Ebook Vascular surgery principles and practice (4/E): Part 1

Part 1 book “Vascular surgery principles and practice” has contents: Clinical examination of the vascular system, clinical examination of the vascular system, thrombolytic therapy, thrombophilia as a cause of recurrent vascular access thrombosis in hemodialysis patients, antiplatelet therapy, acute arterial insufficiency, the pathophysiology of skeletal muscle reperfusion,… and other contents.

VASCULAR SURGERY Principles and Practice F O U RT H E D I T I O N VASCULAR SURGERY Principles and Practice F O U RT H E D I T I O N EDITED BY SAMUEL ERIC WILSON Department of Surgery University of California, Irvine Irvine, California, USA JUAN CARLOS JIMENEZ Division of Vascular Surgery University of California, Los Angeles Los Angeles, California, USA FRANK J VEITH Department of Surgery New York University Medical Center New York, New York, USA and Department of Surgery Cleveland Clinic Cleveland, Ohio, USA A ROSS NAYLOR Department of Vascular Surgery Leicester Royal Infirmary Leicester, UK JOHN A.C BUCKELS Department of Surgery University of Birmingham and Queen Elizabeth Hospital Birmingham, UK CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2017 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S Government works Printed on acid-free paper Version Date: 20160824 International Standard Book Number-13: 978-1-4822-3945-4 (Pack - Book and Ebook) This book contains information obtained from authentic and highly regarded sources While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and not necessarily reflect the views/opinions of the publishers The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint Except as permitted under U.S Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400 CCC is a not-for-profit organization that provides licenses and registration for a variety of users For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com This one is for Ellie, Sam and Camille Samuel Eric Wilson For Dr Carlos and Ana Jimenez, my parents and inspirations for my medical career Juan Carlos Jimenez I have four people who have supported my career throughout and who deserve an acknowledgement: my wife Carol and my associates Jackie Simpson, Julie Harris and Jamie McKay Frank J Veith To my three mentors, Jetmund Engeset, Vaughan Ruckley and Peter Bell A Ross Naylor Contents Preface xi Contributorsxiii Section I:  ASSESSMENT OF VASCULAR DISEASE The evolution of vascular surgery James C Stanley Pathophysiology of human atherosclerosis Christopher K Zarins and Chengpei Xu Hemodynamics and non-invasive testing Doran Mix and Ankur Chandra Clinical examination of the vascular system Michael D Sgroi, Elizabeth L Chou and Samuel Eric Wilson A review for clinical outcomes research: Hypothesis generation, data strategy and hypothesis-driven statistical analysis Laura T Boitano and David C Chang 19 43 61 71 Section II:  MEDICAL TREATMENT 10 11 12 13 Pathology and medical management of atherosclerotic vascular disease 81 Ralph G DePalma Thrombophilia as a cause of recurrent vascular access thrombosis in hemodialysis patients 97 Khushboo Kaushal and Samuel Eric Wilson Anticoagulants 101 Jeffrey D Crawford, Bruce A Warden and Timothy K Liem Thrombolytic therapy 123 Elizabeth L Chou and Nii-Kabu Kabutey Antiplatelet therapy 133 Ian Gordon Vasoactive pharmaceuticals for treatment of peripheral arterial disease 173 Cristine S Velazco, Mark E O’Donnell and Samuel R Money Perioperative evaluation and management of cardiac risk in vascular surgery 183 Nariman Nassiri, Jerry J Kim and Christian de Virgilio The biology of restenosis and neointimal hyperplasia 195 Adam M Gwozdz, Mostafa Albayati and Bijan Modarai Section III:  PERIPHERAL OCCLUSIVE DISEASE 14 15 16 17 Acute arterial insufficiency Mark M Archie and Jane K Yang The pathophysiology of skeletal muscle reperfusion Darin J Saltzman and Dmitri V Gelfand Aortoiliac occlusive disease: Endovascular and surgical therapies Madhukar S Patel, Juan Carlos Jimenez and Samuel Eric Wilson Femoral–popliteal–tibial occlusive disease: Open surgical therapy Frank J Veith, Neal S Cayne, Evan C Lipsitz, Gregg S Landis, Nicholas J Gargiulo III and Enrico Ascher 217 227 245 259 vii viii Contents 18 19 20 21 22 23 24 25 Results of endovascular therapy for femoral, popliteal and tibial disease Adam Z Oskowitz and Brian G DeRubertis In situ saphenous vein arterial bypass Dhiraj M Shah, R Clement Darling III, Benjamin B Chang and Paul B Kreienberg Adventitial cystic disease and entrapment syndromes involving the popliteal artery Juan Carlos Jimenez and Samuel Eric Wilson Extra-anatomic bypass Evan C Lipsitz and Karan Garg Amputation in the dysvascular patient James M Malone and Samuel Eric Wilson Rehabilitation of the vascular amputee Sujin Lee and Sophia Chun Diabetes and peripheral artery disease Robert S.M Davies and Michael L Wall Prevention and management of prosthetic vascular graft infection Max Zegelman, Ojan Assadian and Frank J Veith 267 279 291 301 311 331 351 371 Section IV: ANEURYSMS 26 27 28 29 30 31 32 Abdominal aortic aneurysm: Pathophysiology, endovascular and surgical therapy Denis W Harkin and Paul H Blair Thoracoabdominal aortic aneurysms Germano Melissano, Efrem Civilini, Enrico Rinaldi and Roberto Chiesa Endovascular management of complex aortic aneurysms Giovanni Tinelli, Blandine Maurel, Rafaëlle Spear, Adrien Hertault, Richard Azzaoui, Jonathan Sobocinski and Stéphan Haulon Aortic dissection Benjamin O Patterson and Matt M Thompson Popliteal artery aneurysm Samuel Eric Wilson and Juan Carlos Jimenez Splanchnic artery aneurysms Russell A Williams, Juan Carlos Jimenez and Samuel Eric Wilson Infected aneurysms Michol A Cooper, James