of maximum yaw (modified from [2]).


FIG. 5 AK 47. Usedvery widely throu-Shout the world.Marked yaw besinsabout 25 cm afterpenetration (modi-fied from [2]).

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FIG. 6 AK 74. The bulletyaws early without deforma-tion. As this bullet strikes softtissue, lead flows forwardfilling the air space inside thebullet's tip. This produces anasymmetrical bullet, explai-ning the unusual curve madeby the bullet path in the latterpart of its penetration (modi-fied from [2]).

nonaerodynamic shape causes increased temporarycavity tissue stretch, as does the yawing of the bul-let. The maximum temporary cavity occurs at a shal-lower penetration depth. This soft-point pistolbullet is typical of the type most commonly usedby law enforcement agencies in the United States.It decreases the penetration depth and seldom per-forates the injured (Fig. 7).

+ 7,62 SP. Expansion occurs on impact, butafter this the bullet flattens, its pieces break off andmake their own separate paths of crushed tissue.These bullet fragments penetrate up to 9 cm radi-ally from the bullet path. The following temporarycaptations stretch the muscle already weakened bymultiple perforations. The fragment paths act toconcentrate the force of the stretch, increasing itseffect and causing pieces of muscle to be detached.This synergistic effect is seen only with bullets thatfragment. Very few victims with torso shots survive(Fig. 8).^ .22 CAL FMC. The large permanent cavity

made by the M-193 bullet was observed by surgeons

who served in Vietnam. Its point-forward travel isabout 12 cm, after which it yaws to 90 degrees, flat-tens and breaks around the groove around the bul-let mid section. The bullet point remains a flattenedtriangular piece, and the rear portion breaks intomany fragments that penetrate up to seven cen-timeters radially from the bullet path causing amuch enlarged permanent cavity. The bullet breaksin half at the shooting distance of 80 m. At a rangeof 180 m, the projectile does not break and thewounding mechanism is the same as that of the AK-74 (Fig. 9).

+ M-855 .22 CAL FMC. This is a heavierM-855 bullet used as the standard bullet for the USArmed Forces. The wound profile is similar to thatproduced by the M-193, although the tip does notremain in one piece.

+ The smaller M-193, AK-74, and M-855are susceptible to deflection and disturbance of theirpoint-forward flight. This can result in large yawangles at impact and a shallower location in thebody, but with maximum tissue disruption.


This is an expanding bul-let that makes a larse tem-porary cavity just after itspenetration (modifiedfrom [2]).

FIG. 8 7,62 SOFT-POINT BULLET.The fragmentation of this bullet isresponsible for the massive tissuedisruption (modified from [2]).

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FIG. 9 .22 CALIBER FULL ME-TAL CASED BULLET. This wasthe standard weapon of theUS Armed Forces for a longperiod, but lately has beenreplaced by a new rifle of thesame caliber but with a hea-vier bullet (modified from [2]).


+ 224 Soft-point. This is designed for maxi-mum deformation and fragmentation. The amountand type of damage is similar to that caused by theM-193 bullet, but the location of the maximum dis-ruption is at a shallower penetration depth (Fig. 10).

+ 12-Gauge shotgun, #4 buckshot. This gunloaded with 27 pellets of #4 buckshot at a closerange causes massive crush-type tissue disruption.At this range, soft tissue impact deforms the indi-vidual pellets increasing its section from the origi-nal 6 mm to 10 mm. The 27 perforations result insevere disruption of blood supply to tissue between

the multiple wound channels. Vascular reconstruc-tion is impossible in this case. Maximum soft tissuedisruption is expected at ranges under 25 m. Strik-ing velocity of the projectile decreases with distance.When bone is struck, the penetration depth will beless but the degree of soft tissue disruption will begreater due to increased projectile deformation andthe creation of secondary bone fragment missiles(Fig. 11).^ Fragments from explosive devices (mines,

grenades). The great majority of these projectilesare of blunt and irregular shape, not aerodynamic

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FIG. 10 224 SOFT-POINT BULLET.This is a typical .22 caliber center-firehunting bullet (modified from [2]).

FIG. 11 12-GAUGE SHOTGUN with#4 size buckshot. This weapon isused by the military and law enfor-cement groups for special situations(modified from [2]).


and made of soft material. This causes them to loosevelocity rapidly in the air. Initial fragment velocityis greater than 1800 m/s, but the wounds of sur-vivors indicate that striking velocities were about600 m/s. In cases where the victim is close, such asstepping on a landmine, the injury pattern is sim-ilar to that produced by # 4 buckshot at close range.In this situation, the anatomical integrity is totallydestroyed. If the survivor is at some distance, theprojectile track made by the fragment is consistentwith its size and generally remains constant through-out its part. The temporary cavity stretches a little,while the projectile rotates, flattens and fragments.Rotation produces the grinding effect on soft tis-sues and implicates the vascular repair with run-inand runoff far beyond the wounding area.

Impact of projectile typeon surgical procedure

A shot through the soft tissue of an averagehuman thigh by a 7,62 Nato soft-point bullet canresult in exit wounds up to 13 cm in diameter withmassive tissue loss. If the wound is located in theproximal femoral area, vascular reconstruction isnearly always impossible. If the wound is locatedmore distally on superficial femoral vessels, vascu-lar reconstruction should be performed, but withspecial attention to the possible rupture or severedistension of the sciatic nerve, the disruption ofwhich produces the afunctional, neurotrophic ex-tremity. With such wounds located in the poplitealfossa, amputation is the first choice. If a shot islocated cruraly with a viable foot, debridement andconservative treatment is recommended.

The vascular surgeon must realize that the samedestructive potential is obtained with the Nato 7,62FMC bullet, but the exit wound does not exceed2 cm in its largest dimension.

If a patient presents after leg or arm gunshot witha .22 Long Rifle, .38 Special, or .45 automatic bul-let with entrance and exit holes less than one cen-timeter in diameter, accompanied by vessel injury,vascular reconstruction should always be attempted.The surgical wound treatment rendered should beminimal.

M-193 bullets do not cause any more tissue dis-ruption than the .22 Long Rifle in the first 12 cmof penetration. Reconstruction of neurovascularbundles can therefore be performed, often followed

by muscular flap covering. In the torso wound, ifthe victim survives, the aortic and iliac damage canbe substantial and requires emergent hemostasis,debridement and often extra-anatomical bypasses.

AK-47 and especially AK-74 wounds might beextremely dangerous in the upper thigh or thoracicor abdominal cavity. Due to its directional changein the soft tissues, the bullet can enter the abdom-inal or thoracic cavity through the entry upperthigh wound. Aorto-iliac and thoracic aorta injurycan be missed in such patients. Plain X-ray of theentire torso and neck is therefore recommended.

The .357 Magnum JSP bullet is particularly dan-gerous if it enters the vascular areas. As the maxi-mum of its temporary cavity lies within the first15 centimeters after the point of entry, vascularinjury can be produced not only by destruction,but also with arterial and venous stretching anddistension. Vascular injury can be missed duringthe first exploration by a surgeon with limited ex-perience in vascular surgery.

A 12-gauge shotgun with #4 buckshot producesnonrepairable vascular and soft tissue injury whenfired at a range up to 3 m (close range). Shortranges, if most of the pellets are slowed with bonecontact, can allow a vascular reconstruction ac-companied by external bone fixation. A high in-cidence of associated deep venous injury (82%),nerve injury (37%), fracture (33%), massive tissueloss (43%), and compartmental hypertension (39%)is observed [3].

After vascular injury with fragments from explo-sive devices, in victims with preserved extremityshape, vascular reconstruction should always beattempted. A substantial number of distant mine ormortar vascular injuries present in the late stage,i.e., several months after injury, causing trouble-some access to the vascular structures because ofthe severe fibrosis that occurs as the result of tissuegrinding [2,4,5].

Epidemiologyof vascular trauma

Analysis is limited to hospital trauma victims andresults in a skewed picture of the true epidemio-logy of vascular-injury-related morbidity and mor-tality.

In the recent past, accurate and comprehensiveidentification of gunshot and explosive projectile

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vascular injury cases was difficult and many patientshad complex hospital courses. The creation of com-puterized trauma registries during the past decadehas partially facilitated epidemiological studies ofthose vascular injuries.

In the majority of studies, vascular trauma isdefined on the basis of patients who had blood ves-sels repaired. Thus, the true epidemiology of vas-cular injury is poorly characterized because suchdefinition excludes individuals who die before arriv-ing at the hospital. Furthermore, only a few stud-ies included vascular trauma in persons who die inhospitals before blood vessel repair can be accom-plished, or diagnosed blood vessel injuries that arenot repaired.

Because most epidemiological reports on nonia-trogenic vascular injury have not been populationbased, direct calculation of incidence rates is notpossible [6].

Trends in anatomicaldistribution of

vascular injuries

The reverse proportion of anatomical distribu-tion of vascular injuries can be noticed when mili-tary conflicts are compared with large urban, civil-ian series. In war circumstances, the majority ofvascular injuries are located in the extremities (91%to 97%) and only 1% to 5% and 2% to 4% aresited in the neck and trunk, respectively. In largercivilian series, however, the neck injuries are rep-resented in 12% and trunk injuries in 54%. Injuriesto the blood vessels in the extremities are repre-sented in 34% of individuals [6-10].

Mechanism ofvascular injury

Penetrating trauma is the dominant cause of non-iatrogenic blood vessel injuries, accounting for 50%to 90% of all such injuries. In urban settings, gun-shot wounds that cause nonfatal vascular injury aremost likely to involve the abdominal vessels, fol-lowed by the lower extremities [10-12]. The ballis-tic variable such as missile caliber and velocitytogether with the missile properties influence sub-stantially the mechanism of the blood vessel lesion,

extent of the lesion, operative strategy and patientprognosis.

The outcome is also representatively engravedin patients with gunshot and explosive vascularinjuries when compared with other trauma patients.Injury severity score is 40% higher, hospital stay isprolonged by 30%, intensive care unit stay pro-longed by 20%, and mortality and hospital chargesdoubled [13].

Vascular repair of gunshot and explosive projec-tile vascular injuries can generally be divided into

1 - primary: performed with the time gap needed forthe transport,

2 - secondary: performed several months or longerafter injury.

In general, primary vascular reconstruction isburdened by the emergency setting, shock and itscomplications, primary infection, injury of theadjacent tissues, concomitant injuries, compartmentsyndrome and postischemic syndrome.

Secondary reconstructive procedures are difficultbecause of severe fibrosis that, in some instances,make vascular structures inaccessible, cause troublewith hemostasis, graft stenosis and a longer reha-bilitation period.

Clinical signsof vascular injury

The early, immediate signs of vascular injury canbe dominated by arterial, venous or combinedtrauma. Arterial signs include the 5 Ps (pain, pal-lor, pulselessness, paresthesia, and palsy), pulsedeficit distal to the gunshot wound, decreased cap-illary refill, diminished distal doppler segmentalpressures and arterial hemorrhage. Venous injuryis characterized by edema, numbness, distal hyper-emia, stasis and venous hemorrhage. Late signs ofvascular injury include arteriovenous fistulae andfalse aneurysms. Duplex scanning can locate thedefect in the arterial wall and identify fistulae orfalse aneurysms [4,5,14,15]. Magnetic resonanceangiography or angiography can complete the diag-nostic process.


Treatment of gunshot andexplosive vascular injuries

Prior to the vascular reconstruction, general pre-cautions must be performed, such as adequate treat-ment of hypovolemic shock and anesthesiologicmeasures to combat respiratory distress syndromeand renal failure.

Time is the most important factor determiningthe outcome of the immediate vascular reconstruc-tion [4,16-21]. Ischemia-reperfusion injury can resultin compartment syndrome. If the total ischemic timeis longer than 6 hours in patients older than 60 yearsor longer than 4 hours in young individuals, fas-ciotomy should be considered [4,17,22-25]. In gen-eral, intra-operative doppler can be performed [26,27] but completion angiography is recommended.Because of the high incidence of stenosis, arterio-venous fistulae, or false aneurysms, postoperativesurveillance by means of duplex scanning shouldbe performed [28]. In venous injury, especially ifvenous stasis is present, deep venous reconstruc-tion is the preferred method [23,25,29-33]. Aftersurgery, limb elevation and compressive stockingsdecrease edema formation and anticoagulation isstarted.

Small and limited arteriovenous fistulae can betreated by intraluminal occlusion (stent, coils),whereas large fistulae require surgical occlusion andanatomical reconstruction if possible [4,5,14,15]. Insurgery, severe fibrosis aggravates the exposure andadjacent structures can be incorporated in the fibro-sis. Completion angiography is recommended be-cause multifragment lesions might have causedmore distally located smaller fistulas. False arterialaneurysms also require resection and anatomicalreconstruction.

Diagnostic considerationsfor gunshot and explosive

vascular injuries

Immediately after the injury, assessment of theankle-brachial index is useful. A pressure index lessthan 0.90 predicted arterial injury with 87% sensi-tivity and 97% specificity. Physical examination inconjunction with doppler pressure at a thresholdvalue of 0.90 yielded a sensitivity of 72.5% and aspecificity of 100% [34].

According to recent reports, color-flow duplexhas a 50% to 95% sensitivity, a 99% specificity andaccuracy of 98% in detecting vascular injuries inthe extremities. The accuracy in the thoracic out-let, the axilla and the calf is considered question-able. It is especially useful in detecting occult venousinjuries that would not be detected arteriographi-cally. However, it is highly operator dependent andshould be done exclusively by an interpreter whohas experience in vascular sonography [27,35,36].

If the penetrating injury lies distal to the deltoi-deopectoral groove or inguinal ligament, due to thealgorithm for the arterial trauma with maximumsensitivity while minimizing patient morbidity andcosts, we do not consider diagnostic arteriographynecessary [37-40].

If time allows, arteriography is useful in proximalinjuries, active hemorrhage or expanding hematoma.It is therefore used liberally in abdominal and tho-racic gunshot vascular injuries in stable patients.Arteriography is mandatory when there is uncer-tain suspicion of vascular injury. Furthermore, whenarteriovenous fistulae and/or false aneurysm aresuspected, the diagnosis and endovascular occlusionof these lesions can be obtained during the samediagnostic procedure. Vertebral lesions can be de-tected exclusively by arteriography, which revealsoccult arterial injury in 9% of patients [41]. A selec-tive policy in use of arteriography should be fol-lowed [42,43]. Intra-operative arteriography candemonstrate distal sequential injuries [44].

Gunshot or projectile injuriesof supra-aortic arteries

In another chapter of this book, J. Robbs ad-dresses the treatment of arterial injuries to the neckarteries.

In general, gunshot or explosive projectile carotidinjuries are often associated with injuries of the tra-chea, esophagus, spine and thorax. Associated in-juries are not pathognomonic for carotid injury.Shock at presentation predicts mortality (40% withshock, 8% without), but it does not predict neuro-logic outcome. Coma at presentation predicts mor-tality (higher than 70%) but is not a good predictorof neurologic outcome.

Approximately 50% of patients who are initiallyneurologically intact after partial gunshot injurydevelop neurologic deficit or die. Early diagnosis

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and treatment are imperative for reducing morta-lity and morbidity.

Vertebral arterial injury requires selective man-agement, depending on the type of injury. Nar-rowing or compression is best managed by systemicanticoagulation and/or endovascular stenting. Ver-tebral occlusion only requires exploration in caseof large hematoma. Arteriovenous fistulae requireembolization or, if not successful, surgical ligation.False aneurysms can be managed by endovascularstenting or surgical repair. Innominate artery injuryoccurs less frequently (5.5%) than subclavian arteryinjury (26%). Major, life-threatening bleedings arenot only caused by these arterial lesions but mainlydetermined by internal jugular, subclavian or inno-minate vein injuries [45].

Temporary shunts to maintain cerebral bloodflow, while the innominate or common carotid ar-tery are being prepared, are used infrequently.None of the several reports describe the indicationsfor use or document the results. No valid study hasbeen conducted to clarify this problem but manytrauma surgeons suggest that if there is a scantybackflow from the artery, or stump pressures lessthan 70 mmHg, a temporary shunt may be needed.A variety of shunting techniques have been usedincluding inlaying shunts, combined external andinternal shunts and external ones. The role of eachtechnique has not yet been defined.

Primary ligation may be chosen in some unstablepatients in whom survival depends on prompt com-pletion of the procedure. To ensure normal func-tion, repair of all major arteries is recommendedwhenever possible. In the presence of heavy con-tamination, remote bypass techniques may beemployed in selected patients. Subclavian-carotid,axillary-axillary and carotid-carotid bypasses havebeen used successfully to avoid placing a graftdirectly into a heavily contaminated wound, such asmay be encountered after erosion of a tracheostomytube [46-49].

Gunshot or explosiveprojectile injuries of the

descending thoracic aorta

Patients with direct gunshot injuries of this regionusually die before reaching the hospital. Amongsurvivors with acute injury, we can often find the

brink defect of the aortic wall, while bleeding isstopped by hypotension and temporary clotting.Hypovolemic shock limits the pre-operative diag-nostic work-up and occasionally a computed tomo-graphy scan can be performed in stable patients.Side defects of the aortic wall are associated withlate complications such as pseudo-aneurysms [50].

In emergencies, direct repair is the only choice.When direct pledged sutures are impossible, thebest alternative is partial resection of the thoracicaorta followed by graft replacement. Patching inthis area has not shown encouraging long-termresults. During the resection, the use of a Gottshunt can be beneficial [51].

Abdominal vascular gunshotand projectile injuries

Initial management includes primary and se-condary surveys, resuscitation and diagnostic stud-ies. Many patients with abdominal vascular gunshotinjuries present in hypovolemic shock. Hospitalmortality is up to 75% for the aortic injuries, and66.7% for the inferior vena cava (FVC) injuries [52].Treatment algorithms differ for these patients.When suprarenal aortic injury is suspected, emer-gency thoracotomy for descending thoracic aorticcontrol can be life saving in patients with extremehypotension [53]. It can be done quickly in a blood-less field. However, this maneuver carries highermortality rates and is still in the area of significantdebate. Variables such as recent loss of vital signs,anticipated delay in transfer to the operating roomand requirement for open cardiac massage still arethe indications for emergency thoracotomy [54].

After laparotomy, supraceliac aortic control shouldalways be obtained. Clamping in this area improvesthe hypotension and facilitates further exploration[55]. In injuries of the suprarenal area, distal con-trol can be obtained with second, infrarenal clamp-ing. Then, wide exposure can be obtained by wayof medial visceral rotation of the descending colon,spleen, pancreas, stomach and left kidney. Afterthe division of the left diaphragmatic crus, the newclamp is positioned more proximally (supraceliac)and the previous one removed. The same maneu-ver should be made with the infrarenal clamp.Suprarenal gunshot aortic injury carries high mor-tality rates particularly because it is often associ-ated with additional vascular or visceral injuries.


After debridement and rinsing, simple defects canbe repaired primarily. Larger defects require patchangioplasty. If the circumferential aortic segmenthas been shot or debrided, interposition graftingwill be required, preferably with antibiotic impreg-nated material with re-implantation of the visceraland renal arteries.

Gunshot injury of the infrarenal aorta is ap-proached anteriorly after supraceliac control. Afterapproaching the defect, reclamping below the renalarteries should be performed whenever possible. Ina heavily contaminated field, ligation and extra-anatomical reconstruction is a reasonable alternative,like axillobifemoral or bilateral axillo-unifemoralbypass.

Iliac gunshot/projectile injuries are burdened with ahigh percentage (up to 97%) of associated injuries[56]. Intestinal lesions occur in 88% and genito-urinary in 38%, yielding an average of 2.8 associ-ated injuries per patient. Overall mortality is 23%,mostly attributed to exsanguination. If arterial liga-tion in a contaminated field becomes necessary,early extra-anatomical revascularization should beconsidered because of its improved outcome in com-parison with delayed revascularization. Yet, based onthe experience of prosthetic repairs in the presenceof intestinal injuries where no infection was noted,the repair can be performed even with antibacter-ial prosthesis. Significant postoperative limb swellingoccurs in all patients who undergo venous ligationand venous reconstruction should therefore beattempted.

Portal region gunshot/explosive projectile injuries arevery rare and highly lethal. They are associated withliver and sometimes spinal trauma. Portal vein li-gation has an associated 90% mortality, whereasrepair has a 42% mortality [57]. Extrahepatic arte-rial ligation after the Kocher maneuver is better tol-erated than portal vein ligation, with a mortality rateof 58% (the repair carries 86% mortality). The sur-geon must observe the early development of hepaticischemia, which may necessitate delayed revascular-ization or further parenchyma resection. A repair ofat least one vessel must be seriously considered. Thefirst choice is portal vein repair. Mesenteric vascularinjuries like celiac axis injuries can usually be ligated.The presence of adequate back-bleeding is a posi-tive predictive sign for the uneventful outcome. Sur-gical repair is preferable, performed with autologousvenous material. Repair of the superior mesentericartery has provided better outcomes and should bedone whenever possible [58]. Associated intestinal

injuries should be treated with contemporarystomas.

Precise control of JVC injuries may be difficultbecause of the diffuse nature of the bleeding. Usu-ally, the surgeon is faced with the patient whoseabdominal cavity is filled with blood, and the onlyguidelines to IVC injury are venous blood at thepuncture site and the position of the entry and exitwounds. Digital or sponge stick compression and,at times, balloon tamponade are better methods ofcontrol than the vessel loops or clamps. If the bul-let has perforated the infrarenal IVC, the posteriordefect can be repaired from the surgically extendedanterior one. At times, ligation of the infrarenalIVC can be the only alternative. It is followed bylower extremity edema and leg elevation and com-pression stockings should be employed early in thepostoperative period.

Ligation of the suprarenal-infrahepatic IVC is lesstolerated and repair should be attempted. Thedegree of contamination and the physiologic statusof the patient dictate the appropriate method ofrepair. If the contamination is not severe, the bestresults are achieved with externally supported,large-diameter prosthetic conduits [59,60].

Retrohepatic venous injuries are some of the mostchallenging injuries to treat. The complete vascularisolation of the liver is mandatory, supported withthe packing of the injured veins. During the repair,cavo-atrial shunt has been advised, whereas othersemploy veno-venous bypass [60]. If the hemorrhageis supported by coagulopathy, one may be forced topack the area and address the injury at a later time[61]. Because mortality rates remain overwhelminglyhigh despite attempts of repair, stable hematomasin the retrohepatic area, confirmed by computedtomography scan, should be left unexplored.

Gunshot and explosiveprojectile vascular injuries

in the extremities

Many patients with extremity gunshot/projectilearterial injuries have associated venous, nerve andorthopedic injuries due to the bullet, pellet or frag-ment mechanism of wounding [4,18,24,62,63].

The preferred diagnostic method is still matter ofdebate. Most experienced surgeons, together withthe physical examination and plain X-ray, use duplexscanning for the assessment of the occult arterial

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trauma because of the high sensitivity (95% to100%), specificity (99% to 100%), and predictiveaccuracy (98%) when compared to that of arterio-graphy in the setting of extremity and cervical vas-cular injuries in zone II [59,60]. It also saves time,the most precious constant prerequisite for a suc-cessful vascular repair. It can be used to determinehemodynamic significance of arterial injuries byproviding the real-time assessment of blood flow ve-locities and doppler waveforms. Examples of the ul-trasound findings include luminal narrowing orwidening, luminal defects, vessel occlusion, blunt-ed peak velocities, spectral broadening, arterializa-tion of the venous blood flow, false aneurysms anddeep venous thrombosis. Furthermore, adequatestudies can be obtained in patients with openwounds using the sterile probe covers, and in un-stable patients in the operating room. The majorlimitation to this technique is the availability oftrained vascular technicians.

Respecting the prognosis, in the presence of con-comitant injuries and when the time gap is longerthan six hours, vascular repair should be done first[4]. Bone stability is maintained mainly with exter-nal fixation. Venous repair has been debated exten-sively [64]. Repair of major venous injuries is advo-cated unless there is an overwhelming medicalreason not to do this. The best results are achievedwhen nerve repair is done simultaneously.

ments in order to avoid overly frequent use offasciotomy [73,74]. Physical findings are pain dis-proportionate to the injury, pain with passive stretch-ing, weakness, hypo-esthesia or paraesthesia, para-lysis, tenseness and tenderness to palpation.

Allopurinol, steroids, superoxide dismutase, andmannitol can be of help in preventing and dimin-ishing compartment syndrome with their suppres-sion of xanthine oxidase, inflammatory response,free oxygen and with scavenge of the free radicals,respectively [75].

FASCIOTOMYFasciotomies should be performed according to

the recommended techniques, preferably with dou-ble incision (on both sides of the extremity) [69,76,77]. Open fasciotomy should always be performedafter gunshot injury. Wounds are left open with wet-to-dry dressings. Dressing changes are accomplish-ed at the bedside at a minimum of twice a day.

Postfasciotomy wound management ought not tobe anatomical, following the rule: less and tension-less is better [78]. The complications of fasciotomyarise mainly from its delay rather than the proce-dure itself [20,65-67,79,80]. Fasciotomy woundinfection is primarily related to extent of tissueinjury, duration of ischemia and time gap of fas-ciotomy. Nerve injury (saphenous, posterior tibial,

Compartment syndrome

Compartment syndrome as a condition that existswhen increased pressure within a limited spacecompromises the circulation and function of thetissues within that space most commonly affects thelower extremities, although its occurrence in theupper extremities should not be ignored [43,65-67]. It occurs primarily in response to direct mus-culoskeletal trauma (23% to 50% of cases) [68-70]or vascular injury with resultant ischemia and reper-fusion [68,71].

Fasciotomy is more often required for vasculartrauma (28% in a series of extremity vascular in-juries) than for nontraumatic acute arterial occlu-sions (8% to 14% of patients) [70,72]. The tablesummarizes the different mechanisms of compart-ment syndrome in the extremities.

Diagnosis is based on a high index of suspicionand frequent meticulous clinical examination sup-plemented by compartmental pressure measure-

Decreased compartment size (Extrinsic)

Surgical closure of fascial defects

Large scars

Increased compartment contents (Intrinsic)

Bleeding

Vascular injuries

Fractures

Contusions

Muscular tears

Ischemia/reperfusion edemafrom arterial injuries

Venous thrombosis

Shock


peroneal) may occur during fasciotomy, most com-monly with the subdermal approach. Inadequatedebridement of nonviable muscles may lead towound sepsis and necessitate amputation.

Concomitant venous repairin the management of

the gunshot arterial injuriesin the extremities

The management of concomitant venous injurieshas been controversial for decades [25,81-89]. Oneof the strongest arguments for the immediate repairand preservation of deep venous drainage of theextremity is to facilitate blood flow and prevent sec-ondary complications of the edema that can aggra-vate the condition of the injured limb [80,86,90,91].Barcia et al. [92] found an immediate 50% to 75%decrease in femoral arterial inflow associated withacute venous occlusion. However, Hobson et al. re-ported a return to baseline arterial blood flow afterapproximately 72 hours [93]. Injuries to the femoral,popliteal, iliac and axillar veins should be repaired.In a significantly injured extremity with arterial, ve-nous and extensive soft tissue trauma, venous occlu-sion that is not corrected can significantly affect limbperfusion [94].

After the missile injury, tissue is not only destroyedin its direct path but also in a much wider sur-rounding zone of injury. These cavitation effects areespecially notable when high-velocity weapons areused. Such types of wounds may be seen in militaryconflicts as well as in civilian gunshot wounds. Thesetypes of wounds with the blast effect in the sur-rounding tissue do not easily lend themselves to pri-mary venous repairs.

Most gunshot/explosive projectile venous injuriesmust be managed by interposition graft techniquesor ligation. A duplicated femoral vein exists in 20%,and if a preserved duplicated vein exists, the otherinjured vein may be ligated. Most of the tibial veininjuries may be ligated due to the six outflow veinsin this region; this is not the case with the poplitealvein, which always should be reconstructed becauseof the significant edema after simple ligation. Aftergunshot injury, reconstruction of cubital, brachialand axillary veins is recommended to improve thefunction of the hand. Repair of the iliac vein maynot be an obligation when there is absence ofinguinal injury and the subcutaneous tissue of the

concomitant abdominal part is intact, which is rarelythe case after gunshot/explosive injuries. If thereis a suspicion that collaterals are damaged or con-tused, iliac venous repair is mandatory.

There is often the question which injury shouldbe fixed first. It is most important to repair theinjured artery as soon as possible to minimize theanoxia in the distal extremity. In cases when bloodflow can be temporarily established by an internalshunt, it is better to repair the vein first. In manyclinical situations it may be more expeditious torepair the venous injury first, at least by lateralsuture, to establish hemostasis and permit betterarterial exposure. However, the best way is to doboth repairs as fast as possible.

Personal experience

During a 25-year period we have treated 33 civi-lian gunshot vascular injuries. Wartime and explo-sive projectile vascular injuries were much morefrequent. Between 1991 and 1995 we treated 220 pa-tients with 347 vascular injuries. There were 207 ar-terial and 140 venous injuries as well as associatedfractures and nerve injuries.

The mean prehospital time for this group was7 hours (range 3 to 18 h) [24]. Two hundred andseven (59.6%) arterial and 140 (40.4%) vein lesionswere treated. This is compatible with the previousreports [24,95]. Six percent of these vascular in-juries were caused by high-velocity fragments fromexploding devices and 16.4% by high-velocity soft-point bullets. The mean age of patients was 25 years(range 16 to 47 years). The most common vascularinjury was to the popliteal artery and vein. Injuriesto the superficial femoral and brachial vessels wereslightly less frequent. Ten of the patients had iso-lated venous injuries.

The fractures were stabilized by an external fix-ator in 90.4% of cases. Fractures appear to be theconcomitant injuries that aggravate the vascularrepair because they occur in up to 34% of patientsmaking them candidates for the complex treat-ment. Associated nerve lesions seriously compro-mise the outcome. In our series, they presented in40.4% of casualties. The best results were obtainedafter simultaneous nerve reconstruction during theone procedure.

