Minimal access therapy for vascular disease

Minimal Access Therapy for Vascular Disease

Minimal Access Therapy for Vascular Disease

Edited by

Austin L. Leahy MCh, FRCSI Associate Professor, Department of Surgery

Royal College of Surgeons in Ireland and Consultant Vascular Surgeon, Beaumont

Hospital, Dublin, Ireland

Peter R.F. Bell MB ChB, FRCS, MD Professor of Surgery, University of Leicester, UK

Barry T. Katzen MD, FACR, FACC

Clinical Professor of Radiology, University of Miami School of Medicine

Medical Director, Miami Cardiac and Vascular Institute,

Miami, Florida, USA

MARTIN DUNITZ

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Contents

List of contributors ix Foreword by Professor Josef Rösch xvi Preface xviii

1. Endovascular intervention of the iliac and infrainguinal vessel

M.M. Davidian , G J. Becker and B.T. Katzen 1

2. Extraluminal (subintimal) angioplasty A. Bolia 48

3. Endovascular management of peripheral and visceral aneurysms P.J. Haslam , F.P. McGrath and A.L. Leahy 73

4. Ultrasound-guided angioplasty N.G. Fishwick 99

5. Endoluminal approaches in limb revascularization: techniques and strategies F.J. Criado , E. Wellons , N.A. Paroya , O. Abul-Khoudoud and J.A. Lopes 110

6. Angioplasty and stent application for carotid atherosclerosis P. Bergeron and J. Massonnat 128

7. Thrombolysis techniques and devices M. Narayanswamy and K. Kandarpa 155

8. Endoscopic thoracic sympathectomy C.J. Kelly , D.J. Bouchier-Hayes and A.L. Leahy 197

9. Retroperitoneoscopic lumbar sympathectomy Y.M. Kan , A.W. Darzi and N.J. Cheshire 207

10. Endovascular treatment of aortic diseases J. May , G.H. White and J.P. Harris 218

11. Insertion of an aorto-uni-iliac graft for the treatment of aortic aneurysms P.R.F. Bell and M.M. Thompson 231

12. Endovascular repair of abdominal aortic aneurysm: the aorto-biiliac approach W.S. Moore 261

13. Aneurysm exclusion using hand-assisted laparoscopy R. Kolvenbach and L. Da Silva 283

14. Thoracic aneurysmal disease S.T. Kee and M.D. Dake 295

15. Laparoscopic aorto-femoral surgery S.S. Ahn and K.M. Ro 307

16. Minimal access in situ vein bypass grafting C.H.A. Wittens 316

17. Intravascular ultrasound E.B. Diethrich 332

18. Subfascial endoscopic perforator vein surgery A.D.K. Hill , D. Bouchier-Hayes and A.L. Leahy 346

19. Endoscopic venous valve surgery J.M. Scriven and N.J.M. London 355

20. Minimally invasive varicose vein surgery: transilluminated powered phlebectomy G.A. Spitz

368

21. Dialysis grafts M.A. Mauro and L.L Arnder 375

22. Inferior vena cava filters A.C. Roberts and T.B. Kinney 393

23. Training in endovascular surgery P.R.F. Bell 435

24. The risks of endovascular techniques and the patient’s rights R.N. Baird 438

Index 443

List of contributors

Omran Abul-Khoudoud Senior Surgical Resident, Division of Vascular Surgery, The Union Memorial Hospital, Baltimore, MD, USA

Samuel S.Ahn Clinical Professor of Surgery, Division of Vascular Surgery, and Chief, Endovascular

Surgery, University of California, Los Angeles, LA, USA

Lance L.Arnder Fellow, Vascular/Interventional Radiology, University of North Carolina School of Medicine, Department of Radiology, Chapel Hill, NC, USA

Roger N.Baird Consultant Surgeon, Department of Surgery, Bristol Royal Infirmary, Bristol, UK

Gary J.Becker Miami Cardiac and Vascular Institute, Baptist Hospital, Miami, FL, USA

Peter R.F. Bell Professor of Surgery, Department of Surgery, University of Leiciester, Leicester, UK

Patrice Bergeron Chief, Department of Thoracic and Cardiovascular Surgery, Fondation Hôpital Saint-Joseph, Marseilles, France

Amman Bolia Consultant Vascular Radiologist, Department of Radiology, Leicester Royal Infirmary, NHS Trust

Leicester, UK

David J.Bouchier-Hayes Chairman, Department of Surgery, RCSI, Beaumont Hospital, Dublin, Ireland

Frank J.Criado Director, Centre for Vascular Intervention Chief, Division of Vascular Surgery, The Union Memorial Hospital, MedStar Health Baltimore, MD, USA

Nicholas J. Cheshire Consultant Vascular Surgeon, Regional Vascular Unit, St Mary’s Hospital NHS Trust, London, UK

L. Da Silva Department of Vascular Surgery, Augusta Hospital, Dusseldorf, Germany

Michael D. Dake Associate Professor of Radiology, and Chief, Cardiovascular and Interventional Radiology, Stanford University Medical Center, Stanford, CA, USA

Ara Darzi Professor of Surgery, Academic Surgical Unit, Imperial College School of Medicine, St Mary’s Hospital NHS Trust, London, UK

Mark M.Davidian Miami Cardiac and Vascular Institute, Baptist Hospital, Miami, FL, USA

Edward B.Diethrich Arizona Heart Institute and Arizona Heart Hospital, Phoenix, AZ, USA

N. Guy Fishwick

Consultant Radiologist, X-ray Department, Leicester Royal Infirmary, Leicester, UK

John P.Harris Department of Surgery, University of Sydney, and Department of Vascular Surgery, Royal Prince Alfred Hospital, Sydney, Australia

Philip J.Haslam Department of Radiology, Freeman Hospital, Newcastle upon Tyne, UK

Arnold D.K. Hill Consultant Surgeon, St Vincent's Hospital, Dublin, Ireland

Yuk-Man Kan Research Fellow, Consultant Vascular Surgeon, Regional Vascular Unit, St Mary's Hospital NHS Trust, London, UK

Krishna Kandarpa Associate Professor, Department of Radiology, Division of Cardiovascular and Interventional Radiology, Brigham and Women's Hospital/Harvard Medical School, Boston, MA, USA

Barry T.Katzen Medical Director, Miami Cardiac and Vascular Institute, Miami, FL, USA

Stephen T.Kee Assistant Professor of Radiology, Stanford University Medical Center, Stanford, CA, USA

Cathal J.Kelly Department of Surgery, RCSI, Beaumont Hospital,

Dublin, Ireland

Thomas B.Kinney Assistant Professor of Radiology, UCSD Medical Center, San Diego, CA, USA

Ralf Kolvenbach Chairman, Department of Vascular Surgery, Augusta Hospital, Dusseldorf, Germany

Austin L.Leahy Associate Professor, Department of Surgery Royal College of Surgeons in Ireland and Consultant Vascular Surgeon Beaumont Hospital Dublin, Ireland

N.J.M. London Professor of Vascular Surgery, Department of Surgery, University of Leicester, Leicester Royal Infirmary, Leicester, UK

Joao A.Lopes Medical student, Division of Vascular Surgery, The Union Memorial Hospital, Baltimore, MD, USA

Jérôme Massonnat Vascular Radiologist, Centre Cardio-Vasculaire Valmante Marseilles, France

Matthew A.Mauro Professor of Radiology and Surgery, Department of Radiology University of North Carolina School of Medicine, Chapel Hill, NC, USA

James May Department of Surgery, University of Sydney, and Department of Vascular Surgery, Royal Prince Alfred Hospital,

Sydney, Australia

Frank P.McGrath Consultant Radiologist, Department of Radiology, Beaumont Hospital, Dublin, Ireland

Wesley S.Moore Professor of Surgery, UCLA School of Medicine, Los Angeles, CA, USA

Meena Narayanswamy Research Fellow, Department of Radiology, Division of Cardiovascular and Interventional Radiology, Brigham and Women’s Hospital/Harvard Medical School, Boston, MA, USA

Nadeem A.Paroya Medical student, Division of Vascular Surgery, The Union Memorial Hospital, Baltimore, MD, USA

Anne C.Roberts Professor of Radiology, Department of Radiology, USCD Medical Center/Thornton Hospital, La Jolla, CA, USA

Kyung M.Ro UCLA Center for Health Sciences, Los Angeles, CA, USA

J.M.Scriven Specialist Registrar, Department of Surgery, University of Leicester, Leicester Royal Infirmary, Leicester, UK

Gregory A.Spitz Rush-Copley Medical Center, Aurora, IL, USA

M.M.Thompson Consultant Vascular Surgeon, Leicester Royal Infirmary,

Leicester, UK

Eric Wellons Senior Resident, Division of Vascular Surgery, The Union Memorial Hospital, Baltimore, MD, USA

Geoffrey H.White Department of Surgery, University of Sydney, and Department of Vascular Surgery, Royal Prince Alfred Hospital, Sydney, Australia

Cees H.A.Wittens Vascular Surgeon, Department of Surgery, Sint Franciscus Gasthuis, Rotterdam, The Netherlands

Foreword

Vascular surgery has experienced an explosive evolution over the past 50 years. Theintroduction of endarterectomy, followed by bypass grafting with autologous veins and,subsequently, by the development of fabric prostheses has given surgeons anarmamentarium to treat many types of vascular conditions effectively. Over the past 10years, minimal access surgery, called by some minimally invasive or endovascularsurgery, with its many interventional radiological techniques, has become an importantaddition to this surgical armamentarium. In many cases, it has even become a preferablealternative to the conventional surgical treatment of vascular disease. The combination ofclinical expertise, detailed planning, manual agility, and special devices and instrumentshas made minimal access surgery often as effective a treatment as conventional surgicalmethods, but with less trauma, reduced hospital stay, diminished cost, acceleratedrecovery, and early return to full activity.

Minimal access surgery has a rich history, with contributions from many inventiveinterventional radiologists, vascular surgeons and cardiologists. Medical manufacturers,with their drive to develop new devices and instruments for minimally invasivetreatment, have also played an important part in this evolution. Minimal access surgerystarted in the 1960s with the pioneering work of vascular radiologist Charles Dotter in thetreatment of arterial obstruction by percutaneous transluminal angioplasty using coaxialcatheters. In the 1970s, interventional cardiologist Andreas Grüntzig started the rapid and widespread use of transluminal angioplasty by introducing angioplasty balloons. Rapiddevelopment of medical technology in the 1980s and 1990s accelerated the evolution ofminimal access surgery.

For diagnosis, the introduction of vascular and intravascular ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI) allowed non-invasive vascular diagnosis. Digital subtraction angiography resulted in rapid, detailed diagnosis ofvascular disease shortening the procedures and reducing the amount of required contrastmaterial. For therapy, it was the introduction of expandable stents, stent-grafts, and endoluminal grafts that enabled effective minimally invasive treatment of obstructive andaneurysmal disease in the arterial system. Interventional radiologist Julio Palmaz wasinstrumental in the introduction of expandable stents for the treatment of obstructivedisease, and vascular surgeon Juan Parodi in the introduction of endoluminal grafts forthe treatment of aneurysmal disease. Use of expandable stents, filters, new techniques forvalve transplantation, and interventions on venous perforators improved the treatment ofvenous disease. The introduction of thrombolytic drugs benefited the treatment ofthrombotic obstructions in both the arterial and venous systems. The great success oflaparoscopic surgery of abdominal organs was the incentive to start the use oflaparoscopy and thoracoscopy in the treatment of both obstructive and aneurysmalarterial disease, even of coronary artery lesions. At present, even though minimal accesssurgery has already made great progress, it is only the tip of the iceberg in a new era of

treatment of vascular disease. Much more progress can be expected. New devices andinstruments will be developed; expertise with their use will be improved anddisseminated widely. One can also expect that access sites will become smaller and thateventually most treatments will be done percutaneously. Thus, minimal access surgerywill bring surgeons and their patients closer to the dream of ‘seamless’ surgery—an operation that could be performed without an incision. With the excitement that istypically generated for all new devices and techniques, however, it must not be forgottento test their effectiveness and compare them with a gold standard of conventional surgicaltreatment.

One important aspect, essential for success in minimal access surgery, is harmoniousinterdisciplinary cooperation between involved specialists, particularly vascular surgeonsand interventional radiologists. They should be partners and work together as a team,with relationships based on equity and mutual respect. Teamwork in the evaluation ofpatients, in selection and detailed planning of the most effective method of treatment, andcareful performance of procedures is necessary for safety and the best therapeutic results.Teamwork is particularly important in complex intravascular treatment, such asendoluminal grafting of abdominal and thoracic aortic aneurysms.

This book, with its contributions by highly experienced minimal access surgeons and interventional radiologists, gives both a generalized overview and a detailed inside viewinto multiple techniques of minimal access vascular surgery. All contributions arepresented from a practical viewpoint. They provide technical information and offer datafor decision making regarding the relative advantages and disadvantages of individualtechniques. They also provide the opportunity to obtain a well-informed and very positive opinion about the present status of minimal access vascular surgery and its multipletechniques. Also of great importance is the chapter related to training in endovascularsurgery. It should be emphasized that minimally invasive treatment, like conventionalvascular surgery, must be performed only by those physicians who have undergone aproper course of training.

Josef Rösch, M.D., Ph.D.,Professor of Interventional Therapy and Surgery,

Dotter Interventional Institute,Oregon Health Sciences University,

Portland, Oregon, USA

Preface

This book represents the thoughts of a number of specialists on the current evolution oftherapy for vascular disease. Surgeons, physicians and radiologists have contributed tothese developments and are consequently represented among our contributors.

It is the hope of this book to capture the current changes in the treatment of vascular disease. The principles of minimal access therapy have largely reduced the trauma thatsurgery exerts on patients and frequently facilitated precise treatment of inaccessiblelesions. This has all been made possible by the development of technologies includingendoscopy, angiography and stenting. Therefore it occurs at a crossroads, bringingtogether many divergent skills.

Change is frequently viewed with suspicion. In the area of vascular disease this has ledto a ‘turf war’ between different specialists. Rather than being threatened by the diversityof therapies, we need to see the developments in this book as opportunities. Surgery,medicine and radiology will be changed by these opportunities and the specialist of thefuture will be a hybrid of all three.

We have chosen the words ‘minimal access’ in the title of this book, as this nowrepresents a form of therapy which is believed to be less traumatic. It will only be withthe benefit of time that we can indeed say that what is described are truly advances. Manyof the techniques in this book are so new that it is difficult to estimate their contribution.All of the chapters indicate an evolution in thinking that will undoubtedly inform futuredevelopments.

The editors would like to thank all of the contributors. Many of them are the trailblazers and innovators at whom we can but marvel. The techniques that they describeshould be helpful to the readers and may be included in our therapeutic repertoires.

Our sincere hope is that this book will help physicians, surgeons and radiologists toorganize their thoughts about the changing environment of vascular disease.

Finally we would like to thank Mrs Lesley Gray and Martin Dunitz for their courtesy and attention to detail.

Austin L, Leahy

Endovascular intervention of the iliac and infrainguinal vessels

1 MARK M.DAVIDIAN, GARY J.BECKER AND BARRY T.KATZEN

Background

Charles Dotter was the first to treat an atherosclerotic stenosis by percutaneous means,dilating a stenosis with tapered catheters.1 Since that time, the field of percutaneous intervention has grown tremendously, Some interventional devices and techniques,initially promising, have lost their appeal. The initial enthusiasm for excimer laser andatherectomy, for example, has waned over the past few years. Still, the equipment used iscontinually improving, with better balloons, guidewires, and stents, giving theinterventionalist better tools for endovascular therapy.

Classification of lower limb ischaemia

The indications for intervention in the lower extremities are generally thought of in -terms of two categories: (1) chronic limb ischaemia; and (2) acute limb ischaemia.Rutherford and Becker published their paper concerning the reporting of vascularintervention in 1991.2 This paper described a clinical classification of chronic limbischaemia broken down into seven categories from normal to major tissue loss and restpain (Table 1.1). This was different to the Fontaine classification, used mainly in Europe. Acute limb ischaemia is categorized into three levels:

(1) viable: a limb with intact capillary refill, (2) threatened: slow capillary refill with mild sensory and motor findings; and (3) irreversible: absent capillary refill, profound paralysis and anaesthesia with inaudible

arterial and venous signals.3 The clinical features of chronic and acute lower limb ischaemia are salient to the vascular specialist, as treatment options differ significantly for each patient population.

Results reporting

Rutherford and Becker’s paper attempted to standardize reporting of vascular disease and its treatment.2 They tackled several issues. The first was in handling initial treatmentfailures. It was noted that many series did not include initial failures (i.e. grafts that were

occluded early in the postoperative period, which were re-opened in the immediate

postoperative period) in the final analysis of success rates. They also addressed theconfusion regarding the issue of patency. Rutherford and Becker suggested three differentpatencies: one was primary patency. Primary patency ends when any intervention is usedto preserve or extend patency. Assisted primary patency would be applicable tointervention to a failing but still patent graft. Another was secondary patency (opening agraft that is occluded).

A further area addressed was that of the lack of criteria used for success in theliterature. The example used was the treatment of iliac disease. In some of the reports oftreatment of iliac disease, ankle/brachial indices were used and in some, clinicalquestionnaires and palpation of the femoral pulse were used, with varying results in termsof success. To remedy this, a treatment result is now divided into seven categories basedon a combination of symptoms and non-invasive measurements (see Table 1.3). Thigh/brachial indices are recommended for iliac intervention follow-up. Suggestions regarding life-table analysis, reporting of complications, and procedural mortalityreporting, were also made in this paper.

Lesion classification

The AHA guidelines for lower extremity angioplasty published in 1994 containedrecommendations for certain types of lesions.4 These recommendations were divided intofour categories (see Table 1.2). These four categories of recommended treatments(surgery or percutaneous intervention) were then applied systematically to the aortic,iliac, femoropopliteal, infrapopliteal segments, and infrainguinal bypass grafts, but theserecommendations will obviously evolve as new technologies and techniques are reviewed

Table 1.1 Becker/Rutherford classification of lower extremity chronic ischaemia

Category Symptoms Findings on Non-Invasive Testing

0 Asymptomatic Normal

I Mild claudication Postexercise ankle pressure greater than 50 mmMg

II Moderate claudication

Findings intermediate between categories I and II

III Severe claudication Exercise cannot be completed, with ankle pressure less than 50mmHg

IV Rest pain Flat ankle pressure, pressure, toe pressure <30mmHg, ankle pressure <40mmHg

V Minor tissue loss Ankle pressure <60mmHg, nearly flat ankle waveforms, with toe pressure <40mmHg

VI Major tissue loss

Minimal access therapy for vascular disease 2

in the literature.