H Black III, Bertram M Bernheim, Bruce A Perler and Julius H Jacobson II 387 411 431 449 463 469 477 Section V: CEREBROVASCULAR DISEASE 33 34 35 36 37 38 39 Extracranial vascular disease: Natural history and medical management Ankur Thapar, Ieuan Harri Jenkins and Alun Huw Davies Extracranial carotid artery occlusive disease: Surgical management A Ross Naylor Occlusive disease of the branches of the aortic arch and vertebral artery Gert J de Borst Carotid arterial tortuosity, kinks and spontaneous dissection J Timothy Fulenwider, Robert B Smith III, Samuel Eric Wilson and Dennis Malkasian Extracranial carotid artery aneurysms James A Gillespie, Samuel Eric Wilson and Juan Carlos Jimenez Carotid body tumours J.R De Siqueira and Michael J Gough Carotid angioplasty and stenting Jos C van den Berg 497 513 531 543 555 563 571 Section VI:  VISCERAL ARTERIAL DISEASE 40 41 Renovascular disease George Hamilton Acute and chronic mesenteric vascular disease Stefan Acosta and Martin Björck 589 603 Contents ix Section VII:  VASCULAR DISORDERS OF THE UPPER EXTREMITY AND VASCULITIS 42 43 44 Thoracic outlet disorders: Thoracic outlet compression syndrome and axillary vein thrombosis Michael S Hong and Julie A Freischlag Raynaud’s syndrome and upper extremity small artery occlusive disease Gregory J Landry Vasculitis and dysplastic arterial lesions Aamir S Shah, Hisham S Bassiouny and Bruce L Gewertz 621 633 647 Section VIII:  VENOUS AND LYMPHATIC DISORDERS 45 46 47 48 49 Natural history and sequelae of deep vein thrombosis Meryl A Simon and John G Carson Pathophysiology of chronic venous disease Seshadri Raju Endovenous and surgical management of varicose veins: Techniques and results Juan Carlos Jimenez Deep vein thrombosis: Prevention and management Andrea T Obi and Thomas W Wakefield Surgical management, lytic therapy and venous stenting Anthony J Comerota and Maxim E Shaydakov 669 677 687 699 717 Section IX:  VASCULAR TRAUMA 50 51 52 Thoracic and abdominal vascular trauma Naveed Saqib, Joseph DuBose and Ali Azizzadeh Thoracic outlet and neck trauma David L Gillespie and Adam Doyle Vascular injuries of the extremities W Darrin Clouse 739 753 769 Section X:  COMPARTMENT SYNDROME, VASCULAR ACCESS, MALFORMATIONS AND TRANSPLANTATION 53 54 55 56 Compartment syndrome Caroline A Yao, David A Kulber, Geoffrey S Tompkins and Jonathan R Hiatt Principles of vascular access surgery Samuel Eric Wilson, Juan Carlos Jimenez and Robert Bennion Diagnosis and management of vascular anomalies: The Yakes AVM Classification System Wayne F Yakes, Alexis M Yakes and Alexander J Continenza Vascular aspects of organ transplantation Hynek Mergental, Jean de Ville de Goyet, Jorges Mascaro and John A.C Buckels 799 813 829 845 Section XI:  SURGICAL TECHNIQUES 57 Vascular open surgical techniques Frank J Veith 861 Index 923 454  Aortic dissection Figure 29.4  An acute type A dissection shown at time of diagnosis (above) and after surgical replacement of the ascending aorta Note the persistence of the false lumen beyond the distal aortic arch which will almost certainly need further intervention in the future Figure 29.5  Endovascular treatment of a focal type A dissection using an endovascular stent graft Access was achieved through the right carotid artery and the device covered an entry tear in the mid-ascending aorta MANAGEMENT OF TYPE B DISSECTION If there is evidence from either imaging or physiological monitoring that the dissection is complicated by rupture, malperfusion or impending rupture, then intervention should be planned If the patient remains stable, relatively normotensive and pain free (uncomplicated), then intravenous beta-blockade can be weaned down, whilst oral antihypertensives are introduced If the clinical situation changes, there should be a low threshold for re-imaging After 48–72 hours, further imaging should be arranged to reassess the aorta for expansion, extension of dissection or any clue that the rupture may be imminent, such as a left pleural effusion Early interventional treatment for acute complicated type B dissection Open surgical repair was the mainstay of treatment for acute complicated dissection for many years, but this is associated with high levels of mortality and morbidity The reason for this is the physiological insult caused by posterolateral thoracotomy, single­ -lung ventilation, cross-clamping of the aorta, cardiopulmonary bypass, hypothermia and cerebrospinal fluid drainage to prevent paraplegia With mortality rates as high as 30% reported in multinational registry data, endovascular repair is now seen as an attractive alternative.30 Endovascular treatment is undertaken by placement of a self-expanding endograft into the aorta via peripheral access, with the aim of covering the entry tear and promoting expansion of the true lumen and decompression of the false lumen by sealing the entry tear, preventing aortic branch vessels from being occluded or threatened Secondary interventional procedures may be required to revascularize specific vessels, such as the common iliac artery or the visceral aortic branches The long-term goal is to avoid subsequent aortic dilation that may later lead to rupture or other complications by promoting aortic remodelling Although conceptually endovascular treatment is an attractive first-line treatment for complicated acute type B dissection, there are relatively few good quality prospective studies with appropriate comparator groups This is reflected in the lack of firm consensus in existing guidelines for practice.22 The ongoing pathophysiological process itself and perioperative complications such as retrograde type A Management of type B dissection  455 Figure 29.6 A Retrograde type A