Seventy-four fasciotomies (48% on upper and62% on the lower limbs) were performed because

23_243


of compartment syndrome. This represents 44.5%among all gunshot injuries of the extremity vessels.Vessel injuries repaired within four hours after theincident did not require fasciotomy. The muscle via-bility can be estimated clinically (color, contractil-ity, bleeding). However, in 16 patients muscle biopsywas of help in the decision for fasciotomy.

Arteriovenous fistulae presented in 5.4% vascularinjuries, and false aneurysms were encountered in9.5%. Acute arteriovenous fistulae were present inonly 7 gunshot injuries (2.0%) and acute false aneur-ysms in 6 (1.7%). The rest presented as the late se-quelae of arterial and venous injury. As stated before,peripheral arterial injury was repaired by means ofautologous venous interposition or bypass graftingin most patients.

Eighteen patients who had blood vessel injuryunderwent amputation (8.1%). The indications foramputation were sepsis, deep venous thrombosisand extensive myonecrosis. Concomitant vein, nerve,soft tissue and bone necrosis were present in allamputees. Sixteen patients died. Death was caused

by associated craniocerebral, pulmonary and bowelinjuries, as well as with sepsis.

During follow-up the vascular status in all exam-ined patients was entirely satisfactory and none ofthese patients suffered from ischemic symptoms.One late amputation was done because of the neu-rotrophic limb, not because of ischemia.

Conclusion

Gunshot and projectile vascular injuries are com-plex and require extensive knowledge about the dif-ferent types of bullets and missiles and subsequentsurgical management. Arterial repair is mandatoryin most cases in order to preserve viability. Venousrepair deserves a selective approach, but permanentedema is a threat for healing processes. Associatedsurgical procedures like fasciotomy, bone, organ andnerve repair are extremely important, especially forthe functioning and quality of life on the long term.

23244 R E F E R E N C E S

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40 Gagne PJ, Cone JB, McFarland D et al. Proximity penetratingextremity trauma: the role of duplex ultrasound in the detec-tion of occult venous injuries./ Trauma 1995; 39: 1157-1163.

41 Pasch AR, Bishara RA, Lim LT et al. Optimal limb salvage in pen-etrating civilian vascular trauma. J Vase Surg 1986; 3: 189-195.

42 Degiannis E, Levy RD, Sofianos C et al. Arterial gunshot injuriesof the extremities: a South African experience. J Trauma 1995;39: 570-575.

43 Pillai L, Luchette FA, Romano KS, Ricotta JJ. Upper-extremityarterial injury. Am Surg 1997; 63: 224-227.

44 Roberts RM, String ST. Arterial injuries in extremity shotgunwounds: requisite factors for successful management. Surgery1984; 96: 902-908.

45 Perry MO. The management of acute vascular injuries. Baltimore,Williams & Wilkins, 1981 : pp 55-65.

46 Flint LM, Snyder WH, Perry MO, Shires GT. Management ofmajor vascular injuries in the base of the neck. An eleven-yearexperience with 146 cases. Arch Surg 1973; 106: 407-413.

47 Reul GJ Jr, Beall AC Jr, Jordan GL, Mattox KL. The early oper-ative management of injuries to the great vessels. Surgery 1973;74: 862-868.

48 Calhoon JH, Grover FL* Trinkle JK Chest trauma. Approachand management. Clin Chest Med 1992; 13 : 55-67.

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51 Kram HB, Appel PL, Wohlmuth DA Shoemaker WC. Diagno-sis of traumatic aortic rupture: a ten-years retrospective analy-sis. Ann Thorac Surg 1989; 47: 282-286.

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53 Feliciano DV. Abdominal vascular injuries. Surg Clin North Am1988; 68: 741-755.

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56 Carrillo EH, Spain DA, Wilson MA et al. Alternatives in the man-agement of penetrating injuries to the iliac vessels. / Trauma1998; 44: 1024-1030.

57 Jurkovich GJ, Hoyt DB, Moore FA et al. Portal triad injuries./Trauma 1995; 39: 426-434.

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59 Salam AA, Stewart MT. New approach to wounds of the aorticbifurcation and inferior vena cava. Surgery 1985; 98: 105-108.

60 Rogers FB, Reese J, Shackford SR, Osier TM . The use of ven-ovenous bypass and total vascular isolation of the liver in thesurgical management of juxtahepatic venous injuries in blunthepatic trauma. / Trauma 1997; 43: 530-533.

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62 Radonic V, Baric D, Petricevic A et al. War injuries of the cruralarteries. Br/Swrg 1995; 82: 777-783.

63 Dajani OM, Haddad FF, Hajj HA et al. Injury to the femoralvessels - the Lebanese War experience. EurJ Vase Surg 1988; 2:293-296.

64 lerardi RP, Rich N, Kerstein MD. Peripheral venous injuries: acollective review. J Am Coll Surg 19%; 183: 531-540.

65 Matsen FA 3rd, Winquist RA, Krugmire RB Jr. Diagnosis andmanagement of compartmental syndromes. / Bone Joint SurgAm 1980; 62: 286-291.

66 Myers SI, Harward TR, Maher DP et al. Complex upper extrem-ity vascular trauma in an urban population. / Vase Surg 1990;12: 305-309.

67 Sriussadaporn S. Vascular injuries of the upper arm. JMed Assoc7M 1997; 80: 160-168.

68 Vitale GC, Richardson DJ, George SM Jr, Miller FB. Fasciotomyfor severe blunt and penetrating trauma of the extremity. SurgGynecol Obstet 1988; 166: 397-401.

69 Wrilliams AB, Luchette FA, Papaconstantinou HT et al. Theeffect of early versus late fasciotomy in the management ofextremity trauma. Surgery 1997; 122: 861-866.

70 Abouezzi Z, Nassoura Z, Ivatury RR et al. A critical appraisalof indications for fasciotomy after extremity vascular trauma.Arch Surg 1998; 133:547-551.

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72 Nypaver TJ, Whyte BR, Endean ED et al. Nontraumatic lower-extremity acute arterial ischemia. AmJSurg 1998; 176:147-152.

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74 Field CK, Senkowsky J, Hollier LH et al. Fasciotomy in vasculartrauma: is it too much, too often? Am Surg 1994; 60: 409-411.

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75 Fan tone JJ. Pathogenesis of ischemia-reperfusion injury: anoverview. In: Zelenock G (ed). Clinical ischemic syndromes:mechanisms and consequences of tissue injury. St. Louis, Mosby1990.

76 Mubarak SJ, Owen C. Double-incision fasciotomy of the leg fordecompression in compartment syndromes. / Bone Joint Surgylwl977;59: 184-187.

77 Nghiem DD, Boland JP. Four-compartment fasciotomy of thelower extremity without fibulectomy: a new approach. Am Surg1980; 46: 414-417.

78 Cuschieri J, Anagnostopoulos P, Kralovich KA et al. Fasciotomywound management: less is better. J Trauma (in press).

79 Ernst CB, Kaufer H. Fibulectomy-fasciotomy. An importantadjunct in the management of lower extremity arterial trauma.J Trauma Wl; 11: 365-380.

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81 Borman KR, Jones GH, Snyder WH 3rd. A decade of lowerextremity venous trauma: patency and outcome. Am J Surg1987; 154: 608-612.

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24ENDOVASCULAR TREATMENT OF

BLUNT INJURY OF THE LIMBS

BO RISBERG, LARS LONN

Endovascular treatment of various vascular disorders has been established as part ofclinical routine. Preferentially, endovascular techniques are used in elective cases withstenoses, fistulae, or aneurysms. In recent years, the technique has been applied morefrequently in emergency cases. It has turned out to be lifesaving as well as an attractivealternative to large open exposures. To date, endovascular repair has been performed mostlyfor injuries of central vessels, and reports of its application to limb injuries are sparse [1-4].

2f247

Arterial injury

Traumatic lesions of extremity arteries resultmainly from penetrating injuries and motor vehi-cle accidents. Vascular blunt injuries to the extrem-ities are rare. The literature contains only casereports often related to youth and sports [5,6]. Iso-lated intimal injuries with spontaneous healing havebeen reported after blunt trauma [7].

Blunt vascular lesions occur from external directtrauma to the vessels or from secondary trauma fol-lowing, for example, fractures or joint dislocations.The symptoms usually develop as a consequence ofthe induced ischemia. Bleeding problems followingblunt injuries are extremely rare. The vessel patho-logy after blunt trauma includes wall fractures,hematomas, intimal fractures, dissections, andthrombosis. There can be a wide range of structural

damage and symptoms and there is not necessarilya direct correlation between extent of the injuryand symptoms.

Angiography is the gold standard examination forpatients with documented or suspected vascularlimb injuries. It has been considered important todocument the presence or absence of such injuries,since even small injuries have been thought toprogress to occlusion. [8-11]. Among patients withblunt popliteal injury, angiography was consideredunnecessary in those with normal neurovascularexamination [12].

Standard management at most institutions, how-ever, includes mandatory repair of detected lesions.The indication for intervention must be set by theclinical symptoms and not judged on the angio-graphic images, i.e., do not treat the images. It hasbeen clearly demonstrated in previous studies that


24248

post-traumatic changes as discovered on angiogra-phy can undergo spontaneous resolution [13-15].

Diagnosis

Significant clinical findings in extremity traumainclude pulse deficit, bruit, expanding hematoma,a history of hypotension, or signs of bleeding andeventually neurologic deficit.

The clinical examination must include pulse pal-pation and, in doubtful cases, ultrasound-based pres-sure measurement. Calculating the ankle-brachialindex (ABI) may be helpful in lower extremityinjuries.

Diagnosis is established by duplex-ultrasound,standard arteriography, computed tomographyangiography (CTA), or magnetic resonance angio-graphy (MRA), isolated or in combination. Thedecision of which technique to use must be basedon local organization and routine. In most depart-ments, standard angiography is routine. It has theadvantage that catheters and guide wires willalready be in place if an endovascular procedure isto follow.

Facilities

Modern vascular centers are (or should be) equip-ped with facilities for a variety of urgent endovas-cular procedures. Blunt vascular limb injuries wouldseldom require access to embolization facilities.Large stent graft devices such as used for rupturedaortic aneurysms would never seem to be needed.The shelf in the intervention suite should containvarious guide wires, catheters, stents, and variousembolization materials. The situation may not bedifferent from penetrating injuries, where also avariety of stent-grafts should be available.

Management

Arterial integrity is often threatened in patientswith blunt trauma lesions of the extremities.

Digital subtraction angiography (DSA) quicklyconfirms sites of hemorrhage and other lesions(Table: A). Despite the options available for endo-vascular interventions, acute bleeding is best manag-ed by embolotherapy (Table: B).

Patients with multitrauma are usually examinedwith a spiral CT. Multislice CTA in the evaluationof patients with suspected injuries in the arteries isroutine [16]. Bleeding can often be identified onCT before hemodynamic instability develops, andthis time window can be an opportunity for endovas-cular treatment. If nonsurgical therapy is the firstoption, CTA is unnecessary and it is better to moveforward to angiography as soon as possible.

Color-flow duplex-ultrasound mapping with a lin-ear-array transducer is an option for detection ofvascular injuries. The imaging can be carried outin the emergency room.

The fourth method for diagnosis (Table: C),MRA, has not gained widespread use for acute sit-uations due to logistic problems and availability ofmachines. The two latter techniques are advanta-geous in that neither involves the use of ionizingradiation or iodinated contrast material.

Typesof lesions

A

Rupture,wall fracture

Focalnarrowing

Occlusion,thrombosis

Intimal flap

Intimaldissection

Endothelialirregularities

Intramuralhematoma

AV fistulas

Pseudo-aneurysm

Endovasculartechniques

B

Stent

Stent grafts

Occlusivematerialssuch as:

- coils

- (detachable)balloons

-PVA

- gelfoam

- thrombin,bucrylate

Thrombolysis

Imagingtechniques

C

Angiography(DSA)

Ultrasound

Computedtomographyangiography(DSA)

Magneticresonanceangiography(MRA)

ContrastenhancedMRA(CE-MRA)

ENDOVASCULAR TREATMENT OF BLUNT INJURY OF THE LIMBS

Vascular injuries must be recognized, diagnosed,and treated quickly and accurately at the emergencyward. Occasionally, suspected vascular traumaresults in rapid deterioration of the clinical condi-tion. A surgical approach to control bleeding isthen necessary. In the future, with increasing avail-ability of skills in vascular interventional tech-niques, endovascular treatment should be possiblealso in these severe cases and not only as a guideto surgical treatment. There is a controversy regard-ing whether and to what extent angiography shouldbe carried out. As indicated above, the clinical symp-toms must determine if angiography is going to beperformed or not. In asymptomatic cases, manyangiograms will be negative and conservative man-agement with observation during 24 hours may besufficient. DSA is therefore indicated when:1 - vascular injury is suspected due to clinical symp-

toms2 - multiple lesions are suspected3 - location of injury is uncertain4 - endovascular therapy is feasible5 - abnormal pulse waves on doppler with decreased

ankle-brachial index are at hand.

Technique of angiography

Conventional DSA with selective catheterization,serial imaging, and at least two orthogonal planesshould be obtained on every patient with blunttrauma. These oblique images routinely acquiredwill reduce the risk of missing lesions on single pro-jection images. Superselective angiography is almostalways needed to confirm diagnosis.

LOWER LIMB ANGIOGRAPHYA routine contralateral femoral puncture (Seldin-

ger technique) under local anesthesia is standardapproach for lower extremity lesions. Brachialaccess can be used when femoral pulses are absent.A catheter is positioned in the distal aorta and aflush DSA used to visualize the global arteries incases of lower limb traumas before selective DSA isperformed.

UPPER LIMB ANGIOGRAPHYPatients with upper limb symptoms should have

the brachiocephalic or left subdavian artery andthe more distal arm vessels investigated. For upperlimb injuries, the femoral technique is likewise used

and only in special occasions is the procedure con-tinued with direct antegrade puncture. A flush DSAof the aortic arch in left anterior oblique positionmay be useful to detect any other underlying dis-ease before selective DSA is performed.

Endovasculartreatment options

Embolotherapy is a fundamental aspect of inter-ventional radiology. Treatment of hemorrhage fol-lowing trauma focuses mainly on embolization(Table: B). The word embolus means plug, and em-bolization is a method for plugging vessels in a con-trolled manner via the endovascular route. Embolicagents function by inducing direct mechanicalobstruction of the vessel and provide a frameworkfor thrombus formation. This results in occlusion,and certain agents also incite an inflammatory reac-tion. The material can be divided into permanentor temporary occlusive agents based on its prop-erties. The level of destination from a large vesseldown to capillary levels is determined by the sizeof the product.

Treatment depends on appropriate planning andselection of material, where angiography is the pre-requisite. The technique depends on the locationof the lesion. The collateral network in extremitiesis rich and therefore it is important to embolizeboth proximal and distal to the injury site to pre-vent retrograde filling in certain cases. Intravascu-lar administration of various agents and materials toinduce occlusion is administrated percutaneously.Thus, ongoing hemorrhage will arrest or eliminatevascular supply in order to simplify if a surgical treat-ment is needed.

Particulate material includes coils, gelatin sponge,and polyvinyl alcohol foam (PVA). Coils are madeof steel fragments surrounded by a thrombogenicmaterial (i.e., wool strands) or, as in the case ofdetachable coils, a positively charged electrode (i.e.,platinum coils) promotes clot formation by attract-ing negatively charged cells.

The concept of hemorrhage control by translu-minal balloon catheter tamponade, i.e., detachabletranscatheter balloons, is used primarily in the cere-brovascular regions. An additional role for balloonsis the achievement of temporary hemostasis untilsurgical intervention is allowed in the more globalarteries of the limbs.

249


24250

Gelfoam is a resorbable material used mainly totemporarily control bleeding because of its ten-dency for recanalization.

A liquid tissue adhesive such as bucrylate has lowviscosity and is a very aggressive embolizing agentcausing necrotizing vasculitis. The material can beinfused percutaneously to obliterate traumaticlesions but this requires skill and experience andcertain precautions. It is mainly used in portal veinsfor obliteration before liver surgery.

In cases of pseudoaneurysm formation with nar-row necks, thrombin injection is an option, but itshould be administered percutaneously directly intothe sac [17,18]. There is a potential risk of over-spill of thrombin into the native artery if adminis-tered through the angiography catheter.

Combination of endoluminal stents and stentgrafts can also be applied for minimal arterial re-pair. The concept is to bridge the defect in the ves-sel wall with endoluminal graft supported by a barestent material, usually self expandable. The risk fordevice infection following stent graft repair oftrauma cases is a concern but is not definite.

Survey of the literature

Only few case reports deal with endovasculartreatment of blunt injuries, and none with limbinjuries. Endovascular repair of vascular injuries tothe extremities as reported in the literature domi-nates by penetrating injuries [3]. Still, open repairis the standard of care at most large institutions. Ina recent report on lower extremity injury on 550 pa-tients during a 10-year period, therapy was basedon open surgical reconstruction [19]. In that study,penetrating injuries dominated and 20% were blunttrauma. Open repair is the gold standard for bluntinjuries to the extremities. This is particularly truefor popliteal injuries. Shortcomings in diagnosisand therapy may add to subopdmal results [20,21].

Our survey of the literature has not revealed anyreport on endovascular repair of blunt vascularinjuries to the extremities. One single case fromour own institution is presented below.

The first report of stent treatment of blunt arte-rial injury was by Althaus et al. in 1996. They re-ported successful stent reconstruction of an iliaclesion [22].

In a report by Brandt et al. in 2001, six patientsover a 6-year period had endovascular repair fol-lowing blunt injuries. Each patient had one or more

stents placed. Two patients had injuries to theabdominal aorta, two to the carotid artery, and twoto the subclavian artery. The early and even long-term follow-up was satisfactory [23].

Own case

A 51-year-old man had his right upper arm caughtin the sliding door of a van. At arrival to the hos-pital he had numbness with loss of sensibility onthe medial part of the lower right arm and thehand was cooler. The motor function was not affec-ted. Blood pressure on the left arm was 120 mmHgand on the right 60 mmHg. The radial artery wasnot palpable. Clear doppler insonation was achiev-ed in the right radial and ulnar arteries.

The patient was taken to angiography because ofsuspected intimal tear with occlusion. The angio-graphy was performed by the femoral route. Theright subclavian artery was catheterized. Contrastinjection revealed an intimal tear in the brachialartery with a roll-up for a distance of 2 to 4 cmapproximately 10 cm above the elbow causing com-plete occlusion (Fig. 1). The lesion was easily passed

FIG. 1 Selective digital subtraction angiography (DSA) ofthe right brachial artery: a 2 cm occlusion resulting from anintimal tear is shown (corresponding to the blunt traumaregion).

TTTTTT

by a guide wire and percutaneous transluminalangioplasty (PTA) catheter. The defect was treatedby balloon occlusion for 3 x 2 minutes to seal theintima to the vessel wall. After the first ballooning,a defect was still noticed (Fig. 2). A second bal-looning almost completely restored vessel integrity.A small defect was still seen on contrast injection,but there was free and unhindered blood flowacross this area (Fig. 3). The patient was given gly-cerolnitrat (0.2 mg) four times during the proce-dure. Since there was a clear clinical improvement,no stenting was performed. The introducer was leftin place for a possible re-intervention. Local hep-arin infusion through the introducer as well as lowmolecular heparin subcutaneously was given.

The patient was observed over night with ade-quate heparin administration. The clinical picturewas normalized on the following day, with palpableradial pulse. Blood pressure was identical bilater-ally. A duplex-doppler examination was performedand demonstrated that the brachial artery was openbut a small defect (1 mm) was still seen in the areaof injury.

One-month follow-up with duplex-doppler demon-strated totally normalized conditions. There wereno remaining clinical symptoms.

Discussion

Endovascular techniques have not been usedcommonly for blunt extremity trauma as reportedin the literature. In fact, we have not encounteredany published case. Since blunt injuries are notrare, this is a little bit surprising. The applicabilityof endovascular techniques would seem to be sim-ilar for both penetrating and blunt injuries. Bylarge, many vascular injuries are still treated byopen surgery, but endovascular techniques seem tobe taking over. This is likely to occur also with bluntinjuries.

Blunt trauma to large vessels, as denoted above,has turned out to be a more or less establishedindication for endovascular therapy. Endovasculartreatment of extremity vessels such as brachial andfemoral arteries is next to come.

The dismal results from treatment of atheroscle-rotic patients with long PTA or stents in thefemoral/popliteal/distal arteries may, however,dampen the enthusiasm. The situation may be dif-ferent in the traumatized patient. These patientsmost certainly belong to a much younger agegroup, in which immediate and long-term results

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FIG. 2 After prolonged "gluing" of the dissection into the FIG. 3 Final result: restored vessel integrity with minimalarterial wall by a 6 mm balloon occlusion, the artery is ope- residual defect,ned up. A substantial intimal lesion is visualized.


may be better. There may still be concern aboutintroducing foreign material into young peoplewith long life expectancies.

Conclusion

Endovascular techniques are being increasinglyutilized for emergency vascular cases. There is nodoubt that the immediate success rate is high. Since

this is a novel technology, long-term data are lack-ing. Most experience hitherto is from penetratinginjuries, but as more experience is gained moreblunt injuries will be treated. Of particular concernis the applicability of the technique in growing indi-viduals and people with a long life expectancy. Thisis important since the trauma population differsvastly in age distribution from the aging athero-sclerotic patients in whom endovascular technologyis mostly being applied today.

R E F E R E N C E S

1 Brunkwall J, Lindblad B, Ivancev K et al. latrogenic AV-fistulatreated by a graft-covered self-expandable stent. Eur J VaseEndovascSurgl9%; 12: 243-245.

2 Chuter TA, Ivancev K, Lindblad B et al. Endovascular stent-graftexclusion of an aortobronchial fistula./ Vase Interv Radiol 1996;7:357-359.

3 Marin ML, Veith FJ, Panetta TF et al. Transluminally placedendovascular stented graft repair for arterial trauma. JVasc Surg1994; 20: 466-473.

4 Scharrer-Pamler R, Gorich J, Orend KH et al. Emergentendoluminal repair of delayed abdominal aortic rupture afterblunt trauma. JEndovasc Swrg-1998; 5:134-137.

5 Sarfati MR, Gait SW, Treiman GS, Kraiss LW. Common femoralartery injury secondary to bicycle handlebar trauma./ Vase Surg

JA 2002; 35: 589-591.& ' 6 Sotta RP. Vascular problems in the proximal upper extremity."059 Clin Sports Med 1990; 9: 379-388.

7 Kestenberg WL. Review of intimal arterial injuries. Surgeryversus conservative management. Am Swrgl990; 56: 504-506.

8 Geuder JW, Hobson RW 2nd, Padberg FT Jr et al. The role ofcontrast arteriography in suspected arterial injuries of theextremities. Am Swig 1985; 51: 89-93.

9 Kelly GL, Eiseman B. Civilian vascular injuries. / Trauma 1975;15:507-514.

10 King TA, Perse JA, Marmen C, Darvin HI. Utility ofarteriography in penetrating extremity injuries. Am J Surg 1991;162:163-165.

11 Perry MO, Thai ER, Shires GT. Management of arterial injuries.Ann Surg 1971; 173: 403-408.

12 Abou-Sayed H, Berger DL. Blunt lower-extremity trauma andpopliteal injuries: revisiting the case for selective arteriography.Arch Surg 2002; 137: 585 -589.

13 Dennis JW, Frykberg ER, Veldenz HC et al. Validation ofnonoperative management of occult vascular injuries and

accuracy of physical examination alone in penetrating extemitytrauma: 5 to 10 year follow-up./ Trauma 1998; 44: 243-253.

14 Frykberg ER, Crump JM, Dennis JW et al. Nonoperativeobservation of clinically occult arterial injuries: a prospectiveevaluation. Surgery 1991; 109: 85-96.

15 Frykberg ER, Vines FS, Alexander RH. The natural history ofclinically occult arterial injuries: a prospective evalutation./Trauma 1989; 29: 577-583.

16 Soto JA, Munera F, Cardoso N et al. Diagnostic performance ofhelical CT angiography in trauma to large arteries of theextremities. J Computer Assisted Tomography 1999; 23:188-196.

17 Lonn L, Olmarker A, Geterud K et al. Treatment of femoralpseudoaneurysms. Percutaneous US-guided thrombin injectionversus US-guided compression. Ada Radiol 2002; 43: 396-400.

18 Kang SS, Labropoulos N, Mansour MA, Baker WH. Percuta-neous ultrasound guided thrombin injection: a new method fortreating postcatherization femoral pseudoaneuryms. / Vase Surg1998; 27:1032-1038.

19 Hafez HM, Woolgar J, Robbs JV. Lower extremity arterial injury:results of 550 cases and review of risk factors associated with limbloss./ Vase Surg2001; 33:1212-1219.

20 Gupta R, Quinn P, Rao S, Sleunarine K Popliteal artery trauma.A critical appraisal of an uncommon injury. Injury 2001; 32:357-361.

21 Kwolek CJ, Sundaram S, Schwarcz TH et al. Popliteal arterythrombosis associated with trampoline injuries and anteriorknee dislocations in children. Am Swrgl998; 64:1183-1187.

22 Althaus SJ, Keskey TS, Harker CP, Coldwell DM. Percutaneousplacement of self-expanding stent for acute traumatic arterialinjury./Trawmfl 1996; 41: 145-148.

23 Brandt MM, Kazanjian S, Wahl WL. The utility of endovascularstents in the treatment of blunt arterial injuries./ Trauma 2001;51:901-905.

25RARE CAUSES OF

ACUTE ISCHEMIA OF THE LIMBS

MARK KOELEMAY, DINK LEGEMATE

Acute upper or lower limb ischemia is an urgent condition that requires prompt restorationof blood flow to save the threatened limb. Acute limb ischemia most frequently occurs ^ „unilaterally, but patients may also present with bilateral symptoms. Zi5

With regard to the etiology, a distinction can be made between arterial embolism, arterial 253thrombosis, and dissection. It is estimated that some 60% of acute upper extremity ischemiaand 70% percent of acute lower extremity ischemia is caused by arterial embolism. Some 80%to 90 % of peripheral arterial embolisms are of cardiac origin., such as arrhythmias, cardiacaneurysm, and intracardial thrombus formation after myocardial infarction, dilatorycardiomyopathy, cardiac valve vegetations as in endocarditis or other (innate) cardiac valveanomalies, and atrial myxoma. Acute ischemia due to arterial thrombosis is the result of lowblood flow, increased blood viscosity, or a procoagulative state (Virchow's triad) superimposedon preexistent atherosclerotic changes in the vascular endothelium.

This chapter describes some rare causes of acute limb ischemia, which are listed in the Table.Data were collected by a systematic literature search of the PUBMED database using keywordsarterial, embolism, and thrombosis with references to related articles, and using cross-referencesto complete the search. It was definitely not our aim to present a complete overview of allreported cases on a specific cause of acute limb ischemia.

Anatomic es of peripheral arterial embolism of cardiac ori-gin must be mentioned. Young or middle-aged pa-

CARDIAC tients presenting with acute limb ischemia andWhile the most common cardiac disorders are concomitant venous thrombosis (VTE) or pul-

noted briefly in the introduction, a few rare caus- monary embolism (PE) should raise the suspicion


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AnatomicCardiac

Paradoxical arterial embolismAtrial myxomaMetastatic pulmonary tumorsMetastatic germ cell tumorPeripartum cardiomyopathy

AortaAortic dissectionAortic (aneurysm) thrombosisMural aortic thrombusPrimary malignancy of the aortaInfectious aortitis

Peripheral arteriesPopliteal entrapmentPrimary peripheral artery dissectionOsteochondromaPersistent sciatic arteryExternal compression

DrugsCocaineHuman chorionic gonadotropinAnabolic steroidsHeparinChemotherapyThrombin injection

Prothrombotic stateMalignancy related (Trousseau's syndrome)Anticardiolipin antibodiesLupus anticoagulant antibodiesHyperhomocysteinemiaNephrotic syndromeInflammatory bowel disease

VasculitisTakayasu's diseaseGiant cell arteritisCogan syndromeKawasaki disease

TraumaBlunt abdominal traumaBullet embolism

latrogenicOrthopedic surgerySurgery in high lithotomy positionAortic cannula embolismCatheterizationPuncture sealing devicesIntra-aortic balloon pumpAortic bifurcation endoprosthesis

of paradoxical embolism. This is caused by the pas-sage of a right-sided venous or cardiac thrombusinto the arterial circulation by a patent foramenovale (PFO) or another intracardiac defect, gener-ally at the atrial level. Autopsy studies have revealedthat up to 35% of the population has a PFO, whichhas been suggested to be a risk factor for ischemicstroke. Little is known about the incidence of acutelimb ischemia in patients with a PFO. Travis et al.found paradoxical embolism to be the cause ofacute limb ischemia in 13 of 2764 (0.4%) patientspresenting in a ten-year period [1]. The definitivediagnosis is established by the presence of VTE orPE, arterial emboli, and a right-to-left shunt. Trans-esophageal echocardiography is the investigation ofchoice if transthoracic echocardiography does notidentify an intracardiac thrombus or PFO. Treat-ment modalities for the prevention of further em-boli vary and include observation, antiplatelet ther-apy, anticoagulants, placement of vena cava filters,and closure of the PFO by percutaneous or opera-tive procedures [1,2].

Other sources of cardiac embolism include neo-plasms such as atrial myxoma or primary pul-monary malignancies invading the left atrium orthe pulmonary veins. Occasionally, other malig-nancies cause tumor emboli, as in a young patientwith bilateral acute leg ischemia in whom a germcell tumor invaded the right lung and left atrium[3]; this patient finally died of massive pulmonaryembolus after repeated peripheral embolectomiesand tumor resection.

Dilatory cardiomyopathy is a known risk factorfor peripheral embolism. It is estimated that one ofevery 3000 to 15000 pregnancies is complicated byperipartum cardiomyopathy, with symptoms of dysp-nea, peripheral edema, and fatigue. Whereas suchpatients are at increased risk of venous thrombo-embolism, we found one patient with popliteal andtibial artery embolism that resolved during intra-venous heparin administration [4].