Distribution of disease

In 1991, David Brewster described the influence of distribution of disease on itstreatment.5 He proposed three levels of disease, with type I involving the aorta andcommon iliac arteries, type II involving the external iliacs as well, and type III alsoinvolving the infrainguinal segments. He highlighted the rarity (10%) of patients withisolated, focal aorto-iliac disease and the plethora of patients with infrainguinal disease with concomitant aorto-iliac disease (66%) (type III). This paper dealt only with surgicalprocedures.

Laborde and colleagues published their data on iliac stenting, dividing their patients into the above three categories.6 They had a significantly higher number of patients incategory I (39.6%) than the surgical literature quoted above. Symptom relief was highlycorrelated to extent of disease, with 91.6% of patients in category I and 97.9% of patientsin category-II experiencing benefit. Patients with category-III disease had only 60.8% improvement of symptoms at 3 years. It is clearly seen that patients with multileveldisease and poor run-off have poorer outcome with any intervention than patients withisolated and focal disease.

Grading of clinical status after intervention

Another contribution of Becker and Rutherford was the proposal to standardize outcomemeasures.2 Table 1.3, adapted from their paper, lists the proposed classification scheme, organized into seven categories. This provides a guideline for publications and reportingof vascular intervention so that valid comparisons can be made from the literature.

Table 1.2 AHA task force guidelines for percutaneous intervention

Category I

Lesion for which PTA is procedure of choice

Category II

Lesions well suited, but may be followed by surgery ery

Category III

Lesions that may be treated by PTA, but have a significantly lower chance of initial or long term success than surgery, PTA may be performed due to lack of conduit or increased risk factors for surgery

Category IV

PTA only used in very high-risk surgical candidates or no surgical procedure applicable

Endovascular intervention of the iliac and infrainguinal vessels 3

Complications

Matsi and Manninen recently reported their experience of complications in lower limbinterventions.7 In 410 procedures (192 for claudication and 103 for chronic criticalischaemia), there were 43 complications (10.5%). Broken down into those procedures forstenoses and those for occlusions, the rates were 7% and 18%, respectively.Complications included 22 haematomas (5.4%), six distal embolizations, all associatedwith the treatment of occlusions (1.5%), and five pseudoaneurysms (1.5%). Use ofthrombolytics caused a 30% rate of bleeding complications versus 6% for procedureswithout thrombolytics. Five of the bleeding complications required operative treatmentand one caused the death of a patient. Of note is that the 30-day mortality in patients treated for chronic critical ischaemia was 10%, highlighting the frail nature of thesepatients. These rates of complications compare well with those published by others.

A recent report on outpatient intervention by Criado8 on 151 outpatient interventions demonstrated a very low complication rate, with only three patients kept overnight forcomplications and no re-admissions of discharged patients. They reported a‘conservative’ use of heparin during the procedure. Clearly, with the increased constraints on health-care expenditure, there will be pressure to perform more percutaneous interventions on an outpatient basis.

Levels of disease

Aorto-iliac intervention

Lesions of the iliac and distal aorta are among the most satisfying in percutaneous

Table 1.3 AHA guidelines concerning the reporting of clinical improvement after percutaneous interventions

Grade Description

+3 ABI increased to more than 0.9 with patient markedly improved or asymptomatic

+2 Moderate improvement in symptoms with singlecategory improvement, ABI increased by >0.1

+1 Minimal improvement

0 No change

−1 Mildly worse. No change in clinical category, but ABI decreased by 0.1 or decreased category

−2 Moderately worse clinically. One category worse or unexpected minor amputation

−3 Markedly worse. More than one category worse, or major amputation


vascular intervention. The symptoms of iliac stenosis or occlusion can be debilitating,and the treatment is relatively straightforward and durable. In patients with both iliac andfemoropopliteal segment disease, the iliac lesions are treated first, as this may decreasesymptoms to a point where further intervention (surgical or percutaneous) is unnecessary.Typically, iliac lesions are treated from a retrograde approach. Endovascular alternativesinclude PTA, with selective stenting or primary stent ing. The use of covered stents, orendografts, is covered in a chapter subsequent. Commonly used alternatives for stentinginclude the Palmaz stent (Cordis Endovascular, Johnson & Johnson), Wallstent (BostonScientific), Strecker stent, and more recently, the Symphony stent (Boston Scientific) andthe Smartstent (Cordis Endovascular, Johnson & Johnson). However, a variety of stentsare being developed. At the Miami, we commonly use the Palmaz stent for treatment ofcommon iliac lesions. There is however, Cardiac and Vascular Institute an ongoingclinical trial of the Symphony stent (Boston Scientific) for iliac lesions.

In the late 1970s and early 1980s, iliac angioplasty quickly became an important treatment modality in the treatment of atherosclerotic disease. In 1989, Becker performeda meta-analysis of the literature of iliac angioplasty and found a mean 2-year patency rate of 81% and a 5-year patency rate of 72%.9 In 1994 the American Heart Association(AHA) published their guidelines for peripheral vascular intervention.4 This document provides a categorical division of lesions with treatment recommendations for lesions ofall segments (see Tables 1.1 and 1.2). As can be seen from the tables, occlusions were included under category III lesions. Initially thought to be a contraindication topercutaneous recanalization and treatment, many studies have now shown the lowincidence of distal embolization and other complications with this technique.10–16

In the late 1980s, stenting came to the forefront and provided an important component to iliac intervention. It became useful as a means to treat lesions with recoil, and as a bail-out with haemodynamically significant dissections. A meta-analysis by the Dutch Iliac Stent Trial (DIST) investigators in 1997 found that iliac stenting provided a higherprimary and secondary patency rate compared to PTA alone for both claudication and forcritical ischaemia.17 They used data from six PTA series and eight stent series.10–12, 18–28

The same investigators then published their data from the DIST Study Group,29 which demonstrated equivalent patency rates for primary stenting of iliac lesions compared toselective stenting after PTA. In 1998, this same group (DIST) then published their data,30

demonstrating that primary stenting (versus selective stenting) of all iliac lesions was notcost-effective. They used data from their own trial and their meta-analysis of the literature to come up with cost figures, complications, success rates, patency rates, andquality-of-life scores. Of interest is that this conclusion was valid for a wide range ofcosts for the stent. These conclusions need to be validated by others in large comparativetrials, but at this point it is difficult to justify primary stenting of all iliac lesions on a costbasis. This assumes, however, a high degree of aggressiveness in looking for post-PTA gradients, both at rest and after vasodilatation, as is well doc-umented in the report by Teteroo.31

Current practice in the USA and especially at the Miami Cardiac and Vascular Instituteis to favour primary stenting. Approximately 90% of all iliac stenoses are treated in thismanner at our institution. We perform resting and augmented haemodynamicmeasurements with all iliac interventions.


The AHA guidelines for iliac intervention are as follows:

Femoropopliteal angioplasty and stents

One of the previously described major limitations of femoropopliteal PTA has been therelatively low percentage of success achieved in recanalizing and dilating chronicocclusions. However, two very important studies of femoropopliteal recanalization andPTA have been reported. The first was a report by Morgenstern and colleagues in 1989that documented a 95% success at crossing femoropopliteal occlusions 1–4 cm in length and an 86% success in occlusions 5–10 cm in length using modern imaging, catheters, and guide wires.32 Overall technical success was 91% for occlusions in this report of 160recanal izations. This success rate correlates well with clinical experience today.

Another important paper, written by Murray and colleagues in 1995 provided data onrecanalization and PTA for very long segment femoropopliteal occlusions using moderntechnique and steerable guidewires.33 Lesions ranged from 10 to 40 cm in length, with anaverage of 24–3 cm. Success was defined as <30% residual diameter stenosis and anincrease of >0.2 in the ABI. Patency at follow-up was defined as <50% diameter stenosisby colour flow imaging. Initial success was achieved in 41/44 (93%) of attempts. At the18-month follow-up, the mean ABI had increased from 0.53 (preprocedure) to 0.80. Cumulative primary patency at 18 months was 69%, but clinical symptoms had improvedin 83% of cases.

A study published in 1990 by Jeans and colleagues reported the results of PTA for iliacand femoropopliteal segments.28 They reported the results of angioplasty of 190femoropopliteal segments, including 64 stenoses and 126 occlusions. The overall 5-year patency rate was 41%, with a rate of 61% for stenoses and 31% for occlusions. Calfvessel run-off had a significant impact for both stenoses and occlusions with 5-year patency rates for stenoses with two or more patent vessels 78%, and 5-year patency rate for occlusions with two or more patent vessels, 36% compared to a rate of 25% inpatients with up to one patent calf vessel. Lesion length had an impact for both stenosesand occlusions. The 5-year patency rate for stenoses <1 cm was 76% compared to longer lesions (50%). Of note is that presenting symptoms, critical ischaemia versusclaudication, did not appear to affect 5-year patency of femoropopliteal interventions.

Category 1.

Stenosis is less than 3 cm in length, concentric and non-calcified.

Category 2.

(a) Stenosis is 3–5 cm in length; or (b) calcified or eccentric and less than 3cm in length.

Category 3.

(a) Stenosis is 5–10 cm in length; or (b) occlusion is less than 5 cm in length after thrombolytic therapy with chronic symptoms.

Category4. (a) Stenosis is greater than 10 cm in length; (b) occlusion is greater than 5 cm in length, after thrombolytic therapy and with chronic symptoms; (c) there is extensive bilateral aorto-iliac atherosclerotic disease; or (d) the lesion is an iliac stenosis in a patient with abdominal aortic aneurysm or another lesion requiring aortic or iliac surgery.


Their caseload was evenly split into those with claudication and those with criticalischaemia.

In another study, published in 1991, Capek and colleagues reported the long-term results of 217 PTA procedures in the SFA and popliteal arteries over an 8-year period.34

Patients were followed with serial non-invasive studies and in 71 cases with angiography.Follow-up ranged from 2 to 11 years, with a mean of 7 years. In this study, lifetableanalysis was used to assess factors with potential impact on long-term outcome of PTA. The greatest number of cases in this series was enrolled in 1979 and 1980, before theadvent of DSA, roadmapping, steerable soft-tipped guidewires, and low-profile catheters. Still, the technical success was 93% for stenoses and 82% for occlusions. Excludinginitial failures in 10%, the patencies at 1, 3, and 5 years were 81%, 61%, and 58%, respectively. Inclusion of the initial failures results in overall patencies at 1, 3 and 5 yearsof 73%, 55%, and 52%, respectively. Complications occurred in 10% of cases, but 25%of these were without clinical consequences. Clinical factors that were found tonegatively influence long-term patency included diabetes mellitus, diffuse atherosclerotic cardiovascular disease, and threatened limb loss at the time of initial presentation fortreatment. Morphologic factors found to negatively influence long-term outcome included long lesion length, moderate eccentricity, and residual stenosis on post-PTA angiogram.

In 1992, Johnston re-analysed data from the femoropopliteal angioplasty subgroup inthe Toronto series.35 The author analysed data from 254 femoropopliteal PTAs that were performed for all severities of chronic ischaemia. For stenoses with good run-off, the 5-year cumulative clinical success was 53%; with poor run-off it was 31%. For occlusions, the cumulative clinical success was 36% at 5-years for patients with good run-off and 16% for those with poor runoff. Occlusion may have been a confounding variable in thisstudy, just as it was in the study of Capek and colleagues.34 In other words, in the Capek study, patients with femoropopliteal occlusion who underwent successful recanalizationand PTA were just as likely to have lasting patency as those who began with stenoses.The differences in cumulative clinical success were almost all due to the difference in thetechnical success from the very beginning. The data in Johnston’s re-analysis suggest a similar phenomenon. In the overall study group, cumulative clinical success was 88.8%at 1 month, 62.5% at 1 year, 52.6% at 2 years, 50.7% at 3 years, 44.1% at 4 years, and38.1% at 5 years. When only initially successful cases were included, the cumulativeclinical successes were 70.4% at 1 year, 59.4% at 2 years, 57.1% at 3 years, 49.7% at 4years, 42.9% at 5 years, and 40.2% at 6 years. It seems, from these data, that initialsuccess portends a high likelihood of long-term clinical benefit. Importantly, initialsuccess occurred in 88.8% of cases in the study.

In 1994, Matsi and colleagues published their experience with 140 limbs treated for claudication.36 All patients were claudicants treated with femoropopliteal PTA. Follow-up ranged from 1 to 3 years, and patency was determined by ABIs. Initial success wasachieved in 99% of stenoses (n=71) and 80% of occlusions (n=69), with an 89% success rate overall. Primary patency was 47% at 1 year and 41% at 2 years.

An important study of femoropopliteal intervention was published in 1995 by Huninkand colleagues.37 This was a decision and cost-effectiveness analysis based on a review of procedures performed after 1985. There were 4800 PTAs, and 4511 surgical bypass


operations included in the analysis. They developed a model to examine the choicebetween bypass surgery and PTA for lesions amenable to either procedure. Outcomesmeasured included 5-year patency, quality-adjusted life expectancy (QALE), lifetime costs, and incremental cost-effectiveness ratios. Six treatment strategies were analysed: (1) no treatment; (2) initial PTA, no further revascularization; (3) initial PTA, subsequentPTA; (4) initial PTA, subsequent bypass surgery; (5) bypass surgery followed by nofurther therapy; (6) bypass surgery followed by graft revision. The results showed that fora 65-year-old man with disabling claudication and a femoropopliteal stenosis orocclusion, the initial PTA strategy increased QALE by 2–13 months and resulted in decreased lifetime expenditure as compared to bypass surgery. The same was true forchronic critical ischaemia and a femoropopliteal stenosis. For femoropopliteal occlusionand critical ischaemia, an initial strategy of bypass surgery increased QALE by 1–4 months and decreased lifetime expenditure compared to PTA. Sensitivity analysisshowed that when the 5-year patency of PTA exceeds 30%, PTA is always the preferredinitial strategy. The authors concluded that PTA is the preferred initial strategy in patientswith disabling claudication and femoropopliteal stenosis or occlusion and in those withchronic critical ischaemia and a stenosis. In patients with chronic critical ischaemia andan occlusion, bypass surgery is the preferred initial strategy.

In 1994, Gordon et al. published their experience with recanalizations of 57 superficial femoral artery occlusions in 49 patients.38 They reported an initial success rate of 74%.Included in the analysis were patients with reconstituted proximal popliteal arteries andpatients with at least one patent tibial artery. Patients were not enrolled if they had restpain, gangrene, or ulceration. They tried to correlate score of run-off vessels, occlusion length, and change of ABI with 1-year clinical success. Neither length of occlusion nor status of run-off vessels achieved statistical significance. The patients with patent vessels at 3-month and 1-year followup had a higher change in the initial post-treatment ABI than those with occluded vessels at follow-up. Patients with patent SFA after 3 monthshad an initial change of ABI of 0.21, whereas patients with occluded SFA at 3 monthshad an initial change of ABI of −0.38. This, however, includes initial failures. The change in ABI in patients with patent SFA at 3 months was not significantly differentfrom those patent at the 12-month follow-up (0.21 and 0.246, respectively).

A recent report by Alback39 on femoropopliteal PTA also concludes that PTA is not a procedure of choice for critical limb ischaemia. They used ABI measurements in follow-up and found, as others had before, that ABIs after PTA for limb salvage are worse thanthose for claudication. They do, however, have a lower primary technical success (83%)than most other modern series of femoropopliteal PTA. They also confirm the findings ofothers that poor run-off bodes poorly for the outcome of PTA in the femoropopliteal segment.

In 1992, Sapoval et al. reported their experience with the use of the Wallstent intreating femoropopliteal vascular disease.40 Twenty-two lesions were treated, most of which were occlusions. Four out of the 22 stented segments occluded within the first 30days and five more occurred in the first 5 months. The 1-year patency rate (unassisted) was 49%. Their conclusion was that stenting does not offer any advantage overangioplasty alone. One point that deserves mention is that this study used one type ofstent. A series of 35 treated vessels with the Palmaz stent was reported in 1996 by


Chatelard and Guibourt, but this series was stented because of angioplasty failures.41

Nevertheless, they reported only two cases of acute instent thromboses, and a 1-year primary patency rate of 80%. Gunther et al. did include superficial femoral arteryWallstent placement in their series, but only 14 patients with this stent location wereincluded.13

Based on studies available prior to 1994, an AHA committee comprising membersfrom several different councils reached a consensus in their guidelines document forperipheral PTA.4 Stents were not covered in their recommendations. At the Miami Cardiac and Vascular Institute, we do not primarily stent SFA or popliteal arteries. Theseare used as bail-out devices for severe, flow-limiting dissections and lesions with severe recoil. Care is taken not to stent across areas of flexion and areas of potential kinking,such as seen at the adductor canal. We are currently involved in a clinical trial of acovered stent, the Gore Hemobahn (Gore, Tempe, AZ, USA), that shows promise in thetreatment of superficial femoral artery disease.

The AHA categories for femoropopliteal lesions were as follows:

Tibioperoneal intervention

Indications for tibioperoneal angioplasty include severe claudication, rest pain, andulceration. Improving outflow for more proximal intervention is another commonindication. Diabetic patients with threatened limbs constitute a significant number ofpatients.

Schwarten in 1988 and 1991 described results of treating infrapopliteal disease 42, 43 in 112 threatened limbs. He reported a technical success rate of 100% for stenoses and 88%for occlusions. The limb salvage rate was 83% at 2 years, with amputations onlyoccurring in diabetic patients treated unsuccessfully for occlusions.

Horvath and colleagues reported their results of tibial angioplasty in 1990.44 This report focused on 103 dilatations of crural arteries (15.8% of all of their PTAprocedures). The sites of angioplasty were as follows: 43 in the tibioperoneal trunk; 30 inthe anterior tibial artery; seven in the posterior tibial artery; and 23 in the fibular

Category 1.

(a) Single stenosis up to 5 cm in length not at the origin of the SFA or the distal popliteal artery; or (b) single occlusion up to 3 cm in length not involving the SFA origin or distal portion of the popliteal artery.

Category 2.

(a) Single stenoses 5–10 cm in length, not involving the distal popliteal artery; (b) single occlusion 3–10cm in length, not involving the distal popliteal artery; (c) heavily calcified stenosis up to 5 cm; (d) multiple lesions, each less than 3cm, either stenoses or occlusions; or (e) single or multiple lesions where there is no continuous tibial run-off to improve inflow for distal surgical bypass.

Category3. (a) Single occlusion 3–10 cm in length, involving the distal popliteal artery; (b) multiple focal lesions, each 3–5 cm (may be heavily calcified); or (c) single lesion, either stenosis or occlusion, with a length of more than 10cm.

Category4. (a) Complete common and/or superficial femoral occlusions; (b) complete popliteal and proximal trifurcation occlusions; or (c) severe diffuse disease with multiple lesions and no intervening normal vascular segments.