dissection following TEVAR for acute complicated type B dissection This was managed conservatively as it was asymptomatic, relatively localized and remained stable at follow-up dissection means that all interventions are still associated with significant risk31,32 (Figure 29.6) A meta-analysis of 942 patients showed an in-hospital mortality rate of 9%, with a serious morbidity rate of 8% Re-intervention was required in 10% but subsequent aortic rupture occurred in 162  mm) has been shown to result in more false lumen thrombosis at 36 months in one study, although this did not necessarily translate into reduction in the whole aortic volume.48 Dissection with infrarenal extension displays less tendency to remodel, potentially because treating the segment of aorta above the diaphragm will often not address the main re-entry tear.35 This would s­uggested that longer coverage is necessary, as some re-interventions are linked to patent fenestrations.49 Despite this, high rate of false lumen thrombosis was achieved in the INSTEAD trial where only a single stent graft was used in 83% of patients.42 A short stent graft which ends in the proximal descending thoracic aorta and does not conform correctly to the side walls may pose a risk of damage to the aortic wall due to the distal end moving with the cardiac cycle 50 In combination with generous oversizing of the stent graft, this can traumatize the aortic wall and potentially perforate the intimal flap 51 This may be avoided by sizing the stent graft according to the dimensions of the distal true lumen and may require the placement of tapered devices Retrograde aortic dissection is a particularly lethal complication of TEVAR for type B dissection and occurs in 4% of patients.31 Most of these events occur in the immediate post-operative period and lead to mortality rate of up to 33.6% According to the results of a systematic review, acute aortic dissection (odds ratio 10.0) and device oversizing (odds ratio 1.14 per 1% increase in oversizing above 9%) increase the risk of retrograde dissection significantly The use of endografts with proximal bare stents was not associated with increased risk in the same study, but as it is likely that direct trauma to the aortic wall during TEVAR increases the risk of retrograde type A dissection, they should probably be avoided 458  Aortic dissection There are limited data regarding which type of endovascular device is most suited to treating aortic dissection and how to correctly plan endovascular repair Most stent-graft systems are primarily designed to treat thoracic aortic aneurysms, and their indications for use reflect this There is evidence to suggest that proximal and distal oversizing of endografts should be less aggressive to avoid unnecessarily excessive radial force, which has been associated with damage to the aortic wall and retrograde dissection.31 Stents which employ active proximal fixation with bare stents and barbs should probably also be avoided for the same reason Timing of treatment According to existing published current definitions, the cut-off point at which a dissection becomes ‘chronic’ varies, with some using 14 days from presentation and others using 90 There is no upper limit however, and some studies group patients who are weeks from presentation with those who presented up to 15 years previously.52 The INSTEAD trial intervention arm recruited patients at a median of 3.5 weeks after the diagnosis, meaning many would be categorized as subacute dissections This partially explains why a 90.6% total false lumen thrombosis at 5 years was achieved in a group of patients with chronic dissection Another study treated patients at a mean of 100 weeks post-diagnosis and only achieved false lumen thrombosis in 39% at 3-year follow-up.53 This further supports the idea of a subacute group which may exist for up to a year in some cases.43 Branch vessel involvement and fenestrations More aortic branches arising from the false aortic lumen and more visible fenestrations in the dissection flap may decrease the changes of false lumen thrombosis after TEVAR for chronic dissection.49,52,54 Addressing this with uncovered bare stents may be possible, as placing a fenestrated or branched endograft is not possible if the aorta is not aneurysmal Attempting to individually recanalize aortic branches from the true lumen is possibly not well described If antegrade flow in the false lumen is not sufficiently sealed, then remodelling is unlikely to take place If the entry tear is completely sealed, then flow is ‘to and fro’ locally through residual fenestrations as opposed to linearly in antegrade or retrograde direction, which is likely to produce lower mean pressures in the false lumen and promote remodelling or at least prevent expansion.55 Active false lumen thrombosis If the aorta continues to expand and it is felt that remodelling is unlikely to occur, active management of persistent flow within the aortic false lumen can be considered This may avoid recourse to further invasive surgery in those that may not be fit or where these is no conventional treatment option This can be done using a covered stent, such as an iliac plug, a nitinol embolization plug or custommade spindle-shaped devices that can be easily occluded after placement into the false lumen.56,57 It has not yet been determined if this is a safe and durable technique although early results are promising SUMMARY POINTS • Aortic dissection is diagnosed and managed according to its anatomical extent and chronicity • White men aged over 40  years with hypertension, or those under 40 with Marfan’s syndrome or bicuspid aortic valves, are at highest risk Patients often present with acute