AORTAAortic dissection and aortic thrombosis are well-

known causes of acute extremity ischemia. In ad-dition, peripheral emboli can originate from a dis-eased aorta. The prevalence of nonaneurysmalmural aortic thrombus has been reported to be0.45% in a series of 10671 consecutive autopsies[5]. Eight of these patients had clinical signs ofdistal embolism. To date, 80 cases of distal em-bolization from mural aortic thrombus have been

RARE CAUSES OF ACUTE ISCHEMIA OF THE LIMBS

documented in the literature [6]. One explanationfor mural thrombus formation is a hypercoagula-tive state, whereas local aortic inflammation due topancreatitis, and steroid therapy for Crohn's dis-ease have also been postulated to cause aorticthrombi [7]. Depending on local availability, trans-esophageal echocardiography, magnetic resonanceangiography (MRA), or computed tomographyscanning can be used to establish the diagnosis.The optimal treatment modality for mural aorticthrombus has yet to be established. In the litera-ture several management strategies have been sug-gested including anticoagulation therapy, aorticthrombo-endarterectomy, and graft replacement ofthe diseased aortic segment [6-8]. Primary malig-nancies of the aorta are extremely rare. From 1873to 1997, only 87 cases have been reported in theliterature [9]. In two thirds of these cases, the di-agnosis was made post mortem, whereas the firstmanifestation in the other patients most often wasperipheral tumor embolism. The male: female ratiowas 2:1, the mean age of the patients 60 years.Angiosarcoma, sarcoma, leiomyosarcoma, and ma-lignant fibrous histiocytoma were the most fre-quently found types of aortic tumors. If patholog-ic examination of an embolus reveals an aorticmalignancy, MRA of the aorta can be helpful to de-termine whether the tumor can be resected. Theprognosis, however, remains poor, because some70% of the patients already have distant metastases.

Bacteremia can cause infections of the normalnonaneurysmal aorta. In the pre-antibiotic era, car-diac valve vegetations frequently were the cause ofinfectious aortitis, but now the role of endocarditishas been diminished. At present, patients with acompromised immune system who are 50 to 70 yearsold and have an aortic aneurysm are at risk for in-fectious aortitis, typically caused by Staphylococcus au-reus, Salmonella, or fungal infections. The most se-rious complication of infectious aortitis is ruptureof the aorta, but infectious aortitis should also bekept in mind as a cause for peripheral emboliza-tion. We found case reports on lower limb em-bolization due to infections with S. Pneumoniae andParacoccidiodes brasiliensis [10,11].

PERIPHERAL ARTERIESAn abnormal anatomical relation between the

popliteal artery and the medial head of the gas-trocnemius muscle causes medial displacement andcompression of the artery, known as popliteal en-trapment [12]. It is a rare condition, predominantly

found in young men, who may complain of clau-dication, paresthesia, or numbness of the foot. Arare presentation of popliteal entrapment is embol-ization from the diseased popliteal artery to thefoot arch and digital vessels [13]. Several classi-fications for popliteal entrapment have been sug-gested. In the most common type, the poplitealartery is compressed between the medial head ofthe gastrocnemius muscle and the medial femurcondyle. In the other variants, a slip of gastrocne-mius muscle, a fibrous band, or the popliteus mus-cle may cause constriction of the artery [12]. Fi-nally, physiologic popliteal entrapment may existdue to gastrocnemius, soleus, or plantaris musclehypertrophy in athletes [12,14]. The definitive man-agement depends on the local situation and mayconsist of simple release of the popliteal artery bydivision of the medial head of the gastrocnemiusmuscle or a short venous bypass graft in case of anocclusion.

Primary dissection of the peripheral arteries is arare condition that should be considered in youngpatients with acute onset limb ischemia. In a lite-rature review published in 1969, 110 case reportswere identified [15]. Only nine cases concerned thelower extremity arteries. More recently, additionaldissections of the femoral and popliteal arterieshave been described, with symptoms ranging fromclaudication to acute limb ischemia. Primary dis-section occurs predominantly in patients under 50years of age, more often in men, who are hyper-tensive in 90% of the cases.

Underlying diseases associated with spontaneousdissection include Marfan syndrome, cystic mediadegeneration, and fibromuscular dysplasia. Osteo-chondroma are benign tumors of the metaphysisof long bones that can displace adjacent blood ves-sels such as the superficial femoral and poplitealartery. The majority of patients are younger than25 years and have no manifestations of atheroscle-rotic disease [16,17]. The cartilaginous part of thetumor matures into bone, which continuously da-mages the artery. This may finally result in pseudo-aneurysm formation, arterial thrombosis, luminalstenosis due to extrinsic compression, or arteriove-nous fistula. Some authors therefore advise pro-phylactic resection of osteochondroma in the vicinityof a vessel. A similar mechanism caused embolismof the lower limb in a patient with an osteosynthesisscrew that was used to repair a comminuted femoralfracture. The screw and surrounding callus causedsuperficial femoral artery occlusion and distal

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embolization that did not respond to thrombolytictherapy and resolved only after thrombo-endarte-rectomy and removal of the screw [18].

The sciatic artery is the earliest fetal artery tosupply blood to the lower extremity by connectingthe internal iliac and popliteal artery. The sciaticartery involutes with the development of the super-ficial femoral artery. Its proximal part becomes thesuperior gluteal artery, whereas the distal partforms a plexus on the surface of the great adduc-tor muscle. Based on angiographic studies, the pre-valence of a persistent sciatic artery is estimated tobe between 0.025% and 0.04% [19]. Like otherarteries, the sciatic artery is prone to atherosclero-sis and aneurysmal disease in particular, which maypresent as a pulsatile mass in the gluteal region, aschronic lower limb ischemia, or as acute ischemiadue to distal embolization from a sciatic arteryaneurysm. Management depends on the nature ofthe lesion and comprises surgery in most cases. Ina recently published report, two patients were suc-cessfully treated with placement of a covered stentfor exclusion of an aneurysm, and dilation andstent placement for claudication [20].

Finally, external compression of peripheral arter-ies may lead to acute extremity ischemia, such asin a patient with a proven occlusion by duplexscanning of the right common iliac artery due tomassive fecal impaction of the sigmoid colon andrectum; the symptoms fully subsided after removalof the fecaloma [21].

Drugs

Several drugs have been reported to be associ-ated with acute limb ischemia. Cocaine is a potentvasoconstrictor and is known to cause myocardialinfarction. The use of cocaine, whether taken intra-nasally or smoked as crack, has also been reportedto cause aortic, common iliac, and popliteal arterythrombosis [22,23]. It is hypothesized that cocaineinduces platelet aggregation and that it may aug-ment procoagulants by decreasing protein C andantithrombin III (AT-III) levels, resulting in arterialthrombosis. An additional risk of drug abuse is dis-tal embolization caused by accidental intra-arterialdrug injection.

In a review, Stewart et al. [24] addressed the riskof thrombo-embolic events after ovarian stimulation,in vitro fertilization and gamete intrafallopian trans-

fer, and the use of human chorionic gonadotrophin(HCG). The majority of events were deep VTE andPE, with 15 cases of arterial thrombosis of thecarotid, cerebral, subclavian, and iliac arteries. Poss-ible explanations for arterial thrombosis include de-creased AT-III levels and increased fibrinogen levelsinduced by exogenous HCG or the presence of anunknown thrombophilia in combination with HCG.

Danazol is an androgenic steroid that is used pri-marily for endometriosis and has both prothrom-botic and antithrombotic effects. It influences theclotting cascade by increasing platelet counts andelevating both anticoagulant and procoagulant pro-tein levels. Alvarado et al. described two patientsusing danazol, for endometriosis and idiopathicthrombocytopenic purpura, respectively, with acutelower extremity arterial thrombosis and who hadno risk factors for arterial disease [25]. Both pa-tients were treated successfully with thrombolytictherapy and withdrawal from danazol. Other ana-bolic steroids such as testosterone, nandrolone, sus-tanon, dianabol, and testovarin have also been re-ported to cause diffuse arterial thrombosis or embolifrom left-sided intraventricular cardiac thrombus[26-28], Suggested mechanisms for arterial throm-bosis include platelet activation, increased levels ofprocoagulant factors and a decrease in fibrinolyticactivity.

One of the side effects of unfractionated heparinadministration is the occurrence of heparin-induc-ed thrombocytopenia (HIT) in 2% of patients. Thediagnosis of HIT is established by a decrease in pla-telet count by 50 000/mm3 or an absolute decreasebelow 100 000/mm3 and a positive heparin-depen-dent platelet antibody test. It is estimated that 30%to 75% of patients with HIT develop paradoxicalvenous or arterial thrombosis (heparin-inducedthrombocytopenic thrombotic syndrome [HITTS])or white clot disease [29]. The mechanism of clot for-mation is not fully understood, and it is believed tobe the result of immune activated platelets com-bining with fibrin. A loss of local endothelial integ-rity and heparin-induced immune complex inter-actions may cause thrombosis. A few case reportsdescribe arterial thrombosis of the lower extremityarteries. The optimal treatment of HITTS has not yetbeen established and comprises, apart from heparinwithdrawal, warfarin, dextran, aspirin, low molecularweight heparin, prostacyclin analogues or throm-bolytic therapy with urokinase or streptokinase.

The administration of chemotherapeutic agentssuch as etoposide, cisplatin, vinblastine, methotrex-


ate and bleomycin for treatment of pulmonary andgerm cell cancer has been reported to cause periph-eral arterial thrombosis [30-32]. In addition, pre-menopausal patients receiving adjuvant therapy forbreast cancer were at a 1.6% risk of arterial throm-bosis when tamoxifen was added to chemotherapycompared to 0% in patients receiving chemother-apy alone [33]. The reason for increased risk ofboth venous and arterial thrombosis is not clear.As mentioned in the next section, the presence ofa malignant tumor carries an increased risk of arte-rial thrombosis due to a hypercoagulable state.Suggested mechanisms for chemotherapy-inducedthrombosis include a decrease in proteins C and Sand AT-III levels.

Thrombin injection is an effective and safe treat-ment of pseudoaneurysms, e.g., of the femoral ar-tery, and is associated with a low complication rate[34]. However, arterial thrombosis can result afteraccidental injection of thrombin in the femoralartery [35].

Prothrombotic state

Deficiencies in proteins C and S, AT-III and fac-tor VIII, and factor V Leiden mutation are thrombo-philia that are well known risk factors for sponta-neous venous and arterial thrombosis. A less commoncause of arterial thrombosis is malignancy-relatedhypercoagulability, also known as Trousseau's syn-drome [36]. It has been described predominantly inassociation with malignancies of the lung, pancreas,and intestinal tract, but may be caused by all can-cers. The exact etiology of malignancy-related ar-terial thrombosis is unclear. There is evidence thattumors can produce procoagulant factors, causedeficiencies of proteins C and S and AT-III, andinduce platelet activation. The treatment of arterialthrombosis in such cases is not different from usual.Some authors advocate prompt treatment of theunderlying malignancy, but this is not supported byscientific evidence. A special group of malignanciesare the acute leukemias that cause thrombosis bymeans of leukemic cell sedimentation or dissemi-nated intravascular coagulation [37].

Antiphospholipid antibodies are autoantibodiesthat may cause procoagulant states. The most com-monly detected subgroups are anticardiolipin anti-bodies, lupus anticoagulant antibodies, and anti-B2-glycoprotein-1 antibodies. The prevalence of these

antibodies ranges between 1% and 5% in a younghealthy population and increases with age. Most pa-tients with antibodies will never suffer from athrombo-embolic event. However, 50% to 70% ofpatients with systemic lupus erythematosus and an-tiphospholipid antibodies may develop the anti-phospholipid syndrome, which is characterized byvenous or arterial thrombosis. The majority of throm-boses are venous (55% of cases). Arterial throm-bosis affects the brain (50%), the coronary arteries(27%), and the peripheral arteries (23%). The in-creased incidence of mitral valve vegetations inthese patients causes arterial embolism. The bestprophylaxis and treatment seems to be warfarinmedication, probably lifelong, as withdrawal fromwarfarin leads to a high recurrence of thrombo-embolic events [38].

Hyperhomocysteinemia is an independent, mo-derate risk factor of arterial occlusive disease.Although the relation between hyperhomocys-teinemia and venous and arterial thrombosis is lessclear, it must also be kept in mind as a source ofperipheral arterial thrombosis, as described in apatient with femoral artery thrombus causing acuteischemia of the lower limb; correction of bloodhomocysteine with vitamin suppletion may preventfurther arterial sclerosis and thrombosis.

The nephrotic syndrome has its highest preva-lence in young patients and has been reported tocause arterial thrombosis, mainly of the superficialfemoral arteries. Although rare, there are a few re-ports on arterial thrombosis in adult patients, lo-cated in the cerebral, mesenteric, renal, and aorticand femoral arteries [40,41]. Arterial thrombosis inthe nephrotic syndrome is thought to be a resultof decreased AT-III levels, platelet dysfunction, al-teration in levels of clotting factors, increased bloodviscosity, hypoalbuminemia, and administration ofsteroids.

Inflammatory bowel disease is also associated withthrombo-embolic events with an estimated preva-lence between 1.3% and 6.4%, with two thirds beingvenous thromboses. Patients with Crohn's diseaseand those with ulcerative colitis are at risk of devel-oping aortic or lower extremity arterial thrombosis[42,43]. The origin of arterial thrombosis in inflam-matory bowel disease is as yet unclear because ofits low prevalence. It is hypothesized that a primaryAT-III deficit causes the hypercoagulable state andsubsequent thrombosis. Among other explanationsare increased platelet activation, a decrease in tissueplasminogen activator and elevated anticardiolipin

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antibodies. There is no uniform therapy; the pa-tients described in several case reports and in a sur-vey among members of the American Society of Colonand Rectal Surgeons were all treated with surgicalthrombo-embolectomy.

Vasculitis

Takayasu's disease is a nonspecific inflammatoryprocess of the aorta and its major branches and thepulmonary arteries that causes arterial stenosis oraneurysm formation. The origin of the inflamma-tion that causes changes in all vascular wall layersis unknown. While the majority of symptoms arecaused by alterations in the thoracic aorta and sub-clavian arteries, patients have also presented withacute leg ischemia due to emboli originating fromthe infrarenal aorta [44] and aorto-iliac bifurcation[45]. Therapy comprised thrombolysis in the for-mer case and aorto-iliac bifurcation prosthesis inthe latter, in combination with steroids. Giant cellarteritis is another nonspecific vasculitis of the lar-ger arteries that may cause acute upper or lowerextremity ischemia [46,47]. Like in Takayasu's dis-ease, steroid therapy is the treatment of choice.

Cogan syndrome is a rare condition, character-ized by nonsyphilitic interstitial keratitis and vesti-bulo-auditory symptoms which progress to deafness.In 10% of these patients, vasculitis develops thatmay manifest itself in occlusion or aneurysmal dilata-tion of the coronary arteries, mesenteric ischemiaor neurologic symptoms. One case was describedwith acute onset calf claudication due to a throm-bus in the popliteal artery that was successfully treat-ed with thrombolytic therapy [48]. Kawasaki diseaseis a mucocutaneous lymph node syndrome charac-terized by high, persistent fever, prominence of con-junctival vessels, changes in the oropharyngeal mu-cous membranes, rash and lymphadenopathy. Itoccurs most frequently in children under four years,but it has been described in adults too. A week afterthe initial symptoms, vasculitis develops and aneur-ysms start forming, predominantly in the coronaryarteries and other, similar locations as in Cogansyndrome. One report describes a middle-aged pa-tient with a history of Kawasaki disease who pre-sented with acute ischemia as a result of a throm-bosed popliteal aneurysm [50].

Trauma

The association between vascular injuries andfractures or luxations is well known. Other less com-mon causes of vascular injuries must not be over-looked. Blunt abdominal trauma by seat belt injurywith subadventitial rupture of the common or exter-nal iliac arteries can result in acute leg ischemia[51,52]. It is assumed that shear forces cause a dis-ruption of the intima and subsequent thrombosis.Blunt abdominal trauma can also dislodge throm-bus from an abdominal aortic aneurysm. Onepatient known to have an abdominal aortic aneur-ysm developed an acute ischemic leg from a seatbelt injury [53], while four other patients devel-oped bilateral leg ischemia after the Heimlichmaneuver, as a result of aortic aneurysm thrombo-sis and thrombo-embolism to both legs [54,55].

Bullet fragments must also be considered assources of arterial embolisms because of the in-creasing possession and use of guns. Many papershave reported delayed onset of peripheral arterialischemia due to late migration of bullet fragmentsfrom large caliber arteries to peripheral arteries,including paradoxical bullet embolism in a patientwithaPFO [56,57].

latrogenic

Patients undergoing orthopedic surgery are atrisk for acute peripheral ischemia. Total knee ar-throplasty is associated with a 0.03% to 0.17% riskof vascular complications such as thrombosis,popliteal artery transection and aneurysm forma-tion [58,59]. It is unclear whether the applicationof a tourniquet increases the risk factor for arterialthrombosis. Additional case reports were found oniliac artery occlusion and aortic thrombosis afterretroperitoneal exposure of the spine. Recognitionof this complication could prove difficult becausesensorimotor disturbances may also be caused bytransient nerve damage. In addition, total hip re-placement has been noted to cause bilateral throm-bosis of the iliac arteries.

The ankle-brachial index decreases significantlyby placing patients in the high lithotomy position[60]. Geeraerts et al. described a patient who de-veloped acute external iliac thrombosis superim-posed on preexisting atherosclerotic lesions in the


lower extremity after transurethral bladder tumorresection [61]. Further embolic complications wererelated to femoral artery catheterization for diag-nostic angiographies, percutaneous transluminal(coronary) angioplasties, sealing of the femoralartery punctures with closure devices [62] andembolism by a buffer of an aortic cannula that was

used during coronary bypass surgery in a patientwith acute leg pain [63]. The use of an intra-aor-tic balloon pump was also reported to cause acuteaortic thrombosis. In the near future, patients canbe expected to have acute leg ischemia due tothrombosis of one of the limbs of an endovasculardevice for abdominal aortic aneurysm repair [64].

R E F E R E N C E S

1 Travis JA, Fuller SB, Ligush J Jr. et al. Diagnosis and treatment ofparadoxical embolus./ Vase Surg 2001; 34: 860-865.

2 AbuRahma AF, Downham L. The role of paradoxical arterialemboli of the extremities. AmJSurgl9%; 172: 214-217.

3 Singh A, Jenkins DP, Dahdal M et al. Recurrent arterialembolization from a metastatic germ cell tumor invading theleft atrium. Ann Thome Surg 2000; 70: 2155-2156.

4 Carlson KM, Browning JE, Eggleston MK, Gherman RB.Peripartum cardiomyopathy presenting as lower extremityarterial thrombo-embolism. A case report. JReprod Med 2000; 45:351-353.

5 Machleder HI, Takiff H, Lois JF, Holburt E. Aortic muralthrombus: an occult source of arterial thrombo-embolism. J VaseSwrgl986;4:473-478.

6 Rossi PJ, Desai TR, Skelly CL et al. Paravisceral aortic thrombusas a source of peripheral embolization. Report of three casesand review of the literature. / Vase Surg 2002; 36: 839 - 843.

7 Hahn TL, Dalsing MC, Sawchuk AP et al. Primary aortic muralthrombus: presentation and treatment. Ann Vase Surg 1999; 13:52-59.

8 Bowdish ME, Weaver FA, Liebman HA et al. Anticoagulation isan effective treatment for aortic mural thrombi. J Vase Surg 2002;36:713-719.

9 Seelig MH, Klingler PJ, Oldenburg WA, Blackshear JL.Angiosarcoma of the aorta: report of a case and review of theliterature. / Vase Surg 1998; 28: 732 - 737.

10 Maclennan AC, Doyle DL, Sacks SL. Infectious aortitis due topenicillin-resistant Streptococcus pneumoniae. Ann Vase Surg1997; 11: 533-535.

11 Cherri J, Freitas MA, Llorach-Velludo MA, Piccinato CE.Paracoccidioidomycotic aortitis with embolization to the lowerlimbs. Report of a case and review of the literature. J CardiovascSurg 1998; 39: 573 -576.

12 Lambert AW, Wilkins DC. Popliteal artery entrapmentsyndrome. BrJSurg 1999; 86:1365-1370.

13 Fong H, Downs AR. Popliteal entrapment syndrome with distalembolization. A report of two cases. / Cardiovasc Surg 1989; 30:85-88.

14 Lepori L, Perren A, Gallino A. The popliteal artery entrapmentsyndrome in a patient using anabolic steroids. NEnglJMed 2002;346:1254-1255.

15 Rabkin DG, Goldstein DJ, Flores RM, Benvenisty Al. Spon-taneous popliteal artery dissection: a case report and review ofthe literature. J Vase Surg 1999; 29: 737-740.

16 Eschelman DJ, Gardiner GAJr., Deely DM. Osteochondroma: anunusual cause of vascular disease in young adults. / Vase Interv&Mfio/1995;4:605-613.

17 Vasseur MA, Fabre 0. Vascular complications of osteochon-dromas. / Vase Surg 2000; 31: 532 - 538.

18 Gronefeld G, Zegelmann M, Schulte-Huermann D, Landgraf H.An unusual cause of arterial vascular occlusion with peripheralembolism. VASA 1993; 22: 260-263.

19 Ikezawa T, Naiki K, Moriura S et al. Aneurysm of bilateralpersistent sciatic arteries with ischemic complications: casereport and review of the world literature. J Vase Surg 1994; 20:96-103.

20 Gabelmann A, Kramer SC, Wisianowski C et al. Endovascularinterventions on persistent sciatic arteries. JEndovasc 77^2001;8:622-628.

21 Hoballah JJ, Chalmers RT, Sharp WJ et al. Fecal impaction as acause of acute lower limb ischemia. AmJ Gastroenterol 1995; 90:2055-2057.

22 Mirzayan R, Hanks SE, WTeaver FA. Cocaine-induced thrombosisof common iliac and popliteal arteries. Ann Vase Surg 1998; 12:476-485.

23 Webber J, Kline RA, Lucas CE. Aortic thrombosis associated withcocaine use: report of two cases. Ann Vase Surg 1999; 13: 302-304.

24 Stewart JA, Hamilton PJ, Murdoch AP. Thrombo-embolicdisease associated with ovarian stimulation and assistedconception techniques. Hum Reprod 1997; 12: 2167-2173.

25 Alvarado RG, Liu JY, Zwolak RM. Danazol and limb-threateningarterial thrombosis: two case reports. J Vase Surg 2001; 34:1123-1126.

26 Falkenberg M, Karlsson J, Ortenwall P. Peripheral arterialthrombosis in two young men using anabolic steroids. Eur J VaseEndovasc Surgml; 13: 223-226.

27 McCarthy K, Tang AT, Dalrymple-Hay MJ, Haw MP. Ventricularthrombosis and systemic embolism in bodybuilders: etiologyand management. Ann Thorac Swrg2000; 70: 658-660.

28 Nieminen MS, Ramo MP, Viitasalo M et al. Serious cardiovas-cular side effects of large doses of anabolic steroids in weightlifters. Eur Heart Jim; 17:1576-1583.

29 Murphy KD, McCrohan G, DeMarta DA et al. The heparin-induced thrombocytopenia and thrombosis syndrome: treat-ment with intra-arterial urokinase and systemic platelet aggre-gation inhibitors. CardiovascInterventRadiol 1996; 19:123-127.

30 Cool RM, Herrington JD, W7ong L. Recurrent peripheral arterialthrombosis induced by cisplatin and etoposide. Pharmacotherapy2002; 22:1200-1204.'

31 Molloy RG, Welch GC, Drury JK, Abel BJ. Arterial thrombosisafter chemotherapy with cisplatin, vinblastine and methotrexa-te. BrJ Clin Pract 1995; 49: 50 - 51.

32 Vos AH, Splinter TA, van der Heul C. Arterial occlusive eventsduring chemotherapy for germ cell cancer. NethJMed 2001; 59:295-299.

33 Saphner T, Tormey DC, Gray R. Venous and arterial thrombosisin patients who received adjuvant chemotherapy for breastcancer./Qm Onco/1991; 9: 286-294.

34 Friedman SG, Pellerito JS, Scher L et al. Ultrasound-guidedthrombin injection is the treatment of choice for femoral arterypseudonaeurysms. Arch Swrg-2002; 137: 462-464.

35 Sadiq S, Ibrahim W. Thrombo-embolism complicating thrombininjection of femoral artery pseudoaneurysm: management withintra-arterial thrombolysis./Fast Infers fladio/2001; 12: 633-636.

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36 Rigdon EE. Trousseau's syndrome and acute arterial thrombo-sis. Cardiovasc Surg WOO; 8: 214-218.

37 DiGiovanni RJ, Crilley P, Kerstein MD. Peripheral arterialocclusion in acute promyelocytic leukemia. Cardiovasc Surg1999;7:258-260.

38 Levine JS, Branch DW, Rauch J. The antiphospholipidsyndrome. NEnglJMed20Q2; 346: 752-763.

39 Tan YM, Chia KH. Acute thrombosis associated with hyper-homocysteinemia. EurJ Vase EndovascSurg 2002; 24: 279-280.

40 Nakamura M, Ohnishi T, Okamoto S et al. Abdominal aorticthrombosis in a patient with nephrotic syndrome. AmJNephrol1998; 18: 64-66.

41 Lee CH, Chen KS, Tsai FC et al. Concurrent thrombosis ofcerebral and femoral arteries in a patient with nephroticsyndrome. AmJNephrol 2000; 20: 483-486.

42 Szychta P, Reix T, Sevestre MA et al. Aortic thrombosis andulcerative colitis. Ann Vase Surg2001; 15: 402-404.

43 Novotny DA, Rubin RJ, Slezak FA, Porter JA. Arterial thrombo-embolic complications of inflammatory bowel disease. Report ofthree cases. Dis Colon Rectum 1992; 35:193-196.

44 Buchner N, Sanner B, Tepel M et al. Acute ischemia of the legsand rapidly progressing renal failure in a 39-year-old patient./7iferoirfl999;40:555-560.

45 Pistorius MA, Jego P, Sagan C et al. Arterial embolic mani-festations in the legs revealing isolated aorto-iliac Takayasu'sdisease. JMd Vase 1993; 18: 331-335.

46 Rivers SP, Baur GM, Inahara T, Porter JM. Arm ischemiasecondary to giant cell arteritis. AmJSurg 1982; 143: 554-558.

47 Greene GM, Lain D, Sherwin RM et al. Giant cell arteritis of thelegs. Clinical isolation of severe disease with gangrene andamputations. AmJMed 1986; 81: 727-733.

48 Amatucci G, Del Mastro G, landoli R. Horton giant cell arteritisof the legs. Report of a case. / Cardiovasc Surg 1997; 38: 309 - 312.

49 Bastug DE, Dominic A, Ortiz 0 et al. Popliteal artery thrombosisin a patient with Cogan syndrome: treatment with thrombolysisand percutaneous transluminal angioplasty. Cardiovasc Interv/tofcon997;20:57-59.

50 Bradway MW, Drezner AD. Popliteal aneurysm presenting asacute thrombosis and ischemia in a middle-aged man with ahistory of Kawasaki's disease. / Vase Surg 1997; 26: 884 - 887.

51 Shindo S, Okamoto H, Nagai M et al. Acute ischemia of thelower legs from blunt abdominal trauma: an unusual cause ofatheroembolism. Case report. / Trauma 1994; 36: 451-453.

52 Gupta N, Auer A, Troop B. Seat belt-related injury to thecommon iliac artery: case report and review of the literature./Trauma 1998; 45: 419-421.

53 Jiao LR, Ramanathan A, Ackroyd J. An acute lower limbischaemia with an unusual cause. EurJ Vase Endovasc Surg 1998;15:547-549.

54 Mack L, Forbes TL, Harris KA. Acute aortic thrombosis follo-wing incorrect application of the Heimlich maneuver. Ann VaseSurg 2002; 16:130-133.

55 Ayerdi J, Gupta SK, Sampson LN, Deshmukh N. Acuteabdominal aortic thrombosis following the Heimlich maneuver.Cardiovasc Surg2002: 10; 154-156.

56 Adegboyega PA, Sustento-Reodica N, Adesokan A. Arterialbullet embolism resulting in delayed vascular insufficiency: arationale for mandatory extraction. JTrauma 1996; 41:539-541.

57 Schurr M, McCord S, Croce M. Paradoxical bullet embolism:case report and literature review. J Trauma 1996; 40:1034-1036.

58 Bellemans J, Stockx L, Peerlinck K et al. Arterial occlusion andthrombus aspiration after total knee arthroplasty. Clin Orthop1999; 366:164-168.

59 Ohira T, Fujimoto T, Taniwaki K. Acute popliteal arteryocclusion after total knee arthroplasty. Arch Orthop Trauma Surg1997; 116: 429-430.

60 Canterbury TD, Wheeler WE, Scott-Conner CE. Effects of thelithotomy position on arterial blood flow in the lowerextremities WVmjlWZ; 88:100-101.

61 Geeraerts T, Albaladejo P, Droupy S et al. Acute thrombosis ofexternal iliac artery after short procedure in the high lithotomyposition. Anaesthesiology 2000; 93:1353-1354.

62 Tomlinson MA, Beese R, Banwell M et al. Sequential retro-peritoneal venous hemorrhage and embolism of an angio-sealpuncture closure device complicating iliac artery angioplasty.J Endovasc Surg im; 3: 264-269.

63 Wijesinghe LD, Coughlin PA, Gill K. An unusual cause offemoral embolus. Cardiovasc Surg 2000; 8: 287-288.

64 Parent FN 3rd, Godziachvili V, Meier GH 3rd et al. Endograftlimb occlusion and stenosis after ANCURE endovascularabdominal aneurysm repair. J Vase Surg 2002; 35: 686-690.