(peroneal) artery. Isolated crural intervention was performed in 28 cases, in combination with femoropopliteal intervention in 33 cases, with laser angioplasty in 15, lysis in 11,and surgery in 16 cases. All patients received periprocedural intravenous heparin and oralnifedipine and long-term aspirin. Intravenous nitroglycerin was given for high-risk procedures. Initial technical success was 96%. Patency rates were 79.8% at 1 year and75.3% at 2 years. Five amputations occurred, two as a result of recurrent occlusions, onedespite successful PTA, and in two where the amputation was in the forefoot, where itwould probably have been at a higher level without the intervention. They recommendedcrural angioplasty when the femoropopliteal system is open only in cases of rest pain orulceration. If the femoropopliteal system had been treated as well, then it wasrecommended that crural angioplasty should also be undertaken in severe claudicants, inorder to provide a more durable result to the femoral intervention.

Brown et al. reported their initial experience in 198845 and follow-up data in 1993.46

They reported a technical success rate of 72% in their initial description of 11 patients.However, in their follow-up they reported a clinical success rate of 85% in the group of patients with continuous runoff in at least one trifurcation vessel. Overall, however, theirclinical success rate was a meagre 44% at 26 months average follow-up, highlighting the importance of selecting patients with proper anatomy for tibial PTA.

In 1992, Bull et al reported their data on 168 patients.47 This series included patients referred for claudication (24%) and also included a high number of failing surgical grafts(20%). The clinical success rate was 83% at 3 years for focal disease and 76% formultilevel disease.

Matsi et al., in their report in 1993,48 included 84 infrapopliteal interventions, all inpatients with Fontaine class III or IV disease. Of these, 82% also had simultaneousfemoropopliteal angioplasty. They reported a 77% limb salvage rate at 1 year in patientswith at least one patent tibial vessel to the ankle. This number, however, dropped to 56%if all patients were included, again emphasizing the impact of distal run-off on clinical effectiveness.

In 1994, Durham and colleagues49 reported on their experience with tibial PTA in 14diabetic patients with either no autologous conduit or who were high surgical risk. Allpatients had threatened limbs and six patients also had SFA angioplasty. Their studygroup demonstrated a 57% rate of confirmed coronary artery disease and a 57% rate ofcongestive heart failure, confirming studies of the past showing the high rate ofcomorbidities in diabetics with threatened limbs. They reported a 77% long-term limb salvage rate (10/13). One patient died at day 29 of Myocardial infarction (MI) after toeamputation and is not included in that figure. Three late deaths due to MI occurred at 2, 4,and 24 months following PTA. Seven patients had resolution of ischaemia. Three healedplanned amputations. Two had early failures of their PTA and had major amputations at 6and 8 weeks. One had protracted healing of a wound, but died of an acute MI 17 monthsafter PTA, when the patient underwent a major amputation.

Also in 1994, Sivananthan and colleagues reported their experience with 73angioplasties of crural arteries and reported a technical success rate of 96%.50 All their technical failures occurred in occlusions, whereas all stenoses were treated successfullyangiographically. Most failures also occurred in patients with more severe clinicaldisease. Of the 38 patients treated, 22 had clinical improvement of at least one stage in


the Fontaine classification. Bakal, Cynamon, and Sprayregen, in their review article on tibial angioplasty in

1996,51 reviewed their experience in 53 patients. They reported a 80% limb salvage rateat 2 years in patients in whom inline flow was restored, whereas no patient withobstructed flow derived any clinical benefit. Again, this highlights the importance ofoutflow on durability and efficacy, with restoration of inline flow to at least a partiallyintact pedal arch a requisite for clinical success. As Bakal points out, this datacontradicted earlier beliefs that providing improved tibial inflow to distally obstructedarteries would improve limb salvage.

In 1996, Bakal, Cynamon, and Sprayregen,51 in a response to an article critical of crural PTA by Fraser et al., 52 performed an informative review of the literature of the subject. They noted that approximately 800 patients had been reported in the literature byover a dozen authors. They also noted that infrapopliteal PTA now comprisesapproximately 25% of peripheral PTA by Veith et al. and that they saw a reduction in their amputation rate from 49% to 14%. Clearly, as Bakal et al. point out, infrapopliteal PTA has grown, along with surgical techniques to bypass to crural arteries. As surgeonshave felt more comfortable with these bypasses, they have been more open to crural PTAby interventionalists. The predictions of catastrophic failures of infrapopliteal PTA havenever materialized.

Responding to the article by Fraser, Bakal pointed to problems with infrapopliteal data,which included the following:

1. Poor patient selection. Many patients are reported in the literature with diffuse disease with no inline flow, a factor now known to bode poorly for the results for PTA.

2. The heterogeneity of the ‘poor surgical candidate’ pool. Some are poor candidates because of comorbid medical conditions. Some are poor surgical candidates because of lack of conduit. These are both good candidates for PTA.

3. Patients who are poor surgical candidates because of diffuse arterial disease and no distal anastamotic sites. These patients are poor candidates for PTA as well.

Much of the PTA data, however, comprise patients from all three groups. There is alsothe problem with outcome measures. Angioplasty failures are more commonly treatedwith operation, whereas surgical failures are more often dealt with by percutaneousmeans. The former results in a failure, whereas the latter results in assisted primarypatency or secondary patency.

Stenting in the tibial region is not recommended as a primary tool. At the Miami Cardiac and Vascular Institute, stenting is reserved for flow-limiting dissections and severe recoil. Several coronary stents that are deployed over 0.018 wires are availableand work extremely well for these indications.

The AHA guidelines for infrapopliteal angioplasty are as follows:

Category 1.

Single focal stenosis, 1 cm or less, of tibial or peroneal vessels.

Category 2.

(a) Multiple focal stenoses, each 1 cm or less, of tibial or peroneal vessels; (b) one or two focal stenoses, 1 cm or less, of tibial trifurcation; or (c) tibial or peroneal stenosis


Bypass surgery and endovascular techniques compared

In 1990, Taylor et al. reported their results of reversed vein bypass grafts in 516 limbs ina group of 387 patients,53 with most of the indications for operation being limb-threatening ischaemia (80%). Of these grafts, 58% were to infrapopopliteal arteries.Many of the patients in this cohort did not have adequate ipsilateral saphenous vein andalternate sources of vein were used in 45% of the treated limbs. A primary patency of75% at 5 years was seen overall, with poorer results for infrapopliteal bypasses and thoseperformed with alternative venous conduits. However, 34% of the patients died duringfollow-up. The mean follow-up period was 20 months. This again highlights the frail nature of patients with limb-threatening ischaemia. Grafts were surveyed with ultrasoundduplex during the follow-up period.

Wolf et al. published their results of the Veterans Administration Cooperative StudyNumber 199 in 1993.54 This study was an attempt to perform a randomized trial of endovascular therapy to traditional bypass surgery in lower extremity vascular disease.Inclusion criteria included: (a) angiographic demonstration of at least 80% diameterstenosis or a total occlusion of the iliac, femoral, or popliteal artery less than 10 cm long;(b) ABI of less than 0.90 at rest; (c) intermittent claudication when walking less than twoblocks with rest pain or impending gangrene; and (d) agreement by the vascular surgeonsand the interventionists that the patient was a candidate for both endovascular and bypasstherapy. All patients were men, with about 60% of the patients meeting the criteriaactually consenting for the study (total of 263 patients). The enrollment was between1983 and 1987. Patients were considered in terms of four variables: iliac versusfemoropopliteal disease and claudication versus rest pain/limb threat. Of these patients,73% were claudicants. Only one lesion per patient was randomized, with the other lesion(s) being treated at the discretion of the team involved. Primary patency was defined as asustained increase of 0.15 or more in ABI without further intervention at that lesion site.Median follow-up was 4.1 years, ranging from 2 to 6 years. Neither the primary patency,nor the average increase in ABI was statistically different in the two groups, even whenanalysed in the four subsets mentioned above. However, many advances in catheter, wire,and balloon technology have been made since 1987, and one would expect improved results with the endovascular work done today.

A report by Tunis in the New England Journal of Medicine in 1991 questioned the effects of angioplasty on the rate of amputations and vascular bypass operations in thestate of Maryland.55 As noted in a response in 1993 by Becker et al., however, angioplasty and bypass surgery are often performed for different clinical indications.56

Angioplasty series often have a patient mix of 75% claudicants and 25% with limb-

dilated in combination with femoral popliteal bypass.

Category 3.

(a) Moderate-length stenosis (1–4cm) or moderate-length (1–2cm) occlusion of tib-ial or peroneal vessel; or (b) extensive stenosis of tibial trifurcation.

Category4. (a) Tibial or peroneal occlusions longer than 2 cm; or (b) diffusely diseased tibial or peroneal vessels.


threatening ischaemia, while the opposite is true in most reports of surgical bypass.Angioplasty is often used for lifestyle-limiting claudication, while infrainguinal bypassgrafts are more often used for limb salvage. This report by Tunis highlights the confusionin the medical community regarding the different roles of angioplasty and surgery.

The clinical and preprocedural evaluation of the patient with vascular disease

The evaluation of the patient with vascular disease is, simply stated, challenging. Thepatient with vascular disease can present with a myriad symptoms and findings. Vasculardisease can masquerade as a neurological, orthopaedic, or dermatological problem. It isbecause of these protean manifestations that many patients suffer for long periods of timewithout anyone realizing the vascular nature of the problem. A typical scenario is thepatient with lower extremity ‘aches’ when walking. The internist orders an MRI of the lower spine and a non-invasive study of the lower extremities. The MRI shows that some disc disease and the resting study of the lower extremities is normal. Without exercise,the patient’s iliac disease is never manifested and the symptomatology is ascribed to lumbar disc disease. Aggressive and thorough investigation of a vascular cause of pain isessential to helping these patients.

The clinical interview with the patient is quite helpful and, as in any facet of clinical medicine, will quite often reveal the underlying pathology. Careful attention to the natureof the pain, its location, and its inciting event is crucial. Calf cramping at night while inbed is quite different in aetiology to calf cramping experienced only after walking for 10minutes. The duration of symptoms and their location (uni- or bilateral) is also quite important. A 2-day history of a painful foot in an otherwise asymptomatic patient is quitedifferent to several months of non-healing ulcers in the diabetic patient. While seemingly pedantic and simple, these same historical items can help the interventionalist to decideon treatment strategies, such as when to use lytic agents. Even the patient with long-standing peripheral vascular disease will often give a history of sudden worsening ofsymptoms in the week prior to presentation. This will often imply a thrombotic eventsuperimposed on critical stenoses, which will often respond best to short lytic infusionsbefore recanalization and angioplasty.

In the patient with acute limb ischaemia, a careful notation of the sensory and motor function is essential not only in deciding which patients to treat, but also which limbs arenot salvageable or need emergent surgery. These baseline characteristics help to assessthe response of the patient during the course of lytic therapy.

While beyond the scope of this chapter, the physical examination is extremelyimportant to the interventionalist. The inspection of the skin, pulse examination, andhand-held doppler signal quality often helps the operator in terms of access and indeciding the acuity and severity of the situation. Physiological testing in the non-invasive laboratory is always done before and after any vascular intervention at the Miami Cardiacand Vascular Institute. This includes pulse-volume recordings, directional doppler at thecommon femoral arteries, and postexercise ABI and ankle waveforms. We do not feelthat the use of doppler or colour flow alone in the lower extremities is adequate, as it only


identifies potential lesions and not their physiological importance.

Principles of technique

Iliac intervention

Safe and effective angioplasty of the iliac and femoral arteries is dependent on attentionto detail, and adherence to certain principles of technique. The following representfocused issues of technique that will be of value to the reader.

Diagnostic angiography is generally performed from the patient’s asymptomatic side. This allows maximum flexibility in choosing treatment options. In the iliac circulation,treatment may be performed from the contralateral approach when possible. Theipsilateral approach can also be utilized if necessary. Attempting to cross critical lesionsprior to understanding the underlying lesion in terms of its tortuosity, calcification, andeccentricity may put the operator in potential jeopardy of dissection in a small butdefinite proportion of patients.

Occlusions: recanalization

Total occlusions represent the most technically challenging lesions for theinterventionalist. There are perhaps as many techniques as operators, but over the yearswe have found some to be more effective than others. In addition, the operator must beprepared, in the event of failure, to proceed to another technical option. Some techniquesare effective when others fail and it is often difficult to predict success withoutconsiderable experience. Densely calcified, long-segment occlusions are generally the most difficult to recanalize and are most refractory to angioplasty and stenting in general.The operator should also assess lesion characteristics for the value of preliminarythrombolytic therapy, rather than primary angioplasty. The clinical history can often be oftremendous help in this regard. The more acute the symptom complex, the more likely itis that lytic therapy will be of use.

Carefully assess the angiographic appearance of occlusions at their proximal and distalends. In the iliac arteries, some occlusions are best approached from the ipsilateraldirection and some from the contralateral side. Attempt to begin the recanalization fromthe central portion of the lumen if at all possible. Some lesions have flat or evenlyrounded proximal sections and some have eccentric ‘teats’ at the end of the lumen. When these more pointed ends to the lumen are present, we frequently consider recanalizationfrom the other direction. Figure 1.1 shows an example of successful primary stenting of an iliac occlusion with a Wallstent.


Figure 1.1 Iliac occlusion. (a) Preliminary angiogram of a patient with right leg claudication, showing right common iliac occlusion. (b) completion angiogram showing the results of primary recanalization and stenting using a Wallstent (Boston Scientific).

Stenoses

With the development of modern guidewires and imaging, this step in the endovasculartreatment of peripheral vascular disease has become much safer. The incidence ofguidewire-induced dissection can be reduced by thorough understanding of lesion characteristics and careful choice of approach. Guidewires such as Bentsen, or Wholeywires and other relatively atraumatic wire guides should be used. In general, the safestwire is used first. If unsuccessful, then progressively more stiff wires are used. The LLTwire has been a particularly good wire where the Bentsen or Wholey fail to cross thelesion. Glide wires are then usually used after the LLT wire fails. The operator is advisedto use wires that will buckle at resistance, which can be observed fluoroscopically andfelt at the fingertips. One must carefully observe the real-time image for signs of dissection, such as an unusual course, or resistance with an unusual buckling of the wireover a longer distance than usual.

Kissing balloon technique

Atherosclerotic disease of the iliacs is often a continuation of aortic disease.Consequently, these ostial lesions are often treated by recreating the aortic bifurcationhigher than the native bifurcation with stents. This is most effectively done through abilateral approach with retrograde punctures. This disease is almost always treated byprimary stenting at our institution. This is done with a ‘kissing balloon’ technique, with simultaneous inflation of the balloon-expandable stents. This protects against damaging the other iliac orifice if one was to treat the iliac disease in sequence. An example of this


method is given in Figure 1.2.

Guide wire selection

Most operators use hydrophilic-coated guidewires, such as the angled Glide wire (Terumo, Boston Scientific/Vascular). These wires can be quite effective but have thedisadvantage of decreased or no tactile sensation, and will seek channels anywhere,including subintimal locations. The authors prefer the use of coated moderately ‘floppy’ traditional wires. Specifically, the LLT wire allows penetration of most occlusions, with buckling of the wire when resistance is met. It can also bedirected when used in conjunction with a shaped catheter.

True versus false lumen

Once the guidewire has reached a level, which approximates the length of the occlusion,it is necessary to assess whether one is in an acceptable location. If the wire has had asubintimal course, it generally meets resistance and begins to buckle. Occasionallypatients will have pain associated with subintimal wire passage. If the operator is satisfiedwith the wire position, a small (4 or 5 Fr) catheter should be placed across the occlusionand contrast injected. Once again, resistance is often a sign of subintimal location. Thecontrast injection will confirm the presence within the true lumen, based on angiographicappearance and contrast flow.

Failed recanalization

In the event of failure to recanalize, one can attempt from the same puncture site withdifferent wires and catheters, although this is generally not successful in our experience.Approach from the contralateral direction is most often successful.

External iliac lesions

Lesions of the external iliac are more prone to dissection than are common iliac lesions.These lesions can be treated in a retrograde fashion, or from the contralateral groin.Example of straightforward cases are given in Figures 1.3 and 1.4. Care must be taken, however, in treating lesions close to the inguinal ligament. These can be done from aretrograde approach, but extreme caution should be used in order to avoid certaindisasters. One of these is to pull the sheath out of the artery when preparing to deploy aballoon-expandable stent. Another is to deploy the stent in the sheath by not pulling the sheath back far enough. An example of treating a lesion close to the inguinal ligament isgiven in Figure 1.5. One can encounter dissections here after primary stenting. This can occur if the balloon catheter is longer than the stent, thereby dilating a portion of theartery without stenting. Dissections of the external iliac can also occur after correct sizingof the balloon and stent. An example of a dissection after primary stenting of the externaliliac is given in Figure 1.6.


Figure 1.2 Using ‘kissing’ balloon technique for the aortic bifurcation. (a) Non-invasive testing in a 55-year-old man with right greater than left calf claudication at 50ft. His resting ABI was 0.56 on the right and 0.52 on the left. These dropped to 0.00 and 0.22, respectively after exercise. The postexercise ankle waveforms are flatline. This finding, in conjunction with the severe drop in ABI with exercise, should alert the reader to significant aortoiliac disease, in addition to the SFA occlusions. (b) Preliminary pelvic angiogram showing stenoses at the origins of both common iliac arteries with a 35 mm resting gradient on the right and a 20mm resting gradient on the left. (c) Spot film showing the simultaneous deployment of Palmaz stents (Cordis Endovascular, Johnson and Johnson) using a ‘kissing balloon’ technique. (d) Completion angiogram. (e) (Shown over page).


(e) The postprocedure non-invasive evaluation revealed similar preprocedure resting ABIs (0.65 on the right, 0.57 on the left), again attributable to bilateral SFA occlusions. Now, however, the postexercise waveforms are nearly normal and the postexercise ABIs are 0.79 on the right and 0.70 on the left. The patient walked on the treadmill for 5min with no symptoms. This case demonstrates the fact that use of colour flow alone could have been misleading, as it may only have detected the superficial femoral artery disease.

Treatment of multilevel disease

As discussed above, many patients suffer from multilevel disease. The management ofthese patients should always begin with treatment of the inflow vessels (aortoiliacsegment). As in surgical bypasses (aortobifemoral), treatment of the inflow oftenimproves symptoms to a level tolerable to the patient. Likewise, treatment of the iliaclesions with stenting will often improve the symptoms of the patient dramatically.Conversely, if both the profunda femoral and the superficial femoral arteries are diseased,serious consideration should be given to a staged procedure where the iliac stents arefollowed closely with a vein bypass of the superficial femoral artery. An example of thethis method is given in Figure 1.7. Treatment of iliac disease can also be followed by percutaneous superficial femoral artery intervention. Figure 1.8 illustrates the treatment of multilevel disease.