onset sharp chest pain, sometimes with loss of consciousness or poor perfusion of end organs Computed tomography angiography is the first-line diagnostic investigation Initial management should involve invasive cardiovascular monitoring and intravenous beta-blockade Surgery is the first-line treatment for type A dissection Endovascular treatment is the first-line treatment for acute complicated type B dissection, although some may benefit from a short period of observation prior to this Endovascular repair uncomplicated type B dissection in the subacute phase appears safe and may prevent long-term complications All patients need lifelong antihypertensive therapy and surveillance imaging Chronic type B dissection should be treated if the aorta becomes aneurysmal, with endovascular treatment and open surgery offering effective prevention from aorticrelated death • • • • • • • • REFERENCES Tsai TT, Nienaber CA, Eagle KA Acute aortic syndromes Circulation 2005 December 13;112:3802–3813 Olsson C, Thelin S, Ståhle E, Ekbom A, Granath F Thoracic aortic aneurysm and dissection: Increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002 Circulation 2006;114(24):2611–2618 Allmen von RS, Anjum A, Powell JT Incidence of descending aortic pathology and evaluation of the impact of thoracic endovascular aortic repair: A population-based study in England and Wales from 1999 to 2010 Eur J Vasc Endovasc Surg 2013 February;45:154–159 References 459 Jones DW, Goodney PP, Nolan BW et  al National 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B et al Endovascular approaches to acute aortic type A dissection: A CT-based feasibility study Eur J Vasc Endovasc Surg 2011 October;42:442–447 460  Aortic dissection 29 Ronchey S, Serrao E, Alberti V et al Endovascular stenting of the ascending aorta for type A aortic dissections in patients at high risk for open surgery.  Eur J Vasc Endovasc Surg 2013 May;45:475–480 30 Tsai TT, Fattori R, Trimarchi S et al Long-term survival in patients presenting with type B acute aortic dissection: Insights from the International Registry of Acute Aortic Dissection Circulation 2006 November 21;114:2226–2231 31 Canaud L, Ozdemir BA, Patterson BO, Holt PJE, Loftus IM, Thompson MM Retrograde aortic dissection after thoracic endovascular aortic repair Ann Surg 2014;260(2):389–395 32 Patterson B, Holt P, Nienaber C, Cambria R, Fairman R, Thompson M Aortic pathology determines midterm outcome after endovascular repair of the thoracic aorta: Report from the Medtronic Thoracic Endovascular Registry (MOTHER) database Circulation 2013 January 2;127:24–32 33 Parker JD, Golledge J Outcome of endovascular treatment of acute type B aortic dissection Ann Thorac Surg 2008 November;86:1707–1712 34 Canaud L, Patterson BO, Peach G, Hinchliffe R, Loftus I, Thompson MM Systematic review of outcomes of combined proximal stent grafting with distal bare stenting for management of aortic dissection J Thorac Cardiovasc Surg 2013 June;145:1431–1438 35 Patterson BO, Cobb RJ, Karthikesalingam A et  al A Systematic review of aortic remodeling after endovascular repair of type B aortic dissection: Methods and outcomes Ann Thorac Surg 2014;97(2):588–595 36 Kim KM, Donayre CE, Reynolds TS et  al Aortic remodeling, volumetric analysis, and clinical outcomes of endoluminal exclusion of acute complicated type B thoracic aortic dissections J Vasc Surg 2011 August 1;54:316–325 37 van Bogerijen GHW, Tolenaar JL, Rampoldi V et  al Predictors of aortic growth in uncomplicated type B aortic dissection J Vasc Surg 2014 April;59:1134–1143 38 Tanaka A, Sakakibara M, Ishii H et al Influence of the false lumen status on short- and long-term clinical outcomes in patients with acute type B aortic dissection J Vasc Surg 2013 October 16;1–6 39 Sakalihasan N, Nienaber CA, Hustinx R et al (Tissue PET) Vascular metabolic imaging and peripheral plasma biomarkers in the evolution of chronic aortic dissections Eur Heart J Cardiovasc Imaging 2015;16(6):626–633 40 Brunkwall J, Kasprzak P, Verhoeven E et  al Endovascular repair of acute uncomplicated aortic type B dissection promotes aortic remodelling: year results of the ADSORB trial Eur J Vasc Endovasc Surg 2014 September;48:285–291 41 Shah TR, Rockman CB, Adelman MA, Maldonado TS, Veith FJ, Mussa FF Nationwide comparative impact of thoracic endovascular aortic repair of acute uncomplicated type B aortic dissections Vasc Endovasc Surg 2014 April;48:230–233 42 Nienaber CA, Kische S, Rousseau H et  al Endovascular repair of type B aortic dissection: Long-term results of the randomized investigation of stent grafts in aortic dissection trial Circ Cardiovasc Interv 2013 August;6:407–416 43 Virtue Registry Investigators Mid-term outcomes and aortic remodelling after thoracic endovascular repair for acute, subacute, and chronic aortic dissection: The virtue registry Eur J Vasc Endovasc Surg 2014 October;48:363–371 44 Winnerkvist A, Lockowandt U, Rasmussen E, Rådegran K A prospective study of medically treated acute type B aortic dissection Eur J Vasc Endovasc Surg 2006 October;32:349–355 45 Bashir M, Shaw M, Fok M et al Long-term outcomes in thoracoabdominal aortic aneurysm repair for chronic type B dissection Ann Cardiothorac Surg 2014 July;3:385–392 46 Tian DH, De Silva RP, Wang T, Yan TD Open surgical repair for chronic type B aortic dissection: A systematic review Ann Cardiothorac Surg 2014 July;​ 3:340–350 47 Thrumurthy SG, Karthikesalingam A, Patterson BO et al A systematic review of mid-term outcomes of thoracic endovascular repair (TEVAR) of chronic type B aortic dissection Eur J Vasc Endovasc Surg 2011 November;42:632–647 48 Qing K, Yiu W, Cheng SWK A morphologic study of chronic type B aortic dissections and aneurysms