26ACUTE ARTERIAL THROMBOSIS

OF THE LOWER LIMBS

WILLIAM PAASKE

An arterial thrombus is a clot formed from the constituents of the blood, and arterialthrombosis signifies the formation, or the presence, of a thrombus within the artery indicating ^the dynamic processes leading to partial or complete cessation of blood flow through the vessel £\)and the events thereafter to the static, functional endpoint of that progression. The term acute, 261in clinically detectable situations, relates to the immediate symptoms and/or signs becomingapparent as a consequence of the thrombosis; the transition from acute to chronic thrombosisis not always clear in the temporal domain, but for all practical purposes it would seemreasonable to restrict the term acute to clinical situations in which a sudden deterioration ofthe peripheral arterial circulation is anamnestically and/or clinically evident.

The dynamic nature of the thrombotic process often extends beyond the time of immediatesymptoms or signs; this is particularly evident in some but not all cases of thrombosis resultingfrom atherosclerotic occlusive disease. In other situations, the thrombus-generated symptomsare stable after they have become clinically recognizable, but the clinical course is oftencharacterized with alleviation of symptoms and mitigation of signs in the early hours afterpresentation.

Incidence OI vascular surgery. From 1996 to 2000, the frequencythrombotic events of admissions for acute ischemia was 11 patients

per 100 000 inhabitants of all ages per year, but theThe exact frequency of admissions for acute reporting system does not differentiate between

thrombotic events is not known; the Danish vascu- embolus and thrombosis, and the figure also in-lar surgical registry of procedures, Karbase, covers eludes events on the upper extremities. It is inter-the entire activity of the country in the services of esting to observe that the male/female ratio was


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0.98 in this Danish material. The Swedish vascularregistry, Swedvasc, includes 913 open proceduresfrom acute ischemia in year 2001 (correspondingto 10 per 100 000 inhabitants of all ages per year,remarkably close to the Danish figure in spite ofpronounced regional variations) with half of theseprocedures given as interventions for embolus, theother half for thrombosis. This distribution is sur-prising and must be considered problematic, witha gross overestimation of the embolic etiology. Thepercentage of procedures on the lower extremitieswas 81.7% in the series. Overall, in the Swedish year2001 material, 10.3% of the patients admitted foracute ischemia died within 30 days (average 1995to 2001 around 12% to 13%); 8.1% were ampu-tated within 30 days, and only 58.2% of the patientshad an uncomplicated course within the first monthafter admission followed by some procedure (openoperation, balloon angioplasty). Of the cases re-corded in year 2001 where the procedure was indi-cated as thrombectomy/embolectomy of the leg,12.7% died within 30 days after the procedure (and23.5% occluded). For bypass procedures, the 30-day mortality was 15.3%, and the occlusion rate was21.6%; the cases treated with balloon or catheterin the leg resulted in a 5.1% 30-day mortality anda 30-day occlusion frequency of 26.1%. Thrombo-lysis for lower limb ischemia was performed in208 primary and supplementary cases in Denmarkin the year 2 000; this corresponds to 3.6 lyses per100 000 inhabitants per year (lysis of grafts is in-cluded in this overall figure).

Common to the Danish and the Swedish materi-als was a massive presence of risk factors and comor-bidities in these patients. In Denmark, 47.2% werenoted in the national material from 1996 to 2000as having cardiac disease, 35.2% hypertension,25.1% pulmonary disease, and 17% previous cere-brovascular disease; 15.4% had diabetes mellitus,and 77.6% were frank enough to report that theywere, or had been, smokers. Only 3.7% had beenamputated previously.

The purpose of this chapter is to give a review ofthe mechanisms, diagnosis, and treatment of acutearterial thrombosis in the native arteries of thelower extremities. Considerations on arterial emboliare discussed in another chapter of this book [1].Thrombosis of grafts and of other previously per-formed arterial reconstructions have been discussedpreviously [2] and shall not be repeated here. Sincean interesting clinical problem is the determinationof an embolic or thrombotic cause of the disease

manifestations, some considerations will be inclu-ded with reference to thrombo-embolism.

Mechanisms

ATHEROSCLEROTIC OCCLUSIVEARTERIAL DISEASE

The most frequent etiological factor for throm-bus formation in the legs is atherosclerotic occlu-sive arterial disease where complex pathogeneticprocesses lead to changes of the morphology, thebiochemistry, the physiology, and the biomechanicsof the vessel wall together with local disturbancesof the blood to vessel wall interface interactions,and generalized changes in the blood constituents[3]. It has been demonstrated that different ath-erosclerotic plaques contain varying proportions ofthe plaque components. From several studies, main-ly on coronary and carotid arteries, it has becomeclear that the main plaque constituents are the con-nective tissue extracellular matrix (collagen, proteo-glycans, fibronectin, elastic fibers), crystalline choles-terol, cholesteryl esters and phospholipids, and cells(monocyte-derived macrophages, T lymphocytes,smooth muscle cells) [4]. The precise nature of thespecific details of the atherosclerotic processes inthe lower extremity arteries is less well known, butthere is evidence to suggest that the practical clas-sification of the plaques based on their histologicalcomposition and structure as suggested by theCommittee on Vascular Lesions of the Council on Arterio-sclerosis, American Heart Association [5] can be gen-eralized and applied to lower extremity arteries aswell. Although this classification has been criticized[6] and updated [7], the concept of the vulnerablearteriosclerotic plaque [8, 9] seems suitable for in-terpretation of infrainguinal arterial pathologiestoo, since the lesions now [7] denoted types VI (sur-face defect, hematoma, thrombosis), VII (calcifica-tion predominates [10]), and VIII (fibrous changespredominate) appear applicable for the purposes ofperipheral vascular surgery. The term vulnerable im-plies vulnerability to plaque disruption with the proba-bility of subsequent acute thrombosis.

The question of stable versus unstable athero-sclerosis has, for obvious reasons, attracted enor-mous attention for coronary and carotid arteries[11], and the notion of a high-risk or vulnerableatherosclerotic plaque with superpositioned throm-bus formation [12] must be investigated in detailin the lower extremities to decide whether it will

ACUTE ARTERIAL THROMBOSIS OF THE LOWER LIMBS

be clinically meaningful to extend this interestingconceptual framework to the patients with vasculardisease in the legs. However, there can be no doubtthat plaque disruption is often the crucial, finalcommon process that converts a nonocclusive,often clinically silent atherosclerotic lesion to a po-tentially limb-threatening, invalidating, or fatal con-dition [13]. The recent developments in clinicalimaging, especially high-resolution multicontrastmagnetic resonance (MR) technology and electronbeam computed tomography (for assessment of cal-cification), should be applied for plaque imagingand characterization in extremity arteries as a nextstep to the investigations performed on the aorta,coronary, and carotid arteries [4]. The effect ofearly detection of peripheral lesions as markers oflocalized and possibly generalized atheroscleroticdisease followed by risk reduction and modificationtogether with targeted medical therapy, for the timebeing notably statins [14], is an apparent and ur-gent subject for concerted international multicen-ter trials comprising large-scale cohorts.

The presently available experimental evidenceobtained on autopsy-based models with doppleranemometry [15] as well as with advanced nonin-vasive MR techniques in vivo [16,17] has definitelyshown an association between atherosclerosis devel-opment and low and oscillating wall shear stress onthe interface between the blood and the endothe-lium. This means that there are now firm observa-tions to support the theory of a relation betweenthe physical forces acting on the arterial wall andthe development of atherosclerosis in certain pre-disposed segments of the arterial tree. Extrapola-ting from these data, one must assume that theclinical correlates of the atherosclerotic process tothe thrombotic mechanisms, at least to some un-specified degree, reflect the uneven distribution ofthe frictional forces acting on the arterial wall inthe lower extremity as well as in the aorta [17] andcarotid arteries [18,19].

Arterial remodeling also in connection with ath-erosclerotic stenosis development is well known.The anatomical changes induced by the remodel-ing process may add risk for thrombosis with hyper-tension, unstable shape of plaque, thickness ofplaque, and the extent of the stenosis as risk fac-tors for outward remodeling at least of carotid arter-ies [20]. This is probably of clinical importance inrestenosis following angioplasty in leg arteries too,and whether new, experimental drugs such assirolimus [21] will be useful for extremity arterial

disease is open to speculation. In a recent study,pairs of atherosclerotic femoral arteries showedconcordance in plaque size, expansive remodeling,and occurrence of plaques containing a lipid-richcore, but no concordance in plaque inflammationbetween right and left arteries. These findingsstrongly suggest that not only the amount of ath-erosclerosis but also arterial remodeling and plaquelipid deposition is influenced by systemic factors[22].

Thrombosis leads to endothelial dysfunction[23]. These phenomena are evidently secondaryand obligatory to the atherosclerotic degenerationof the vessel wall, but the pathophysiologic conse-quences have not been clarified in details specifi-cally with regard to the leg arteries [24]. It is ofhigh theoretical interest that modest hyperinsu-linemia, mimicking fasting hyperinsulinemia of in-sulin-resistant states, abrogates endothelium-de-pendent vasodilatation in large conduit arteries,probably by increasing oxidant stress [25]. Since ni-trous oxide, which is formed in normal endothe-lial cells, is of great importance for the modulationof the peripheral vascular resistance, especially indiabetics [26], there is evidence for the fact thatvasodilatation (by NO-induced reduction of intra-cellular calcium) together with autoregulation ofblood flow and the veno-arteriolar sympatheticaxon reflex are disturbed in patients with athero-sclerosis in the legs [27]. Oxidation of lipids con-sumes NO in itself, and the overall effect of de-creased NO in atherosclerosis is then increased riskof platelet aggregation, increased platelet adhesionto the endothelial surface, increased invasion ofmonocytes, higher arterial muscular tonus, and hy-pertrophy of the smooth muscle cells in the vesselwall.

Finally, it has been shown that patients with inter-mittent claudication have disturbances in variousrheological variables (red blood cell aggregation,hematocrit, viscosity; leukocyte and platelet activa-tion in atherosclerotic regions) [28-30] that will addto the thrombogenic potential. Also, the amountof exercise-provoked micro-albuminuria in claudi-cants is associated with the degree of ischemia[31,32], an interesting observation, since micro-al-buminuria is a marker of endothelial dysfunction[33].

Local arterial thrombosis secondary to athero-sclerosis is the crucial stage of multiple, extremelycomplex, local, and generalized processes leadingto blood flow interruption and, possibly, to acute

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clinical presentation; it is, however, not the end pointof the pathological process as is well known [5].

ARTERIAL THROMBOEMBOLISM AND EMBOLIIn the view of this author, the concept of arterial

thrombo-embolism is dangerous. In the classical lit-erature, it is repeatedly envisaged that a thrombuscan cause embolization in the more distally locatedvascular tree by partial or complete loosening ofthe thrombus at the site of formation with subse-quent symptoms or signs arising de novo or beingaccentuated by a deterioration of the pre-embolicclinical condition. This is certainly of high clinicalimportance in the carotid artery territory [34], oftenresulting in focal neurologic deficits such as amau-rosis fugax, transitory ischemic attacks, and stroke.In patients with atherosclerosis causing thrombosisof the major arteries of the leg, there are frequentlysynchronous atherosclerotic lesions in the cruralarteries as well. The development of thrombosis inthe major leg arteries may lead to perfusion reduc-tion in the more distal arteries and decrease of thelinear blood flow velocities, so this multifacetedcondition, often accompanied by congestive heartdisease, hypotension, and dehydration, causes a stag-nant, intra-arterial blood pool causing favorableconditions for distal thrombosis. It seems to me thatan embolic etiology can rarely be established withconfidence in patients with suspected or sympto-matic occlusive arterial disease in the legs, whereassecondary crural artery thrombosis arising as des-cribed rather than caused by thrombo-embolismgives a more meaningful interpretation of the clin-ical situation. In other cases, of course, peripheralthrombosis may be secondary to embolization. Inwell-established situations such as in the presenceof an ulcerated aortic plaque or a shaggy aorta,thrombo-embolism may be a relevant underlyingmechanism behind for example blue toe syndrome(most frequently cholesterol athero-embolism); it isoften obvious after percutaneous transluminalangioplasty [35], and occasionally after open recon-structions [36]. Overall, the incidence of primaryembolization of the leg arteries is rapidly decreas-ing because of the improved medical treatment ofrheumatic heart disease, atrial fibrillation, andmyocardial infarction.

ANEURYSMThe development of nonspecific abdominal aor-

tic aneurysms can no longer be attributed to sim-ple atherosclerotic wall degeneration because mul-

tiple studies have shown complex disturbances inthe normal molecular biology of the aortic wall inthese aneurysm patients [37]. The debate on a pos-sibly genetic etiology has not been settled as yet[38] although generalized aneurysmal disease (andsystolic blood pressure) are associated with poly-morphic variation in the fibrillin-1 gene [39]. Also,the expression of angiogenic factors such as vascu-lar endothelial growth factors [40] and the oxida-tive stress [41] seem to be involved in the patho-genesis of aneurysms. Autoimmune [42,43] or eveninfectious pathogeneses (notably Chlamydia pneu-moniae) have also been suggested, the latter beinghighly controversial [44]. Since there is some de-gree of concordance between abdominal aortic andpopliteal aneurysms (around 10% of patients withabdominal aneurysm also have popliteal aneur-ysm) , it seems reasonable to suggest common etio-logy and pathogenesis for development of someaneurysmal types. Recently, this notion has foundexperimental substantiation, since the architectur-al changes in the vessel wall (primarily fragmenta-tion of the elastic lamellae), the loss of vascularsmooth muscle cells, and the increased amount ofinflammatory infiltrate seem to be analogous; be-sides a number of biochemical markers, includingthose of apoptosis, support a unifying theory for ar-terial aneurysm development [45]. Experimental evi-dence has also pointed toward generalized involve-ment of the arterioles as well as the larger arteries[46]. There is also reduction in tensile strength andstiffness in venous tissue from patients with ab-dominal aortic aneurysm that is associated with dis-ruption and reduction of the elastin contents of thevein wall; these changes are analogous to those ob-served in the arterial aneurysmal wall and confirmthe systemic nature of this disorder [47]. Further,it has been shown that aortic aneurysms appear tobe an important source of circulating interleukin-6where the concentration is influenced by genotype[48], but it remains to be examined whether thisholds true for popliteal aneurysms as well.

It has been demonstrated that there is a surpris-ingly high occurrence of popliteal aneurysm in pa-tients with the popliteal entrapment syndrome [49].These aneurysms are seen in young patients, pre-dominantly below 30 years of age, and it seems rea-sonable to infer that the cause of the developmentof aneurysm in this situation is the hemodynamicdisturbances induced by the stenotic compressionof the artery leading to poststenotic aneurysm for-mation, a remodeling response.


As with other aneurysms, those in the poplitealartery may thrombose; while the frequency is notknown, older materials suggest that it is around40% [50] with one quarter presenting with signs ofacute and one quarter with chronic ischemia.Thrombosis must be conceived as being due to thepathologic blood flow patterns within and belowthe aneurysmal sac, but it cannot be excluded thatemboli loosened from the aneurysm may impederun off in a progressive manner and result in a vari-ant of stagnant flow thrombosis.

Cystic adventitial disease of the popliteal arteryrarely leads to thrombosis whereas claudication iscommon [51]. At least in the United States, lesionsof the popliteal artery in high-performance athletesseem rather frequent [52].

ARTERIAL TRAUMAThe mechanisms of arterial trauma with subse-

quent acute thrombosis and the patterns of com-plications of vascular injury management are welldocumented in the literature [53]. In civilian prac-tice in Denmark and Sweden, only 0.5 and 1.0 pro-cedures are performed per 100 000 inhabitants peryear for vascular trauma [54], respectively. Aroundtwo thirds affect the lower limb arteries [55]. Theexact frequency of interventions performed by vas-cular surgeons for iatrogenic trauma is not knownbut it probably exceeds 40% of all vascular injuriesin European countries without armed conflicts[56]. The increasing volume of invasive examina-tions and treatments (cardiac catheterizations,angiographic procedures, percutaneous translumi-nal angioplasty, orthopedic and neurosurgical pro-cedures) has led to an increasing frequency ofsymptomatic lesions that need open, vascular sur-gical interventions. The mechanisms behind theacute thrombosis are multifactorial, and spasmmust always be kept in mind. Local thrombosis canoccur after contusion damages or in the vicinity ofthe path of a projectile through the vessels. Evenwith minimal endothelial damage, thrombosis canresult as a consequence of local platelet aggrega-tion and fibrin accumulation. The conditions forlocal thrombosis also occur after fracture of theintima, either partial or complete (blunt violenceor penetrating trauma). Thrombosis is likely tooccur when a local dissection and coiling of theintima reduces blood flow, and even a small, local-ized, intramural hematoma changes the propertiesof the overlying endothelium to make it highlythrombogenic. Local lacerations are frequently ac-

companied by pulsating hematomas, local spasms,and intramural bleeding. Under unfavorable cir-cumstances, hematomas in surrounding soft tissuescan compress the artery with local occlusion andthrombosis. After stretching of the artery, and, ofcourse, transection, thrombosis may occur. A spe-cial case occurs in drug addicts who inject varioussubstances into the arteries. These arterial traumashave their highest prevalence in younger patientswithout notable collateral vessel formation whichgive rise to deep, distal ischemia that often neces-sitates urgent attempts of revascularization.

PHLEGMASIA CERULEA DOLENSThis is a rare but important cause of acute arte-

rial thrombosis of the lower limbs. Phkgmasia ceruleadolens is the term for the clinical picture seen inmassive, acute venous ilio-femoral thrombosis withlife-threatening obstruction of the venous return,included the microvascular collaterals; occasionallycompartment syndrome accompanies the seriousstate. The disease is most often seen on the leftside in critically ill patients with medical problemssuch as hypercoagulation, serious infections (strep-tococcal fasciitis, Staphillococus aureus sepsis), incom-pensated heart disease, cancer or other chronicconditions that interfere with the clotting of theblood or the patient's mobility (postoperativestate), but it can also occur rapidly and sponta-neously in previously healthy individuals, such aspregnant or post partum women, and in children[57]. The reason for the accompanying secondaryarterial thrombosis is stagnant flow due to the pri-mary outflow obstruction.

Miscellaneous

AORTIC DISSECTION [58]Aortic dissection occasionally or often (12% to

55%, materials vary) affects inflow to the legs, exclu-sively or in combination with ischemia of other endorgans [59]. The ischemia is produced by obliter-ation of the peripheral vessel origin (s) into the dis-section or obliteration of the true lumen by anexpanding false lumen. Marfan's syndrome some-times causes lower limb ischemia [60-62], whereasleg ischemia due to Ehlers-Danlos syndrome seemsmore often to be caused by rupture of the oftenaneurysmatic aorta or iliacs [63,64]. Spontaneousdissection of the infrarenal aorta is very rare but it

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should be known that 50% extend into the iliac orfemoral arteries [65].

FlBROMUSCULAR DYSPLASIAFibromuscular dysplasia of the lower limbs is

rare [66] and can be unilateral as well as bilater-al and give rise to hypoplasia and anisomelia inchildren [67]. The literature contains a few reportson isolated crural artery affection [68]; the pro-funda femoris artery can also be diseased [69],whereas iliac artery disease seems to be a bit morefrequent. It has not been investigated whether theendothelial properties are deranged in this disease,but due to the very nature of the wall changes,local vasomotor control must be assumed to be se-verely compromised.

CYSTIC ADVENTITIAL DISEASECystic adventitial disease most often affects the

popliteal artery [70] but can also be found in veins;it is characteristic that the lesions appear near anarticulation (knee, ankle, elbow, wrist) [71], butlesions in the common femoral artery have alsobeen described [72]. Ultrasound will provide thediagnosis, although MR scanning will probably beindicated for precise visualization.

EXTERNAL COMPRESSIONExternal compression of the arteries with subse-

quent thrombosis in the lower limbs can be seenin the popliteal entrapment syndrome [73-75], thecompartment syndrome [76], in pregnancy withaortic dissection [77], and in combination withtrauma.

ARTERITISTakayasu's disease, which has recently been de-

scribed with simultaneous occurrence of Marfan'ssyndrome [78], Buerger's disease (thromboangiitisobliterans) [79], and Horton giant cell arteritis [80]are unusual and rare causes of thrombosis in west-ern countries. Adamantiades-Behcet's disease in theangio variant is characterized by venous thrombo-sis and, on the arterial side, aneurysms (often mul-tiple) are frequently encountered together with lo-calized or more widespread arterial thromboses[81,82]. Due to the huge number of immigrants tonorthwestern Europe from the Middle East andAsia, the prevalence and incidence will increasehere to approach that of the Mediterranean re-gions. Raynaud's disease occasionally causes throm-bosis in distal arteries [83]. Patients with periar-

teritis nodosa with aneurysms and those with sys-temic lupus erythematosus are seldom seen by vas-cular surgeons, but one should be aware that thesediseases occasionally include secondary thrombosisin the clinical pattern. Cannabis as a cause of ar-teritis in young smokers seems to be forgotten asa cause of thrombosis and distal necrosis but shouldbe kept in mind [84].

COAGULATION DISORDERS,TOBACCO, DRUGS

It is beyond the scope of this chapter to discussthese states; long, systematic lists can be found in re-levant textbooks and in recent reviews [85]. Spasmsmust, as always, be kept in mind (ergotism, cocaine,heroin, temazepam, digitalis).

Diagnosis

Acute arterial thrombosis of the lower limbs is aclinical diagnosis that can be made with a high de-gree of certainty if based on a careful, analyticalsynthesis of anamnesis, symptoms, and signs. Onlyin selected cases, it should be considered to ordersupplementary examinations. Besides, it is essentialto decide whether treatment should be initiated in-stantly, or whether it is advisable to postpone treat-ment as a consequence of one or more delayingdiagnostic procedures. In other cases, waiting withtreatment can be indicated after a balanced judg-ment (watchful waiting). The overriding consider-ation must always be that the risk to limbs and lifefor each and every patient must be minimized. Ajudgment of the safety of the system in which thesurgeon is compelled to act must, as usual, be ba-lanced toward the aggregated risk to which the pa-tient is exposed.

The clinical picture is well known: it can varyfrom the asymptomatic to the catastrophic. The de-velopment of symptoms is dependent on theanatomical localization and extent of the throm-bosis, the degree of a possible collateral circulation,and the general state of the patient. One extremeis the sudden appearance of intense Pain withPallor, Paresthesia, Paralysis, Pulselessness, andPoikilothermia (the six P); in other cases, a sud-den occlusion of for example the superficial fem-oral artery can occur asymptomatically in an eld-erly patient with slowly progressing atherosclerosiswith gradual development of compensatory collat-


eral circulation. The conventional sign of pallor ismisleading, cyanosis may be elicited or supercedepallor. An estimation of the venous filling or of thecapillary return may be helpful. In many cases thesymptoms will be relieved within hours, but otherpatients will have to be revascularized within a timespan of four to six hours, less in children and youngadults. Usually, the muscles will exhibit histologicalsigns of warm ischemia after some four hours withedema (macroscopic fish flesh appearance) where-as the skin commonly can tolerate a more extend-ed time span before necrosis develops, except inphlegmasia cerulea dolens where bullae as a sign ofskin necrosis can occur rapidly. In a pathophysio-logic context, it must be remembered that throm-bosis in the major arteries, where adequate collat-erals are not present or not adequate, will befollowed by thrombosis in the microcirculation. Thismeans that there is a possibility for the postopera-tive occurrence of the no reflow phenomenon, i.e.,the capillary perfusion will not show signs of im-provement in spite of even perfect blood deliverythrough the revascularized arterial system. Pulse pal-pation is a difficult art and meaningful interpreta-tion is difficult.

In light cases there will be moderate pain andpale skin with no effect on motor or sensory ner-vous function. The next step is more intense painand development of paresthesia with numbness pro-gressing to loss of sensation. The sense of light touchwill be diminished and proprioception may disap-pear, whereas decreased temperature sense andtwo-point discrimination will disappear later (butbefore the deep pain and pressure senses are lost)since these sensory modalities are conductedthrough less hypoxia-sensitive fibers. The most seri-ous case is a livid, anesthetic foot without capillaryperfusion and venous filling together with rigidityof the crural muscles (rigor mortis) causing lack ofdorsiflexion and plantar flexion of the toes aloneor in combination with paresis of the ankle joint.In these patients, amputation may be an immedi-ate option. A special variant is present in diabeticswith preexisting sensory deficits.

The Joint Council of The Society for Vascular Surgeryand the North American Chapter of the InternationalSociety for Cardiovascular Surgery have approved a setof recommended standards for reports dealing withlower extremity ischemia [86]. These are, however,problematic since presence or absence of arterialand venous doppler signals are included in the al-gorithm for classification into the clinical cate-

gories. The purely clinical descriptors for catego-rization of this type of ischemia are appropriate andmay help to decide the plan of action. In some em-inent textbooks (for example the standard work ed-ited by Rutherford [87]), emphasis is laid on doc-umenting the doppler segmental pressures. Thiscan also be questioned since the methodologicaluncertainties [88] in combination with the erro-neous measurements in certain patient groups (no-tably diabetics [89,90]) make it dangerous to inter-pret these recordings in a meaningful way. Evenstandardized ankle and toe blood pressure meas-urements performed in specialist laboratories withstrain gauge equipment cannot be relied upon fordiagnosis of acute thrombosis, especially in athero-sclerotic patients, because of the wide standard vari-ations [91]. The point is that acute thrombosis is aclinical diagnosis and that reliance on seemingly"objective" vascular laboratory measurements isdangerous.

To supplement the clinical examination, ultra-sound duplex scanning can be performed with rea-sonable confidence as a pre-operative procedure inat least chronic atherosclerotic occlusive disease[92,93], but in the acute situation its use is moreproblematic for arterial affection. In highly spe-cialized laboratories, duplex may obviate the needfor pre-operative angiography [94], but some sys-tematic series are not so optimistic [95-97] with re-gard of getting precise, and usable, information asto the run off in distal, crural and pedal arteriesfor potential bypass procedures. Angiography, asduplex, should only in rare cases be considered asdiagnostic but rather as a necessary pre-operative,or preinterventional, tool for detailed planning ofthe therapeutic procedure.

Ultrasound duplex is the diagnostic procedure ofchoice for phlegmasia cerulea dolens, with veryhigh sensitivity and specificity (around 95%) [98,99]. It should be performed absolutely at once with-out delay as soon as clinical suspicion has arisen,and on liberal indications.

The standard imaging technique for arterialthrombosis remains digital subtraction angiography(DSA) with intra-arterial injection of a contrastagent. The newer digital subtraction techniques[100] combined with contrast (signal to noise) en-hancing agents have made MR angiography anoption [101-104], but where thrombolysis or otherendovascular procedures (for example suction/as-piration [105]) are possibilities, the first choice re-mains DSA, except in diabetics and patients with

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impaired kidney function. The new spiral or mul-tislice computed tomography scanners can providegood three-dimensional multiplanar reconstruc-tions of the major arteries by bench postprocessing;experience with crural and pedal arteries is limit-ed but promising [102,106,107].

In selected difficult cases, we have occasionallyfound it helpful to visualize the degree of ischemiain the crural skeletal muscles by plain MR imaging(estimates of muscle edema) or by MR spectroscopy.

Advanced indicator kinetic methods such as thesingle injection, residue detection method [108,109] have been used experimentally in humans,and animals, to determine the capillary permeabil-ity of selected indicators in the peripheral tissuesand the heart [110,111]. We recently attempted tocombine these methods (which are based on theprinciples of irreversible thermodynamics and sto-chastic black box analysis) with the investigativeoptions presented by positron electron tomogra-phical scanning and apply them to patients withintermittent claudication and critical ischemia. Thework is in progress in our institution and has notas yet been published. These technologies, whichare very expensive and time consuming, open newwindows of opportunity to assess objectively thedegree of acute ischemia.

Treatment

The decision to treat acute thrombosis of the legarteries is dependent on a complex set of factorsof which not all can be subjected to a strict scien-tific analysis. The available literature is, also in thiscase, often not clear with respect to essential data[112,113].

The starting point is to decide whether treatmentis indeed indicated. In an unknown proportion ofcases, acute thrombosis of the superficial femoralartery is entirely asymptomatic, presumably oftenwith absence or very discrete signs of clinical man-ifestations, as already noted by Fontaine [114]. Thegray zone, where slight clinical symptoms and signsdecline into minimal or absent problems after aperiod of observation, presents itself as an oppor-tunity for the vascular surgeon to contemplaterestraint of therapeutic enthusiasm: It can be done,but should it? For example, acute onset of claudi-cation will frequently, if not always, merit a phaseof observation and conservative treatment (stop

smoking and keep walking [115]). Often, strict sci-entific information for an informed clinical riskassessment is simply not available, and the strategymust be left to best clinical judgment, which maylater be the subject of forensic controversy, com-plaints or litigation. Of the 424 claims recordedagainst vascular surgeons in the United Kingdom,36 cases regarded alleged failure to recognize ortreat ischemia [116].

Acute limb ischemia was defined by the Trans-Atlantic Inter-Society Consensus (TASC) as any suddendecrease or worsening in limb perfusion causing apotential threat to extremity viability [117], andacute arterial thrombosis was identified as one ofthe two major causes of acute limb ischemia, theother one being embolus. If the acute ischemia is,or potentially or manifestly becomes, a threat forlimb viability, vascular surgical treatment is often,but not always, contraindicated. If the general stateof the patient makes vascular surgical interventionproblematic, or if the result of a considered analy-sis of the comorbidities is destructive, primary am-putation might be indicated; this is generally thecase in situations where the leg shows signs of motorparalysis as a result of extreme ischemia. Since athrombosis may show signs of progression, some au-thors [85] advocate the immediate routine admin-istration of intravenous heparin. If time permits,the general state of the patient should be optimizedafter consultation with experienced medical col-leagues, notably anesthesiologists and cardiologists.