Figure 1.3 Isolated external iliac artery stenosis. (a) Retrograde injection of contrast, showing a stenosis of the proximal external iliac involving the origin of the internal iliac. (b) Simultaneous haemodynamic recording of the. catheter and sheath showing the resting gradient and then equalization of pressures as the catheter is pulled across external iliac lesion. (c) Deployment of a Palmaz 394 stent across the lesion. (d) and (e) (Shown over page).


Femoropopliteal angioplasty

Many of the above generalizations of wire selection and catheter technique apply here aswell. However, these interventions are typically performed via an antegrade approach.Common femoral lesions or lesions of the very proximal SFA are often treated from acontralateral appoach or with surgery. Femoropopliteral interventions can often beperformed through a 4 or 5 Fr sheath. AS with iliac interventions, it is always wise tobegin with the safest wire and progress to wires such as the angled Glide wires only ifwires such as the Bentsen or LLT fail. An example of recanalising an occludedsuperficial femoral artery is given in Figure 1.9. Here a J-tipped wire is used for safety.

Proper sizing of the balloon with regard to the diameter of the artery and the length of disease is crusial. Dissections here are extremely common and are often flow limiting.Rather than resorting to stent deployment, a trial of prolonged ballon inflation is alwaysattempted. This is typically done for 3 min with the guidewire removed. The end-hole of the balloon cathether can then be perfused with normal saline during the inflation. Anexample of the utility of prolonged balloon inflation is given in Figure 1.10. Angioplasty of normal segments of artary is counterproductive. The choice of an 0.035 or 0.018/0.014 system is determined by vessel size. Often, popliteal artery intervention can be done with0.014 systems and 3.5–4.5 mm ballons. Nitroglyserin, nifedipine, and heparin are oftenused as adjuncts to intervention. Nitroglyserin, is especially useful to treat or preventspasm; an example is given in Figure 1.11. As with iliac intervention, care is taken to carefully elicit a history from the patient and to scrutinize the angiograms for signs ofacute occlusions and emboli needing thrombolytic therapy. Crossing occlusions here ingeneral follow the same guidelines described above for iliac occlusions: begin with thesoftest and safest wire. Again, there is no advantage to primary stenting. At the MiamiCardiac and Vascular Institute, we use stents for angioplasty failures, such as flow-limiting dissection and lesions with serve recoil. An example of a stents used for such asituation is given in Figure 1.12. We are currently involved in a trial of a covered stent—the Hemobahn (W.L. Gore and Associates, Inc.). This has shown promise in thetreatment of superficial femoral artery disease; an example is given in Figure 1.13. While not the focus of this chapter, treatment of femoropopliteal vein bypasses can be treatedwith many of the same principles outlined above. Often, the disease occurs at theproximal or distal anastamosis and angioplasty can be quite useful, as in Figure 1.14.


(d) Completion angiogram shows excellent angiographic result. Note the preservation of the internal iliac artery. (e) Haemodynamic tracing done with nitroglycerin showing abolition of the gradient. Pharmacological augmentation of gradients is essential when the resting pressures are normal, especially after treatment with stents.


Figure 1.4 Primary stenting of the external iliac artery. (a) Preliminary pelvic oblique angiogram in a 72-year-old man with right leg claudication showing severe distal common and proximal external iliac stenotic disease with occlusion of the hypogastric. Resting ABI was 0.48, which dropped to 0.00 after minimal exercise on the treadmill. Resting pressure gradient across this lesion was 45 mm. (b) Spot film showing ipsilateral retrograde deployment of a self-expanding nitinol Smartstent (Cordis Endovascular, Johnson and Johnson). The stent requires balloon dilatation for full deployment. (c) Spot film showing the stent after dilatation with a 7mm balloon. The stented segment now appears fully dilated and the stenoses evident on the prior spot film are gone. (d) Completion angiogram showing an excellent angiographic and haemodynamic result. The patient also had a dramatic clinical improvement.


Figure 1.5 Treating lesions near the inguinal ligament. (a) Preliminary angiogram in a 6l -year-old. woman with left leg claudication, showing tandem lesions in the very distal external iliac artery. She had a history of pelvic radiation and this raised the issue of postradiation-induced vasculopathy. (b) The lesion was approached in an antegrade fashion and predilated to 5 mm. This is the angiographic appearance after the initial 5 mm angioplasty. (c) Completion angiogram with Palmaz 154 stents (two) deployed on a 7 mm×2 cm balloon under trace angiography, showing excellent angiographic results. Her symptoms were completely relieved by the procedure. Lesions in this location are in general quite prone to dissection and should be approached with great caution.


Figure 1.6 Poststent dissection and its treatment. (a) Injection of the contralateral iliac on pull-back demonstrates a gradient across the iliac straddling the internal iliac origin. (b) Angiogram after deployment of bilateral iliac stents, both through retrograde approaches, showing a good result to the right external iliac (confirmed by measuring gradients with nitroglycerin), but a dissection limiting flow on the left. (c) Completion angiogram after deployment of another Palmaz stent (Cordis Endovascular, Johnson and Johnson) in the left external iliac artery to treat the dissection. This shows an excellent angiographic result.


Figure 1.7 Percutaneous iliac intervention followed by surgical femoropopliteal bypass. (a) Preliminary angiogram in a man with left leg chronic ischaemic ulcers, showing no discreet stenosis (incidental finding of a pelvic kidney). (b) Careful interrogation of the iliac system on the left revealed a high resting gradient (40mm) across the proximal external iliac artery. (c) The patients left common femoral artery was then punctured and deployment of a Palmaz stent on an Opta LP balloon (both Cordis Endovascular, Johnson and Johnson) was performed. (d) Completion angiogram showing excellent angiographic results with abolition of gradient, even with nitroglycerin. Nitroglycerin augmentation is crucial for detection of lesions responsible for claudication. This was done as a staged procedure, with the patient undergoing femoropopliteal bypass for a long-segment superficial artery occlusion the following day.


Providing good inflow for lower leg bypasses is crucial for their long-term patency.

Figure 1.8 The approach to multilevel disease. (a) Pulse volume recordings of a 65-year-old man with left leg claudication at one block. Severe dampening is seen at the calf level, indicating haemodynamically significant disease of the femoropopliteal segment. The ankle and metatarsal levels are nearly flatline, indicating severe trifurcation disease as well. (b)-(k) (Shown on the following pages.)


(b) Preliminary angiogram showing bilateral common iliac disease with ulcerative, stenotic lesions. High resting pressure gradients were measured across both iliacs at their origins. (c) Preliminary angiogram, showing a 4 cm occlusion of the left popliteal artery. (d) Spot film showing simultaneous deployment of Palmaz 394 stents with Opta LP 8mm×4cm (Cordis Endovascular, Johnson and Johnson), all through 6Fr sheaths (Pinnacle, Terumo) using ‘kissing balloon’ technique. (e) Completion angiogram, showing an excellent angiographic result of the reconstruction of the bifurcation and treatment of the iliac stenoses. (f)-(k) (Shown on the following pages.)


(f) Pulse volume recording after iliac stent placement, showing severe dampening of the waveforms at the femoropopliteal level. The patient was still symptomatic in the left leg. (g)-(k) (Shown on the following pages.)


(g) The patient was brought back for treatment of the left popliteal artery occlusion. The groin was punctured antegrade and a trace angiogram performed. This image shows the use of a J-tipped Rosen wire (Cook Inc.) to cross the occlusion. This tip provides a safe means to cross the lesion, with minimal chance of dissection. (h) Spot film showing balloon inflation across the lesion. Again, balloon length is matched to the diseased segment. (i) Angiogram after initial angioplasty. This shows a dissection causing compromise of the


lumen. It is our practice always to attempt prolonged balloon inflation in these cases, rather than to go immediately to stenting. (j) Angiogram after balloon inflation for 3 min. During these long inflation times, the wire is removed and the end-hole of the balloon catheter infused by hand with flush heparinized saline. (k) (Shown on the following page.)

(k) Pulse volume recording showing normal waveforms on the left. The patient is now asymptomatic. This illustrates an uncommon occurrence, where treatment of inflow (iliac) disease did not decrease the patient’s claudication.


Figure 1.9 Superficial femoral artery occlusion. (a) Non-invasive study in a woman with right leg claudication, showing dampening of the pulse-vol ume recording at the right calf level indicating significant femoropopliteal occlusive disease. (b)-(e) (Shown on the following pages.)


(b) Preliminary angiogram showing a short segment occlusion of the distal superficial femoral artery at the adductor canal. This treatment was done in an antegrade fashion via the ipsilateral common femoral artery. (c) Roadmapped image of balloon inflation. Balloon length is selected to match the length of disease to minimize angioplasty-induced injury to non-diseased segments, Balloon diameter is selected to minimize overdilation, in general 10% over native artery diameter. Marking catheters or ‘tape measure’ guides can be used for these determinations. (d) Completion angiogram of angioplasty site showing minimal dissection and good flow through the vessel. The completion angiogram should be viewed dynamically to evaluate flow characteristics through the treated segment. (e) (Shown on the following page.)


(e) Postintervention showing improvement in the right calf waveform and improvement in the ABI from 0.55 to 0.74, with markedly reduced symptoms.


Figure 1.10 The value of prolonged inflation. (a) Preliminary angiogram showing a short segment occlusion of the distal right superficial femoral artery in a woman with claudication. (b) Roadmappped image showing an LLT wire (Cook, Inc.) crossing the lesion. Notice how the wire shows no abnormal buckling and follows a straight course. (c) Angiogram after initial angioplasty. Flow-limiting dissection is seen. (d) Angiogram after prolonged inflation to 3 min, showing marked improvement in flow through the PTA site.


Figure 1.11 Utility of nitroglycerin in lower extremity angioplasty. (a) Preliminary angiogram showing short-segment occlusion of the popliteal artery in a 53-year-old woman with a history of smoking and a 6-month history of right calf cramping at 100ft. (b) Angioplasty was performed with an 0.018 Flex-T guidewire and a 4.0 mm Savvy balloon (Cordis Endovascular, Johnson and Johnson). (c) Arterial spasm was noted on the postangioplasty angiogram, as depicted here (arrow). (d) Angiogram after 100 µg of nitroglycerin, showing resolution of the vasospasm.


Figure 1.12 Suboptimal angioplasty and flow-limiting dissection. (a) Preliminary angiogram in a 49-year-old man with right leg claudication, showing distal superficial artery stenosis. (b) Angioplasty with a 5 mm×10cm-length balloon. (c) Postangioplasty angiogram, showing a severe flow-limiting dissection. (d) Angiogram following prolonged balloon inflation in an attempt to ‘tack’ down the dissection flap. The flow is improved somewhat, but the dissection is still limiting flow to a significant degree. (e) Lateral femoral angiogram with leg flexed to better determine the site of the adductor canal This shows a minimal margin of normal vessel beyond the dissection, a margin that is essential for stent deployment. (f) Deployment of an 8 mm×38 mm Wallstent. (g) Completion angiogram showing excellent angiographic result.


Figure 1.13 Treatment with endografts. (a) Preliminary angiogram in a 71-year-old woman with left worse than right leg claudication, showing an 8cm-length occlusion of the distal superficial femoral artery. (b) Angioplasty performed from an antegrade approach with a 5mm×10cm balloon, showing the waist of the balloon as it is inflated. (c) Postangioplasty angiogram, showing a good result. There is a dissection, but it did not limit flow. (d) The patient underwent placement of a Hemobahn (W.L. Gore and Associates, Inc.) covered stent, which gave an excellent result, demonstrated on this completion angiogram. (e) Follow-up angiogram at 6 months, showing continued patency with no instent stenosis.


Figure 1.14 Treatment of femoropopliteal graft stenosis. (a) Preliminary angiogram in a 76-year-old woman with claudication 2 years following femoropopliteal bypass with reversed saphenous vein. Shown on this pelvic oblique angiogram is a high-grade stenosis of the proximal vein graft. (b) Spot film of the ballaon catheter going over the aortic bifurcation. (c) Spot film of the initial balloon inflation. This shows the waist centred between the markers an the end of the balloon catheter, thereby eliminating the tendency for the balloon to be pushed either distal or proximal to the lesion on inflation. after giving up wire access across the lesion. With the Balkin sheath around the bifurcation, one can inject easily through a Touhy-Borst adapter (Cook (d) Postangioplasty angiogram. Without a Balkin sheath (Cook Inc.), as in this case, a good completion angiogram is usually done with a diagnostic catheter Inc.) with the wire still across the lesion. In case of severe dissection, this wire access becomes a tremendous advantage.


Tibioperoneal angioplasty

Tibial angioplasty is again usually performed via an antegrade puncture of the commonfemoral artery. Anatomical data has shown that the common femoral artery usually liesover the femoral head and therefore punctures should be directed in a manner that allowsthem to enter the artery in this location. Periprocedural aspirin is usually given andcontinued for at least 2 months after the intervention. Newer antiplatelet agents such asclopidogrel and ticlopidine have not been studied in native artery intervention to date, butwill most likely be shown to be of some use. Nitroglycerin is used for spasm selectivelyby some and routinely by others. It has been given through the catheter by some andsublingually by others. Nifedipine has also been used in this manner. Heparin is mostcommonly given as the lesion is crossed. At our institution, however, heparin is not givenroutinely, but only to selected cases with poor run-off, multilevel disease, and difficult lesions. A variety of steerable 0.018 inch guidewires and low profile balloons areavailable and can help reduce the introducer sheath size to 4 or 5 Fr. An example of thisis given in Figure 1.15. Balloon sizes vary, but peroneal or posterior tibial vessels usually vary between 2.0 and 3.0 mm. Tibioperoneal trunk diameters are slightly larger. Kissingballoon technique can be used to treat ostial lesions simultaneously at branch points byplacing the wires and balloon catheters in tandem through the sheath. This provides somedegree of safety in preventing damage to the ostia of one tibial vessel, while treating theostia of another. Some loss of the haemostatic function of the sheath is seen, but isusually minimal if the procedure is carried out quickly; an example is given in Figure 1.16. Roadmapping, low ionic contrast and pre- and postprocedural angiography are essential for success. A variety of coronary stents have been developed and can be usedto treat extensive dissections in the tibial circulation. These typically track over 0.014 or0.018 guidewires. An example is given in Figure 1.17.


Figure 1.15 The use of small-vessel technique (a) Preliminary right leg angiogram in a 71 -year-old man with diabetes and ischaemic ulceration of the foot and a history of left above-knee amputation. Focal stenosis of the SFA is noted. (b) Preliminary angiogram at the trifurcation, showing severe stenosis of the tibioperoneal trunk and proximal peroneal arteries. Chronic occlusion of the anterior tibial is also noted. (c) The right groin was punctured in an antegrade fashion and the proximal peroneal artery was dilated with a 2.5 mm Savvy balloon (Cordis Endovascular, Johnson and Johnson) over an 0.018 Flex-T wire. (d) The balloon was pulled back into the tibioperoneal trunk and inflated again. (e) The balloon was then exchanged for a 5.0 mm×2 cm Symmetry (Meditech, Boston Scientific) balloon and the SFA lesion dilated. (f) Completion angiogram showing an excellent angiographic result with preservation of the posterior tibial origin. (g) Completion angiogram of the SFA stenosis, showing an excellent result with no flow-limiting dissection.


Figure 1.16 The treatment of tibial bifurcation disease. (a) Preliminary angiogram in a 72-year-old man with severe left calf claudication. This shows a critical stenosis in the distal popliteal artery involving the origin of the anterior tibial artery (open arrow). Less severe stenoses are seen in the tibioperoneal trunk (closed arrow). (b) Trace angiogram showing angioplasty of the distal popliteal artery over a Flex-T wire (open arrow), with an additional Flex-T wire placed parallel through the sheath and into the origin of the anterior tibial artery for safety and access (closed arrow). (c) Trace angiogram, showing angioplasty of the origin of the anterior tibial artery. (d) Completion angiogram, showing excellent angiographic results. The patient experienced a dramatic improvement in his symptoms.


Figure 1.17 Bailout tibial stenting. (a) Pulse volume recordings of an 81-year-old man with diabetes and a gangrenous second toe of the right foot. Dampened waveforms at the ankle and metatarsal level consistent with trifurcation disease worse on the right with falsely elevated ABI values bilaterally due to non-compressible, calcified vessels, 0.84 on the right and 1.48 on the left. (b)–(h) (Shown opposite.)


(b) Preliminary angiogram, showing the trifurcation on the right with the main run-off being a diseased posterior tibial artery. (c) Angioplasty of proximal posterior tibial stenosis with a 3 mm×4cm Savvy (Cordis Endovascular, Johnson and Johnson) balloon. (d) Angioplasty of distal posterior tibial stenosis with the same balloon. A Hi-Torque Floppy II guidewire (0.014) was used (Advanced Cardiovascular Systems, Inc., Temecula, CA, USA). (e) Postangioplasty injection, showing persistent narrowing of the proximal lesion, which was seen to limit flow on real-time observation. (f) Spot film showing deployment of 3 mm AVE stent, a stent used primarily for coronary lesions, but excellent for tibial work. (g) Completion angiogram, showing an excellent angiographic result. (h) Shown over page.


(h) Pulse-volume recordings after posterior tibial angioplasty and stenting. Improvement in the ankle and metatarsal levels is seen. The patient went on to heal the ulcer of his right second toe.

Conclusion

Lower extremity endovascular intervention is certainly an area of clinical and technicalchallenge, but one of tremendous potential reward, both for the patient and theinterventionalist. While the guidelines above provide a framework and knowledge basefrom which to begin, each patient has unique features in terms of clinical presentationand anatomy, which comes to bear on the intervention used. With continued advances intechnology there promises to be a march towards ever-increasing success and reduced risk of lower limb endovascular intervention.


References

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Extraluminal (subintimal) angioplasty

2 AMMAN BOLIA

Introduction

Since the first description of percutaneous endoluminal treatment by Dotter in 19641 and subsequent development of the balloon catheter and its application by Gruntzig in 1974,2the treatment of peripheral vascular disease has been transformed. Percutaneoustransluminal angioplasty (PTA) has been employed extensively in the treatment ofperipheral vascular disease, with a highly successful outcome.3–10 However, the results of recanalization of long occlusions have been perceived to be poor in terms of primarysuccess rates and long-term outcome.3,4 Conventionally, occlusions of the superficialfemoral artery (SFA) or the popliteal artery of more than 10 cm or flush occlusions of theSFA have been treated by a surgical bypass. Since the development of the technique ofsubintimal angioplasty,11 the vast majority of the occlusions can be treated, whether they are full-length occlusions of the superficial femoral artery or flush occlusions.12–17 Tibial artery occlusions can be treated successfully in the majority of cases,18–20 thusmaking an impact onthetreatment of critical limb ischaemia where the disease tends to be distal.21, 22

Extraluminal angioplasty, commonly known as percutaneous subintimal angioplasty (PSA), has been experienced accidentally by most operators. However, there have onlybeen a few reports of intentional extraluminal recanalization. Following the first reportsof recanalizations through a dissection with a laser probe23, 24 and an early report in the form of a letter to the editor,25 the first significant publication occurred in 1990, presenting the experience of 71 procedures.11 A number of reports has since beenpublished, which has included the experience of recanalization of femoropoplitealocclusions in the majority of cases.11–16 However, the procedure has also been extendedto crural artery occlusions,18–21 iliacocclusions,26,28 and, in some cases, common femoral, profunda, subclavian and brachial artery occlusions.29

The procedure is simple, inexpensive, offers a low complication rate, good primary success rates and long-term results. It has made a significant impact on the treatment of chronic critical limb ischaemia,21, 22 being applicable in up to two-thirds of patients with this condition.