after thoracic endovascular stent grafting J Vasc Surg 2012 May 1;55:1268–1276 49 Hughes GC, Ganapathi AM, Keenan JE et al Thoracic endovascular aortic repair for chronic DeBakey IIIb aortic dissection Ann Thorac Surg 2014 December;​ 98:2092–2098 50 Manning BJ, Dias N, Ohrlander T et al Endovascular treatment for chronic type B dissection: Limitations of short stent-grafts revealed at midterm follow-up J Endovasc Ther 2009;16:590–597 51 Zhang L, Zhou J, Lu Q, Zhao Z, Bao J, Jing Z Potential risk factors of re-intervention after endovascular repair for type B aortic dissections Cathet Cardiovasc Intervent 2016;16(1):59 52 Kitamura T, Torii S, Oka N et al Key success factors for thoracic endovascular aortic repair for non-acute Stanford type B aortic dissection Eur J Cardiothorac Surg 2014 September;46:432–437, discussion 437 53 Kang WC, Greenberg RK, Mastracci TM et  al Endovascular repair of complicated chronic distal aortic dissections: Intermediate outcomes and complications J Thorac Cardiovasc Surg 2011 November 1;142:1074–1083 References 461 54 Tolenaar JL, Kern JA, Jonker FHW et al Predictors of false lumen thrombosis in type B aortic dissection treated with TEVAR Ann Cardiothorac Surg 2014 May;3:255–263 55 Rudenick PA, Bijnens BH, García-Dorado D, Evangelista A An in  vitro phantom study on the influence of tear size and configuration on the hemodynamics of the lumina in chronic type B aortic dissections J Vasc Surg 2013 February;57:​464–474.e465 56 Idrees J, Roselli EE, Shafii S, Reside J, Lytle BW Outcomes after false lumen embolization with covered stent devices in chronic dissection J Vasc Surg 2014 December;60:1507–1513 57 Kölbel T, Lohrenz C, Kieback A, Diener H, Debus ES, Larena-Avellaneda A Distal false lumen occlusion in aortic dissection with a homemade extra-large vascular plug: The candy-plug technique J Endovasc Ther 2013 August;20:484–489 30 Popliteal artery aneurysm SAMUEL ERIC WILSON and JUAN CARLOS JIMENEZ CONTENTS Epidemiology 463 Clinical features 464 Diagnosis 464 Management 464 Conclusions 466 References 466 Popliteal artery aneurysms are the most common peripheral aneurysms accounting for approximately 70% Surgical treatment dates back to Antyllus, a third-century Greek physician who ligated both poles of the aneurysm and incised and packed the aneurysm sac In 1785, John Hunter treated a coachman with a popliteal aneurysm by simply ligating the superficial femoral artery above the aneurysm (in what today is called Hunter’s canal).1 Matas performed endoaneurysmorrhaphy by ligating all branch vessels from within the aneurysm and suturing the walls of the aneurysm together He performed this operation on 154 popliteal aneurysms between 1888 and 1920 In the 1950s, aneurysm exclusion and bypass with reversed saphenous vein interposition became the primary method of treatment More recently endovascular repair has become common EPIDEMIOLOGY Although popliteal aneurysms (Figure 30.1) are the most common form of peripheral artery aneurysms, the prevalence in the general population is low In Detroit, at Henry Ford Hospital, popliteal aneurysm accounted for in 5000 hospital admissions; there was popliteal aneurysm per 15 abdominal aortic aneurysms Popliteal aneurysm is a disease found almost exclusively in men, most often in the sixth decade of life (Table 30.1) Most popliteal aneurysms are fusiform and associated with atherosclerosis They can also occur after trauma such as posterior knee dislocation, operative injury such as knee replacement or knee arthroscopy, popliteal artery entrapment syndrome, inflammatory arteritis such as Behcet’s or Kawasaki disease3 and infected emboli and as a complication of bacteremia with organisms such as Staphylococcus and Salmonella.4–9 Diseases associated with atherosclerosis are found in patients with popliteal aneurysm Coronary artery disease and cerebral vascular disease occur, respectively, in 35% and 10% of patients; hypertension is present in 45% and diabetes mellitus in 13%.3,7–13 There is an astonishingly high rate of additional aneurysms in patients with popliteal aneurysm (Table  30.1) Bilateral popliteal aneurysms are found in about 50% of patients Extrapopliteal aneurysms are found in 40%–75% of patients with a single popliteal aneurysm, and if bilateral popliteal aneurysms are present, there is a 68%–87% incidence of extrapopliteal aneurysm disease.5,6,14,15 The abdominal aorta is most often affected, followed by the femoral and iliac arteries The specific genetic defects that lead to arterial dilation are yet to be fully elucidated.16,17 In the patient found to have a popliteal aneurysm, a thorough examination must be made for additional aneurysms, particularly of the abdominal aorta and contralateral popliteal artery 463 464  Popliteal artery aneurysm DIAGNOSIS Figure 30.1  A typical angiogram of a popliteal aneurysm Physical examination of the popliteal fossa and p­a lpation of the popliteal pulse is usually an accurate and adequate screening test for low-risk patients; however, a very prominent popliteal pulse may signify dilation of the artery Occasionally, a nonvascular mass such as a Baker’s cyst may be mistaken on exam for an aneurysm Duplex ultrasound provides non-invasive confirmation of the diagnosis A popliteal artery greater than 2 cm in diameter is usually considered aneurysmal.14 To avoid misinterpretation of a general dilatation, as in patients with arteriomegaly, it is appropriate to compare the diameter of the dilated vessel to the diameter of the distal superficial femoral artery In such instances a vessel with a diameter 1.5–2.0 times the diameter of the proximal vessel is considered aneurysmal.12,14 Before elective intervention, it is