In the acute phase, the overall strategy is to in-tervene in order to convert the acute situation intothat immediately prior to this acute episode; thismeans that definite lege artis arterial reconstructionshould be postponed and undertaken as an elec-tive procedure, if at all possible. At the preliminarystage, the intra-arterial catheter-directed throm-bolytic therapies are presumed helpful accordingto vascular surgical mainstream thinking to allevi-ate the acute symptoms, occasionally to dissolve thethrombus, to increase or restore distal perfusion,and to make visualization of the run off possible,either immediately or after a period of drug infu-sion where the window of therapeutic expectancythus becomes widened [118]. Translated, thismeans that thrombolysis can be indicated in theacute patient coming in the evening and going onovernight to convert the patient's treatment froma possibly risky emergency operation to a moresafer, considered, and elective daylight case afterproper visualization of the run off options. This has


the additional advantage of giving more time to al-leviate or remove associated generalized risk factors.It must be stressed, though, that a recent Cochranereview addressed the question of whether the pre-ferred initial treatment for acute limb ischemia wassurgery or thrombolysis; embolic, thrombotic andother cases were included in the analysis [119]. Allin all, five trials were identified for inclusion ac-cording to the Cochrane entry criteria, and the ag-gregated material comprised 1 283 patients, notablythe STILE 1994 [120-123] and TOPAS 1996 [120,124-126] series; also included was the small (n=20)Swedish material [127]. The conclusion was as fol-lows: "Universal initial treatment with either surgeryor thrombolysis cannot be advocated on the avail-able evidence. There is no overall difference in limbsalvage or death at one year between initial surgeryand initial thrombolysis. Thrombolysis may be as-sociated with a higher risk of ongoing limb ischemia,and of hemorrhagic complications, including stroke.The higher risk of complications must be balancedagainst risks of surgery in each patient." This at-tempt at a structured meta-analysis from the present-ly available literature must be considered most prob-lematic. As the Cochrane reviewers themselves note,there were major differences in patient demo-graphics, including severity of ischemia, site of oc-clusion, prosthetic or native vessel, and lytic regimeand agent, and caution is required in interpretingthe results of the meta-analysis of the data. It is nec-essary to point out in this connection that the datafrom the STILE study have indicated that for pa-tients with subacute limb ischemia due to nativevessel occlusion, surgery is both more effective andmore durable than thrombolysis, as pointed out bythe Leicester group [128]. Recently reported stud-ies continue to report heterogeneous materials[129,130], although smaller but more focused se-ries [131] seem to corroborate the view that throm-bolysis has its place in the acute phases. Whetheradvancing age is a risk factor for lysis is controver-sial [132,133]. A Markov decision tree analysisbased on the TOPAS series information and ex-penditures in a New York environment concludedthat initial surgery provided the most efficient andeconomical use of resources for acute lower ex-tremity arterial occlusion; besides, the high cost ofthrombolysis was related to the expense of the lyticagents, the need for subsequent interventions inpatients treated with initial lysis, and the long-termcosts of amputation in patients who fail lytic ther-apy [134]. In conclusion, and in line with the

Thrombolysis Consensus Document of 1998 [135], thescientific evidence for thrombolysis simply is not yetavailable but the data must nevertheless be con-sidered to be sufficiently cogent for approval ofagents. Finally, it should be noted that systemicintravenous infusion of thrombolytic agents for na-tive artery occlusion must be considered obsolete[135]. The problem of lysis of thrombosed poplitealaneurysms, and the distal vasculature, has been verymuch debated, but there seems to be a growingconsensus for lysis followed by permanent recon-struction [136-138] and also for elective operationof nonthrombosed aneurysms at that location[139]. Recent European series maintain the im-portance of an aggressive surgical approach toacute thrombosis [128].

The most common site of thrombosis in athero-sclerotic patients is the superficial femoral artery.In these cases, the proper strategy is revasculariza-tion with an in-situ or reversed saphenous vein graft[113]; the second choice is implantation of a syn-thetic graft. There is still controversy as to whetherPTFE (polytetrafluoroethylene) is preferable to da-cron (polyester; polyethyleneterephthalate) [140,142], and a recent Cochrane review [143] con-cluded that there is no clear evidence which typeof graft is best for femoropopliteal grafting, that interms of autologous graft patency in-situ andreversed vein grafts are equally successful whilehuman umbilical vein performs better than PTFE,and that a distal vein cuff may improve primarypatency for below-knee PTFE femoropopliteal graft-ing. In a very recent study, obviously not includedin the Cochrane review, the two-year results of thePop-Up multicentered (Denmark, Norway, Finland)and randomized study comprising 427 patientswere presented [144]: 413 patients with 208 dacron(Uni-Graft, B-Braun Aesculap) and 205 PTFE (Go-retex; W.L. Gore Inc.) grafts were available foranalysis. The two-year primary patency rates were68% for Dacron and 57% for PTFE (p=0.05), andthe secondary patency rates were 76% and 63%respectively (p=0.01); amputations, mortality, and30-day complications occurred at identical rates.However, this series did not focus on surgery foracute ischemia due to thrombosis, but it seems rea-sonable to extrapolate the results.

Isolated thromboses of the common femoral arteryand the deep femoral artery are rarer and can usu-ally be managed by local thrombo-endarterectomythrough groin incisions; they are not suitable forendovascular procedures, whereas the newer stent

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graft endoprostheses [145-148] might prove theirefficiency for recanalization of the superficial fem-oral artery, but their place in the treatment of acutethromboses has not been settled.

The Amplatz thrombectomy device has been usedfor recanalization of acute occlusions of both thesuperficial and the deep femoral arteries, but thereports are anecdotal [149]. The Rotarex rotationalthrombectomy catheter has been deployed in acuteand subacute thromboses with occlusions of themiddle or distal third of the superficial femoralartery or the popliteal artery; the results seem towarrant further studies [150]. Generally speaking,percutaneous thrombectomy may prove to becomean option for treatment of acute thromboses [151],also for more distal pathology [152].

There is still controversy regarding whether shortor long reversed saphenous vein grafts should beapplied for treatment of a localized popliteal throm-bosis. Some surgeons prefer to use the distal super-ficial femoral artery or the proximal popliteal ar-tery as the inlet site for the bypass whereas othersadvocate mounting of a conventional saphenousvein in-situ graft from the groin to the infragenicu-lar popliteal artery. The case for the long graft iscorroborated by the fact that later development ofatherosclerosis in the superficial femoral artery maynecessitate further procedures in the long term.The short-term results seem to be identical. Theendovascular techniques with endografts and/orstents are not yet established procedures [153].

The in-situ long saphenous vein graft technique(with or without the new endoscopic techniques[154] or blind valvulotomy [155]) is eminently suit-able for thromboses necessitating a distal anasto-mosis below the knee joint, even for reconstructionof the foot arteries, as documented by a wealth ofliterature reports. The strict scientific evidence, how-ever, as to the superiority of the in-situ technique

in preference to the reversed method, is not avail-able [113], and presently the choice of proceduremust be left to the discretion of the surgeon [156,157]. Implantation of synthetic prostheses with dis-tal anastomosis below the knee joint should be re-stricted to limb salvage cases after consideration ofother options, for example the use of, spliced, armveins [158] or other venous conduits.

The efficacy of subintimal angioplasty of isolatedinfragenicular lesions is well documented [159,160], but the place of this sophisticated treatmentis not settled for acute cases.

Finally, one should always exert a high level ofsuspicion for the development of revascularizationcompartment syndrome whether after thrombolysisor open surgery for acute thromboses [161].

Conclusion

Surgical treatment of acute lower limb throm-boses is one of the core areas in clinical vascularsurgery accounting for around 10 open proceduresper 100 000 inhabitants of all ages per year in theScandinavian countries corresponding to 10% to15% of the total workload. Thrombolysis accountsfor 3.6 cases per 100 000 per year (graft lysis in-cluded) . Typical patients are high-risk old age pen-sioners with complex histories, previous interven-tions, together with presence of multiple risk factorsand comorbidities. The diagnosis is made on clini-cal grounds, and whereas the available diagnosticprocedures can establish the precise location of thethrombotic processes and clarify the treatment op-tions, the clinical decision of whether, when, andhow to treat is highly complex and dependent ona multitude of factors, of which only a few havesolid scientific evidence.

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113 Paaske WP. Femoropopliteal reconstruction. In: BranchereauA, Jacobs M (eds). Critical limb ischemia. Armonk, FuturaPublishing Co, 1999: pp 147.164.

114 Fontaine R, Kim M, Kieny R. Die chirurgische Behandlung derperipheren Durchblutungsstorungen. Helvetica Chirurgica Ada1954; 5/6: 499-533.

USHousley E. Treating claudication in five words. Br Medjl%8;296: 1483-1484.

116 Campbell WB, France F, Goodwin HM. Medicolegal claims invascular surgery. Ann R Coll SurgEngl 2002; 84: 181-184.

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118 Hall TB, Matson M, Belli AM. Thrombolysis in the peripheralvascular system. Eur Radiol 2001; 11: 439-445.

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122 Weaver FA, Comerota AJ, Youngblood M et al. Surgical revas-cularization versus thrombolysis for nonembolic lower extrem-ity native artery occlusions: results of a prospective randomizedtrial. The STILE investigators. Surgery versus thrombolysis forischemia of the lower extremity. J Vase Surg 1996; 24: 513.523.

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126 Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinanturokinase with vascular surgery as initial treatment for acutearterial occlusion of the legs. Thrombolysis or PeripheralArterial Surgery (TOPAS) investigators. NEnglJMed 1998; 338:1105-1111.

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128Pemberton M, Varty K, Nydahl S, Bell PR. The surgical man-agement of acute limb ischaemia due to native vessel occlu-sion. EurJ Vase Endovasc Surg 1999; 17: 72-76.

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130 Swischuk JL, Fox PF, Young K et al. Transcatheter intra-arterialinfusion of rt-PA for acute lower limb ischemia: results andcomplications. / Vase Interv Radiol 2001; 12: 423-430.

131 Suggs WD, Cynamon J, Martin B et al. When is urokinase treat-ment an effective sole or adjunctive treatment for acute limbischemia secondary to native artery occlusion? Am J Surg 1999;178: 103.106.

132 Braithwaite BD, Davies B, Birch PA et al. Management of acuteleg ischaemia in the elderly. BrJSurg 1998; 85: 217-220.

133 Lambert AW, Trkulja D, Fox AD et al. Age-related outcomefor peripheral thrombolysis. EurJ Vase Endovasc Surg 1999; 17:144.148.

134Patel ST, Haser PB, Bush HL Jr, Kent KG. Is thrombolysis oflower extremity acute arterial occlusion cost-effective? J SurgRes 1999; 83: 106-112.

135 Anonymous. Thrombolysis in the management of lower limbperipheral arterial occlusion. A consensus document. Workingparty on thrombolysis in the management of limb ischemia.Am/Carrfw/1998;81: 207-218.

136Dorigo W, Pulli R, Turini F et al. Acute leg ischaemia fromthrombosed popliteal artery aneurysms: role of pre-operativethrombolysis. EurJ Vase Endovasc Surg 2002; 23: 251-254.

137 Steinmetz E, Bouchot 0, Faroy F et al. Pre-operative intra-arte-rial thrombolysis before surgical revascularization for poplitealartery aneurysm with acute ischemia. Ann Vase Surg 2000; 14:360.364.

138Greenberg R, Wellander E, Nyman U et al. Aggressive treat-ment of acute limb ischemia due to thrombosed poplitealaneurysms. EurJ Radiol 1998; 28: 211-218.

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142 Post S, Kraus T, Muller-Reinartz U et al. Dacron vs. polytetra-fluoroethylene grafts for femoropopliteal bypass: a prospectiverandomised multicentre trial. EurJ Vase Endovasc Surg 2001; 22:226.231.

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146Bauermeister G. Endovascular stent-grafting in the treatmentof superficial femoral artery occlusive disease. / Endovasc Ther2001; 8: 315-320.

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148 Rubin BG, Sicard GA. The Hemobahn endoprosthesis: a self-expanding polytetrafluoroethylene-covered endoprosthesis forthe treatment of peripheral arterial occlusive disease after bal-loon angioplasty. / Vase Surg ZOO}; 33 (2 Suppl): S124-S128.

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ARTERIAL EMBOLIOF THE LOWER LIMBS

MICHAEL HORROCKS

It is now well recognized that acute leg ischemia is a dangerous condition leading to loss oflimb and loss of life. In a major review of acute leg ischemia reported by the Vascular SurgicalSociety of Great Britain and Ireland, limb salvage rates were only 70 % and there was a 22%mortality rate during the same hospital stay [1], With the declining incidence of rheumaticheart disease and increased evidence of acute on chronic ischemia, an accurate and speedydiagnosis is essential so that the appropriate treatment can be given.

Acute arterial ischemia is caused either by an embolusfrom a proximal source or by primarythrombosis of the artery itself. It is important to try and distinguish between these twoprincipal causes, as the outcome may be quite different and the treatment required may beselected according to etiology.

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Background

In a review of intra-arterial thrombolysis in theUnited Kingdom, it was shown that there were ap-proximately 5 000 patients presenting annually withacute lower limb ischemia [2]. The etiology wasfound to be thrombo-embolic disease in the vast ma-jority of cases, and thrombosis had now replacedembolism as the principal cause of acute ischemia.Thrombosis accounted for approximately 60% of allcases with embolism accounting for less than 30%.The review also showed that intra-arterial throm-bolysis was being used increasingly as a first line

treatment for acute lower limb ischemia, even whenthe evidence suggested that the cause was embolic.

In a review of acute and acute on chronic leg is-chemia, Kauhanen et al. emphasized the impor-tance of distinction between acute embolic ischemiaand acute on chronic ischemia caused by thrombussuperimposed on an atherosclerotic stenosis [3]. Ina series of 194 acutely ischemic lower limbs of which189 underwent balloon catheter thrombo-embol-ectomy, even in retrospect, the diagnosis of acuteembolic ischemia was only made in 48% of patients,the remainder being acute on chronic ischemia. In22% of the patients, the emergency surgeon was


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unable to distinguish between acute embolic is-chemia and acute on chronic ischemia. The resultsof these studies emphasize the difficulties of clin-ical assessment and suggest that routine diagnos-tic angiography would be an important evaluationtool in planning optimum management, particu-larly as many patients can be treated by catheter-based techniques.

Presentation

The classic presentation of acute embolic arteri-al ischemia is the six P's: Pain, Paresthesia, Pulse-lessness, Pallor, Paralysis and Perishing cold. There isoften an obvious source of an embolus such as car-diac arrhythmia (usually atrial fibrillation), recenthistory of myocardial infarction, or an alternativesource such as a large abdominal aortic aneurysm.There is usually evidence that the rest of the pe-ripheral vascular tree is normal with no history ofprevious claudication and a full compliment of puls-es in the other limbs. When clot or atherosclerot-ic plaque from a proximal source embolizes intothe arterial tree, the embolus usually lodges at thebifurcation of an artery. The common sites for lod-ging are the bifurcations of the aorta, the commoniliac artery, the common femoral artery and thepopliteal artery. This usually produces sudden andvery severe ischemia of the limb below the embo-lus and, as there has been little opportunity for thedevelopment of collateral circulation, the ischemiais usually profound. This clear-cut pattern of pres-entation is easy to recognize and should be treatedwith great urgency.

The classic picture of acute embolic ischemia isbecoming increasingly rare with the decline in rheu-matic heart disease and the better treatment of atri-al fibrillation. More commonly, patients presentwith a more complicated picture. Patients with atri-al fibrillation may also have peripheral vascular dis-ease giving rise to a less acute picture because ofpreexisting collaterals around the site of the em-bolus. In the presence of such peripheral vasculardisease, even if an embolus has caused the suddenonset of ischemia, the results of embolectomy aremuch less certain. In these cases, making the diag-nosis is more difficult and treatment is associatedwith increased risk of postoperative complications.

While atrial fibrillation associated with ischemicheart disease or rheumatic heart disease remainsthe most common source of peripheral embolism,

it should be remembered that there are less com-mon causes giving rise to arterial emboli. In a reportby Pereira et al., infective endocarditis was foundin 24% of patients causing arterial emboli second-ary to heart disease, and a further 28% secondaryto dilating cardiomyopathy [4].

Investigations

In the presence of clear-cut criteria for an embo-lus like sudden onset of leg pain, clinical evidenceof heart disease like myocardial infarction or atrialfibrillation, and no evidence of peripheral vasculardisease (normal pulses in the other leg), it is usu-ally considered safe to proceed straight to surgicalembolectomy. If there is doubt as to the diagnosis,urgent arteriography is mandatory, with a provisionto treat by catheter techniques if appropriate.

Techniques of embolectomy

It has now been almost fourty years since the firstembolectomy technique was recorded by Fogarty etal. [5]. More recently, new percutaneous thrombec-tomy techniques have been used for removing em-boli including aspiration thrombo-embolectomy, an-gioscopic thrombo-embolectomy and mechanicalthrombectomy with or without fibrinolytic infusions.

BALLOON THROMBO-EMBOLECTOMYAlthough balloon embolectomy is a well-tried and

proven technique, problems remain with its use. Itis well recognized that after removal of an embolusfrom an arterial wall by embolectomy catheter, resid-ual thrombus may well be left behind. Furthermore,secondary thrombosis of runoff vessels may be in-adequately cleared, giving rise to poor flow and thepossibility of secondary thrombosis. Thrombo-em-bolectomy using a Fogarty catheter may also causearterial perforation and pseudo-aneurysm forma-tion, and may at a later stage give rise to intimalhyperplasia [6,7]. The degree of endothelial dam-age that leads to intimal hyperplasia appears to beindependent of the type of balloon catheter used.It increases with increasing sheer force (pressure)on the vessel wall and with multiple passages of theballoon [8]. It has been suggested that the passageof an embolectomy catheter over a guide wire underX-ray control might reduce the incidence of arterial

ARTERIAL EMBOLI OF THE LOWER LIMBS

perforation, although there are no randomized datato support this. There is little evidence that the typeof embolectomy catheter used has any influence oncomplication rate or outcome [9].

Recently, mechanical thrombectomy has beenpromoted as an effective way of clearing thrombo-embolic material in an occluded artery. These me-chanical devices either combine clot macerationwith suction removal (Angiojet Hydrolysor, Oasis)or use clot maceration alone (Amplatz thrombec-tomy device). Most of this experience appears to re-late to acute on chronic ischemia rather than em-bolic disease and there are no separate data foremboli as opposed to thrombosis. There are manyreports of successful removal of the embolized ma-terial following mechanical disruption from the dis-tal vessel.

SURGICAL EMBOLECTOMYIn cases of a saddle embolus, there is sudden oc-

clusion of the aorta by a large embolus sitting atthe aortic bifurcation. This is best approached by abilateral femoral route. It is important not to tryand remove the embolus through one single fem-oral artery, as there is a real danger of dislodgingclot into the contralateral leg. A bilateral femoralapproach can be done perfectly adequately underlocal anesthetic although a regional or general anes-thetic may be preferable in a very distressed patient.

For a patient who has an embolus in either theiliac or common femoral arteries, a femoral ap-proach is satisfactory. It would be normal practiceto give heparin 5 000 international units intrave-nously once the decision has been made to do anembolectomy, but this may be delayed if the pa-tient is to have a spinal or epidural anesthetic. Localanesthesia by direct infiltration is adequate, allow-ing full mobilization of the common femoral arteryand the origin of the superficial and profundafemoris artery.

Following arteriotomy, an appropriately sizedFogarty catheter should be passed upward to en-sure that the inflow is clear, and then distally downboth the profunda femoris and the superficialfemoral artery. Pressure on the balloon should bekept to a minimum compatible with removal of theclot. For emboli that have gone to the popliteal ar-tery or more distally, it may be advantageous to ex-plore the popliteal artery rather than the femoralartery. This is best done by a medial approach. Ifthere is evidence that there is thrombus going intothe individual calf vessels, then exploration of the

popliteal artery with control of the origin of eachof the calf vessels is essential. This allows direct con-trol of the embolectomy catheter with passage intoeach of the calf vessels. Following an arteriotomyof the popliteal artery, it is wise to repair the arterywith a vein patch to prevent narrowing and second-ary thrombosis.

Quality control

On completion of what appears to be a satisfac-tory embolectomy, it is essential to do an on-tableangiogram or similar investigation to ensure thatthe artery is adequately cleared. It is well recognizedthat up to 70% of embolectomies are incompleteafter the surgeon feels he or she has a satisfactoryresult, angiography showing residual thrombus orfurther thrombus in a more distal part of the limb.In the author's experience, it is a good idea to in-clude intra-arterial thrombolysis inserted distallyafter successful embolectomy. This can remain inthe distal circulation while the upstream part of theembolectomy is performed and during the periodof arteriotomy closure. Completion angiographyshould be completed prior to closure of the groinwound.

Results

In a review of lower limb emboli in a single vas-cular unit, Burgess et al. found a mean delay be-fore diagnosis of 29 hours in 71 lower limb emboli(range 1 to 264 hours) [10]. Two thirds of the caus-es were atrial fibrillation and one third was othersources. Thirty-day mortality was 45% with an am-putation rate of 15% and an overall complicationrate of 62%. There was no evidence of improvingfigures over a ten-year period.

Factors that increased mortality were a delay be-fore diagnosis, grade of surgeon performing theoperation, and inadequate inflow or outflow at op-eration. Factors found to affect limb salvage rateadversely were intermittent claudication, lack of im-mediate pre-operative heparinization and juniorityof operating surgeon.

In a study of 397 patients, Becquemin and Kovarskyreviewed their experience of lower limb arterial em-bolism. The in-hospital mortality rate was 15%. Riskfactors for amputation were comorbidity, severity of

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ischemia, distal embolus and delay in treatment[11].

The role of thrombolysis in the treatment of em-bolic occlusion of the lower extremity was report-ed from the STAR Registry by Huettl and Soulen[12] in which 45 of 306 consecutive cases of lowerlimb arterial occlusion were treated with urokinaseand registered in the Society of Cardiovascular Radio-logy Transluminal Angioplasty and RevascularizationRegistry. The diagnosis of embolus was based on thecombination of clinical and angiographic data. Fiftyof the patients had atrial fibrillation, 40% previousmyocardial infarction and 35% had a prior cere-brovascular event. At the time of presentation 71%of the limbs were deemed to be viable, 27% werethreatened and one had irreversible ischemia. Themean duration of symptoms to treatment was 8.6days and the average length of occlusion was 17 cen-timeters. The distribution of the emboli was 4% inthe aorto-iliac segment, 65% in the femoropoplitealsegment, 24% in the tibial segment and 7% wereinto an arterial graft. There was a technical successrate of 69% with a one-year primary patency rateof 79%. These results are similar to those reportedfor surgical embolectomy and appear to confirm noadvantage over surgical procedure.

Much of the data related to the management ofacute critical ischemia with thrombolysis do notclearly differentiate between embolic and primarythrombotic ischemia. In their review of surgery ver-sus thrombolysis for acute limb ischemia for theCochrane database, Berridge et al. reviewed 1283patients in five trials [13]. They found no signifi-cant difference in limb salvage or death at 30 days,6 months, or one year between initial surgery andthrombolysis. Thrombolysis was thought to be asso-ciated with a higher risk of ongoing limb ischemiaand hemorrhagic complications including stroke.They concluded that the higher risk of complica-tions must be balanced against the relative risk ofsurgery in each patient. These patients were main-ly acute on chronic ischemia rather than embolic,and no differentiation is made between the resultsin those who were found in retrospect to have anembolus and those with a primary thrombosis.

A further study of 204 patients (107 female,97 male) with 224 episodes of lower limb ischemiatreated surgically between 1993 and 1997 is report-ed by Ilic et al. [14]. Admission and operation werewithin 6 hours in 9% of the patients, 6 hours to24 hours in 33% of the patients and greater than24 hours in 56% of the patients. More than half

the patients had motor and sensory deficit at thetime of admission. The majority of their emboli werediscovered in the popliteal artery; a transfemoralapproach was used in 60% of cases and a transpopli-teal approach in 40%. In addition to doing an em-bolectomy, they had to perform a bypass operationin 14 cases, fasciotomy in 43 cases, and administerintra-operative streptokinase in two cases. Qualitycontrol was performed using continuous wave dop-pler and occasionally intra-operative angiography.Early amputation rate was 10% and subsequentlylimb salvage was recorded at 77% at one year. Com-plete recovery was recorded in 90% of the limbssalvaged, but there was a peroneal nerve palsy in5% of cases. The one-month mortality rate was 12%.Factors that indicated a worse prognosis were lo-cation of the embolus in the abdominal aorta orthe popliteal artery, delay in presentation or pres-entation with neurologic deficit. There was a smallincidence (2%) of further emboli occurring re-quiring treatment within one year despite appar-ently adequate anticoagulation.

Trash foot

One form of embolism into the foot that is relat-ed to operative procedures is trash foot, which usu-ally occurs following repair of abdominal aorticaneurysm. In a review, Kuhan and Raptis studied1601 aortic reconstructions performed between 1976and 1995 [15]. Trash foot occurred in 32patients(44 limbs, 23 cases following aortic aneurysm repairand 9 cases following an aortofemoral bypass for oc-clusive disease): 13.6% underwent an early ampu-tation and 20% required a delayed amputation. Thir-ty-day mortality was 25%. There was no suggestionthat surgical embolectomy improved the outcome.

COMMENTSIn a review of thrombolysis in lower extremity

acute arterial occlusion, Patel et al. looked at therelative costs of surgery versus thrombolysis [16].Although this study was aimed at acute on chron-ic thrombosis rather than embolic thrombosis, theirconclusions were that surgery was more efficientand more cost effective than thrombolysis in treat-ing acute lower limb ischemia.

In a review of percutaneous aspiration embolec-tomy in acute embolic occlusion of the infrainguinalarteries, Wagner and Starck [17] reviewed 102 pa-tients, 62% of whom had limb-threatening ischemia.

Eighty-six percent had cardiac disease as the sourceof their embolus. The initial clinical success rate ofpercutaneous aspiration embolectomy was 87% withmajor complications occurring in 9% of cases. Thethirty-day mortality was 4%, comparing well withsimilar results with Fogarty catheter embolectomy.In their hands percutaneous aspiration embolecto-my had a higher success rate and a lower mortality.They advocated percutaneous aspiration embolec-tomy because it was a simpler technique combin-ing diagnosis with therapeutic procedures and en-abling the treatment of tibial and pedal vessels aswell as femoral and popliteal arteries.

In a review of 159 cases of arterial embolism be-tween 1991 and 1993, Wolosker et al. reported thatthe patients were almost equally split between maleand female [18]. In most cases, the cause of theembolus was well established, with the most com-mon cause (78%) being atrial fibrillation. The siteof occlusion was most frequently the femoral ar-tery, and although all patients presented with se-vere lower limb ischemia, none had gangrene onadmission. Seventy percent of patients presented tothe hospital within 24 hours, and all patients weresubmitted to lower limb embolectomy with a Fog-arty catheter, 70% of which were done through thefemoral artery. Fasciotomy was performed on 48 pa-tients because of compartment syndrome. Nineteenpatients died immediately after operation, most ofthese due to heart failure. Twenty-three (16%) of the140 surviving patients were submitted to amputa-tion after the occlusion of artery branches that hadundergone embolectomy. One hundred twenty-sevenlimbs were preserved in the 117 patients (83%).

Those patients with muscle tenderness, paralysisor ischemia lasting longer than 24 hours, had theworst results in relation to limb preservation. It wasconcluded that patients who presented with lowerlimb embolism who were in a good general condi-tion and who did not have any necrosis of the limbor neurologic deficit, had a good outcome fromthe point of view of both their limb and their life.A very low complication rate was recorded from thesurgical Fogarty catheter.

Conclusion

Embolization of the lower limb is a relatively un-common but limb- and life-threatening problem re-quiring urgent surgical and radiological manage-ment. In those patients who have a clear-cut history

of sudden onset of acute ischemia with no evidenceof cardiac disease and no evidence of peripheral vas-cular disease, surgical embolectomy with a Fogartyembolectomy catheter seems the most appropriatetreatment. In many cases, however, the differentialdiagnosis between a surgical embolus and throm-bosis of a previously diseased artery may be diffi-cult to tell. If there is doubt, the patient should besubmitted for urgent arteriography with a view toeither thrombolysis, catheter embolectomy or sur-gical embolectomy. If the embolus is localized andsmall with relatively normal vessels, then surgicalembolectomy may seem the most attractive way ofremoving the embolus. Completion angiography ismandatory before wound closure. If there is moreextensive thrombus, and other catheter techniquesmay be more helpful, then a radiological solutionis more appropriate.

Care must be taken to pass an embolectomy cath-eter as few times as possible, minimizing the dam-age to the endothelium. In those institutions inwhich there is experience and radiological expert-ise in catheter techniques for removing emboli, theresults are largely similar to those of surgical em-bolectomy. If these techniques fail, however, it isimperative that there is vascular surgical expertiseto perform a surgical embolectomy or to do someform of reconstruction to revascularize the limb.Factors that affect limb salvage and survival are ageof patient, comorbidity, delay in presentation, sen-iority and experience of the surgical staff, and thepresence of neurosensory deficit at the time of pres-entation. The management of surgical embolus re-mains a high-risk and challenging procedure bestdealt with by vascular surgeons.

R E F E R E N C E S

1 Campbell WB, Ridler BMP, Szymanska TH. Current mana-gement of acute leg ischemia: results of an audit by the VascularSurgical Society of Great Britain and Ireland. Br J Surg 1998;85: 1498-1503.

2 Golledge J, Galland RB. Lower limb intra-arterial thromboly-sis. Postgrad AW/1995; 71: 146-150.

3 Kauhanen P, Perakyla T, Lepantalo M. Clinical distinction ofacute and acute on chronic leg ischaemia. Ann Chir Gjnaecol1995; 84: 335-338.

4 Pereira Barretto AC, Nobre MR, Mansur AJ et al. Peripheralarterial embolism. Report of hospitalised cases. Arq Bras Cardiol2000; 74: 324-328.