The technique offers a number of advantages to the conventional surgical bypass operation. Patients who are poor candidates for general anaesthesia or who do not havean adequate vein for a distal bypass may be successfully treated. The procedure rarelycompromises a subsequent surgical option in case of a failed angioplasty, and is alsomore readily repeatable compared to surgery.

Indication

• Long occlusions. When a long occlusion is present, it is very unlikely that the guidewire/catheter could be maintained intraluminally; hence, dissection is likely to ensue.

• Hard/long-standing occlusions. When an occlusion is long standing, the feel imparted to the guidewire will indicate that the occlusion is hard and any forward advancement of the guidewire is likely to result in a dissection, because the guidewire will tend to take the path of least resistance, which is in a dissection.

• Occlusions in diffuse disease. When there is underlying diffuse disease and an occlusion present, it is unlikely that the guidewire will be able to negotiate the true lumen throughout the length of the occlusion. Therefore, dissection is likely to ensue and PSA becomes appropriate.

• Occlusion in a moderately calcified vessel. In a moderately calcified vessel the presence of calcification generally indicates long-standing disease and therefore the occlusion is likely to be hard. Dissection is likely to occur in such situations.

• Previously failed intraluminal approach. Any previously failed intraluminal approach is unlikely to succeed intraluminally again, hence PSA is indicated.

• Perforation during a previous attempt at PTA. If perforation occurred during an intraluminal recanalization, it is very unlikely that a successful outcome could be achieved, because the guidewire/catheter will tend to follow the path into the perforation. With PSA, it is possible to find an alternative dissection, which is likely to result in a successful outcome.

• Large proximal collateral. When a large proximal collateral is present, the resultant anatomy may not allow the guidewire or catheter to engage into the origin of the occlusion. PSA allows this to be achieved by initiating a dissection with the use of a hard end of the guidewire above the level of the occlusion. Once an intimal flap has been lifted, it is possible to continue the dissection, which usually follows the main vessel rather than the collateral, and in this way a collateral entry can be avoided.

• Popliteal occlusion extending into the trifurcation. PSA allows recanalization of a popliteal occlusion that extends into the trifurcation by recanalizing into all three run-off vessels, assuming that these are patent distally.

• Common femoral occlusion extending into the bifurcation. PSA allows the recanalization of an occlusion extending into the bifurcation to be recanalized into both vessels, the superficial femoral artery and the profunda artery.

• Long stenosis. PTA of long stenoses produces poor results due to a high incidence of recurrence of disease. Where there is a reasonable proximal and distal vessel, a long stenotic segment may be treated by PSA. PSA allows the exclusion of the diffusely disease segment, thus creating a new channel.

• Flush SFA occlusion. Total SFA occlusions with no stump can be treated by PSA. • Tibial artery occlusion. Full-length tibial artery occlusions can be recanalized by PSA,

which is particularly useful in the treatment of patients with critical limb ischaemia. • Iliac occlusions. During attempted retrograde recanalization of an iliac occlusion,

dissection frequently ensues and re-entry proximally into the lumen is often difficult,

Extraluminal (subintimal) angioplasty 49

possibly because of the relatively thick intima towards the aorta. In such situations, PSA is possible by the crossover approach.

• Brachial, subclavian, common femoral and profunda occlusion. Depending on how long these occlusions have been present, it may be impossible to make an intraluminal approach, due to the hardness of the occlusion. PSA is effective, even in very hard occlusions.

• Previously occluded femoropopliteal or femorodistal graft. In patients who have had a previous femoropopliteal or femorodistal graft that has subsequently occluded, recanalization of the indigenous vessel occlusion may be possible with PSA.

Relative contraindications

• Fresh occlusions of less than 3 months’ standing. It is difficult to determine the age of an occlusion. However, when the patient gives a history of an acute event, it may be possible to determine when an occlusion occurred. This being the case, and as long as the patient’s symptoms are not severe, we would recommend that a minimum of 3 months is allowed for the occlusion to ‘mature’ before PSA is attempted. If the occlusion is less than 3 months old, recanalization is likely to be unsuccessful because the occluded segment may fail to remain open, but also because there is a chance that an embolic complication from fresh thrombus may occur.

• Short occlusion. If the occlusion is short, then generally it is easier to pass the wire intraluminally. However, if dissection ensues in these cases, then PSA is pursued.

• Occlusion within severe diffuse disease. When an occlusion is present within a severely diffusely diseased vessel, then re-entry into the lumen beyond the occlusion may become difficult, because the wire loop will have the tendency to continue the dissection further down the leg without having the tendency to come back into the lumen. While an attempt has to be made to recanalize the occlusions in such situations, if the dissection has extended too far and there are risks of compromising important collaterals, then the procedure has to be abandoned.

• Long stenosis with extensive diffuse disease. When there is a long stenosis and extensive diffuse disease in the proximal and distal vessels, it becomes difficult to determine where to begin the dissection and where to end it. Such cases are perhaps best dealt with intraluminally.

Materials

The materials required are listed in Table 2.1.

Table 2.1 Materials required for extraluminal angioplasty

Guidewires

Teflon-coated ordinary 3 cm floppy guidewire (0.035, 180 cm long)


Technique

Femoropopliteal occlusions

Following an antegrade puncture, a Van Andel catheter is introduced and advanced up tothe level of the occlusion. The occlusion is entered with the help of an ordinary straight-tipped Teflon-coated guidewire, on which a small curve has been introduced. The angledtip of the guidewire is directed towards the wall of the artery, away from any importantcollaterals. Advancing the tip of the wire usually results in a dissection, because the wiretakes the path of least resistance. Once the wire is in a dissection, the catheter is advancedinto this position and its location in the dissection is confirmed with a small amount ofdilute contrast medium. Most of the length of the occlusion is traversed using a

1.5 mm, J-Teflon coated guidewire with 3 cm floppy tip.

Curved-tip hydrophilic guidewire; (Terumo),

Curved-tip stiff hydrophilic guidewire (Terumo)

2 mm J-half-stiff hydrophilic guidewire (Terumo)

Catheters

Van Andel catheter

4 French dilator

Coeliac/sidewinder catheter

Balloon Cathetets (5 French shafts)

2.5, 3 and 3.5 mm diameter with 2 cm balloon length and

120 cm shaft

4–10 mm diameter with 4cm balloon length and 80 cm shaft shaft

Inflation device

Drugs

Aspirin 150mg per day

Heparin up to 5000 units during procedure

Tolazoline 25 mg

Glyceryl trinitrate 500µg

Glyceryl trinitrate patch 5 mg per 24 h

Aspiration/embolectomy system

6–8 French sheath with removable valve ,

5–8 French non-tapered widebore catheter

50 ml luerlock syringe


combination of a 1.5 mm J-tipped guidewire and the Van Andel catheter. This may be done either with the 1.5 mm J-tipped guidewire protruding at the end of the catheter or with the straight tip of the wire. Traversing the length of an occlusion through adissection plane is usually not difficult, since the wire/catheter will progress along thepath of least resistance. Surgeons who perform endartectomy are familiar with the easewith which occluding atheroma can be excised in this plane.

When most of the occlusion has been traversed, the J-tipped wire is manipulated to form a large loop in the wire. It is this loop in the wire that allows re-entry into the lumen of the artery distally. A disease-free segment beyond an occlusion is a favourable factorand allows re-entry to happen easily. However, if there is diffuse disease beyond the occlusion, then the loop may not re-enter immediately beyond the occlusion, but thedissection may have to be extended beyond the area of diffuse disease until a diseasefreesegment of the artery is approached, and then the loop will have a natural tendency to re-enter the lumen. Recanalization in the subintimal plane can be likened to the situation inacute aortic dissection where the dissection either re-enters the true lumen spontaneously or is surgically fenestrated. In this situation, the false lumen is often larger, and has ahigher blood flow than the true lumen.

Once in the lumen, the Van Andel catheter is substituted for a balloon catheter and thewhole dissected segment dilated with a balloon. Short but high-pressure inflations (up to 12 atm pressure and 10s inflations) are used throughout the length of the occlusion(Figures 2.1a, b).

When a successful outcome has been achieved, any contrast injection done beyond thelevel of the occlusion will show rapid clearance of the contrast. Any reluctance in thewashout of the contrast should be carefully assessed and corrected. Further inflations,possibly using even higher pressures, may be necessary in order to remove any residualstenoses. The success of the procedure is judged on how rapidly the contrast clears fromthe angioplastied artery (haemodynamic success), rather than the anatomical appearancesof the recanalized segment (Figure 2.2).

Perforation in the femoropopliteal segment

When perforation occurs, an advantage of the subintimal technique is that an alternativedissection can be found in the majority of cases, thus bypassing the site of the perforationand allowing the procedure to continue as before. The alternative dissection can be foundeither with the angled tip of the wire directed away from the site of the perforation andalternative dissection pursued, or a large loop introduced in the wire which would thennot enter the site of the perforation (Figure 2.3).


Figure 2.1 (a) The occlusion is approached in the direction away from any important collaterals. The catheter/wire combination is advanced into the dissection space. A large loop is created within the dissection. This loop allows the dissection to be extended throughout the length of the occlusion and also allows re-entry back into the arterial lumen distally. (b) The cross-section shows the position of the catheter and the occluding material, having been displaced eccentrically after balloon dilatation.


Figure 2.2 There is an occlusion of the profunda artery and a flush occlusion of the superficial femoral artery which extends up to the mid-popliteal level. A successful subintimal recanalization was achieved with good result.


Iliac occlusions

Iliac occlusions are difficult to recanalize, due to the frequency with which a dissectionoccurs when a retrograde

Figure 2.3 A short mid-popliteal occlusion is present. During attempted recanalization, a perforation occurred. An alternative dissection channel was negotiated through the subintimal space and a successful recanalization achieved.

approach is made to cross the occlusion. As a result, a method has been developed thatallows a controlled dissection to be made in the occluded segments.26 In the first instance, a retrograde approach and dissection from the ipsilateral approach is carried outand an attempt made to reenter the artery proximal to the occlusion. However, this isfrequently unsuccessful, presumably because as we approach the aorta the intima is muchthicker than in the distal artery and it is therefore difficult to break back into the lumen.

To overcome this difficulty, a puncture is made in the contralateral femoral artery and the occlusion is approached in an antegrade fashion using a sidewinder or a coeliac-shaped catheter. The tip of the catheter is engaged against the occlusion and the tip of aguidewire, usually a curved hydrophylic guidewire, is directed towards the wall of theartery in order to initiate a dissection. Once the wire is advanced into the dissection, thewire is manipulated so as to meet up with the dissection caused from the retrogradeapproach. Since both these dissections are in the same plane, usually after manipulations,a common channel is found and the lesion crossed. The occlusion is usually balloondilated from the crossover approach (Figures 2.4 and 2.5).


Figure 2.4 An initial attempt at recanalization of an iliac occlusion is made from the ipsilateral approach. This frequently results in a failure, by not being able to re-enter the lumen proximally. Hence an approach is made from the contralateral side and a dissection initiated at the origin of the iliac occlusion. This dissection is in communication with the dissection created from below and, after manipulations, a common channel is usually found and successful recanalization achieved.


Figure 2.5 A right external iliac occlusion was successfully recanalized by percutaneous subintimal angioplasty. Notice a dissection flap at the origin of the external iliac occlusion.

Crural artery occlusions

There are several differences in how a crural artery recanalization is carried out. First, itis very important to get a good quality diagnostic arteriogram, not only to show theproximal vessels, but, importantly, the quality of the distal vessels with which thedissection will have to meet up. Secondly, an antispasmodic in the form of tolazoline isgenerously used. Prior to crossing the lesion, 10mg tolazoline and subsequent doses maybe required, up to a total amount of 25 mg. Prior to crossing the lesion, 5000 units ofheparin are also introduced.

There is an important difference in how a tibial occlusion is crossed in comparison to the other occlusions described above. A balloon catheter is introduced from the start ofthe procedure, usually 3 mm in diameter, and 2 cm long on a 5 French shaft and 120 cmlong. Unlike the occlusions in the femoropopliteal segment whereby the lesion is crossedwith a Van Andel catheter before a balloon catheter is introduced, in the case of tibialarteries, the balloon catheter is introduced at the beginning of the procedure because thecrossing of a tibial artery occlusion, especially if it is a full-length occlusion, becomes difficult. The difficulty arises because of the distance at which one is working from thefemoral puncture to the tibial artery occlusion. For this reason, a 5 French system basedon an 0.035 guidewire is used, which is inherently stronger than the other smaller systemsused for tibial angioplasty. The idea of a balloon catheter used for crossing the lesion isthat when the forward progression of the catheter comes to a halt, the balloon is used to


dilate the segment of the artery that has already been crossed. This has the advantage ofeliminating all the resistance to the progression of the balloon catheter so that whenforward pressure is applied to the catheter, it moves forward within the occlusion. Whenthe catheter comes to a halt again, the resistance may be eliminated in a similar fashionby multiple dilatations above the level of the area of resistance. In this fashion, the wholelength of the occlusion may be crossed and the artery dilated, once again using highpressures (12 atmospheres) but very short inflations of 3–5 s per inflation (Figure 2.6).

A hydrophilic guidewire (Terumo) is used in a looped fashion in order to cross thewhole length of the occluded tibial artery. In some instances, the ordinary hydrophilicguidewire may prove not to be strong enough; in such situations a stiff hydrophilicguidewire is used. However, care must be taken when the stiff guidewire is used as thereis a possibility that this would cause a perforation. Perforation of the tibial artery is acommon complication (occurring in approximately 5–10% of cases) and when perforation occurs, it is impossible to negotiate the site of the perforation in the majorityof cases and this may therefore result in a failed procedure.

Figure 2.6 This patient with critical limb ischaemia presented with proximal occlusion of all the run-off vessels. The recanalization was first carried out into the peroneal artery successfully. Subsequently, recanalization of the posterior tibial artery was carried out, thus achieving a good two-vessel run-off. Notice the disappearance of the extensive collateral circulation following a haemodynamically good result.


Popliteal occlusion extending into the trifurcation

Many patients with critical ischaemia have disease in the run-off vessels, and a significant proportion of the patients may have popliteal occlusions that extend into all the runoff vessels. If this is the case, subintimal angioplasty offers the option ofrecanalizing the popliteal occlusion into one or more of the run-off vessels and, in most cases, all three run-off vessels. Once again, the technique involves a loop in theguidewire, usually a hydrophilic guidewire, that is advanced into one of the run-off vessels.

The peroneal artery is in a straight line with the popliteal artery and this is the artery that is frequently entered by the loop. Once re-entry has been achieved, the occlusionfrom the popliteal artery into the peroneal artery is dilated using a small balloon (usually3 mm diameter). Then an attempt is made at finding the origins of the other vessels—the anterior tibial and the posterior tibial arteries—using the curved tip of the hydrophilic guidewire. When the origin of one of these vessels is found, once again a loop is createdin the guidewire and re-entry achieved distally. This segment is again ballooned using the small balloon. The other run-off vessel is recanalized in a similar fashion. Finally, a larger balloon (usually 5mm diameter) is used to dilate the popliteal artery and in thisway all three run-off vessels may be recanalized. This has the advantage of achieving flow in all three vessels from a recanalized popliteal segment, the equivalent of whichcannot be achieved with a surgical distal bypass, whereby the distal limb of theanastomosis may be done to only one of the run-off vessels. The advantage of having a recanalization into all the run-off vessels is that the angioplastied segment will have abetter chance of a patency, having a three-vessel run-off rather than a onevessel run off (Figures 2.7 and 2.8).

Aftercare

The use of an introducer sheath is unnecessary in the vast majority of cases of subintimalangioplasty. Hence, the hole created in the femoral artery for access is usually no morethan 5.5 French. As a result, the majority of the patients can be dealt with on a day-case basis. After 5 or 6 h of bed rest within the department after the procedure, the patients areable to leave for home.

Most patients with critical ischaemia are treated on an inpatient basis. They generallytend to be elderly and require further care for the management of other problems relatedto critical ischaemia, such as local treatment of leg ulceration.

No special aftercare is required in the majority of the cases. Most patients are onaspirin 150 mg per day on a continual basis but if they are not, it is usuallyrecommended. If the procedure has been difficult in view of a long occlusion or apossible complication that has been dealt with, then the patient receives 5000 units of


Figure 2.7 The schematic diagram shows a popliteal occlusion extending into all the three run-off vessels. Dissection is first extended into one of the vessels; in this case, the anterior tibial artery. Subsequently, the peroneal and then the posterior tibial arteries are recanalized, thus achieving all three run-off vessel recanalizations.

subcutaneous heparin every 6 h for 24 h. At the same time, a glyceryl tri nitrate patch (5mg per 24 h) is administered after a successful procedure. This ensures a sustainedvasodilation, which helps to improve flow through the angioplastied segment. Thenursing staff are informed of any high puncture that may have been carried out, in casesof flush superficial femoral artery occlusions, so that a very careful eye is kept on theblood pressure and pulse measurements, and action taken immediately if there is anyevidence of significant blood loss in the retroperitoneum.

Results

Femoropopliteal occlusions

The experience of PSA has been widest in the femoropopliteal segment, and over 700procedures have been carried out since January 1987, when the first procedure wascarried out accidentally. After this first accidental recanalization, a number of arterieswere recanalized, some accidentally and some intentionally, As time went by, more andmore procedures were carried out intentionally through a dissection. At present, it isalmost an exception to carry out an intraluminal recanalization for a femoropopliteal


Figure 2.8 There is an occlusion extending from the mid-popliteal level into the anterior tibial and the peroneal arteries. Recanalization was first achieved into the peroneal artery. Subsequently, with wire and catheter manipulations, the channel into the anterior tibial artery was created and angioplasted, with a good result.

occlusion. Primary success rates of over 80% can be expected, irrespective of the lengthof occlusion. The rate of significant complications is quite low and long-term results are promising.

The first 200 procedures in 176 patients over a period of 64 months were carried out between 1987 and 1992 and have been reported elsewhere.12 The results are presented here briefly. Of the 176 patients, the mean age was 69 (22–92) years, 130 (74%) were males, 33 (19%) were diabetics, 62 (35%) were hypertensive and 61 (35%) weresmokers.