prudent to screen for other aneurysms because of their relatively high coincidence Depending on the findings of these screening tests, the order of treatment may need to be altered Ultrasound provides adequate sensitivity and specificity for most clinical decisions Preoperative computed tomographic angiography, especially given recent advances to allow 3D reconstruction, gives high-quality images to the level of the popliteal artery and often below Arteriography is reserved for the operating room to guide endovascular repair MANAGEMENT CLINICAL FEATURES Approximately 70% of patients with popliteal aneurysms present with symptoms, often complications of thromboembolic disease ranging from claudication to rest pain and ischemic gangrene Popliteal aneurysms, in contrast to aortic aneurysms, present with rupture less than 5% of the time.13,17–19 Symptoms may also be caused by compression of neighbouring structures such as the sciatic nerve and popliteal vein in up to 10% of patients.13,15,18,19 Compression may lead to radiculopathy, venous thrombosis and rarely arteriovenous fistula.20 Symptomatic aneurysms Thromboembolic disease arising from the popliteal arterial aneurysm typically causes ischemic symptoms and physical findings Given the relatively low rates of limb salvage once extensive embolization has occurred, any embolization should be considered a strong indication for surgery Complete aneurysm thrombosis without embolization may also occur The natural history of this condition is worsened by the relative paucity of collateral vessels around the bony and ligamentous knee joint Table 30.1  Epidemiology and percentage of additional aneurysms in patients with popliteal aneurysm Percentage of other aneurysms Series Reilly et al Whitehouse et al.12 Vermillion et al.13 Shortell et al.21 Halliday et al.5 11 Number of patients Mean age Male–female ratio AAA Iliac Femoral 70 61 87 39 40 70 67 60 63 64 15:1 30:1 28:1 39:0 19:1 32 62 40 39 30 36 25 18 15 38 34 14 22 Bilateral popliteal 53 44 68 24 50 Management 465 Despite  surgical intervention, 16%–50% of extremities that present with acute thrombosis or thromboembolism go on to minor or major amputation as either a primary or secondary procedure.5,12–14,21 Asymptomatic aneurysms The management of asymptomatic popliteal aneurysms is more successful than treatment once symptoms have occurred Accumulation of prospective natural history data on asymptomatic popliteal aneurysms is difficult as even large centres usually see fewer than 10 of these lesions per year Retrospective analyses suggest that between 29% and 59% of popliteal aneurysms will become symptomatic over time.6,22–24 The variables that will predispose to thromboembolism likely include size and extent of intraluminal thrombus, but this is not well defined Dawson et al.24 studied 42 patients over an average of 6.2 years who had asymptomatic popliteal aneurysms with an average aneurysm size of 3.1 cm After 18 months, 59% developed symptoms, culminating in three leg amputations, one peroneal nerve palsy and eight limbs with claudication Delaying therapy until the onset of symptoms avoids operation in high-risk individuals, but adversely effects surgical outcome because of the pruning of outflow vessels Varga et  al.25 followed 137 patients who were newly diagnosed with popliteal aneurysms to examine variables affecting results of repair Grafts placed emergently had a 10% early bypass failure rate as opposed to 1.2% of those placed electively With regard to safety and efficacy, in four series reporting operations on patients with asymptomatic aneurysms, there were no operative deaths; long-term limb loss was 0%–3%, and 89%–97% of patients remained symptom-free for years.5,11,13,14 In summary, the indications and timing of popliteal aneurysm repair require astute surgical judgement In contrast to aortic aneurysms, the complications of popliteal aneurysms are limb but not life-threatening In the high-risk patient, a case can be made for nonoperative management; however, this is less common today given the low risk of endovascular repair For most patients, elective repair of a popliteal aneurysm (femoral–popliteal bypass or interposition with autologous vein) or exclusion by a stent graft is a definitive, safe operation that has clinical results that equal or exceed similar operations done for occlusive disease.26 We recommend that an isolated asymptomatic popliteal aneurysm large enough to cause arterial turbulence or thrombus formation be considered for operative repair These criteria would typically include aneurysms greater than 2.5  cm The presence of thromboembolism discovered either clinically or radiologically should be considered a strong indication for surgery to avoid limb loss Repair of the asymptomatic popliteal aneurysm has results much superior than intervention after ischemic symptoms develop Thrombolytic therapy Thrombolytic agents, such as tissue plasminogen activator, catalyze endogenous fibrinolytic pathways They have demonstrated efficacy in lysis of thrombus both acute and chronic, venous and arterial and in situ and embolic Whether vascular patency will be preserved after thrombolytic recanalization depends on the nature of the primary lesion The use of thrombolytics in the treatment of popliteal aneurysms has a strong appeal since the most frequent cause of reconstruction failure is thromboembolic occlusion of outflow vessels The use of surgical thrombectomy is not necessarily easier because of frequent concomitant atheroocclusive disease and the difficulty in rescuing inframalleolar thromboembolism operatively Thrombolysis may release additional embolism from the aneurysm sac Catheterbased infusion directly