5 Fogarty TJ, Cranley JS, Krause RJ et al. A method for extrac-tion of arterial emboli and thrombi. Surg Gynecol Obstet 1963;116: 241-244.

279


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6 Nevelsteen A, Suy R. Arterial rupture and pseudoaneurysm for-mation secondary to the use of the Fogarty balloon catheter.Ada ChirBelg 1987; 87: 300-303.

7 Cronenwett JL, Walsh DB, Garrett H. Tibial artery pseudoa-neurysms: delayed complication of balloon catheter embolec-tomy. J Vase Surg 1988; 8: 483-488.

8 Gloor B, Schopke C, Largiader J. Damage to the vessel wall bythe Fogarty balloon catheter. Helv ChirActa 1994; 60: 749-752.

9 Schwarcz TH, Dobrin PB, Mrhdcka R et al. Balloon embolec-tomy catheter-induced arterial injury: a comparison of fourcatheters. / Vase Surg 1990; 11: 382-388.

10 Burgess NA, Scriven MWT, Lewis MH. An 11-year experience ofarterial embolectomy in a district general hospital./,/? Coll SurgEdinb 1994; 39: 93-96.

11 Becquemin JP, Kovarsky S. Arterial emboli of the lower limbs:analysis of risk factors for mortality and amputation. AssociationUniversitaire de Recherche en Chirurgie. Ann Vase Surg 1995;9 (Suppl): S32-S38.

12 Huettl EA, Soulen MC. Thrombolysis of lower extremityembolic occlusions: a study of the results of the STAR Registry.Radiology 1995; 197: 141-145.

13 Berridge DC, Kessel D, Robertson I. Surgery versus thrombol-ysis for acute limb ischaemia: initial management. CochraneDatabase Sjst Rev 2002; CD002784.

14 Ilic M, Davidovic L, Lotina S et al. Arterial embolisms of thelower limb extremities. Srp Arh Celok Lek 2000; 128: 276-280.

15 Kuhan G, Raptis S. "Trash foot" following operations involvingthe abdominal aorta. Aust N ZJ Surg 1997; 67: 21-24.

16 Patel ST, Haser PB, Bush HL, Kent KG. Is thrombolysis of lowerextremity acute arterial occlusion cost-effective? J Surg Res 1999;83: 106-112.

17 Wagner HJ, Starck EE. Acute embolic occlusions of the infrain-guinal arteries: percutaneous aspiration embolectomy in 102 pa-tients. Radiology 1992; 182: 403-407.

18 Wolosker N, Kuzniec S, Gaudencia A et al. Arterial embolec-tomy in lower limbs. Rev Paul Med 1996; 114; 1226-1230.

28ACUTE THROMBOLYSIS OF

PERIPHERAL ARTERIAL ANEURYSMS

LUDWIG KARL VON SEGESSER, BETTINA MARTY, PATRICK RUCHATPHILIPPE GERSBACH, SALAH QUANADLI, DANIEL HAYOZ, ADAM FISCHER

Acute thrombosis of peripheral arterial aneurysms is a serious problem. In contrast to still ^ _patent peripheral arterial aneurysms, where rupture and consecutive bleeding can be an issue, ZiOthe main problem after thrombotic aneurysm occlusion is, in general, the lack of distal runoff 281due to previous micro-embolization with progressive occlusion of the more distal arterial bed.Hence, standard aneurysm repair, i.e., resection in combination with interposition of anautologous or other graft, often results in recurrent occlusion. In order to increase the successrate under such circumstances, the therapeutic approach must be more specifically tailored tothe problem of distal malperfusion and not only the issues related to the peripheral aneurysmper se. Pre-operative thrombolysis has been recommended [1] under such circumstancesbecause it has the potential to not only recanalize a peripheral aneurysm, but also to re-openat least a part of the distal vascular bed, thus allowing for an improved runoff after surgicalaneurysm repair. In this chapter we will discuss our experience with pre-operative thrombolysisfor acute popliteal aneurysm thrombosis and its background.

for lower lysis in the management of lower limb peripherallimb peripheral artery arterial occlusion are well defined. These include

nr»rlii«inn in o-ptipral the end Points of the studies'the clinical Presenta'ucciubioii in geuei ai tion of the patients ̂ ischemia, the definition ofterms used in conjunction with fibrinolytic thera-

The Working Party on Thrombolysis in the Management pies, the description of the catheter systems, theof Limb Ischemia has produced an excellent docu- available thrombolytic agents, the recommendedment [2] in which the relevant issues for thrombo- choice and dose of lytic agents (appendix A of this


28282

document includes over 40 reported dosage schemesin catheter thrombolysis), the indications for throm-bolysis, the centra-indications, adjunctive treatments,monitoring and complications.

Thrombolysis for acuteischemia after popliteal

aneurysm occlusion(personal experience)

In our hands, routine work-up in patients withacute ischemia of the lower limbs includes, in addi-tion to the clinical assessment, an ultrasonographicstudy prior to angiography. As a result, the presenceof a peripheral arterial aneurysm is often knownprior to the initial angiography and the latter canbe planned accordingly. In this setting, angiographyis usually started through a contralateral femoral ap-proach and a cross-over maneuver is performed toreach the superficial femoral artery of the affectedischemic limb. As previously reported [3], the stan-dard technique was to embed the catheter first inthe distal part of the aneurysm and to inject an ini-tial bolus of 200 000 international units (IU) ofurokinase in order to achieve some degree of throm-bus lacing for accelerated thrombolysis. After posi-tioning the tip of the catheter in the proximal partof the thrombus, this maneuver is followed by a con-tinuous infusion of 75 000 to 100 000 lU/h of uroki-nase. Simultaneously, intravenous heparin (standarddosage is 15 000 IU/24h for a 70 kg adult patient)is given systemically. In addition to clinical follow-up, angiographic assessment with distal catheter tipadvancement in accordance to the progression ofthrombolysis is performed every 6 to 24 hours.Throughout the fibrinolytic therapy, the patients aremonitored in our intermediate care unit and theprotocol includes systematic assessment of conscious-ness, noninvasive blood pressure measurement,quantification of diuresis, clinical status of the lowerlimb, the puncture site, as well as lab work with afocus on coagulation parameters and indicators ofmyolysis and renal function.

PATIENTSAll patients hospitalized in our institution are sys-

tematically registered in our patient analysis and ina tracking system. By retrospective analysis we iden-tified 59 admissions to our unit for popliteal aneur-ysms (age 36 to 91 years).

The most frequent risk factors in this group ofpatients were arterial hypertension (42%), activesmoking (24%), hypercholesterolemia (22%), over-weight (19%), pre-operative renal failure (14%),former smoking (7%; together with active smoking:31%) and others. Additional aneurysms were de-tected at the level of the abdominal aorta in 26 pa-tients (44%), iliac artery (20%), femoral artery(19%), thoracic aorta (7%) and elsewhere.

Previous surgical procedures related to the car-diovascular system were documented in 61% ofpatients, including previous femoral artery proce-dures in 22%, aneurysm repair in 17% and coro-nary artery bypass grafting in 17%.

PATIENTS UNDERGOING THROMBOLYSISThirteen patients (mean age 76±10 years) with

documented popliteal aneurysm by means ofduplex ultrasound underwent thrombolysis prior tosurgical aneurysm repair as described previously[3]. Duration of ischemia prior to hospital admis-sion was less than 6 hours in 6 of 13 patients (46%)and more than 6 hours in 7 of 13 patients (54%).Twelve patients had ischemia of category Ha [4]with slight sensomotoric disturbance. One patienthad severe ischemia category lib with an immedi-ately threatened limb. A typical image of an initialangiography is shown in Fig. 1.

RESULTSMean duration of lysis was 32±15 hours with in-

fusion of 2 400 000 ± 800 000 IU of urokinase.Thrombolysis resulted in a patent popliteal arterywith one- or two-vessel runoff in 10 of 13 patients(77%). A typical angiographic control with reper-meabilization of the popliteal axis after 22 hours ofintra-arterial lysis is shown in Fig. 2. Fig. 3 showsthe result after 44 hours of intra-arterial thrombo-lysis in the same patient. Clean inflow and outflowsegments have been restored prior to surgical aneur-ysm repair.

In contrast, Fig. 4 shows an angiographic controlexamination after 60 hours of intra-arterial throm-bolysis without restoration of distal outflow. Thistype of persistent lytic failure was documented inthree of 13 patients (23%).

Ten patients underwent subsequent bypass graft-ing. A reversed saphenous vein was used in eightpatients and a prosthetic graft was implanted in twopatients. The distal anastomosis was performed atthe infragenicular popliteal artery in seven patientsand at the tibial artery in three patients. In seven

ACUTE THROMBOLYSIS OF PERIPHERAL ARTERIAL ANEURYSMS

patients the outcome was successful. There werefour bypass graft occlusions in three patients be-cause of insufficient runoff. One patient with a ve-nous conduit and one with a prosthetic conduithad lytic failure with absence of runoff. The thirdpatient underwent venous bypass grafting twice butboth failed. An overview of the outcome in thesepatients is given in Table I.

For this small series of patients who underwentintra-arterial thrombolysis prior to surgical poplitealaneurysm repair, patency rate at one month was 68%and limb salvage rate was 83%, whereas early mor-tality was 15%. Mean follow-up was 15 ± 9 months

and the 12-month patency rate was 46%. Threepatients have completed the 24-month follow-up andhad a patent femoropopliteal graft (two veins andone endoprosthesis).


Popliteal aneurysm occlusion is a serious event.In the past, direct surgical aneurysm repair withintra-operative exploration of the distal vascular bedwas routine. However, distal tibial artery occlusion

FIG. 1 Preprocedural angiosraphy showing distalsuperficial femoral artery occlusion.

283

FIG. 2 Angiographic control after 22 hours ofintra-arterial thrombolysis showing repermabiliza-tion of the femoropopliteal axis and residual intra-luminal thrombotic material (same patient as Fig. 1).


28284

FIG. 3 Angiographic control after 44 hours ofintra-arterial thrombolysis: clean inflow and out-flow prior to popliteal aneurysm repair (samepatient as Figs. 1 and 2).

FIG. 4 Angiographic control examination after 60hours of intra-arterial thrombolysis documentingfailure of distal vessel repermeabilization: aneu-rysm repair is not indicated.

Successful lysisFailed lysisAneurysm repairOcclusionAmputationDeath

Success

10/13

9/101/100/101/10

Failure

3/132/32/32/31/3

due to previous embolization from the poplitealaneurysm is not uncommon. In our opinion, intra-procedural attempts to re-open the distal vascularbed using balloon catheters and/or intra-operativelysis are not a reliable approach in patients withthrombosed popliteal aneurysms. The experiencepresented here shows that the mean duration ofthrombolysis required for re-opening the arterialbed and achieving a clean inflow and outflow is usu-ally more than 24 hours (see also Figs.l through 4)and requires considerable doses of intra-arterialurokinase application (superior to 2 000 000 IU).

In contrast, intra-operative thrombolysis allowingfor a few doses of 100 000 IU of urokinase over a

ACUTE THROMBOLYSIS OF PERIPHERAL ARTERIAL ANEURYSMS

short period is quite limited in its potential and cantherefore not reach the same degree of reperme-abilization. As a matter of fact, Fig. 2 shows that the22 hours of thrombolysis allows for repermeabiliza-tion of the distal vascular bed. However, continuedthrombolysis over more than 40 hours is necessaryto clean out the proximal femoral inflow (Fig. 3).

The limb salvage rate of 83% reported here foracute occlusion of popliteal aneurysms must becompared with the results reported in the litera-ture for similar patient populations. Bowrey et al.[5] report a limb loss rate of 24% in their group(pre-operative thrombolysis was used in 9 of 17 pa-tients), whereas Dawson et al. [6] describe a medianlimb loss rate of 25% (range 9% to 36%).

Marty et al. [3] compiled the results of 12 seriesfrom the literature in which pre-operative throm-bolysis was performed prior to surgical poplitealaneurysm repair. In the cited reports, the numberof patients included varied between 1 and 18. Earlygraft patency was between 73% and 100%, whereas

the limb salvage rate varied between 70% and 100%(Table II). Unfortunately, many parameters neces-sary for thorough analyses are not available in a sub-stantial number of studies cited and therefore theconclusions made must be considered with caution.

There are a number of arguments in favor of theconcept proposed by Marty et al. [3] to use the suc-cess of thrombolysis as predictor for outcome ofsurgical repair of thrombosed popliteal aneurysm.The images reproduced here speak for themselves.Figs. 1 through 3 document successful thromboly-sis prior to successful surgery and are in sharp con-trast to Fig. 4, in which no reliable peripheral per-fusion was obtained after 60 hours despite increaseddosage of thrombolytic agents. For the latter case,the final outcome could be expected to be nega-tive, and finally was. Although further validation ofthis approach is recommended for the future, forthe time being, based on our experience and com-mon sense, we have adopted the described ap-proach for our current practice.

First author[ref.]

Schwarz [7]

Ferguson [8]

Bowyer [9]

Thompson [10]

Ramesh [11]

Carpenter [12]

Varga [13]

Garramone [14]

Hoelting [15]

Debing [16]

Taurino [17]

Greenberg [18]

Personal experience [3]

Year

1984

1986

1990

1993

1993

1994

1994

1994

1994

1997

1997

1998

2001

Numberof patients

1

10

9

6*

12

7 including 1*

18 including 9*

3

9

2

8

6 including 1*

13

Failure%

0

NA

33

0

17

0

11

0

0

0

13

0

23

Mortality%

0

0

11

0

0

0

0

0

NA

0

NA

0

15

Earlygraft patency

%

100

NA

100

100

NA

100

73

100

100

100

NA

83

68

Limb salvage%

100

70

100

100 at 30 days

83 at 18 months

100 at 62 months

73 at 30 days

100

100 at 5 years

100 at 5 years

87

100 at 2 years

83 at 30 days

285


28286

R E F E R E N C E S

1 Callum K, Bradbury A. ABC of arterial and venous disease.Acute limb ischemia, fir Afed/2000; 320: 764-767.

2 Anonymous. Thrombolysis in the management of lower limbperipheral arterial occlusion. A consensus document. WorkingParty on Thrombolysis in the Management of Limb Ischemia.Ajn/Carrfio/1998;81: 207-218.

3 Marty B, Wicky S, Ris HB et al. Success of thrombolysis as apredictor of outcome in acute thrombosis of poplitealaneurysms. / Vase Surg 2002; 35: 487-493.

4 Anonymous. Transatlantic Inter-Society Consensus (TASC)Working Group. Management of peripheral arterial disease.EurJ Vase Endovasc Surg 2000; 19: S115-S143.

5 Bowrey DJ, Osman H, Gibbons CP, Blackett RL. Atheroscleroticpopliteal aneurysms: management and outcome in forty-sixpatients. EurJ Vase Endwasc Swrg2003; 25: 79-81.

6 Dawson I, Sie RB, van Bockel JH. Atherosclerotic poplitealaneurysm. BrJSurg 1997; 84: 293-299.

7 Schwarz W, Berkowitz H, Taormina V, Gatti J. The pre-opera-tive use of intraarterial thrombolysis for a thrombosed poplitealartery aneurysm. J Cardiovasc Surg 1984; 25: 465-468.

8 Ferguson L, Paris I, Robertson A et al. Intra-arterial streptoki-nase therapy to relieve acute limb ischemia. / Vase Surg 1986;4: 205-210.

9 Bowyer R, Cawthorn S, Walker W, Giddings A. Conservative

management of asymptomatic popliteal aneurysm. Br J Surg1990; 77: 1132-1135.

10 Thompson J, Beard J, Scott D, Earnshaw J. Intra-operativethrombolysis in the management of thrombosed poplitealaneurysm. BrJ Surg 1993; 80: 858-859.

11 Ramesh S, Michaels J, Galland R. Popliteal aneurysm: mor-phology and management. BrJ Surg 1993; 80: 1531-1533.

12 Carpenter], Baker C, Roberts B et al. Popliteal artery aneurysms:current management and outcome. / Vase Surg 1994; 19: 65 - 72.

13 Varga Z, Locke-Edmunds J, Baird R. A multicenter study ofpopliteal aneurysms. / Vase Surg 1994; 20: 171-177.

14 Garramone R, Gallagher J, Drezner D. Intra-arterial throm-bolytic therapy in the initial management of thrombosedpopliteal artery aneurysms. Ann Vase Surg 1994; 8: 363-366.

15 Hoelting T, Paetz B, Richter G, Allenberg J. The value of pre-operative lytic therapy in limb-threatening acute ischemia frompopliteal artery aneurysm. Am] Surg 1994; 168: 227-231.

16 Debing E, Brande PVD, Tussenbroek FV et al. Intra-arterialthrombolysis followed by elective surgery for thrombo-embolicpopliteal aneurysms. Acta Chir Belg 1997; 97: 137-140.

17 Taurino M, Calisti A, Grossi R et al. Outcome after early treat-ment of popliteal artery aneurysms. IntAngio 1998; 17: 28-33.

18 Greenberg R, Wellander E, Nyman U et al. Aggressive treat-ment of acute limb ischemia due to thrombosed poplitealaneurysms. EurJ Radial 1998; 28: 211-218.

29ENDOVASCULAR APPROACH

TO ACUTE ARTERIAL OCCLUSIONS

ANDREA STELLA, MAURO GARGIULO

Peripheral artery occlusion preventing blood flow to a limb is caused by embolism or thenatural progression of peripheral arterial disease, usually atherosclerosis. Progression of _ ̂arterial disease is characterized by the gradual extension of occlusion and is manifested by &Jconcomitant change in the clinical symptoms. The progression from claudication to rest pain, 287ischemic ulcers or gangrene may be the result of a single acute event exacerbating existingchronic ischemia. However, even if progression may be correlated with acute events, thisclinical condition cannot be defined as true acute ischemia as it is induced by segmentarythrombosis.

True acute limb ischemia (ALI) is the sudden and unheralded occlusion of a vessel. It is alimb- and often life-threatening condition. The thrombosis causing ALI does not remainsegmentary but extends rapidly especially to the limb extremity. Mortality can be as high as20 % and if treatment is delayed, amputation may be required in some 30 % of cases. Thefactors triggering ALI are not so much insufficient collateral pathways as the development ofthrombosis, the severity of the underlying disease and, hence, the extension of peripheralatheromatous lesions, the occlusion site, the speed of onset and the presence of venousthrombosis. If these factors are accompanied by spasm and a fall in blood pressure, the clinicalcondition may rapidly become one of irreversible ischemia.

.treatment Options lar results, variations depending largely on the typeof presenting thrombosis and time to treatment.

The various disease management procedures pro- After the introduction of the Fogarty catheter, manyposed such as direct surgery, thrombectomy and thromboses were treated with simple thrombec-endovascular treatment have all shown fairly simi- tomy, a procedure that gave acceptable results in


29288

the short term but high thrombus recurrence ratesdue to persistence of the primary cause of occlu-sion. Endovascular treatment, especially fibrinolyticdrug therapy, achieves artery revascularization inmost cases and successfully resolves most periph-eral thromboses. Vessel revascularization usuallyallows identification of the cause of thrombosis andso enables a decision as to possible definitive treat-ment with endovascular procedures or open sur-gery. Despite the numerous studies conducted inthe 1990s to establish the best treatment of acuteperipheral ischemia, management regimens stillvary considerably. Although partly due to the ini-tial treatment carried out by the receiving hospital,these discrepancies are also due to the varying pro-fessional skills of the surgeon charged with the case.Moreover, not all hospitals have a vascular radiolo-gist with the equipment necessary to perform en-dovascular procedures. These variables have beenevidenced by a study carried out among membersof the Vascular Surgical Society of Great Britain andIreland (VSSGBI) [1]. Questionnaires were returneddescribing 539 events in 474 patients: 55% of pa-tients admitted to the hospital were placed in thecare of a vascular surgeon, 25% under a generalsurgeon with no vascular specialization and 20%under other medical staff. Forty percent of delaysin presentation were attributable to the patient, thegeneral practitioner or the transfer. Delayed refer-rals were the result of a late decision on the partof the admitting team (35%), or delay by the vas-cular team because no vascular surgeon or radiolo-gist was present in the hospital.

Because the most effective means of dissolving clotis activation of plasminogen bound to fibrin withinthe matrix of the clot, it is natural that current ther-apy approaches to vessel thrombolysis for acuteischemia are based on catheter delivery of the plas-minogen activator directly into the thrombosis(Table I). If delivered into the thrombus, the plas-minogen activator is protected from neutralizationby circulating plasminogen activator inhibitors. De-spite the local or regional delivery, ongoing intra-thrombus infusion of lytic agents often results in sys-temic activation of plasminogen with breakdown offibrinogen, clotting factors and other plasma protein[2]. Therefore lysis of the thrombus is obtained withdirect infusion of thrombolytic agents or with per-cutaneous mechanical thrombectomy.

Streptokinase was the most frequently used agentuntil the landmark article of McNamara and Fischerin 1985 documented improved results with locallyadministrated high-dose urokinase (UK) [3].

Appropriate medical treatment can achieve revas-cularization of an occluded artery in a procedurethat can constitute a scheduled treatment of choice.Today lesions causing occlusion, stenosis or aneu-rysm can be successfully treated with endovascularprocedures, with reduced trauma and overall risk ofcomplications.

Important additional goals of thrombolytic the-rapy are to provide a complete diagnosis of the dis-ease, restore patency of branch vessels inaccessibleto mechanical thrombectomy or direct surgery, andavert major vascular reconstruction surgery in favorof a limited, less extensive procedure or endovas-cular therapy.

Arterial thechniques forperipheral thrombolysis

After Dotter's report on the use of the coaxialcatheter to restore flow to the extremity of the limb[4], Gruentzig in 1974 introduced a double-lumenballoon catheter which revolutionized endovascular

Thrombolytic therapy

Streptokinase

Urokinase

Recombinant tissue-type plasminogen activator(rt-PA)

Single-chain urokinase-type plasminogenactivator (scu-PA)

Acylated plasminogen-streptokinase activatorcomplex (APSAC)

Percutaneous mechanical thrombectomy

Percutaneous aspiration thrombectomy

Fullback thrombectomy and trapping

Rotational and hydraulic recirculationthrombectomy

Non-recirculating mechanical thrombectomy

ENDOVASCULAR APPROACH TO ACUTE ARTERIAL OCCLUSIONS

therapy [5]. Introduced in the late 1980s, percuta-neous transluminal angioplasty can now be con-verted to a successful procedure with the placementof a stent. In 1974 Dotter reported the use of strep-tokinase for selective clot lysis [6].

When treating patients with ALI, most interven-tional radiologists choose to access the vascularsystem through the common femoral artery con-tralateral to the symptomatic limb. This approachfacilitates thrombolysis while not precluding subse-quent procedures on the affected limb. The inferiorepigastric artery and deep circumflex iliac arteryare the landmarks to locate the inguinal ligament.Access is through the common femoral artery belowthe inguinal ligament. A puncture site that is tooproximal may lead to retroperitoneal hematomas,dangerous complications of thrombolytic therapy.To avoid this, a basic arteriogram should be per-formed from the renal level up to both femoralarteries.

Once the arterial occlusion has been identified,it is important to determine if the clot is lysable.McNamara described the guide wire transversal testin which an attempt is made to pass a floppy-tippedguide wire into the clot. If the guide wire cannotbe easily advanced into the clot, there is only a 10%likelihood of success [7]. Smith et al. then showedthat an initial 2- to 4-hour lytic infusion at the prox-imal edge of the clot will soften it up sufficientlyto allow the passage of a guide wire through andsubsequently and increase the likelihood of suc-cessful thrombolytic therapy [8].

Depending on the occlusion site, antegrade orretrograde puncture may be performed: antegradeaccess is more suitable for femoropopliteal throm-bosis, whereas retrograde access is indicated for iliacand aortic artery occlusions. Acute iliac occlusionsare treated from the original puncture site. Super-ficial artery and popliteal artery occlusions can betreated from either the initial puncture point orfrom the affected limb. Using the original puncturesite eliminates the risk of bleeding from an addi-tional puncture point, which would render proce-dures such as angioplasty and stenting in thepopliteal or tibial area more difficult. For occlusionsbelow the common femoral artery, an antegradepuncture can be performed. This technique can bechallenging, however, especially in obese patients,as the guide wire preferentially advances into theprofunda femoral artery. Several techniques havebeen developed to conduce the guide wire into thesuperficial femoral artery. After documenting that

the common femoral artery has been effectivelyentered, the needle should be redirected to the con-tralateral wall and the wire re-advanced. Alterna-tively, the floppy tip of a moveable core wire canbe advanced into the profunda and allowed to her-niate into the superficial femoral artery. A thirdmethod is to exchange the needle for a directionalcatheter, retract it under fluoroscopy and redirecta wire into the superficial femoral artery. Once thewire is placed in the superficial femoral artery, avascular sheath is introduced to facilitate the pro-cedure and reduce local complications. Infusion of5000IU heparin is recommended to prevent throm-bus formation induced by partially obstructed flowand catheter manipulations. After assessing the clotwith the guide wire transversal test, the next step isto advance a catheter with multiple side holes intothe occluded artery. The catheter should be posi-tioned so that the proximal side hole is at or closeto the top of the clot and the distal side hole is justproximal to the end of the clot. Follow-up arterio-graphy should be performed as necessary and whenpractical, i.e., in the afternoon if the therapy wasstarted in the morning, or the next morning if com-menced in the afternoon. Patients often may expe-rience increased pain during lysis. This is due tothe embolization of small clots into the peripheralvascular field. Symptoms are short lived, however,and resolve with prolonged infusion. When theangiographic follow-up identifies emboli down theleg, the catheter should be advanced into the tib-ial arteries and infusion continued until the embolidissolve. Inability to pass the guide wire through theocclusion is indicative of either atherosclerotic dis-ease, neointimal fibroplasias or a highly organizedand calcified thrombus that will not respond to alytic agent. Therefore primary operative reconstruc-tion is recommended in these cases.

Certain safety guidelines and important techni-cal aspects are fundamental during intra-arterialthrombolytic therapy. Patients should be carefullyselected and include only those who are coopera-tive and able to endure the prolonged bed restinvolved (24 to 36 hours) with minimal movement.All invasive procedures and needle puncturesshould be kept to a minimum. When thrombolytictherapy is selected, it is preferable, when techni-cally feasible, to puncture and cannulate throughthe contralateral groin to minimize bleeding aroundthe catheter insertion site.

In the event of an endovascular protocol beingadopted, many factors are predictive of the success

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of intra-arterial thrombolysis: the guide wire pass-ing into the clot, short duration of the occlusion,localization of the occlusion (iliac, femoral, orpopliteal) and visualization of distal vessels. Aftersuccessful infusion, an arteriogram should be per-formed and blood studies repeated. If the cause ofocclusion is identified it can be managed immedi-ately with standard interventional techniques. Ifpercutaneous correction is not possible, systemicanticoagulation should be continued until thedefinitive operative procedure is completed. Thetechnique selected to repair the lesion may havesubstantial impact on long-term results.

Complications ofthrombolytic therapy

Complications of thrombolytic therapy includehemorrhage, allergic reactions, embolism, stroke,reperfusion syndrome and arteriography complica-tions. As numerous complications result from theinvasive nature of intra-arterial thrombolytic ther-apy, there are several absolute and relative contra-indications that must be complied, most impor-tantly severe ischemia with neurologic changes anddevitalized limb with irreversible ischemic damage(Table II). Patients with profound ischemia char-acterized by pallor, paresis and decreased sensationcannot sustain the length of time required forthrombolytic therapy to have an effect and are besttreated with emergency surgical intervention.

Bleeding is the most common and feared com-plication of thrombolytic therapy; it occurs as theresult of the active lytic state, but can also resultfrom the induced coagulopathy. The systemic effectof lytic agent and heparin therapy used to reducethe risk of pericatheter thrombosis is monitored bythe fibrinogen level, prothrombin time, partialthromboplastin time, and fibrin degradation pro-ducts during infusion. Although bleeding can occurin any patient receiving lytic therapy, patients withsignificant hypofibrinogenemia appear to be atgreatest risk of a serious hemorrhagic complication.If the fibrinogen level drops below 100 mg/dL,infusion should be slowed or stopped to allow therestoration of circulating fibrinogen and clottingfactors. However, the efficacy of catheter throm-bolysis is evaluated angiographically and clinicallyand does not depend on laboratory markers of sys-temic fibrinolysis. In general, laboratory values do

not correlate with hemorrhagic complications orthe efficacy of lysis.

Some bleeding occurs because of the trauma du-ring invasive diagnostic or therapeutic procedures.Since catheter-directed thrombolysis is by definitionan invasive procedure, an albeit minimal numberof bleeding complications is inevitable. The NationalAudit of Thrombolysis for Acute Limb Ischemia (NATALI)database reports an 8.1% incidence of major hem-orrhage compared to 5.1% reported for the seriesreviewed by Berridge et al. and 12.5% reported byTOPAS [9,10].

Although intra-arterial urokinase has been de-monstrated to increase the salvage of acutely is-chemic skeletal muscle in an experimental model,thrombolytic therapy in the setting of acute is-chemia introduces certain potential complications.Myonephropathic syndrome (acidosis, hyperkalemiaand myoglobinuria), compartment syndrome and

Absolute

Active bleeding source

Cerebrovascular accident or otherintracranial process (< 2 months)

Relative

Recent major surgery, eye surgery, organ

biopsy, postpartum status

Recent trauma

Severe and uncontrolled hypertension

Coagulation deficits

Pregnancy

Hemorrhagic retinopathy

Hepatic failure

Endocarditis

Absolute contra-indications for intra-arterialthrombolytic therapy

Severe ischemia with neurologic changes

Devitalized limb with irreversible ischemicdamage


hemorrhagic necrosis may result when profoundlyischemic tissue is reperfused after thrombolysis.Occasional complications of arteriography and arte-rial cannulations, such as arterial wall injury, muraldissection, or thrombosis, must also be taken intoaccount.