Technical success was defined as recanalization with 30% or less residual stenosis and antegrade flow at the conclusion of the procedures. Technical failures resulted frominability to either enter, traverse or exit the subintimal space. The common reasons forabandoning the procedure were usually failure to progress with a catheter in a heavilycalcified vessel, an occurrence of a perforation, or failing to re-enter the lumen distally. Major complications were defined as those that altered the patient’s clinical state, whereas minor complications did not. Patient followup consisted of clinical examinationand ankle brachial pressure index (ABPI) only. These were performed at 24 h, 1, 3, 6, 9and 12 months, and thereafter at 6-monthly intervals.

The technical success rate was 80% (159/200) and there were no significant differences between the technical success and failure group with respect to the incidenceof diabetes, critical ischaemia, claudication, occlusion site or occlusion length. The


technical success rate for occlusions less than 10 cm was 81%, for occlusions 11–20 cm was 83%, and for occlusions more than 20 cm 68%, with no significant statisticaldifference in terms of ability to cross a short or a long occlusion.

There were two major (1%) and 13 minor (6.5%) complications. The major complications were one retroperitoneal and one scrotal haematoma, and although bothrequired surgical evacuation there were no long-term sequelae. These two major complications were puncture related and not related to the technique of the subintimalangioplasty. The minor complications were two groin haematomas, seven distal emboliand four vessel perforations. The groin haematoma resolved spontaneously. Two of theperforations require no treatment and two were treated by embolization usingembolization coils. Of the seven distal emboli, six were aspirated using an 8 Frenchnontapered aspiration catheter and, in addition, one required regional fibrinolysis withstreptokinase (5000 units per h) for 24 h. There were no deaths or limb loss directlyrelated to the angioplasty procedure. The 30-day mortality was 3/200 (1.5%), all three deaths resulting from myocardial infarction (Figure 2.9).

After this study period, 275 subsequent procedures were analysed (resultsunpublished). There were 31 failures (11%), giving a primary success rate of 89%. Themean length of occlusion in this group was 15 cm.

The failures in these 31 procedures were due to failure to re-enter distally in 15 (5%), heavy calcification in six (2%), perforation in four (1.5%), fresh occlusion in two (1%)and damage to important collaterals without reconstitution of flow in four (1.5%). In thelatter four cases, emergency bypass surgery was required. There were 10 emboliccomplications, of which eight were aspirated percutaneously and the other two werehaemodynamically insignificant. Surgical embolectomy was not required in any case.

The long-term haemodynamic patencies of all the successfully treated cases (159 procedures) are shown in Figure 2.9. The haemodynamic patencies at 12 and 36 months for all procedures were 56% and 46%, respectively; the symptomatic patency were 58%and 48%, respectively. Of the technically successful procedures, 3% failed within 24 h.

Tibial occlusions

The published literature on angioplasty of tibial occlusions is limited and a few availableseries have combined the treatment of stenoses and occlusions.30–34 A smallstudy carried out at the Leicester Royal Infirmary of tibial occlusions treated by PSA has beenpublished elsewhere.20 Thirty-two infrapopliteal artery occlusions in 28 critically ischaemic limbs in 27 patients have been recanalized by PSA. Of the treated occlusions,25 (89%) were of a single vessel, whereas in three limbs (11%) multiple occlusions wererecanalized, and median (range) length of occlusion was 7 (2–30) cm. Of the 28 limbs, four (14%) had rest pain, 17 (61%) had ulceration and seven (25%) had gangrene.


Figure 2.9 The graft shows cumulative patency rates of the 159 successfully treated femoropopliteal occlusions over a 3-year period.

The immediate technical success rate was 26 of 32 (81%) occlusions. There were no failures at 24 h and 30-day mortality was 0. Three complications

included one puncture-related retroperitoneal haematoma, which required surgical intervention, a vessel perforation that was of no consequence to the patient, and wasregarded as a failed procedure and one distal embolization after a successfulrecanalization that was aspirated percutaneously.

Although long-term results are not available yet, the 1year haemodynamic and symptomatic patencies were 50% and 54%, respectively.

In patients with critical limb ischaemia, tibial vessel patency is only desirable to relieve rest pain, heal ulceration or demarcate gangrene to allow localized surgery. In themajority of cases, PSA allows this to happen.


The impact of PSA on critical ischaemia

PSA has made a major impact on the treatment of chronic critical limb ischaemia at theLeicester Royal Infirmary. Recent prospective survey of all critical limb ischaemiapatients who presented at the Leicester Royal Infirmary was carried out during a 12-month period in 1994.21 There were 222 referrals in 188 patients. This survey showed that the majority of the patients were treated with angioplasty (42%), 6% of the patientshad a combined treatment of angioplasty and surgery (minor amputations) and 24% ofthe patients has reconstructive surgery. Of the total number of patients, 17% were treatedconservatively and 10% had primary amputation. The mean (range) hospital stay forpatients treated by surgery was 16 (3–97) days, for angioplasty 4.5 (1–73) days, and for amputation 18 (7–91) days. The in-hospital mortality rate was 10%, with a limb salvagerate of 79%. The complication rate of angioplasty requiring surgery was 5.5% (Figure 2.10).

A further prospective 12-month study was carried out as a continuation of this previous study.22 The aim of the study was to assess and compare the efficacy of angioplasty andsurgery in the treatment of severe lower limb ischaemia. Of the 188 patients (222critically ischaemic limbs), complete 12-month follow-up data could be obtained in 180 patients (187 limbs).

Figure 2.10 The pie chart indicates the modes of treatment of 222 critically ischaemic limbs treated during the year 1994 at the Leicester Royal Infirmary.


The overall 12-month patient survival was 75%. The 12month survival rates for surgery and angioplasty were significantly higher (91% and 78%, respectively),compared to those of primary amputation and conservative management (57% and 52%,respectively). The overall 12-month limb salvage rate was 71%. The limb salvage for patients treatedwith either angioplasty or surgery was 76%.

The policy to attempt angioplasty whenever possible enabled 46% of the patients in the study to be revascularized by this modality, compared to a national average of 22%.35

Furthermore, the limb salvage rates for angioplasty compare very favourably withsurgery.22

The data for this study strongly supports the use of angio plasty as first-line treatment for severe lower limb ischaemia, with no major evidence that angioplasty is detrimentalto subsequent surgery if required. In the context of a 12-month survival of 75% and a 3-year survival of only 50–60%, a long-term solution is not what many of these elderly frail patients require. This study highlights that as minimally invasive procedures, PTA andPSA serve the majority of patients very well, with a short hospital stay, and 12-month limb salvage rates that equate with those achieved by surgery.

Iliac occlusions

The experience of PSA in iliac occlusions has been fairly limited. Primary success ratesof 80% have been achieved, which is similar to what can be achieved in thefemoropopliteal segment and tibial artery occlusions. However, data for long-term results are lacking.

Complications

The incidence of major complications is 1–15%. The four common complications can becovered under the headings of perforation, embolism, puncture site haematoma, and (themost serious of all) compromising important collaterals without achieving a successfuloutcome. The management of these complication is described.

Perforation

This is a fairly common complication occurring in approximately 10% of cases. Themajority of these can be dealt with at the time of the procedure with a successfuloutcome. However, in some cases the true dissection channel cannot be negotiated and asa result the procedure has to be abandoned. A subsequent attempt at recanalization isusually successful. In some cases, in patients where either the perforation has beensubstantial and/or the patient is hypertensive, embolization of the perforated segmentbecomes necessary in order to contain the formation of a large haemotoma. This can beeffected with a use of an embolization coil. The presence of a coil in the occludedsegment is no bar to a subsequent attempt. Once again, a further attempt at recanalizationis made at a later date, usually with a successful outcome (see Figure 2.11).


Embolism

This complication can occur in approximately 5% of cases. The vast majority of theemboli can be aspirated using a large-bore aspiration catheter. In the large vessels (the superficial femoral artery and the popliteal artery) an 8 French catheter is used. However,for distal emboli in the tibial artery a 5 French catheter usually suffices. In rare sit

Figure 2.11 Summary of perforation.

uations, an embolic complication may result, whereby the embolus is such that it fails toengage at the end of the aspiration catheter. This may be due to the fact that the embolusis rather large and has a hard consistency and that its shape may be such that whenvacuum is created in the aspiration catheter, the embolus fails to engage around thecatheter tip and therefore effective vacuum cannot be created. As such, the embolus failsto be pulled out and would normally require surgical removal. However, there is analternative option whereby, instead of pulling the embolus, it may be pushed down intoone of the run-off vessels, usually the peroneal artery, which is in a straight line with the popliteal artery. This obviously compromises flow through the proximal part of theperoneal artery but if there are one or two other run-off vessels, then such an action is of little consequence to the patient’s distal circulation and saves an operative intervention.However, if there is only a single vessel run-off then surgical embolectomy would become necessary.

In the majority of cases, the emboli can be dealt with by the above two methods. Rarely, if there is a soft embolus that cannot be aspirated, then thrombolysis may be anoption. Thrombolysis is indicated where there has been more extensive embolism of freshthrombus. This may occur when recanalization of a fresh occlusion is attempted, and thismust therefore be avoided.

Generally, only in rare circumstances is surgical embolectomy necessary, where allother methods of percutaneous management have failed (see Figure 2.12).

Puncture site haematoma

A puncture site haematoma may occur following an endovascular intervention. Patientswho have had a large puncture hole, are hypertensive, or who are on anticoagu-


Figure 2.12 Summary of embolism.

lants are more likely to develop a haematoma. This may be exacerbated in patients whoare obese and, as a result, manual compression on the puncture site may have beenineffective. It may have been difficult to assess the size of the haematoma early on and itmay subsequently become rather large before it becomes detectable. In the majority ofpatients, this complication is self-limiting, and may not require any intervention otherthan prolonged compression either manually or by some mechanical device (for examplewith ‘Femostop’ or ‘Colapinto belt’). If there has been a substantial blood loss, blood transfusion may be required. If, however, the puncture site continues to extravasate,manual compression under ultrasound guidance may help to control the bleeding. If thisfails, surgical repair may become necessary.

A high puncture is required for the treatment of disease in the proximal SFA, flushSFA occlusions or profunda disease. In such cases, there may be a substantial risk of asilent retroperitoneal haemotoma. Since bleeding from a high puncture may not beevident at the puncture site, the only evidence of a significant bleed may come fromdetection of significant fall in blood pressure and a rise in pulse rate of the patient, and/orsymptoms of significant blood loss. Hence, the nursing staff must be well informed if ahigh puncture was made, with sufficient instructions for frequent blood pressure, pulsecheck and symptomatic assessment of the patient (see Figure 2.13).

Compromising important collaterals without achieving a successful outcome

This is the most serious complication of subintimal angioplasty, whereby the extension ofa dissection in the distal artery has resulted in compromise of important collaterals, thuscutting off the blood flow to the distal limb. If such an event has occurred withoutachieving a successfully recanalized channel, then the patient’s circulation has been compromised and, as a result, the patient will require emergency bypass surgery. Sincethe circulation will have stopped in the distal limb, thrombosis of the run-off arteries occurs, which complicates the subsequent bypass surgery. Distal embolectomy, togetherwith intraoperative thrombolysis, is required before a successful bypass operation can becarried out. There is an approximate incidence of 1–1.5% of this occurring.


Discussion

During our early experience11 PSA was only performed if the guidewire entered the subintimal space accidentally. However, it soon became evident that it was quite safe toenter the subintimal space deliberately with the intention of performing subintimalrecanalization. Nowadays, PSA is a routine procedure in almost all cases of occlusivedisease of the femoropopliteal, tibial and iliac arteries. It is also applicable in occlusionsof the subclavian, brachial and profunda arteries.

Although it has been standard teaching that inadvertent subintimal dissection duringconventional intraluminal angioplasty is an indication to withdraw and relocate theguidewire or even to abandon the procedure,36 there are theoretical reasons why PSAmight be advantageous. The subintimal plane is the path of least resistance and theguidewire therefore has a tendency to enter this space, particularly when the occlusion ishard or long. Surgeons who perform endarectomy are familiar with the ease with whichoccluding atheroma can be excised in this plane. During PSA, the occlusion is traversedin an extraluminal plane and this may explain why we found the technical success

Figure 2.13 Summary of puncture site haematoma.

rate to be the same for long and short occlusions. Recanalization in the subintimal planecan be likened to the situation in an acute aortic dissection where the dissection either re-enters the true lumen spontaneously or is surgically fenestrated. In this situation, the falselumen is often larger and has a higher blood flow than the true lumen.

Another potential advantage of subintimal angioplasty is that the thrombogenic,crushed atheroma is displaced to one side of the new lumen, whereas in conventionalintraluminal angioplasty, the new lumen is entirely surrounded by thrombogenic material.In achieving the new lumen of PSA, there is very little mechanical trauma involved,unlike other modes of recanalization, whereby mechanical injury or thermal injury (laserangioplasty) occurs. Such injury is likely to have a tendency to platelet adhesion and apossibility of acute reocclusion or early intimal hyperplasia. The minimal injury thatoccurs during PSA might be expected to minimize the restenosis rate of angioplasty.

Against these advantages, there is a serious disadvantage of PSA, which may make thepatient worse rather than better. There is a potential risk of damage to importantcollaterals distal to the occlusion when these are included in the dissected portion.


When important collaterals are compromised without achieving a haemodynamicallyviable channel in the main artery, the patient’s distal circulation will be compromised andurgent bypass surgery will be required to restore circulation to the distal leg. It istherefore crucially important that a dissection is not extended too far distal to theocclusion, particularly early on in a doctor’s experience.

Primary success rates of around 80% can be expected in any occluded segment with a low complication rate of 1–1.5% of major complications. In the femoropopliteal segment a patency rate of approximately 50% of all successful procedures can be expected at 4years.

In critical limb ischaemia, PSA appears to have made a major impact on the treatment of this condition, being applicable in up to two-thirds of the patients who present with this condition. The 1-year salvage rates are comparable to those achieved with distal bypass surgery.

On the basis of the data gathered from our experience of the technique of PSA, thetechnique can be expected to provide excellent results in the femoropopliteal and tibialsegments, the latter being for the treatment of chronic critical limb ischaemia. In the iliacvessels, experience has been rather limited, but success rates of 80% have been achieved.

Conclusion

PSA offers a number of advantages. In terms of the technique, no specialized equipmentor materials are necessary. It does not require extensive experience by the operators, theprocedure is inexpensive, it is relatively non-traumatic and does not preclude subsequent surgery should it fail to recanalize an occlusion.

It is applicable in a large number of situations where other techniques are likely to fail, for example in long occlusions, moderately calcified vessels, previously failedintraluminal approach and in hard occlusions of long standing. For long occlusions of thetibial artery, flush SFA occlusion, popliteal occlusions extending into the trifurcation, inthe presence of a large proximal collateral, common femoral occlusions extending intothe bifurcation, and when a perforation occurs in an attempted SFA recanalization, PSAis probably the only technique that allows a successful outcome to be achieved in the vastmajority of cases.

In critical limb ischaemia, the data from the study carried out at the Leicester Royal Infirmary strongly supports the use of angioplasty as a first-line treatment, with no major evidence that angioplasty is detrimental to later surgery if required. Angioplasty offers ashort hospital stay and 12-month limb salvage rates that equate with those achieved by surgery. It therefore offers an excellent alternative to distal reconstructive surgery for thetreatment of tibial artery occlusion in patients with critical limb ischaemia.

References

1. Dotter CT and Judkins MP. Transluminal treatment of arteriosclerotic obstruction: description of a new technique and a preliminary report of its application. Circulation 1964; 30:654–70.


2. Gruntzig A, Hopff H. Perkutame rekanalisation chronischer artererieller verschlusse mit einem neuen dilatationskatheter: modifikation der Dotter Technick. Deutsch Med Wochenschr 1974; 99: 2502–11.

3. Johnston KW, Rae M, Hogg Hohnstono SA et al. Five year results of a prospective study of percutaneous transluminal angioplasty. Ann Surg 1987; 206:403–13.

4. Johnston KW. Femoral and popliteal arteries: reanalysis of results of balloon angioplasty. Radiology 1992; 183:767–71.

5. Murray RR, Hewes RC, White RI et al. Long segment femoropopliteal stenosis: successful angioplasty a boon or a bust. Radiology 1987; 162:473–6.

6. Krepel VM, Van Andel GJ, Van Erp WF, Breslau PJ. Percutaneous angioplasty of the femoropopliteal artery: initial and long-term results. Radiology 1985; 156:325–8.

7. Capek P, Mclean GK, Berkowitz HD. Femoropopliteal angioplasty. Factors influencing long-term success. Circulation 1991; 83: 170–80.

8. Pell JP, Whyman MR, Fowkes FGR, Gillespie I, Ruckley CV. Trends in vascular surgery since the introduction of percutaneous transluminal angioplasty. Br J Surg 1994; 81:832–5.

9. Skotnicki SH. The vascular surgeon and transluminal angioplasty. Eur J Vasc Surg 1988; 2:143–4.

10. Motarjeme A. PTA and thrombolysis in leg salvage. J Endovasc Surg 1994; 1:81–7. 11. Bolia A, Miles KA, Brennan J, Bell PRF. Percutaneous transluminal angioplasty of

occlusions of the femoral and popliteal arteries by subintimal dissection. Cardiovasc Intervent Radiol 1990; 13:357–63.

12. London NJM, Srinivasan R, Sayers RD et al. Subintimal angioplasty of femoropopliteal artery occlusion: the long-term results. Eur J Vasc Surg 1994; 8:148–55.

13. Reekers JA, Kromhout JG, Jacobs MJHM. Percutaneous intentional extraluminal recanalization of the femoropopliteal artery. Eur J Vasc Surg 1994; 8:723–38.

14. Heenan SD, Vinnicombe SJ, Buckenham TM et al. Percutaneous transluminal angioplasty by a retrograde subintimal transpopliteal approach. Clin Radiol 1994; 49:824–8.

15. Nasim A, Sayers RD, Dunlop P et al. Intentional extraluminal recanalization of the femoropopliteal segment following perforation during percutaneous transluminal angioplasty. Eur J Endovasc 1996; 12:246–9.

16. Nasim A, Sayers RD, Bell PRF et al. Recanalization of the native artery following failure of a bypass graft. Eur J Vasc Surg 1995; 10: 125–7.

17. Berengoltz-zlochin SN, Mali WP, Borst C et al. Subintimal vesus intraluminal laser assisted recanalization of occluded femoropopliteal arteries: one year clinical and angiographic follow-up. J Vasc Intervent Radiol 1994; 5:689–96.

18. Bolia A, Sayers RD, Thompson MM, Bell PRF. Subintimal and intraluminal recanalization of occluded crural arteries by percutaneous balloon angioplasty. Eur J Vasc Surg 1994; 8:214–19.