into the distal embolus may help prevent or resolve this complication Preoperative thrombolysis of a known thrombosed popliteal aneurysm which has not caused embolization is unnecessary and perhaps unwise The diagnosis of popliteal aneurysm is occasionally made incidentally after therapeutic thrombolysis for presumed atherosclerotic occlusion The overall effect of thrombolytics in a patient with thromboembolic outflow compromise appears to be beneficial For example, Hoelting et al.27 retrospectively compared 11 patients who received primary bypass surgery for acute popliteal aneurysm–related ischemia to nine similar patients who received thrombolytics prior to bypass surgery There were five “occlusive complications” and one secondary amputation in the primary bypass group as opposed to none in the thrombolytic group In a similar retrospective review, Carpenter et  al.26 compared 38 patients who received primary bypass surgery for acute popliteal aneurysm–related ischemia to seven similar patients who received thrombolytics prior to bypass surgery These seven patients were described as having thrombosis of all three of their run-off vessels The patients treated with preoperative thrombolysis had better graft patency and limb salvage than the patients that underwent emergency primary operation Varga et  al prospectively compared 23 patients who received thrombolytics to 56 patients who had primary bypass surgery and concluded that “intra-arterial thrombolysis is of value in restoring the distal run-off before bypass in popliteal aneurysms presenting with acute limb-threatening ischemia.”25 Surgery The open operation of choice for popliteal aneurysm is construction by a reversed saphenous vein arterial bypass and exclusion of the aneurysm (should an autologous vein not 466  Popliteal artery aneurysm be available, a polytetrafluoroethylene graft may be used as the arterial conduit.) A medial approach to the popliteal artery is taken, as classically described by Szilagyi et al.15 Definitive treatment of popliteal aneurysms consists of aneurysm ligation and bypass The typical bypass usually consists of an above-knee popliteal to below-knee popliteal bypass, although this can vary considerably in either direction, depending on the extent of aneurysmal disease The best conduit for bypass is autologous vein The popliteal aneurysm can be exposed and bypassed by either the medial or posterior approach The medial approach allows exposure of the greater saphenous vein, the above- and below-knee popliteal artery and the tibial vessels for selective tibial thrombectomy or more distal bypass Without division of the hamstring tendons, the medial approach does not permit surgery directly on the aneurysm sac When direct sac exposure is required, as in a patient with compressive symptoms requiring sac debridement, and when the extent of the aneurysm is clearly defined, many surgeons find the posterior approach simplest The posterior approach allows a bloodless and superficial dissection of the entire popliteal artery This exposure readily allows dissection and debridement of the aneurysm off neighbouring structures For aneurysms limited to the popliteal fossa, the posterior approach may also permit a shorter interposition because of the better exposure When necessary an additional 4–5 cm of superficial femoral artery can be exposed posteriorly by division of overlying adductor muscle fibres Distal tibial exposure through the posterior approach, whilst possible, is more difficult than from a medial approach One disadvantage of the posterior approach is that an additional incision will be required for harvesting of the greater saphenous vein In general, patients with repaired asymptomatic aneurysms have higher long-term graft patency rates than patents with symptomatic aneurysms.18,21 grafting of popliteal aneurysms seems still to be reserved for elderly and poor condition patients’ Contemporary outcomes are more favourable Spesiale et al treated 53 popliteal aneurysms using the peripheral Viabahn endograft with neither in-hospital mortality nor reintervention resulting in a primary patency of 74% after a mean follow-up of 3  years.31 Wagenhauser et  al were cautious in their 2015 report, considering endovascular treatment ‘an alternative’ but pointing out that ‘long-term results are pending’ and stating that surgery was still the gold standard.32 The Cochrane 2014 analysis concluded that ‘endovascular repair should be considered as a viable alternative to open repair’ and called for a randomized, multicentre trial.33 Endovascular repair Schechter DC, Bergan JJ Popliteal aneurysm: A celebration of the bicentennial of John Hunter’s operation Ann Vasc Surg 1986;1:118 Potter D, Morris-Jones W Popliteal artery injury complicating arthroscopic meniscectomy Arthroscopy 1995;11(6):723 Bradway MW, Drezner AD Popliteal aneurysm presenting as acute thrombosis and ischemia in a middle-aged man with a history of Kawasaki disease J Vasc Surg 1997;26(5):884 Wilson P, Fulford P, Abraham J, Smyth JV, Dodd PD, Walker MG Ruptured infected popliteal artery aneurysm Ann Vasc Surg 1995;9(5):497 Halliday AW, Taylor PR, Wolfe JH, Mansfield AO The management of popliteal aneurysm: The importance of early surgical repair Ann R Coll Surg Engl 1991;73:253 Farina C, Cavallaro A, Schultz RD et  al Popliteal aneurysms Surg Gynecol Obstet 1989;169:7 The advantages of lowered morbidity and earlier recovery are especially important in popliteal aneurysm, where many of the lesions are asymptomatic and none are lifethreatening Early reports include that of Puech-Leaao et al., who, through a posterior popliteal artery exposure, passed a Palmaz stent sewn to a saphenous vein graft