As the intra-arterial thrombus is lysed and bloodflow through the vessel restored, embolization ofthe clot into the distal vasculature may occur. Thenumerous reports in the literature show a wide vari-ation of distal embolization incidence rates rang-ing from 16% to 65% [11,12].

Belkin and O'Donnell [13] have characterizedthe resulting clinical picture as "the storm beforethe calm" since these patients usually suffer anacute worsening of their ischemic symptoms thatalmost always resolves with continued thrombolyticinfusion. Thus, when the patient suffers suddenclinical deterioration with distal embolization, thereflex to discontinue therapy should be resisted.

Pericatheter thrombosis remains a significantclinical problem when the patient does not receiveconcomitant heparinization. Before heparin use,pericatheter thrombus occurred in 36% of cases.Today the routine administration of heparin hasreduced this to less than 5% [11].

Results ofthrombolytic therapy

Some patients develop acute leg ischemia as apreterminal event. Recognition of these patientsand thoughtful conservative treatment are part ofgood medical practice. In these cases, the associa-tion between nonviable limbs and mortality coun-sels appropriate management that does not includeamputation. Conversely, other patients presentingwith unsalvageable legs are best managed with earlyamputation.

Publications on the management of acute leg is-chemia tend to reflect the practices of specialist units.The management of acute ischemia has changedradically in recent years. Many general surgeons nowrightly consider themselves insufficiently experienc-ed to manage the condition.

The results of the current treatment reflect tech-nical advances such as the development of multi-side-hole catheters ensuring infusion of high-doseUK directly into the thrombus. Assessing the suit-ability of thrombolytic management of an ischemic

leg must be based on a clear definition of the sever-ity of the presenting ischemia and the under-standing that thrombolytic therapy alone is seldomsufficient. The ischemia scoring system generallyused in the literature refers to Rutherford's three-category classification: viable (not immediatelythreatened), threatened (salvageable if promptlytreated) and irreversible (major tissue loss, ampu-tation regardless of treatment) [14]. In 1998 anintercontinental consensus paper was published onthe use of thrombolytic therapy in occlusive periph-eral arterial disease affecting lower limbs. Theseauthors broadened category II into a) salvageableif threatened, and b) salvageable if threatened asemergency [15]. Although many randomized trialscompare surgery with lysis, the results are unfortu-nately inconclusive. In one severely ischemic groupof patients, while mortality was higher in patientsundergoing initial surgery, no difference was seenbetween the two groups in regard to limb salvage.

In the single-center Rochester study, the rate oflimb salvage was identical at 80%. More cardiopul-monary complications were reported in patientstaken directly to surgery, which explains the higherlong-term mortality rate in the surgical group: at12 months follow-up, 84% of patients randomizedto UK were alive compared to only 58% of patientsrandomized to primary surgery. Mortality was com-parable in patients without cardiopulmonary compli-cations, averaging approximately 10% at 12 monthsirrespective of treatment. In conclusion, thrombo-lytic therapy was associated with a reduction in cardio-pulmonary complications, improved survival andlimb salvage [16].

There were no differences in mortality and ampu-tation rates when lysis and surgery were comparedin the 392 patients included in the Surgery versusThrombolysis for Ischemia of the Lower Extremity (STILE;three treatment groups: rt-PA, UK or primary oper-ation) study. However, this study contained manypatients with late presentation [17]. Post hoc analy-sis of surrogate end points, such as death and ampu-tation, hemorrhage and peri-operative complicationsfavored surgery. The rate of major amputation washigher in native arterial occlusions treated withthrombolysis: 10% thrombolysis versus 0% surgeryat one year. Recurrent ischemia was also morecommon in the lysis group. When recent occlusions(below 14 days) were considered separately, how-ever, fewer amputations were reported in the pa-tients who underwent lysis. This study suggests thatthrombolysis provides greatest benefit to patients

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with acute occlusion of bypass graft if treated beforeday 14. In this study, UK and rt-PA are equivalent.ALI (within 14 days) was best treated with throm-bolytic therapy, as amputation rates were lowerwhen infusion was instituted promptly. Primary sur-gical intervention was seen to be more effective inpatients with recent ischemia (above 14 days) andnative arterial occlusions which respond poorly tothrombolytic therapy.

The Thrombolysis or Peripheral Arterial Surgery(TOPAS) study, conducted at 113 centers in theUnited States, Canada and Europe and includingpatients with lower limb arterial occlusion (within14 days), reports similar amputation and mortalityrates at discharge and at one year in 544 patients,(68.2% and 68.8% for UK and surgical patients,respectively) [18]. At 6 months follow-up, 31.5% ofpatients undergoing a thrombolytic percutaneousprocedure were amputation-free. This figure fell to25.7% at one year. In conclusion, 4000 lU/minrecombinant UK (rUK) for 4 hours followed by2 000 lU/min would appear to be a safe treatmentregimen, achieving limb salvage and patient sur-vival rates similar to peripheral arterial surgery.Generally, concomitant heparin therapy increasesthe risk of hemorrhagic complications: major bleed-ing occurred more frequently with thrombolysis(12.5% versus 5.5%), with intracranial hemorrhagedeveloping in 1.6% of the thrombolytic group.

Nevertheless the TOPAS findings confirm thatALI may be treated with catheter-directed throm-bolysis, achieving similar results while avoiding theneed for open surgery in many patients.

Although the STILE and TOPAS studies bothclaimed better results for graft occlusions comparedto native vessel occlusions, adjuvant procedureswere usually required to maintain patency.

Mechanical thrombectomy

Percutaneous mechanical thrombectomy (PMT)avails itself of a heterogeneous group of devices andtechniques designed to clear intravascular throm-botic occlusion using a combination of mechanicaldissolution, fragmentation and aspiration. Whilethrombolytic therapy is the standard treatment forocclusion, it is associated with a definite risk of hemo-rrhage and embolic complications. ConsequentlyPMT may be required in a number of patients. PMTdevices are of variable complexity, design, mecha-nism of action, efficacy and cost. Several ones are

now gaining favor among European practitionersand have been approved by the Food and DrugAdministration. Many PMT devices work with recir-culation, trapping and lysing the thrombus. Thefirst device to use hydrodynamic recirculation wasthe Kensey (Trac-Wright) athero-ablative catheter.Dr Kurt Amplatz of the University of Minnesota hasdesigned several recirculation prototypes using dif-ferent techniques. There are now two categories ofrecirculation mechanism: rotational recirculation inwhich the vortex is produced by high-speed rota-tion, and hydraulic recirculation in which high-speed fluid jets create a stagnation pressure gradient(venturi effect), trapping and dissolving the evacu-ated thrombus. Another class of PMT techniquesconsists of devices whose primary function is directthrombus fragmentation and aspiration. However,these simple devices with negligible recirculationcarry high risks of embolization and vascular injury.A further class of PMT instrumentation uses ultra-sound energy for selective thrombus ablation.

The efficiency of mechanical thrombectomy couldbe defined as the percentage weight or volume ofthrombus cleared or fragmented by the treatment.This effect depends on technique, thrombus vol-ume, composition, organization, wall adherence, theextent of atherosclerotic disease and the coagula-tion activity of the patient. Another problem is ves-sel wall damage: there is no standardized system foracute vascular injury. The chronic manifestations ofvascular injury from transcatheter applications in-clude intimal hyperplasia, atherosclerosis, pseudo-aneurysm and fistula. These complications seemto occur less as compared to the Fogarty ballooncatheter.

Catheter clot lysis is now gaining increasing ac-ceptance as it becomes evident that not all cases ofcritical ischemia are best treated surgically or withthrombolysis alone.

Thromboaspiration was first developed by Starcket al. in 1985 to treat infrainguinal embolic occlu-sions [19].

A 5F to 8F catheter is introduced into an 8Fsheath and advanced to the thrombus, where aspi-ration is performed manually with a syringe. Whileaspiration is certainly more rapid (less than onehour), it does not carry the contra-indications ofthrombolysis and is also suitable for long occlusion.It can only be used on recently formed thrombus(within a day). Desgranges et al. [20] report a suc-cess rate of 43% using thrombus aspiration aloneand 81% when thrombus aspiration is associated


with thrombolysis and lesion repair using angio-plasty or surgery.

Castaneda et al. [21] report promising results intheir study comparing the Fogarty embolectomycatheter, the Arrow-Trerotola peripheral thrombec-tomy device and the MTI-Castaneda over-the-wirebrush. While all devices proved effective in remov-ing the thrombus from the iliac arteries treated,they all caused lesions extending into the media.Other multicenter clinical studies and case reportshave shown factors such as lateral wall pressure,catheter size, catheter tip sharpness, balloon ec-centricity, fluid- versus gas-filled balloons, syringesize, velocity of catheter motion and presence ofblood in the vascular lumen to be regularly un-derestimated as a cause of vascular injuries that areincriminated for failure.

In 1997 Henry et al. [22] reported their results withthe Hydrolyser catheter: technical success was ob-tained in 79% of all the primary arterial thrombosestreated. While this catheter has the advantage thatit can be used during the same endovascular pro-cedure, it does not allow complete debridement ofthe artery and must be associated with complemen-tary interventional and/or fibrinolytic procedures.

Hopfner et al. [23] reported their results in 51 pa-tients with the shredding embolectomy throm-bectomy catheter (S.E.T. catheter, now OASIS throm-bectomy system), performing hydromechanicalthrombectomy (venturi effect). The procedure en-tails the introduction of an ipsilateral antegrade 8Fsheath and monitoring of systemic blood pressureand heart rate. The S.E.T. catheter proved com-pletely successful in 12% of the patients, requiringa mean time of 6.4 minutes. Rapid reduction ofthrombus mass was achieved in the other patients.Revision procedures were required in 88% and pe-ripheral embolization in 10%, compared with the5% reported in the literature for thrombolysis.

The above results justify the still limited use of thesedevices, even though removing part of the thrombusremains an interesting theoretical proposal. Furthertechnical improvements to these devices should makethem suitable for regular use, thereby cutting thetime and cost of treating acute thrombosis.


Many studies show that lytic therapy offers an ef-fective therapeutic option for the treatment of ALLThe principal objective of thrombolytic therapy is

to remove the occlusion, thus restoring the vascu-lar patency and to make the diagnosis of the dis-ease. There are many potential attractions of throm-bolytic therapy over an initial surgical approachbecause these findings confirmed that ALI couldbe treated with catheter-directed thrombolysis,achieving similar results but avoiding the need foropen surgery in many patients. The distal arterialbed can be cleared of small thrombi more effi-ciently with a balloon preparing the artery for finaltreatment.

Intra-arterial UK infusions have been proposedas the first-choice treatment for acute arterial andgraft thrombosis [24]. Immediate success rates withintrathrombus UK can be as high as 88% in nativearteries, and meta-analysis of the English literaturereveals an average success rate of 85% in the mostrecent series with a complication rate of 20% [25].

Nevertheless, acceptance of thrombolytic therapyas the procedure of choice is not yet universal. Oneof the major potential advantages of thrombolysisis to limit the extent of subsequent major surgicaltherapy and, if possible, to conduce the patient intothe endovascular treatment. In the experience ofSuggs et al. [26], in 23% of their patients it provedto be the sole therapy required for limb salvage,and in a number of other cases successful lysisuncovered stenotic lesions that were amenable toangioplasty and stenting.

Long-term follow-up revealed that successfulthrombolytic therapy with or without a required sub-sequent endovascular procedure resulted in durablearterial patency. Similar results have been reportedby Wholey et al. [27], with a one-year patency rate of87% for native vessels following successful lysis andangioplasty in patients with ischemia of less than14 days duration. The STILE and TOPAS trials didnot analyze the long-term patency of successfully ly-sed native arteries. Moreover Faggioli et al. [25] clear-ly reported data supporting the need of adjunctivetherapy to improve long-term patency, confirmingthe failure of thrombolysis as sole therapy. Clinicalfactors such as duration of ischemia and severity oflimb ischemia have been suggested as important as-pects of lytic results. A post hoc analysis of the STILEtrial (entered only patients with ischemia within14 days) which stratified all patients by duration ofischemia, showed the significant benefit of throm-bolysis for the acutely ischemic limbs. Nevertheless,amputation rate was similar in patients with is-chemia longer than 14 days and patients who hada shorter period of ischemia: 14% versus 10% [17].

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When evaluating the thrombolysis, the length ofthe occlusion has an important impact on the re-sults: a multifactorial analysis of the TOPAS datashowed that lesions with a length greater than thirtycentimeters predicted better amputation-free sur-vival than surgery.

ConclusionIn conclusion, patients with significant motor or

sensory deficits, femoropopliteal occlusion and dia-

betes must be treated by emergent angiography andsurgery if possible. Unfortunately the results forthese patients tend to be worse than for those withless profound ischemia. Thrombolysis should havea role as a treatment option for ALI secondary tonative artery occlusion, for patients with extensivethrombus rapidly occluding the distal bed, and foryoung patients with minimal atherosclerotic dis-ease. In addiction, short focal lesions are besttreated with an endovascular approach reducingthe impact of the surgery.

R E F E R E N C E S

1 Campbell WB, Ridler BM, Szymanska TH. Current manage-ment of acute leg ischaemia: results of an audit by the VascularSurgical Society of Great Britain and Ireland. BrJ Surg 1998;85: 1498-1503.

2 Comerota AJ, Malone MD. Simplified approach to thrombolytictherapy of arterial and graft occlusion. In: YaoJST, Pearce WH(eds). Practical vascular surgery. Stamford, Appleton & Lange,1999: pp 321-334.

3 McNamara TO, Fischer JR. Thrombolysis of peripheral arterialand graft occlusions: improved results using high-dose uroki-nase. AJR Am J Roentgenol 1985; 144: 769 - 775.

\/ O 4 Dotter CT, Judkins MR Transluminal treatment of arterioscle-*** *^ rode obstruction: description of a new technique and prelim-004 inary report of its application. Circulation 1964; 30: 654.

5 Gruntzig A, Hopff H. Percutaneous recanalization afterchronic arterial occlusion with a new dilator-catheter (modifi-cation of the Dotter technique) Dtsch Med Woehenschr 1974; 99:2502-2511.

6 Dotter CT, Rosch J, Seaman AJ. Selective clot lysis with low-dose streptokinase. Radiology 1974; 111: 31-37.

7 McNamara TO, Bomberger RA. Factors affecting initial and six-month patency rates after intra-arterial thrombolysis with high-dose urokinase. Am J Surg 1986; 152: 709-712.

8 Smith DC, McCormick MJ, Jensen DA, Westengard JC. Guidewire traversal test: retrospective study of results with fibrinolytictherapy. / Vase Interv Radial 1991; 2: 339-342.

9 Campbell B, Kinsella D. Complications of thrombolytic therapyand their avoidance. In: Greenhalgh RM, Powell JT, MitchellAW (eds). Vascular and endovascular opportunities. London, W.B.Saunders, 2000: pp 505-516.

10 Berridge DC, Makin GS, Hopkinson BR. Local low dose intra-arterial thrombolytic therapy: the risk of stroke or major haem-orrhage. BrJ Surg 1989; 76: 1230-1233.

11 Belkin M, Belkin B, Bucknam CA et al. Intra-arterial fibrinolytictherapy. Efficacy of streptokinase vs urokinase. Arch Surg 1986;121: 769-773. '

12 O'Donnell TFJr, Coleman JC, Sentissi J et al. Comparison ofdirect intra-arterial streptokinase to urokinase infusion in themanagement of failed infrainguinal ePTFE grafts. In: Veith FJ(ed). Current critical problems in vascular surgery. St. Louis, QualityMedical Publishing, 1989: pp 80-88.

13 Belkin M, O'Donnell TFJr. Complications of thrombolytic ther-apy. Bernhard VM, TowneJB (eds). Complications in vascular sur-gery. St. Louis, Quality Medical Publishing, 1991: pp 433-441.

14 Rutherford RB, Flanigan DP, Gupta SK et al. Suggested stan-

dards for reports dealing with lower limb ischemia. / Vase Surg1986; 4: 80-94.

15 Anonymous. Thrombolysis in the management of lower limbperipheral arterial occlusion. A consensus document. Workingparty on thrombolysis in the management of lower limbischemia. Am] Cardiol 1998; 81: 207-218.

16 Ouriel K, Shortell CK, DeWeese JA et al. A comparison ofthrombolytic therapy with operative revascularization in the ini-tial treatment of acute peripheral arterial ischemia. J Vase Surg1994; 19: 1021-1030.

17 Anonymous. Results of a prospective randomised trial evaluat-ing surgery versus thrombolysis for ischemia of the lowerextremity, the STILE trial. Ann Surg 1994; 220: 251-268.

18 Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinanturokinase with vascular surgery as initial treatment for acutearterial occlusion of the legs. Thrombolysis or PeripheralArterial Surgery (TOPAS) Investigators. NEngJMed 1998; 338: 1105-1111. '

19 Starck EE, McDermottJC, Crummy AB et al. Percutaneous aspi-ration thromboembolectomy. Radiology 1985; 156: 61-66.

20 Desgranges P, Ernenwein D, Kobeiter H et al. Ischemiesaigues spontanees des membres inferieurs. In: Kieffer E (ed).Urgences vasculaires non traumatiques. Paris, AERCV, 1998: pp163-179.

21 Castaneda F, Li R, Patel J et al. Comparison of three mechan-ical thrombus removal devices in thrombosed canine iliac arter-ies. Radiology mi; 219: 153-156.

22 Henry M, Amor M, Henry I, Alloaoui M. Thrombectomy withthe hydrolysing catheter. A propos of 50 cases. Arch Mai CoeurVaiss 1997;' 90: 797-804.

23 Hopfner W, Vicol C, Bohndorf K, Loeprecht H. Shreddingembolectomy thrombectomy catheter for treatment of acutelower-limb ischemia. Ann Vase Surg 1999; 13: 426-435.

24 McNamara TO, Bomberger RA, Merchant RF. Intra-arterialurokinase as the initial therapy for acutely ischemic lower limbs.Circulation 1991; 83 (2 suppl): 1106-119.

25 Faggioli GL, Ricotta JJ. Thrombolysis therapy for lower extrem-ity arterial occlusion. Ann Vase Surg 1993; 7: 297-302.

26 Suggs WD, Cynamon J, Martin B et al. When is urokinase treat-ment an effective sole or adjunctive treatment for acute limbischemia secondary to native artery occlusion? Am J Surg 1999;178: 103-106.

27 Wholey MH, Maynar MA, WTioley MH. Comparison of throm-bolytic therapy of lower-extremity acute, subacute, and chronicarterial occlusions. Cathet Cardiovasc Diagn 1998; 44: 159-169.

30THROMBOLYSIS FOR

OCCLUSION OF BYPASS GRAFTS

ROBERT HINCHLIFFE, BRUCE BRAITHWAITE, BRIAN HOPKINSON

The standard surgical management of bypass graft occlusion has been thrombo-embolectomywith additional procedures performed as necessary to treat any underlying occlusive lesion.This approach yields rather disappointing results. Alternatively, some authors advocate graftremoval and replacement in an attempt to improve the outcome.

The surgical management of bypass graft occlusion is associated with significant morbidityand mortality. Many patients are simply too frail to undergo further major arterial bypasssurgery. With an aggressive surgical approach only 12% of patients will be alive at five years

HIThrombolysis was popularized in the 1970s by Dotter as an endovascular method of

restoring patency in native artery occlusions. The minimally invasive nature of thrombolysisand its potential to reveal occlusive lesions amenable to endovascular therapy and to restoreflow in thrombosed distal vessels became established. Later, reports emerged regarding its usein the management of bypass graft occlusion.

The evidence

Despite the widespread use of thrombolysis inlower limb ischemia, a recent systematic review ofpublished data found only ten reports of random-ized, controlled trials [2]. The majority concernthrombolysis of native arterial occlusions. Only oneof these publications, a subgroup of patients iden-tified from the Surgery versus Thrombolysis for Ischemia

of the Lower Extremity (STILE) trial, specifically re-ported the results of surgery or thrombolysis in pa-tients with occluded bypass grafts of less than sixmonths duration [3]. Other studies of thrombolysisfor bypass graft occlusions are retrospective and con-sist of small groups of heterogeneous patients. Inaddition to these studies, a large national databaseof thrombolysis, the National Audit of Thrombolysis inAcute Leg Ischaemia (NATALI), was maintained in theUnited Kingdom.


296

Delivery and type of lytic agent

The delivery of the thrombolytic agent to its tar-get site may be achieved via a systemic route or di-rectly into the occluded bypass graft. The formertechnique has been abandoned in peripheral arte-rial (both native and bypass) occlusions due to thehigh number of bleeding problems and the morefavorable results achieved by direct intrathrombusdelivery. The ability to catheterize the graft andcross the occlusion with a wire has a significant ef-fect on outcome. Failure to catheterize an occludedgraft occurred in 39% of patients in the STILE trial[3]. Sullivan et al. found that difficulties cath-eterizing an occluded graft could be negotiated byplacing the tip of the thrombolysis catheter at theorigin of the graft thus creating a stump throughwhich a wire could be manipulated in to the oc-clusion [4]. An alternative technique to facilitatedelivery of intrathrombus lysis is to perform directgraft puncture. This technique is particularly usefulin patients with extra-anatomical prosthetic bypassgrafts. Prophylactic antibiotics are required wheredirect puncture of prosthetic grafts is undertaken.

A number of thrombolytic dosing regimens havebeen reported. In Braithwaite's report of native arte-rial thrombolysis, there was no difference with re-spect to limb salvage or complications following low-or high-dose therapy, however, more secondaryprocedures were performed in those patients receiv-ing the high-dose regimen [5]. There is no evidenceto suggest which may be the preferred techniquefor bypass graft occlusion.

The pulse-spray technique achieves thrombolysisthrough the delivery of lytic agent under pressurevia a multi-side-hole catheter. The pressure createdcontributes to the mechanical lysis of thrombus. Inthe study by Hye et al. using pulse-spray for bypassgraft occlusion, only 27% of patients required aninfusion of thrombolytic agent outside the radiol-ogy suite [6]. Lysis using pulse-spray alone took 118minutes, whereas requirement for an infusion in-creased the time to 13.5 hours. In the Thrombolysisor Peripheral Arterial Surgery (TOPAS) trial, all nativeand bypass graft occlusions were pooled togetherbut higher doses of lytic agent were required forpatients with bypass graft rather than native arteri-al occlusions.

There is no clear evidence to suggest whichthrombolytic agent should be used in graft occlu-sion. In one study streptokinase was successful in

clearing thrombus in only 57% of cases, whereas inother studies, almost 90% of grafts have been suc-cessfully opened with tissue plasminogen activator(tPA) [7,8]. In the STILE trial there was no differ-ence between the efficacy of urokinase and rt-PAwith respect to the composite outcome measure.

Heparin is a useful adjunct during thrombolysisalthough it may increase the hemorrhagic compli-cations. In our institution it is infused alongside theindwelling sheath to prevent peri-catheter throm-bus during infusion of lytic agent.

Outcome of graft thrombolysisand prognostic factors

There is a significant shortfall of patients who failto undergo graft catheterization or in whom throm-bolysis is prematurely terminated due to complica-tions. The United Kingdom NATALI database de-monstrated that successful lysis was achieved in 70%of attempts. Complete lysis was achieved in 48%and partial lysis in 22% of patients. The one-yearpatency of lysed grafts was 33%. On an intention-to-treat basis, this figure dropped to 20% [9]. A30% one-year patency following initial successfulgraft thrombolysis is remarkably similar among dis-parate studies.

The role of thrombolysis is primarily to restoreflow and reveal the underlying lesion that con-tributed to the occlusion. Lesions may be amenableto endovascular treatment such as angioplasty andare multiple in a third of cases [6]. Gardiner et al.found that one-year patency rates were better inthose patients who had a correctable underlying le-sion (86% versus 37%) [10].

Alternatively, lysis may direct traditional surgicaltherapy and allow a minimal access approach. In-deed, some studies have shown that intimal hyper-plasia or vein graft stenosis may be better managedby open surgery rather than endovascular tech-niques [11].

One study found a tendency for a higher initialrecanalization rate in patients with prosthetic by-pass grafts, although these did not reach statisticalsignificance [4]. Immediate success may be greaterwith suprainguinal grafts than their infrainguinalcounterparts [12].

Arterial bypass grafts that occlude in the firstpostoperative year are usually a result of either tech-nical error or an incorrect choice of operation.

THROMBOLYSIS FOR OCCLUSION OF BYPASS GRAFTS

Consequently, it may be expected that thromboly-sis will have less favorable results in patients withgrafts that are less than one year old. Nackman etal. were able to demonstrate by multivariate analy-sis that grafts less than 12 months old were a sig-nificant predictive factor in the failure of throm-bolysis [13]. If lysis was undertaken successfully ingrafts less than one year old, 44% required an ampu-tation, rising to 69% where lysis has failed.

The duration of ischemia has a major impact onthe outcome of thrombolysis. Thrombolysis is moreeffective in acute graft occlusion. Comerota et al.demonstrated a clear reduction in major amputa-tion at one year (48% versus 20%) in patients un-dergoing thrombolysis compared to surgery wherethe duration of ischemia was less than 14 days [3].Conversely, the same data from the STILE trial wasunable to detect any difference if the ischemia hadbeen present for greater than two weeks.

At one year, there was little difference in com-posite clinical outcome whether the patient was un-dergoing thrombolysis of a graft above (80%) orbelow (81%) the inguinal ligament. A review of theavailable results in the literature by Browse et al.appeared to demonstrate an improved outcome inpatients undergoing thrombolysis for suprainguinalbypass occlusion compared with those obtainedfrom infrainguinal lysis [14]. Galland's analysis ofthe NATALI database was unable to support thisfinding. There was no difference in patency betweenthe two sites [9].

Thrombolysis may restore the patency of occlud-ed collateral vessels and improve lower limb circu-lation without fully opening the graft. This may besufficient to permit limb salvage. In one study, inexcess of 60% of limbs were salvaged at one yeareven though only 30% of grafts were patent [13].However, long-term patency is significantly greaterif lysis was complete. Galland et al. [9] demon-strated a 12-month patency of 39% where graft pa-tency had been restored with at least one vesselrunoff. Where lysis was incomplete, the patency wassignificantly less (17%).

predictor of outcome. The length of occlusion ap-peared to be a more important factor. Patients withlonger occlusions appear to fare better with throm-bolysis, which may be related to the difficulty ofchoosing an outflow site for a bypass graft [15].

Diabetic patients appear to respond poorly to at-tempts at graft thrombolysis and do badly follow-ing graft lysis. They were less likely to undergosuccessful initial thrombolysis and had inferiorlong-term patency if recanalized. Although the pres-ence of diabetic distal disease was suspected as thecause, it could not be proven. Runoff was similarin both groups.

Hye et al. [6] suggested that venous bypass oc-clusions may have a worse outcome compared totheir synthetic counterparts because of vein wall is-chemia. This observation appears to be born outin other author's experience [16,17]. One study,however, found that venous bypass occlusions re-spond well to thrombolysis [4]. The results of thelatter study may be misleading because of con-founding factors such as the state of the runoff andthe presence of underlying occlusive lesions.

No firm conclusions can be drawn about the useof warfarin following the successful restoration ofgraft patency by thrombolysis. Both Nackman et al.[13] and Galland et al. [9] demonstrated that long-term patency was not affected by the use of war-farin, although the number of patients was smalland anticoagulation was prescribed at the discre-tion of the surgeon. Our own feeling is that aspirinshould be used for the prevention of other car-diovascular events but the mainstay of graft preser-vation remains mechanical.

If a bypass graft reoccludes following thromboly-sis, further attempts at lysis are associated with apoor outcome. An analysis of the NATALI databasefound that five of eight such grafts reoccluded atthree months. Subsequent surgical attempts at limbsalvage following failed thrombolysis similarly havea low chance of success. In Sullivan's series, of the11 thrombolytic failures only three were successfullytreated by revision or graft replacement [4].

Life table analysesfor long-term patency

Following the STILE trial, a multifactor analysisof patients undergoing thrombolysis found that thenature of the occlusion was not an independent

Periprocedural mortality

The reported peri-operative mortality for the sur-gical management of bypass occlusion is surpris-ingly low (no deaths in Comerota's series). It isprobable that a significant number of patients are


not offered revascularization due to their comor-bidity, although results from the STILE trial sug-gested 92% of designated procedures were carriedout on an intent-to-treat basis.

The accepted overall mortality from thromboly-sis in the periprocedural period is in the area of3% to 5%. The majority of patients will perish fromstroke, myocardial infarction, or hemorrhagic com-plications.

The long-term survival following lysis of occludedgrafts is encouraging. In Nackman's paper [13], 89%of patients were still alive at two years and 84% ofpatients in another study were alive at 42 months [6].

Logistics

Thrombolysis is a labor-intensive technique. Pa-tients may require multiple visits to the interven-tional radiology suite. In a study by Browse et al.[14], an average of four angiograms were requiredin every patient. Furthermore, graft occlusions ap-pear to take longer to successfully lyse than theirnative arterial counterparts. Pulse-spray techniquesmay reduce the time to achieve patency and thelabor intensity of lysis by means of its mechanicalaction on thrombus. However, even when pulse-spray techniques are employed, graft occlusions ap-pear to take longer to lyse than their native arterialcounterparts (93 minutes versus 65 minutes in onestudy) [18].

The incidence of complications means that medi-cal and nursing staff must be familiar with the tech-nique. The patient is usually nursed on a high de-pendency unit. A protocol for the treatment ofthrombolysis complications may reduce their sever-ity and simplify patient care.

The general impression might be that there is lit-tle cost difference between bypass surgery andthrombolysis in native vessel occlusion. However,Rickard et al. found that on average they werespending $ 2440 Australian more per patient withgraft occlusion (1997) [19].

Complications of thrombolysisfor occluded grafts

Thrombolysis requires a great deal of patientcooperation. The procedure requires that the pa-tient lies still for a number of hours and it is asso-

ciated with significant pain. Thrombolysis should notbe considered in patients whose grafts have occludedless than four weeks following insertion. The poros-ity of prosthetic grafts poses risk of major hemor-rhage through the graft wall and anastomosis.