19. Nydahl S, London NJM, Bolia A. Technical report: recanalization of all three infrapopliteal arteries by subintimal angioplasty. Clin Radiol 1996; 51:366–7.

20. Nydahl S, Hartshorne T, Bell PRF, Bolia A, London NJM. Subintimal angioplasty of infrapopliteal occlusions in critically ischaemic limbs. Eur J Vasc Endovasc Surg 1997; 14:212–16.

21. Varty K, Nydahl S, Butterworth P et al. Changes in the management of critical limb ischaemia. BRJ Surg 1996; 83:953–6.

22. Varty K, Nydahl S, Nasim A, Bolia A, Bell PRF, London NJM. Results of surgery


and angioplasty for the treatment of chronic severe lower limb ischaemia. Eur J Vasc Endovasc Surg 1998; 16:159–63.

23. Rosenthal E, Curry PVL, Reidy J. Subintimal dissection and false tract formation during successful laser thermal probe (‘hot tip’) angioplasty. J Intervent Radiol 1989; 4:19–22.

24. Belli A-M, Proctor AE, Cumberland DC. Peripheral vascular occlusions: mechanical recanalization with a metal laser probe after guide wire dissection. Radiology 1990; 176:539–41.

25. Bolia A, Brennan J, Bell PRF. Recanalization of femoropopliteal occlusions: improving success rate by subintimal recanalization (letter). Clin Radiol 1989; 40:325.

26. Bolia A, Fishwick G. Recanalization of iliac artery occlusion by subintimal dissection using the ipsilateral and the contralateral approach. Clin Radiol 1997; 52:684–7.

27. Murphy TP, Marks MJ, Webb MS. Use of a curved needle for true lumen re-entry during subintimal iliac artery revascularization. JVIR 1997; 8:633–6.

28. Murphy TP. Subintimal revascularization of chronic iliac artery occlusions. JVIR 1996; 7:47–51.

29. Bolia A, Nasim A, Bell PRF. Percutaneous extraluminal (subintimal) recanalization of a brachial artery occlusion following cardiac catheterization. Cardiovasc Intervent Radiol 1996; 19:184–6.

30. Bakal CW, Sprayegen S, Scheinbaum K et al. Percutaneous transluminal angioplasty of the infrapopliteal arteries: results in 53 patients. AJR 1990; 154:171–4.

31. Flueckiger F, Lammer J, Klein GE et al. Percutaneous transluminal angioplasty of crural arteries, Acta Radiol 1992; 33:152–5.

32. Schwarten DE. Clinical and anatomical considerations for nonoperative therapy in tibial disease and the results of angioplasty. Circulation 1991; 83(Suppl. 1): 86–90.

33. Schwarten DE, Cutliff WB. Arterial occlusive disease below the knee: treatment with percutaneous transluminal angioplasty performed with low-profile catheters and steerable guidewires. Radiology 1988; 169:71–4

34. Buckenham TM, Loh A, Dormandy JA, Taylor RS. Infrapopliteal angioplasty for limb salvage. Eur J Vasc Surg 1993; 7:21–5.

35. The vascular surgical society of Great Britain and Ireland. Critical limb ischaemia: management and outcome. Report of a national survey. Eur J Vasc Endovasc Surg 1995; 10:108–13.

36. Deutsch L-S. Techniques of percutaneous balloon angioplasty including aortoiliac and femoropopliteal systems: indications, results and complications. In: WS Moore, SS Ahn (eds), Endovascular Surgery. Philadelphia, PA: W.B. Saunders, 1989; 163–208.


Endovascular management of peripheral and visceral aneurysms

3 PHILIP J.HASLAM, FRANK P.McGRATH AND AUSTIN L.LEAHY

Introduction

The management of peripheral and visceral aneurysms and pseudoaneurysms haschanged considerably over the past 20 years. This has largely come about due toadvances in endovascular techniques, and imaging modalities such as ultrasound,computerized tomography (CT) and magnetic resonance imaging (MRI). Peripheralarterial pseudoaneurysms are presenting with increasing frequency, often caused byendovascular procedures such as coronary angio plasty and stenting. The treatmentprinciple is the same for all types of peripheral aneurysms. They are excluded from thecirculation, by whatever means, while maintaining an adequate circulation distally.Clearly, some aneurysms lend themselves more readily to endovascular techniques due totheir morphology and location, whereas others require open operation. The aim of thischapter is to heighten the aware’ ness of the reader to the range of endovascularmanagement options available.

Aetiology and natural history

Peripheral true aneurysms

The most common peripheral true aneurysms encountered are popliteal aneurysms. Thesemay remain asymptomatic for many years, but complications have been reported in 18–31% of patients.1 Popliteal aneurysms, for example, are usually found in men during theirsixth and seventh decades and are bilateral in up to 64%. They are also associated withischaemic heart disease and abdominal aortic aneurysm in up to 62%.2 Their importance stems from the high incidence of distal embolization and thrombosis they cause, leadingto critical ischaemia and limb loss (Figure 3.1). Other patients may present withclaudication, com pressive symptoms and occasionally rupture (Table 3.1). It is important that even asymptomatic popliteal aneurysms are treated because of the high risk ofcomplications, especially limb loss.

True femoral aneurysms are rare and, like popliteal aneurysms, are often bilateral and associated with

Figure 3.1 Popliteal aneurysm with thrombosis of the distal calf vessels (a) pre and (b) post-local thrombolysis with tissue plasminogen activator (TPA).

Table 3.1 Complications of aneurysms and pseudoaneurysms

1. Rupture

2. Thrombosis leading to distal vessel thrombosis

3. Distal embolization

4. Local pressure effects

● nerve compression

● ischaemia of surrounding tissues

● compression of vessels, leading to venous thrombosis


abdominal aortic aneurysms. The usual cause is atherosclerosis. Sapienza and colleaguesencountered only 22 cases over a 20-year period and 18 of these had associated noncontiguous abdominal aortic aneurysms.2 Other causes of peripheral arterialaneurysms include fibromuscular dysplasia, connective tissue disease includingneurofibromatosis, Kawasaki disease, giant cell arteritis, polyarteritis nodosa, Beςhet’s disease and Takayasu’s arteritis.3

Peripheral pseudoaneurysms

The most frequently encountered aneurysms in the peripheral circulation arepseudoaneurysms, which result from femoral artery catheterization. The majority occurfollowing coronary angiography, with the incidence depend’ ing on the complexity of the procedure. In cardiac intervention this varies from 0.2% for coronary angioplasty to 3.2%for stenting.4 Katzenschlager and colleagues recently reported a prospective study whereall patients underwent ultrasound Doppler study after angiography, and they foundpseudoaneurysms in 7.7% of patients.5

Peripheral pseudoaneurysms are most likely to occur when the patient is anticoagulated, receiving thrombolytic therapy, when a large sheath has been used, or dueto inadequate compression after the procedure. Indeed, Katzenschlager and coworkersmanaged to reduce the incidence to less than 1%, with a further 5 min of manualcompression once haemostasis had been achieved.

Traditionally, femoral pseudoaneurysms were thought to be unstable and were surgically repaired on discovery.6 There is now evidence that many small asymptomatic aneurysms will spontaneously thrombose and require no intervention.7, 8 In a series of16 pseudoaneurysms, Kent and colleagues found that nine spontaneously thrombosedafter a mean interval of 22 days. Most of the aneurysms that thrombosed were less than1.8cm in diameter. Thrombo sis did not occur in seven anticoagulated patients, and theserequired surgical repair.

Infection is another cause of pseudoaneurysms and noniatrogenic trauma can cause pseudoaneurysms in any location. These traumatic pseudoaneurysms can pose a difficultsurgical management problem due to associated trauma and contamination of tissuesadjacent to the pseudoaneurysm. In this situation, endovascular treatment from a distalaccess site is particularly attractive.

Visceral true aneurysms

The precise incidence of visceral true aneurysms is unknown. There are approximately3000 reported cases in the literature and the natural history is thought to be gradualexpansion leading to rupture, haemorrhage, and often death. In a series reported byStanley and coworkers, nearly 22% of all visceral artery aneurysms presented as clinicalemergencies, including 8.5% that resulted in death.9 The most commonly involved

● and arterial ischaemia

● obstructive jaundice

Endovascular management of peripheral and visceral aneurysms 75

vessels, in order of decreasing frequency, include splenic, hepatic, superior mesenteric,coeliac, gastroepiploic, jejunal-ilial-colic, pancreaticoduodenal, pancreatic, gastroduodenal, and inferior mesenteric arteries.10

In the past, visceral artery aneurysms were rarely diagnosed before rupture, but now they are frequently identified earlier using modern non-invasive imaging techniques. Up to 63% of patients may present with symptoms, usually of vague abdominal pain.Symptoms may include Quincke’s classic triad, described in 1871, of abdominal pain,haemobilia and obstructive jaundice caused by a hepatic artery aneurysm. Historically,visceral aneurysms were usually due to syphilis or mycoisis and patients commonlypresented with rupture. Current literature suggests that they are now generally due toarteriosclerosis/medial degeneration, leading to true aneurysms, which are mostlyasymptomatic.10–11

The main complication of visceral aneurysms is that of catastrophic rupture. Gastroduodenal artery (GDA) aneurysms are the most likely to present in this way, with amortality of up to 50%.10 Hepatic artery aneurysms are thought to rupture in less than20%, but the associated mortality may be as high as 35%.10, 12 These visceral aneurysms should therefore be managed aggressively.

Splenic artery aneurysms are the most common visceral aneurysms, but tend not to rupture if they are less than 2.5 cm in diameter. The greatest risk of rupture occurs duringthe third trimester of pregnancy, due to circulatory and hormonal changes. For thisreason, treatment of splenic artery aneurysm is indicated in pregnant patients or inwomen of child-bearing age who might become pregnant.13 Splenic artery aneurysms greater than 2.5 cm in diameter should also be treated, especially in younger patients.9

Visceral pseudoaneurysms

Symptomatic visceral pseudoaneursysms are typically due to trauma and inflammation.Iatrogenic trauma is becoming an increasingly common cause, mainly due to the greatercomplexity of hepatic and biliary interventions undertaken today.11 Examples include pseudoaneurysms of the hepatic artery secondary to percutaneous placement of biliarystents for malignant disease and pseudoaneurysms of the right hepatic artery followinglaparoscopic cholecystectomy.10, 14

Pseudoaneurysms of the gastroduodenal and pancreaticoduodenal arteries are three or four times more common in males and commonly associated with chronic pancreatitis.15

The cause is thought to involve autodegradation of the arterial walls secondary topancreatic elastase and trypsin action. It has been reported that up to 10% of patients withrecurrent pancreatitis have associated visceral aneurysms.16 Although it is not known at what stage these aneurysms will rupture, the mortality rate associated with free ruptureapproaches 50%.

Endovascular management of peripheral true aneurysms

Endovascular methods have a limited role in the current management of true femoral andpopliteal aneurysms. These are frequently fusiform in nature and are not suitable for


embolization techniques. There are several reports in the literature of the successfulplacement of uncovered and covered stents across popliteal and femoral aneurysms.17–19

Uncoveredstents presumably slowthe blood flow within the sack sufficiently to lead tothrombosis. The major problem is the unknown longevity of these stents when placedacross a joint. It is likely that in the long term they will fracture and neo-intimal hyperplasia will lead to stenosis. Stent design is constantly changing, with newer deviceshaving lower profiles, smaller introducer sheaths and more resistance to fracture. It islikely that covered stents will take a more prominent role in the future treatment ofperipheral aneurysms. Currently, the authors would only advocate the use of stent graftsin peripheral vessels if surgery was not a viable option.

Endovascular management of peripheral pseudoaneurysms

Ultrasound-guided compression

This technique is non-invasive and not strictly an endovascular procedure; however, ithas low morbidity and is successful in 75–97% of patients.4, 20, 21 It should be attempted in all femoral pseudoanuerysms prior to considering minimally invasive procedures.Figure 3.2 shows a suggested algorithm for the management of post-catheterization pseudoaneurysms.

Duplex ultrasound of the groin is initially performed to confirm the presence of apseudoaneurysm. The typical appearances are of a single or multi-loculated chamber, closely associated with the femoral artery and joined to it by a narrow tract of variablelength. Within the aneurysm, swirling blood gives the so-called Yin-Yang sign of red and blue, showing blood flowing in opposite directions (Figure 3.3). The Doppler gate can then be placed across the neck of the pseudoaneurysm and the to-and-fro flow can be demonstrated (Figure 3.4). Gradual pressure is then applied to the pseudoaneurysm withthe ultrasound probe until the lumen has been obliterated and no flow is demonstratedwithin the aneurysm cavity (Figure 3.5). It is important to attempt to maintain flow withinthe underlying vessel during this procedure, as compression may have to be applied forup to 60 min. This is often a painful procedure, requiring adequate sedation andanalgesia.

After 15 min the pressure on the probe is eased to check if the cavity has occluded. Ifflow returns, pressure should be reapplied for a further 10–15min. Compression may need to be applied for longer in anticoagulated patients. This procedure can be successfulin patients who have a pseudoaneurysm that has been present for many days. Factorsassociated with failure include high levels of anticoagulation, operator fatigue and severepain during the procedure, which may indicate femoral nerve compression.


Figure 3.2 Algorithm for the management of post-catheterization pseudoaneurysms.


Figure 3.3 A large pseudoaneurysm secondary to percutaneous biopsy within a failed renal transplant. The image shows the typical Yin-Yang sign.

Figure 3.4 A superficial femoral artery pseudoaneurysm post-coronary angiography demonstrating to-and-fro flow across the aneurysm neck.

Percutaneous tissue adhesive injection

This recently described technique involves the placement of an angioplasty balloonacross the neck of the pseudoaneurysm within the lumen of the artery, to occlude flowwithin the cavity. Following this, under ultrasound guidance, thrombin or tissue adhesive(thrombin, fibrinogen, aprotinin and antithrombin 3) is slowly injected percutaneously tocause very rapid thrombosis of the pseudoaneurysm (Figure 3.6).22


Figure 3.5 Femoral pseudoaneurysm precompression (left) and during ultrasound guided-compression (right). Note that the superficial femoral artery is not completely occluded.

Figure 3.6 Direct percutaneous treatment with either tissue adhesive/thrombin or coils.

The aneurysm neck is first precisely located using angiography. For a common femoral false aneurysm it is usually necessary to puncture the contralateral femoral artery andcross the aortic bifurcation. An antegrade puncture can be used for more distalaneurysms. A suitable-sized angioplasty balloon is placed across the neck of the


aneurysm and the balloon is inflated (Figure 3.7). Cessation of flow is confirmed withDoppler ultrasound. Throughout inflation, the balloon catheter is intermittently flushedwith heparinized saline to help prevent distal vessel thrombosis.

The aneurysm cavity is then directly punctured percutaneously under ultrasound control using an 18 G needle. The two components of the tissue adhesive are injected intothe aneurysm either sequentially or simultaneously using the supplied twin-syringe injector. The rapid development of highly reflective thrombus is observed withultrasound. This begins immediately and is seen to progress over approximately 15 min(Figure 3.8). The balloon catheter is deflated and the cavity is monitored with Doppler ultrasound for recurrent flow. A repeat angiogram is then performed either via the sheathor the catheter, to confirm aneurysm occlusion (Figure 3.9).

The technique described has several advantages over previously described techniques. The balloon virtually eliminates the chance of distal embolization and decreases thelikelihood of the tissue adhesive having any effects on the patient’s coagulation status. The tissue adhesive does not rely on the patient’s own clotting factors and is thereforemore likely to work in anticoagulated patients. The technique leaves a temporaryhaematoma, which is then degraded in the normal way by fibrinolysis and phagocytosis.

A similar technique was described by Cope and Zeit in 1986.23 They directly thrombosed aneurysms with percutaneous injections of diluted thrombin, but with noprotective balloon across the neck of the aneurysm. They treated four patients withaneurysms of the iliac femoral and peroneal arteries, and a true aneurysm of an accessoryhepatic artery. Liau and coworkers have also used thrombin injected directly into falseaneurysms without balloon protection.24 In the authors’ experience, the placement of an angioplasty balloon across the neck of the pseudoaneurysm is a useful modification.Instead of using thrombin, our preference is to use ‘tissue adhesive’. This is a commercially available product consisting of fibrinogen, thrombin, aprotinin, anti-thrombin 3 and calcium (Beriplast, P. Centeon Ltd, UK; Tisseel, Immuno AG, Austria).

Coil embolization

Another means of excluding aneurysms and pseudoaneurysms from the circulation is bypacking the aneurysm with coils. There is a variety of different types of coil suitable fordeployment through either standard 5 F catheters or micro-catheters, including the Tracker™ catheter (Boston Scientific Europe, Parc Industrial de Petit—Rechain B.4800, Verviers, France). Some of the most frequently used coils are Tornado coils (WilliamCook Europe, Bjaeverskov, Denmark). These consist of a platinum coiled spring withattached polyvinyl alcohol (PVA) strands, which promote thrombosis. Another morerecently introduced coil is the Target coil (Boston Scientific), which is a complex helical-fibred platinum coil. Other available coils are made from tungsten or stainless steel.These can additionally be soaked in thrombin before deployment. Coils may be placedwithin the aneurysm by one of two methods: catheter coil deployment or directpercutaneous coil deployment.


Figure 3.7 Superficial femoral pseudoaneurysm with angiogram (a) and road-mapped view (b), showing the angioplasty balloon inflated across the pseudoaneurysm neck.

Figure 3.8 The renal transplant pseudoaneurysm shown in Figure 3.3, post-thrombin injection. Note the presence of reflective thrombus within the aneurysm cavity.


Figure 3.9 Angiograms showing a superficial femoral pseudoaneurysm (a) pre- and (b) post-tissue adhesive injection.

In the first method, a catheter must be negotiated into the aneurysm cavity in a stable position so that the coils may be deployed with minimal risk of being displaced into theparent artery. The aneurysm neck must be of sufficient diameter to allow passage of thecatheter and the neck must arise at a suitable angle from the artery. Coil embolizationmay not be successful in high-flow situations, where there may be persistent flow aroundthe coils and the aneurysm may fail to thrombose. Additionally, coils should not beplaced in pseudoaneurysms that are in close proximity to joints, as flexion of the jointmay become uncomfortable (Figure 3.10). Furthermore, it is possible that the pressureeffect of the coils could cause problems with erosion through to the skin.

Direct percutaneous coil placement is an elegant way to occlude superficial aneurysmsor pseudoaneurysms.25 The aneurysm is first localized with angiography and can then be punctured percutaneously using a standard arterial puncture needle and an angiogram as aroad map. The authors prefer direct ultrasound-guided puncture. Following this, a guidewire is used to replace the needle with a sheath, or catheter, through which the coilscan be placed. Balloon occlusion of the aneurysm neck may be used to help preventinadvertent embolization of the underlying vessel.