superiorly into the superficial femoral artery to perform a proximal anastomosis (stent expansion) beyond the limits of surgical exposure.28 May et  al reported successful deployment of an endovascular graft to exclude a popliteal pseudoaneurysm caused by knee replacement surgery.29 These early interventions were not uniformly successful Mercadae reported six patients with popliteal aneurysms that were percutaneously treated with an endoluminal graft.30 In this series, with follow-up less than year, there was one case of thrombosis and one case of incomplete exclusion with recurrence Mercadae concluded that ‘stent CONCLUSIONS Popliteal aneurysms are not uncommon in the older male The natural history consists of progression to aneurysm thrombosis or embolic occlusion of the infrapopliteal vessels Approximately one third of untreated patients will become symptomatic within 3  years If treatment is delayed until the onset of limb-threatening ischemia, the rate of limb loss is higher than if treated electively when asymptomatic Popliteal aneurysms may be managed by ligation and bypass or endovascular repair When outflow vessels are compromised, consideration should be given for preoperative thrombolytic therapy Open repair of popliteal aneurysms can be accomplished through either the medial or posterior approaches Endovascular exclusion is replacing open surgery but some reservations remain about long-term outcome REFERENCES References 467 Jimenez F, Utrilla A, Cuesta C et  al Popliteal artery and venous aneurysm as a complication of arthroscopic meniscectomy J Trauma 1988;28:1404 Gillespie DL, Cantelmo NL Traumatic popliteal artery pseudo-aneurysms: Case report and review of the literature J Trauma 1991;31:412 Rosenbloom MS, Fellows BA Chronic pseudoaneurysm of the popliteal artery after blunt trauma J Vasc Surg 1989;10:187 10 Cole CW, Thijssen AM, Barber GG et  al Popliteal aneurysms: An index of generalized vascular disease Can J Surg 1989;32:65 11 Reilly MK, Abbott WM, Darling RC Aggressive surgical management of popliteal artery aneurysms Am J Surg 1983;145:498 12 Whitehouse WM, Wakefield TW, Graham LM et al Limb-threatening potential of arteriosclerotic popliteal artery aneurysms Surgery 1983;93:694 13 Vermilion BD, Kimmins SA, Pace WG, Evans E A review of one hundred forty-seven popliteal aneurysms with long-term follow-up Surgery 1981;90:1009 14 Dawson I, Van BJ, Brand R, Terpstra JL Popliteal artery aneurysms Long-term follow-up of aneurysmal disease and results of surgical treatment J Vasc Surg 1991;13:398 15 Szilagyi DE, Schwartz RL, Reddy DJ Popliteal arterial aneurysms Arch Surg 1981;116:724 16 Kontusaari S, Tromp G, Kuivaniemi H et al A mutation in the gene for type III procollagen (COL 3AI) in a family with abdominal aneurysms J Clin Invest 1990;86:1465 17 Kuivaniemi H, Tromp G, Prockop DJ Genetic causes of aortic aneurysms: Unlearning at least part of what the textbooks say J Clin Invest 1991;88:1441 18 Schellack J, Smith RB, Perdne GD Nonoperative management of selected popliteal aneurysms Arch Surg 1987;122:372 19 Hands LJ, Collin J Infra-inguinal aneurysms: Outcome for patient and limb Br J Surg 1991;78:996 20 Reed MK, Smith BM Popliteal aneurysm with spontaneous arteriovenous fistula J Cardiovasc Surg (Torino) 1991;32:482 21 Shortell CK, DeWeese JA, Ouriel K, Green RM Popliteal artery aneurysms: A 25-year surgical experience J Vasc Surg 1991;14:771 22 Gifford RW, Hines EA, Janes JM An analysis and follow-up of one hundred popliteal aneurysms Surgery 1953;33:284 23 Wychulis AR, Spittel JA, Wallace RB Popliteal aneurysms Surgery 1970;68:942 24 Dawson I, Sie R, van Baalen JM, van Bockel JH Asymptomatic popliteal aneurysm: Elective operation versus conservative follow-up Br J Surg 1994;81(10):1504 25 Varga ZA, Locke-Edmunds JC, Baird RN A multicenter study of popliteal aneurysms Joint Vascular Research Group J Vasc Surg 1994;20(2):171 26 Carpenter JP, Barker CF, Roberts B, Berkowitz HD, Lusk EJ, Perloff LJ Popliteal artery aneurysms: Current management outcomes J Vasc Surg 1994;19(1):65 27 Hoelting T, Paetz B, Richter GM, Allenberg JR The value of preoperative lytic therapy in limb-threatening acute ischemia from popliteal artery aneurysm Am J Surg 1994;168(3):227 28 Puech-Leaao P, Kauffman P, Wolosker N, Anacleto AM Endovascular grafting of a popliteal aneurysm using the saphenous vein J Endovasc Surg 1998;5(1):64 29 May J, White GH, Yu W, Waugh R, Stephen MS, Harris JP Endoluminal repair: A better option for the treatment of complex false aneurysms Aust NZ J Surg 1998;68(1):29 30 Mercadae JP Stent graft for popliteal aneurysms Six Cases with Cragg Endo-pro System I Mintec J Cardiovasc Surg 1996;37(Suppl 1):41 31 Spesiale F, Siriggnano P, menna D et  al Ten years’ experience in endovascular repair of popliteal aneurysm using the Viabahn prosthesis: A report from two Italian registries Ann Vasc Surg 2015;29:941–949 32 Wagenhauser MU, Herma KB, Sagban TA et al Long term results of open repair of popliteal artery aneurysm Ann Med Surg (Lond) 2015:4(1):58–63 33 Joshi D, James RL, Jones L Cochrane Database Syst Rev 2014 August 31;8:CD010149 .. .VASCULAR SURGERY Principles and Practice F O U RT H E D I T I O N VASCULAR SURGERY Principles and Practice F O U RT H E D I T I O N EDITED BY SAMUEL ERIC WILSON Department of Surgery. .. strategy and hypothesis-driven statistical analysis Laura T Boitano and David C Chang 19 43 61 71 Section II:  MEDICAL TREATMENT 10 11 12 13 Pathology and medical management of atherosclerotic vascular. .. Veith 267 279 2 91 3 01 311 3 31 3 51 3 71 Section IV: ANEURYSMS 26 27 28 29 30 31 32 Abdominal aortic aneurysm: Pathophysiology, endovascular and surgical therapy Denis W Harkin and Paul H Blair