The complications of arterial thrombolysis are notinsignificant. In a study from Nottingham, majorhemorrhage occurred in 5% of patients, minor in15%, and stroke in 1% [20]. In Hye's study of pulse-spray thrombolysis of occluded bypass grafts [6],27% of patients had a complication directly attrib-utable to thrombolysis. The axilla is a more frequentsite of bleeding complications than the groin be-cause of the lack of supporting connective tissue[14]-

Direct graft puncture offers an alternative ap-proach. In experienced hands it is associated withlow rates of local complication. It is especially use-ful in patients with prosthetic extra-anatomical femo-rofemoral bypass grafts in whom local complicationsmay be high [21].

Evidence from the UK NATALI database suggeststhat bleeding complications were higher in patientsundergoing graft thrombolysis [9]. Prosthetic graftsin particular seem to have more local complications[3]. In another series, more complications were ex-perienced with prosthetic graft lysis (53%) com-pared to vein graft (41%) and native artery bypass(29%), although these figures did not reach statis-tical significance. Furthermore, acute worsening ofischemia due to embolization appeared to be almosttwice as common in graft thrombolysis (2.7% versus1.5%) [22]. In that study of 19 patients, 11 patientsrequired amputation and two patients died despitefurther lysis or surgery. Paradoxically, lower rates ofhemorrhagic complications occurred in patientswith bypass graft occlusions in the TOPAS trial andno difference could be demonstrated with regard tomajor morbidity at one year in the STILE trial.

Alternative indications

Occlusion of the body and iliac limbs of en-dovascular stent grafts is not an uncommon com-plication. The conventional management of endo-vascular stent graft occlusion is a femorofemoralbypass, an axillobifemoral graft, or conversion toopen repair. Conversion to open repair carries amortality of at least 20%. Unfortunately, thrombol-ysis may cause significant complications. A case from

THROMBOLYSIS FOR OCCLUSION OF BYPASS GRAFTS

the Malmo group demonstrated that thrombolysiscaused loss of graft seal with the aortic wall, aneur-ysm expansion and subsequent rupture [23]. In ad-dition, thrombolysis has been used to good effectin patients with occluded hemodialysis fistula. Themost important predictor of successful restorationof patency with lysis in these cases appears to be theadequacy of venous outflow.

Conventionalsurgical management

The diagnosis of bypass graft occlusion does notmandate revascularization. In the absence of criti-cal ischemia (30% of occluded grafts in the STILEtrial), nonoperative management may be appro-priate. Alternatively, primary amputation should beconsidered if the graft has occluded due to globalprogression of atherosclerotic disease in the runoffvessels or if the patient is too frail to survive majorarterial surgery.

Standard surgical practice for the revascularizationof critically ischemic limbs following bypass involvesone of two approaches. First is graft thrombectomy(with or without an adjunctive procedure), and sec-ond is graft removal and replacement. Robinson et al.[24], however, reported a cumulative secondary pa-tency rate of 47% at one year in patients undergoingsurgical thrombectomy and an adjunctive procedure(in those patients treated for early graft failure).Twenty-six percent of patients required amputationat 1 month and 41% at one year in that study.

Graft thrombo-embolectomy alone is akin tothrombolysis. Both involve removal of the throm-bus without treatment of the underlying cause.One study reported a 29% patency at one year in40 occluded above-knee prosthetic grafts under-going revision surgery [25], The majority had graftthrombectomy with or without patch angioplasty.Others have demonstrated a two-year patency ofless than 40% with thrombectomy and graft revi-sion, decreasing to less than 30% at five years [26].

Where the population of patients is matched withrespect to patient demographics, graft type and oc-clusion, short-term patency rates were better withthrombolysis than thrombectomy alone (86% versus42%) [27]. Some authors have attained good long-term outcomes using graft replacement surgery.Edwards et al. [1] achieved a 5-year secondary pa-tency of 71% and limb salvage of 90% using graft

replacement with a venous conduit, whereas othershave generally found limb salvage rates of 40% atthree years [28]. Gardiner et al. [10] suggested thatgraft replacement with a venous conduit offeredsubstantially better patency than prosthetics. Sev-enty-seven percent of vein grafts were patent at16 months compared with 45% of prosthetic graftsat 14 months. However, the results may be ex-plained in part by the large numbers of underlyingcorrectable lesions that were found in those under-going replacement with vein (85% versus 39%) [9].

Conclusion

The results from repair of failing bypass graftsare superior to those of grafts that are occluded.Graft replacement provides more durable resultsthan thrombectomy alone or with angioplasty, espe-cially if performed using autogenous vein.

Patients who appear to benefit from thromboly-sis are those with occluded grafts where the dura-tion of ischemia has been short. Grafts greater thanone year old and in which an underlying cause ofthe occlusion can be treated also appear to do well.Those patients without distal runoff and in whomgraft replacement cannot be performed with anautogenous venous conduit may also be consideredin a favorable light for thrombolysis. Diabetics andpatients with venous bypass graft occlusions dopoorly following successful thrombolysis.

More evidence is required before absolute con-clusions can be drawn regarding the indications forthrombolysis in bypass graft occlusion. The deci-sion to perform thrombolysis for bypass graft occlu-sion will depend, in part, on the experience anddistribution of resources in individual centers.

R E F E R E N C E S

1 Edwards JE, Taylor LM Jr, Porter JM. Treatment of failed lowerextremity bypass grafts with new autogenous vein bypass graft-ing. / Vase Surg 1990; 11: 136-145.

2 Palfreyman SJ, Booth A, Michaels JA. A systematic review ofintra-arterial thrombolytic therapy for lower limb ischaemia.EurJ Vase Endavasc Surg 2000; 19: 143-157.

3 Comerota AJ, Weaver FA, Hosking JD et al. Results of a prospec-tive, randomised trial of surgery versus thrombolysis foroccluded lower extremity bypass grafts. Am J Surg 1996; 172:105-112.


30300

4 Sullivan KL, Gardiner GA Jr, Kandarpa K et al. Efficacy ofthrombolysis in infrainguinal bypass grafts. Circulation 1991; 83(2suppl):I99-1105.

5 Braithwaite BD, Buckenham TM, Galland RB et al. Prospec-tive randomized trial of high-dose bolus versus low-dose tissueplasminogen activator infusion in the management of acutelimb ischaemia. Thrombolysis Study Group. BrJ Surg 1997; 84:646-650.

6 Hye RJ, Turner C, Valji K et al. Is thrombolysis of occludedpopliteal and tibial bypass grafts worthwhile? J Vase Surg 1994;20: 588-597.

7 Seabrook GR, Mewissen MW, Schmitt DD et al. Percutaneousintra-arterial thrombolysis in the treatment of thrombosis oflower extremity arterial reconstructions. / Vase Surg 1991; 13:646-651.

8 van Breda A, Robison JC, Feldman L et al. Local thrombolysisin the treatment of arterial graft occlusions. / Vase Surg 1984;1:103-112.

9 Galland RB, Magee TR, Whitman B et al. Patency followingsuccessful thrombolysis of occluded vascular grafts. EurJ VaseEndovasc Surg m\; 22: 157-160.

10 Gardiner GA Jr, Harrington DP, Koltun W et al. Salvage ofoccluded arterial bypass grafts by means of thrombolysis. J VaseSwrgl989;9: 426-431.

11 Berkowitz HD, Fox AD, Deaton DH. Reversed vein graft steno-sis: early diagnosis and management. / Vase Surg 1992; 15:130-142.

12 Berridge DC, al-Kutoubi A, Mansfield AO et al. Thrombolysisin arterial graft thrombosis. EurJ Vase Endovasc Surg 1995; 9:129-132.

13 Nackman GB, Walsh DB, Fillinger MF et al. Thrombolysis ofoccluded infrainguinal vein grafts: predictors of outcome./ Vase Surg 1997; 25: 1023 -1032.

14 Browse DJ, Torrie EP, Galland RB. Low-dose intra-arterialthrombolysis in the treatment of occluded vascular grafts. BrJSttrg-1992;79:86-88.

15 Ouriel K, Veith FJ. Acute lower limb ischemia: determinants ofoutcome. Surgery 1998; 124: 336-342.

16 Durham JD, Geller SC, Abbott WM et al. Regional infusion ofurokinase into occluded lower-extremity bypass grafts: long-term clinical results. Radiology 1989; 172: 83-87.

17 Parent FN 3rd, Piotrowski JJ, Bernhard VM et al. Outcome ofintraarterial urokinase for acute vascular occlusion. J CardiovascSurg 1991; 32: 680 -689.

18 Valji K, Roberts AC, Davis GB, Bookstein JJ. Pulsed-spray throm-bolysis of arterial and bypass graft occlusions. AJR Am JRomtgmol 1W1; 156: 617-621.

19 Rickard MJ, Fisher CM, Soong CV et al. Limitations of intra-arterial thrombolysis. Cardiovasc Surg 1997; 5: 634-640.

20 Berridge DC, Makin GS, Hopkinson BR. Local low dose intra-arterial thrombolytic therapy: the risk of stroke or major haem-orrhage. BrJ Surg \m; 76: 1230-1233.

21 Guest P, Buckenham T. Thrombolysis of the occluded prostheticgraft with tissue-type plasminogen activator. Technique, resultsand problems in 23 patients. Clin Radiol 1992; 46: 381-386.

22 Galland RB, Earnshaw JJ, Baird RN et al. Acute limb deterio-ration during intra-arterial thrombolysis. Br J Surg 1993; 80:1118-1120.

23 Resch T, Lindblad B, Lindh M et al. Aneurysm expansion andretroperitoneal hematoma after thrombolysis for stent-graftlimb occlusion caused by distal endograft migration. J EndovascThermO; 7: 446-450.

24 Robinson KD, Sato DT, Gregory RT et al. Long-term outcomeafter early infrainguinal graft failure. J Vase Surg 1997; 26:425-438.

25 Anonymous. Results of a prospective randomized trial evalua-ting surgery versus thrombolysis for ischaemia of the lowerextremity. The STILE trial. Ann Surg 1994; 220: 251-268.

26 Whittemore AD, Clowes AW, Couch NP, Mannick JA. Secondaryfemoropopliteal reconstruction. Ann Surg 1981; 193: 35-42.

27 Graor RA, Risius B, Young JR et al. Thrombolysis of periph-eral arterial bypass grafts: surgical thrombectomy comparedwith thrombolysis. A preliminary report. J Vase Surg 1988; 7:347-355.

28 Bartlett ST, Olinde AJ, Flinn WR et al. The reoperative poten-tial of infrainguinal bypass: long-term limb and patient survival./ Vase Swrg 1987; 5: 170-179.

ACUTE PROBLEMSOF THE DIABETIC FOOT

JAN RAUWERDA

Diabetes mellitus (DM) is a metabolic disease caused by hereditary as well as environmentalfactors. There are two different types of DM. DM type 1 (10% to 20%), also known asinsulin-dependent diabetes, is caused by a destruction ofthefl-cells of the pancreas, due to anautoimmune response. It leads to insulin deficiency and hyperglycemia. It affects primarilychildren and adolescents. The so-called type 2 DM (80% to 90%) is characterized by agradual defect in insulin production in the f-cells as well as an insulin resistance caused bya diminished response of the receptors in the target organs and an increase of glucoseproduction by the liver. Before the diagnosis of DM type 2 is made, the disease is alreadypresent for four to seven years. It was calculated that in 2000 more than 755 million peopleworldwide would suffer from DM. This number will increase to more than 250 million in2010, with immense consequences for vascular surgeons [1].

301

DM and foot problems

The annual incidence of foot ulcers is 2% to 3%.Cross-sectional studies showed that the prevalenceof a foot ulcer and/or amputation is 3% to 5%.The local recurrence rate of foot ulcers is high,varying from 34% after one year to 70% after5 years. This means that, of all the individuals withDM, 15% to 25% will develop a foot ulcer [2].

There is a country-based variation in the relativerisk of diabetes-related lower extremity amputation

(Table I). It is not surprising that 40% to 60% of allamputations are performed in patients with DM [3].

Within 3 years of amputation, 30% to 50% of thepatients undergo an amputation of the contralat-eral leg. Even the life expectancy is influenced bythe amputation. The 5-year survival rate of a patientwith DM and a healed ulcer is 58%. After an ampu-tation due to ischemic lesions it is only 27%, reflect-ing the end stage of the disease.

It has been calculated that almost 20% of all thehospitalizations and costs of patients with diabetesare related to foot ulceration and/or amputation.


1st author[ref.]

Gujral [4]

Trautner [5]

Siitonen [6]

Lawee [7]

Anonymous [8]

Deerochanawong [9]

Most [10]

Miller [11]

Lee [12]

Nelson [13]

Van Houtum [14]

Location

Leicestershire, United Kingdom

Leverkusen, Germany

Eastern Finland

Ontario, Canada

Washington State, USA

Newcastle upon TyneUnited Kingdom

Six states in the USA

New Jersey, USA

Oklahoma Indians, USA

Pima Indians, USA

Dutch population

Year

1980-1985

1990-1991

1978-1984

1987-1988

1988

1989-1991

1976-1978

1979-1981

1972-1980

1972-1984

Incidence per year

14/10 000

21/10 000

Men: 35/10000Women: 24/10000

44/10000

51/10000

57/10000

60/10000

77/10000

180/10000

241/10000

25/10 000

The International Working Group of the Diabetic Footshowed that the primary healing costs varies from7 000 to 10 000 dollars. The direct costs related toamputation, in association with the diabetic footproblem, varies from 30 000 to 60 000 dollars. Theindirect costs, which result from the loss of jobs,reduced productivity, the individual patient costsand not even calculating the loss of quality of life,for the diabetic foot in the United States has beenestimated as 4 billion dollars per year. So the dia-betic foot is not only a specific patient problem butit is also of significant economic interest [15]. Thecosts associated with diabetic foot ulceration andlower extremity amputations are shown in Table II.

To reduce the incidence of amputations, the St.Vincent Declaration has been adopted. The goal ofthis declaration is to reduce the amputation rate ofpatients with DM by 50%. In this respect, a coor-dinated multidisciplinary screening or even thestart of so-called Diabetic Foot Clinics has been shownto be successful.

Neuropathic ulcers can be healed in 68% of pa-tients, ischemic ulcers in 72%, and an amputationrate reduction of 50% has been achieved. Com-pared to the individual costs of primary healing,

the multidisciplinary approach to prevent amputa-tion is cost effective [24-26].

Pathogenesis of foot problemsDiabetic foot ulcers are the result of al least two

risk factors. This pathway is shown in Table III.Diabetic peripheral neuropathy involves mostly

all fibers of the nervous system (sensory, autonomicand motor fibers). Sensory neuropathy leads to dim-inished sensation of pain, pressure awareness andpropriocepsis.

Motor neuropathy results in atrophy of the intrin-sic foot muscles leading to flexion deformity of toesand even a disturbed walking pattern. All those fac-tors lead to high-pressure zones, mostly on the plan-tar surface of the metatarsal heads I and V anddorsal side of toes.

The autonomic neuropathy leads to diminishedsweat secretion, which is responsible for vulnerabledry skin with cracks and fissures.

Angiopathy also plays a role. The so-called micro-angiopathy is responsible for a hampered circu-lation by opening the arteriovenous shunts. This

ACUTE PROBLEMS OF THE DIABETIC FOOT

1st author[ref.]

CountryCosts

A. Primary healingBouter [16] 1988 The Netherlands1

Apelqvist [17] 1994 Sweden3

B. Healing with amputationConnor [18] 1987 United Kingdom1

Bouter [16] 1988 The Netherlands1

Bild [19] 1989 United States1

Reiber [20] 1992 United States2

Thompson [21] 1993 New Zealand1

Apelqvist [2] 1993 Sweden3

Van Houtum [22] 1995 The Netherlands1

C. Long-term costs (3-year period)Apelqvist [23] 1995 Sweden3

100007000

1400015000

8000-1200020000-25000

110001100014500

Primary healing16 1006-26 7007

Healing with anamputation43 1004-63 1005

1 In-hospital costs2 In-hospital costs, rehabilitation included3 Total direct costs until healing4 Minor amputation5 Major amputation6 Without ischemia7 With ischemia

31303

leads to edema noticed as a warm foot with dis-tended veins, but also a diminished capillary flow.It is not certain whether this microcirculatory dis-turbance can be influenced.

Another specific pattern is the so-called macroan-giopathy. In comparison with the distribution ofatherosclerotic lesions in non-diabetics, it is morecommon, affects younger individuals without sexdifference, is multisegmental, but most strikingly itis a pattern of multisegmental crural vessel occlu-sions with surprisingly often intact foot arteries. In40% of cases, the popliteal artery is palpable. Thenatural history of these atherosclerotic lesions showsmuch faster progress than in non-diabetics. Besidesthese atherosclerotic lesions, the media calcinosis(Monckenberg disease) is found more often in dia-betics, with a frequency up to 30 times. This calci-nosis of the muscular layer of the arterial wall,probably due to neuropathy, has no influence onthe peripheral circulation, but makes it difficult to

use the standard noninvasive vascular laboratorytests because of the noncompressibility of the cruralarteries. Beside neuropathy and angiopathy, littlefoot trauma as well as infections can lead to severelimb-threatening complications.

The diabetic foot andassociated complications

The World Health Organization's definition of thediabetic foot refers to foot problems in patients withDM, associated with ulceration and/or infection,with or without destruction of deep tissues, relatedto neurological abnormalities and varying degreesof peripheral vascular disease in the lower limb.

Diabetic foot problems can be limb and life threat-ening, caused by infection, ischemia, or a combi-nation of these complications and most oftenrequire urgent surgical intervention.


OKimDmMncFQ&r 1999 [IS]

DIABETESMELLITUS

NEUROPATHY

1\

11

Postural andcoordination

deviation

Decreased painsensation andpropriocepsis

Automatic

r i

Inadequatefoot wear,

non-compliance,neglect,

unawareness, lack ofpatient and staff

education

Diminishedsweating

i r

Foot deformities,stress and

shear pressures


Although there is not much written about emer-gent foot surgery in patients with DM, Taylor et al.described the principles of treatment [27]. Theseprinciples are:1 - debridement with or without phalangeal and/or

ray amputation,2 - broad-spectrum antibiotics (intravenous),3 - noninvasive vascular testing and angiography,4 - revascularization procedures.There are three groups of diabetic foot problemsthat require urgent intervention:1 - septic diabetic foot without ischemia,2 - septic diabetic foot with ischemia,3 - tissue loss with ischemia.

SEPTIC DIABETIC FOOT WITHOUT ISCHEMIAPatients with a septic foot show an infected ulcer,

arthritis, osteomyelitis or even a subplantar abscesscombined with general symptoms of infection (fever,deregulated glucose metabolism, etc.). Even in pa-tients with an uninterrupted arterial circulation (pal-pable pedal pulses, biphasic arterial signals on dop-pler examination, ankle-brachial index [ABI] higherthan 0.9), this infection can be limb threatening.

This is mostly caused by the special foot anatomyas well as metabolic disturbances aggravated byinfection.

FOOT ANATOMYThe purpose of the human feet is to support the

entire body weight, to absorb forces, to accommo-date propulsion, and to facilitate rotational move-ments. Our feet are well adapted for this monu-mental task. These adaptations are reflected inspecial anatomical features such as a thickened epi-dermis and subcutaneous tissue consisting of fattypads, which provide protection of the underlyingsoft tissues and bony structures and effectivelycushion the high-stress forces.

Moreover, the foot muscles are adapted to per-form their task, by means of arrangement in sepa-rate anatomical compartments.

FOOT COMPARTMENTSFour separate foot muscles are recognized: a

medial plantar, a central plantar, a lateral plantarcompartment, and an interosseus compartment(Figs. 1 and 2).

3051 - Lateral compartment2 - Central compartment3 - Medial compartment

it - Interosseus compartment5 - Lateral compartment6 - Central compartment7 - Medial compartment

FIG. 1 The plantar aspect of the foot. FIG. 2 Transverse section of the foot.


306

The borders of the foot compartments are dor-sally formed by the metatarsal bones and the inter-osseus fascia and, on the plantar side, by the fasciaplantaris. Medially, the intermuscular septum ex-tends from the calcaneus to the head of the firstmetatarsal bone, and on the lateral side, the inter-muscular septum ranges from the calcaneus to thefifth metatarsal. Finally, on the central side, indi-vidual muscles are divided by the intermuscular sep-tum. Proximally, there is a fibrous attachment be-tween the navicular bone, the posterior tibial musclesand the medial cuneiform bone. The lateral neu-rovascular bundle penetrates this septum. The lat-eral plantar compartment houses the intrinsic footmuscles of the fifth toe, such as the flexor digiti min-imi brevis and abductor muscle.

The medial plantar compartment contains the in-trinsic foot muscles of the big toe, including the flex-or hallucis brevis and abductor hallucis muscles aswell as the flexor hallucis longus muscle. The plan-tar compartment contains all the intrinsic foot mus-cles of the other toes: the adductor hallucis muscle,the quadratus plantae muscles, the flexor digitorumbrevis muscle, as well as the tendons and muscles ofall the long flexor muscles. The interosseus com-partment contains only the interosseus muscles.

Walking on a deformed foot leads to high-pres-sure zones. This can result in a foot ulcer. Prefer-ential ulcer locations are the planter side of metatar-sophalanges I and V. If this ulcer becomes infected,

edema increases the pressure in the adjacent com-partment leading to a compartment syndrome.

Metabolic changes

Another predisposing factor for elevated com-partment pressure are metabolic changes. In dia-betic patients, glucose is preferentially metabolizedby means of the so-called sorbitol pathway. This maylead to an excess conversion of glucose to sorbitol,which in turn is responsible for increased tissueconcentration of several split products. Together,these products and the hydropholic molecules, sor-bitol in particular, are responsible for edema withinthe compartments, leading to a higher compartmentpressure.

Another metabolic change in patients with dia-betes is caused by greater affinity of HbAlC for oxy-gen than normal for hemoglobin. This phenome-non, which lowers the tissue oxygen concentration,is known as pseudohypoxia. All these factors are re-sponsible for an increased capillary permeability[28]. A foot infection results in edema and, evenin case of a normal arterial circulation, can resultin digital arterial thrombosis causing wet gangreneof a toe or even a compartment syndrome of thefoot with necrosis with the whole content of thatof a specific compartment (Fig. 3).

FIG. 3 Necrosis example of theinternal compartment of the foot.


This explains why an infected foot ulcer can causeextensive tissue necrosis, even in a normal vascu-larized foot.

TREATMENTThe treatment consists of broad-spectrum anti-

biotics (intravenous) and a drainage procedure. Foradequate debridement, knowledge of the anatomyof the foot is mandatory.

When the infection is over, healing by secondaryintervention is to be expected. Recently some goodresults with use of vacuum therapy have beendescribed [29].

The septic diabetic footwith ischemia

This group of patients shows an acute diabeticfoot problem related to ischemia and infection.Also in this category, aggressive debridement andbroad-spectrum antibiotic treatment is required.Noninvasive tests, if not performed pre-operativelythan shortly after the primary operation, can pro-vide information of the arterial circulation.

Although there is lack of prospective trials, thereis scarce evidence that transcutaneous oxygen pres-sure measurements as well as ABI/or toe pressuremeasurements can proclaim wound healing.

Fig. 4 shows the relation between probability ofwound healing and noninvasive measurements.

These tests allow for the probability of woundhealing to be estimated and also indicate additionalangiography and revascularization procedures [15].Absent foot pulses, ABI less than 0.6, abnormal toepressure (ATI) less than 0.4, or noncompressiblecrural vessels are indications for angiography.

This strategy appears not to be routine in all hos-pitals. A retrospective analysis of 283 diabetics from18 hospitals in the Netherlands in 1994 showed thatoptimal vascular evaluation concerning palpation offoot pulses, noninvasive testing, duplex scanning ofthe vessels, angiography, etc., were only performedin 53% of patients undergoing a major amputationand in 45.3% undergoing a minor amputation.

Only the university hospitals showed adequatevascular investigations and revascularization proce-dures [30].

Angiography

In case of impaired renal function with goodfemoral pulses and an uninterrupted blood flow inthe aortofemoral segment on duplex examination,antegrade puncture of the ipsilateral femoral arterycan be performed to make an angiography of theleg and foot to diminish the total amount of the

307

0 20 40 60 80 100 120 140

TcPo2

Toe pressure

Ankle pressure

mmHg

FIG. 4 Wound healing versus different noninvasive measurements.


308

nephrotoxic contrast medium to avoid renal fail-ure. In obese patients, a Seldinger technique fromthe contralateral groin is preferable.

Characteristically, angiography shows multiple seg-mental crural occlusions, but surprisingly often thepedal arteries are patent and suitable for revascu-larization. If angiography shows no pedal arteries,duplex and/or magnetic resonance angiographycan be helpful [31].

An angiographic scoring system of the foot arter-ies, advised by the Joint Vascular Society Councils, isassociated with bypass graft patency and limb sal-vage. In a prospective series, a foot score greaterthan 7 correlated with a bypass failure rate of 2%,and a score less than 7 correlated with a bypass fail-ure rate of 30%. However, this scoring systemproved not to be able to discriminate between can-didates for a pedal bypass procedure or a primaryamputation [32].

Not every patient with an acute foot problem andischemia should be a candidate for revasculariza-tion. In this respect, the prehospital state of mobil-ity is a very helpful scoring system to discriminatebetween primary amputation and revascularization(Table IV).

Patients who are pre-operatively scored in cate-gories 4 and 5 are probably better off with a pri-mary major amputation [33]. Treatment also con-sists of aggressive debridement and antibiotics. Inthe other groups, revascularization should be per-formed soon after the debridement in order to pre-vent a major amputation.

Because there is often multilevel disease, a com-bination of percutaneous transluminal angioplasty(PTA) and/or stent implantation for inflow im-provement combined with outflow procedures(femorocrural, popliteal crural, or pedal bypasses)

fabtel? DEGREES OF MOBILITY

1 Free mobility in- and outdoors

2 Free mobility outdoors with support

3 Free mobility indoors with support

4 Wheelchair dependency

5 Bed: not able to move around

must be performed. A combination of infra-ingui-nal revascularization surgery and PTA of aortoiliacor even femoropopliteal segment shows to be effec-tive and there is no evidence that diabetes per seis a limiting factor [34].

Tissue loss without ischemia

The third category is patients presenting withacute ischemia and/or gangrene without infection.Noninvasive testing with angiography and revascu-larization are the best ways to prevent a major am-putation. From this category, excellent results aredescribed in the literature (3-year patency higherthan 70%, limb salvage superior to 80%) [35,36].In case of large soft tissue defects, even the use ofa free flap transfer combined with crural or pedalbypass is effective, although reconstructions on theplantar side without restoration of sensibility haveshown to be of less value [37].

However, the five-year life expectancy of patientswith neuro-ischemic foot defects in diabetic patientsis less than 25%. From the literature it is knownthat there is no evidence that crural pedal recon-struction in diabetics have a worse prognosis thanin non-diabetics [38]. In case of crural stenotic le-sions, PTA is recommended.

Although there are some reports of good resultsof durability of PTA of multiple crural lesions, oth-ers report only a patency of 55% after one monthand 32% after one year [39,40]. Nevertheless, theimproved arterial inflow by means of PTA of crurallesions can be sufficient diabetic foot healing.

Personal results of urgent footsurgery in diabetic patients

In a retrospective analysis of all consecutive ad-missions for urgent foot surgery in diabetic patientsin our tertiary referral center during a five-year pe-riod, 198 patients were analyzed. The patient char-acteristics are shown in Table V.

In 127 (64%) patients, the indication for urgentfoot surgery was ischemia with or without infection.One hundred and seventeen patients underwent175 vascular procedures.

Peri-operatively, 14 patients died, eight patientsas a result of sepsis and/or respiratory insufficiency,two patients because of myocardial events, and four


TdileV PATIENT CHARACTERISTICS OF ?$irt&i

PeriodNumber of patientsNumber of involved legs

Duration of Diabetes millitus - YearsAge (range) - YearsVascular involvement - NPrimary amputation - NVascular procedures - N

Primary assisted patency - %Peri-operative mortality - %Two-year limb salvage rate - c ,Two-year survival - %

1996-2001198

199

17.1

67.9(41-94)127

10

117

Septic footSeptic ischemic footIschemic foot

727849

6212.681.152

InflowOutflowCombinedTotal

45

10030

175

patients, mostly young ones, refused further treat-ment because they had end-stage diabetic diseasewith blindness, dialysis dependency and an impend-ing major amputation.

The two-year primary assisted patency of crural/pedal reconstruction was 62%, with a limb salvageof 81.1%, comparable to the results in the literature.

Routine postoperative control

After secondary wound healing with or withoutrevascularization, the plantar surface of the foot isdeformed. This deformity again leads to high-pres-sure zones. These high-pressure zones are a poten-tial risk for development of recurrent foot ulcersand, consequently, a risk for amputation. This am-putation risk is expressed in the risk profile for thediabetic foot, also known as the Simms classifica-tion, which determines the frequency of postoper-ative control (Table VI).

In a two-year follow-up study, the amputation riskin patients within category 3 was 25% [41].

Also in a prospective controlled trial, this risk clas-sification showed to be effective.

In a series of 225 diabetic patients during a three-year follow-up, ulceration occurred in 5.1% in cat-egory 0, in 14.3% in category 1, in 18.8% in category2, and 54.8% in category 3 (bilinear associationp < 0.001). All amputations took place in group 2and 3 (respectively, 3.1% and 20.9%; p < 0.001) [42].

In general, a multidisciplinary approach is effec-tive in lowering the amputation rate in diabeticpatients and the frequency of control depends onthe risk profile [43].

309

fttteYTSIMMS CMSSIHCATI0NQREKEP1OHLE

Category Neuropathy Footdeformity

Footsurgery


R E F E R E N C E S

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