The coils usually come preloaded on a stylet or within an introducer, which is used to place the coil within the catheter. The central stylet is then removed and the coil can bepushed into the catheter using a guidewire, or the coils can be flushed with normal salinealong the length of the catheter into the aneurysm. This latter technique has limitations asthere is no control over the rate of deployment of the coil and displacement of thecatheter tip could occur, resulting in the coil being placed in the feeding artery.


Figure 3.10 Coils placed via a catheter into a femoral pseudoaneurysm prior to our use of tissue adhesive injection.

Table 3.2 Covered stents

Advantages of covered stents

1. Placed

2. Minimally invasive

3. Reduced anaesthesia requirements

4. Reduced/absent dissection of traumatized area

5. Will provide haemostasis in the event of vessel/aneurysm rupture

6. Successful exclusion with a large aneurysm neck

Disadvantages of covered stents


Stents and stent grafts

Stent grafts have been used successfully for repair of abdominal aortic aneurysms since1991.26 Stent grafts provide an excellent means of excluding aneurysms andpseudoaneurysms from the peripheral circulation, particularly when there is a wide neck(Table 3.2; Figure 3.11). Stent graft placement is minimally invasive and they can beplaced from an easily accessible site remote from the location of trauma. Standardsurgical repair can be difficult in traumatized patients, due to inaccessibility of centralvessels, distorted anatomy due to pseudoaneurysm formation, AV fistulae, and venoushypertension.27

The earlier stents produced include numerous ‘homemade’ devices constructed by covering balloon expandable stents, such as the Palmaz stent, which is made fromstainless steel (Johnson & Johnson, New Broomswick, NJ, USA). These stents could besutured inside a segment of a standard polytetrafluoroethylene (PTFE) graft (W.L. Goreand Associates Inc., Elkton, MD, USA). The stent graft is then mounted on a balloonangioplasty catheter and delivered to the site of the aneurysm within a 12 F introducersheath. The advantage of such homemade devices is that they can be manufactured in avariety of different lengths and diameters. Of course, the graft itself need not be limitedto PTFE, and there are several reports in the literature of autologous brachial andsaphenous veins being used as coverings for such stents.28

Commercially available covered stents usually come preloaded on a long introducercatheter/sheath. These are frequently of large diameter and require the placement of alarge arterial sheath up to 12 F. There are two main varieties of covered stent. The first isa self-expanding stent, which is made using stainless steel or a metal with thermal memory properties such as nitinol. The covering, which is usually made of PTFE or woven dacron, is then applied to the stent. When the stent reaches body temperature, itattempts to regain its original annealed shape, thus giving a good radial force forexpansion and apposition against the vessel wall. The Wallgraft (Boston ScientificVascular) is a covered, self-expanding stent graft and is demonstrated in Figure 3.12.

The second type of stent requires balloon expansion for deployment. An example of this, the JOSTENT (JOMED) is demonstrated in Figure 3.13. The advantage of a balloon expandable stent is that it can be placed very precisely and can be expanded to therequired diameter with a high degree of radial force.

Stent deployment is straightforward, but accurate positioning is very important. The stent, preloaded on its catheter/sheath, is passed over the guidewire until it lies across theneck of the aneurysm. The outer sheath/ catheter is then slowly withdrawn over thecentral catheter, which allows the stent to expand. An intra-arterial injection of approximately 3000 units of heparin is usually given to help prevent thrombosis within

1. Unknown long-term durability

2. Neo-intimal hyperplasia reduces lumen diameter

3. Not suitable for small vessels due to hyperplasia

4. Not suitable for placement across a joint prone to high degrees of movement


the deployed stent. Some stents will require further balloon expansion to complete’ ly oppose the stent with vessel wall. Some of the more recently introduced stent grafts arecovered with a rolling membrane, which is withdrawn over the stent while holding thestent in position with forward pressure on its rigid central mount (Figure 3.12b). This variety does not initially require a long sheath to cover the neck of the aneurysm prior todeployment. Balloon expandable stents are readily deployed by inflation of the balloonupon which the stent has been mounted. This allows for highly accurate positioning.Figure 3.14 shows the placement of a covered stent in the subclavian artery.

All stents and stent grafts are prone to neointimal hyperplasia, leading to restenosis.This is particularly problematic in smaller vessels. Stents placed in certain locations, suchas the common femoral artery, popliteal artery and subclavian artery, are subject toconstant mechanical stress forces as the limb flexes and extends. It is therefore importantthat the interventionalist considers the likely life expectancy of both the stent and patient,and the relative risks of alternative open surgical procedures in the light of this. Theauthors would advocate that stent grafts are only used in peripheral vessels when thepatient is of poor surgical risk or the long-term patency of the vessel is not of primaryimportance (Table 3.2).

Figure 3.11 Stent graft aneurysm occlusion.


Figure 3.12 The Wallgraft (Boston Scientific, USA). (a) The stent part-ly deployed. (b) The central metal strut is held in place and the outer covering (with sideport for flushing) is slowly withdrawn, uncovering the self-expanding stent. (c) The fully expanded stent.


Figure 3.13 The JOSTENT balloon expandable peripheral stent graft (JOMED), Showing (a) the stent as it would be mounted on an angioplasty balloon for deployment, and (b) expanded following deployment.


Figure 3.14 Subclavian artery pseudoaneurysm secondary to tumour invasion. (a) and (b) demonstrate the aneurysm pre and post placement of a covered stent. (c) shows the opaque stent in position.


Surgical options

Some peripheral pseudoaneurysms are not suitable for endovascular techniques. Figure 3.15 shows a pseudoaneurysm caused by a small avulsion fracture (pull-off lesion) in ayoung soldier on a forced march. The sharp bone fragment has punctured the artery andthe expanding haematoma has displaced the vessel medially away from the fragment.Such a lesion can only be repaired surgically, since the underlying fragment must also beremoved.

Endovascular management of visceral arterial aneurysms and pseudoaneurysms

By their nature, visceral arteries are smaller than peripheral arteries, and it is necessary toconsider the various collateral pathways by which blood could fill the aneurysmretrogradely or supply distal tissues if the feeding vessel was occluded. For example, it ispossible to temporarily occlude a gastroduodenal artery aneurysm by placing a coilproximally. However, collateral circulation from the superior and inferiorpancreaticoduodenal arteries would cause refilling of the aneurysm and failure of theprocedure. These aneurysms therefore need to be treated by either complete occlusion ofthe aneurysm by packing it with coils or by placing coils distal to the neck, across theneck and proximal to the neck, thereby isolating the aneurysm from the circulation(Figure 3.16). In contrast, this technique should not be used for aneurysms of the common hepatic artery, as the patient would run a risk of hepatic necrosis. Location isprobably one of the most important features when considering therapy for visceral arteryaneurysms.

Hepatic artery

When hepatic artery aneurysms present with rupture and life-threatening haemorrhage, angiography should only be considered if the patient can be stabilized. Angiographyprovides the precise anatomy of the aneurysm and its collateral blood supply. Themorphology of the aneurysm is also important, as sacular aneurysms with a neck lendthemselves readily to percutaneous catheter embolization with coils, whereas fusiformaneurysms cannot be treated by this method without occlusion of the hepatic artery.Good-risk patients with hepatic artery aneurysms are better treated by open surgicalaneurysmectomy, followed by reconstruction with a reversed saphenous vein graft.29


Figure 3.15 Pseudoaneurysm of the superficial femoral artery due to an avulsion fracture of the distal femur.


Figure 3.16 (a) CT; (b) ultrasound; and (c) angiogram of a gastroduodenal artery pseudoaneurysm due to pancreatitis. (d) Shows the coils in situ occluding the pseudoaneurysm.

Intrahepatic aneurysms, which are more often pseudoaneurysms resulting from trauma, are very difficult to treat surgically. Prior to the development of catheter embolizationtechniques these were treated by liver resection, with substantial morbidity. Intrahepaticaneurysms arising from lobar and segmental branches of the hepatic artery can usually beselectively embolized using either a 5 F catheter or a micro-catheter (Tracker™ and Fast-Tracker™, passed through a 5 F guiding catheter). More peripheral aneurysms can be treated with complete occlusion of the parent vessel, with only minimal adverse effectson the hepatic paren chyma (Figure 3.17). These should be followed up with duplexultrasound or contrast-enhanced CT to detect any residual flow within the aneurysmcavity. Lumsden and colleagues would advocate treatment of all extra hepatic aneurysmsgreater than 2 cm in diameter, as these are thought to be at increased risk of rupture.Intrahepatic pseudoaneurysms greater than 1 cm in diameter should be embolized withcoils or Gelfoam plugs (Pharmacia and Upjohn, Kalamazoo, MI, USA). The directtranshepatic percutaneous approach can also be used for the placement of coils in aperipheral intrahepatic aneurysm, but it should be second-line treatment after failed transarterial embolization.30


Splenic artery

Splenic artery aneurysms are the most commonly encountered type of visceral arteryaneurysm. The technique of choice for embolizing splenic aneurysms is catheter coilembolization, with packing of the aneurysm sack. This frequently leads to occlusion ofthe splenic artery at the point of origin of the aneurysm; however, there is usually a goodcollateral arterial supply to the distal splenic artery, which prevents significant splenicinfarction. 31 It is also possible to use gelfoam with smaller aneurysms. Thedisadvantages of gelfoam are that as a particulate material it could be dis lodged from the aneurysm sac, causing distal embolization of the splenic bed.Furthermore, it often requires high pressure to inject the gelfoam, so there can be a risk ofrupture during the procedure.

Superior mesenteric artery (SMA)

Traditionally, superior mesenteric artery (SMA) aneurysms have been treated withsurgical resection. Aneurysms of the SMA must be treated with extra caution due to therisk of small and large bowel infarction from inadvertent occlusion of the vessel. Theonly endovascular technique that can realistically be considered for SMA aneurysms isthat of catheter coil embolization, and in this case the aneurysm must be saccular, with aneck that can be selectively catheterized for coil deployment (Figure 3.18). This is a difficult procedure, made hazardous by the risk of vessel occlusion and the theoreticalrisk of aneurysm rupture during coil deployment.

Gastroduodenal artery and pancreaticoduodenal arteries

Aneurysms of the gastroduodenal and pancreaticoduodenal arteries are most often causedby pancreatitis and atherosclerosis. True aneurysms are more frequently associated withvisceral occlusive disease involving the coeliac axis and are distributed equally betweenthe sexes. Pseudoaneurysms are three to four times more common in males andfrequently associated with chronic pancreatitis. The usual management of suchaneurysms has been open surgery, with the most common technique involving ligation ofboth antegrade and retrograde feeding vessels, accompanied by a pancreatic drainageprocedure when associated with a pseudocyst. Embolization is associated with asignificantly lower morbidity and mortality than surgery.15

The gastroduodenal and pancreaticoduodenal arteries are vessels that can safely be occluded, as they have multiple collaterals. For the same reason, it is also important thatthe interventionalist does not merely occlude the parent vessel proximal to the aneurysmneck, as it is almost inevitable that a collateral pathway will be established, thus refillingthe aneurysm in a retrograde direction. This may not be immediately apparent. If theaneurysm itself cannot be packed with coils due to either its size or location, then it canbe successfully excluded from the circulation by placing coils proximal and distal to theaneurysm neck or across the aneurysm neck (Figure 3.16d).


Figure 3.17 Embolization of a peripheral hepatic pseudoaneurysm using a micro-catheter passed through a 5F guiding catheter.


Figure 3.18 This 32-year-old soldier presented with haematemesis and melaena due to erosion of a superior mesenteric artery pseudoaneurysm into the duodenum. The pseudoaneurysm (a) arose from the site of a jump graft used to repair a previous pseudoaneurysm following a knife wound. (b) shows its precise origin and emphasizes the importance of selective angiography for diagnosis. (c) shows coils placed within the sac. Note that there is initially persistent flow around the coils. Subsequent ultrasound confirmed aneurysm thrombosis.

Conclusion

The endovascular treatment of peripheral and visceral aneurysms/pseudoaneurysms is achallenging area. In most situations the aneurysm must be excluded from the circulation.When the parent vessel can be safely sacrificed, then it may be occluded completely withcoils or other embolization material. Saccular aneurysms can be thrombosed with tissueadhesive, packed with coils via a catheter, or coils placed percutaneously. Fusiformaneurysms are not suited to these methods, but can be excluded by the placement of acovered stent. Advances in stent design are likely to lead to their more frequent use in themanagement of peripheral aneurysms and pseudoaneurysms. Each patient must becarefully assessed clinically and with good highquality imaging prior to making adecision as to the most appropriate therapy.

References

1. Carpenter JP, Barker Clyde F, Roberts B, Berkowitz K, Lusk EJ, Perloff LJ. Popliteal artery aneurysms: current management and outcome. J Vasc Surg 1994; 19:65–73.

2. Sapienza P, Mingoli A, Feldhaus RJ et al. Femoral aneurysms: long term follow-up and results of surgical treatment. Cardiovasc Surg 1996; 4:181–4.

3. Shipolini AR, Wolfe JHN. Case report fibro muscular dysplasia and aneurysm formation in the brachial artery. Eur J Vasc Surg 1993; 7: 740–3.

4. Chatterjee T, Do DD, Kaufmann U et al. Ultrasound-guided compression repair for treatment of femoral artery pseudoaneurysm: acute and follow-up results. Cathe Cardiovasc Diagn 1996; 38:335–40.

5. Katzenschlager R, Ugurluoglu A, Ahmadi A et al. Incidence of pseudoaneurysm after diagnostic and therapeutic angiography. Radiology 1995; 195:463–6.

6. Mills JL, Wiederman JE, Robinson JG, Hallett JW. Minimising mortality and morbidity from iatrogenic arterial injuries: the need for early recognition and prompt repair. J Vasc Surg 1986; 4:22–7.

7. Kresowik TF, Khoury MD, Miller BV et al. A prospective study of the incidence and natural history of femoral vascular complications after percutaneous transluminal coronary angioplasty. J Vasc Surg 1991; 13:328–35.

8. Kent KG, McArdle CR, Kennedy B, Baim DS, Anninos E, Skillman JJ. A prospective study of the clinical outcome of femoral pseudoaneurysms and arteriovenous fistulas induced by arterial puncture. J Vasc Surg 1993; 17:125–33.


9. Stanley JC, Wakefield TW, Graham LM, Whitehouse WM, Zelenock GB, Lindenauer SM. Clinical importance and management splanchnic artery aneurysms. J Vasc Surg 1986; 3:836–40.

10. Carr SC, Pearce WH, Vogelzang RL, McCarthy WJ, Nemcek AE, Yao JST. Current management of visceral artery aneurysms. Surgery 1996; 120:627–34.

11. Graham ML, Stanley JC, Whitehouse WM et al. Celiac artery aneurysms: historic (1745–1949) versus contemporary (1950–1984) dif ferences in etiology and clinical importance. J Vasc Surg 1985; 2: 757–64.

12. Graham LM, Mesh CI. Celiac, hepatic, and splenic artery aneurysms. In: CB Ernst, JC Stanley (eds). Current theory in vascular surgery. 3rd edition. St Louis, MO: Mosby Year Book Inc., 1995, 714–8.

13. Holdsworth RJ, Gunn A. Ruptured splenic artery aneurysm in pregnancy: a review. BRJ Obstet Gynaecol 1992; 99:595–7.

14. Siablis D, Tepetes K, Vasiou K, Karnabatidis D, Perifanos S, Tzorakoleftherakis E. Hepatic artery pseudoaneurysm following laparoscopic cholecystectomy: transcatheter intraarterial embolization. Hepatogastroenterology 1996; 43:1343–6.

15. Coll DP, Ierardi R, Kerstein MD, Yost S, Wilson A, Matsumoto T. Aneurysms of the pancreaticoduodenal arteries: a change in management. Ann Vasc Surg 1998; 12:286–91.

16. White AF, Baum S, Buranasiri S. Aneurysms secondary to pancreatitis. Am J Roentgenol 1976; 127:393–6.

17. Kudelko PE 2nd, Alfaro-Franco C, Diethrich EB, Krajcer Z. Successful endoluminal repair of a popliteal artery aneurysm using the Wallgraft endoprosthesis. J Endovasc Surg 1998; 5:373–7.

18. Manns RA, Duffield RG. Case report: intravascular stenting across a false aneurysm of the popliteal artery. Clin Radiol 1997; 52:151–3.

19. Beregi JP, Prat A, Willoteaux S, Vasseur MA, Boularand V, Desmoucelle F. Covered stents in the treatment of peripheral arterial aneurysms: procedural results and mid term follow-up. Cardiovasc Intervent Radiol 1999; 22:13–19.

20. Fellmeth BD, Roberts AC, Bookstein JJ et al. Postangiographic femoral artery injuries: non surgical repair with US-guided compression [see comments]. Radiology 1991; 178:671–5.

21. Kazmers A, Meeker C, Nofz K et al. Non-operative therapy for postcatheterization femoral artery pseudoaneurysms. Am Surg 1997; 63: 199–204.

22. Loose HW, Haslam PJ. The management of peripheral arterial aneurysms using percutaneous injection of fibrin adhesive. Br J Radiol 1998; 71:1255–9.

23. Cope C, Zeit R. Coagulation of aneurysms by direct percutaneous thrombin injection. AJR 1986; 147:383–7.

24. Liau CS, Ho FM, Chien MF, Lee TY. Treatment of eatrogenic femoral artery pseudoaneurysm with percutaneous thrombin injection. J Vasc Surg 1997; 26:18–23.

25. Murray A, Buckenham T, Belli AM. Direct puncture coil embolisation of iatrogenic pseudoaneurysm. J Interven Radiol 1994; 9:183–6.

26. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991; 5:491–9.

27. Marin ML, Vieth FJ, Panetta TF et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vasc Surg 1994; 20:466–73.

28. Sullivan TM, Bacharach JM, Perl J, Gray B. Endovascular management of unusual aneurysms of the axillary and subclavian arteries. J Endovasc Surg 1996; 3:389–95.

29. Lumsden AB, Mattar SG, Allen RC, Bacha EA. Hepatic artery aneurysms: the


management of 22 patients. J Surg Res 1996; 60: 345–50. 30. Goldblatt M, Golden AR, Chaff MI. Percutaneous embolisation for the management

of hepatic artery aneurysms. Gastroenterology 1977; 73:1142–6. 31. Reidy JF, Rowe PH, Ellis FG. Technical report: splenic artery aneurysm

embolisation—the preferred technique to surgery. Clin Radiol 1990; 41:281–2.


Ultrasound-guided angioplasty

4 N.GUY FISHWICK

Duplex-guided angioplasty is an alternative to conventional angioplasty techniques, utilizing the same wires and catheters as conventional techniques and, in place of aradiographer and screening equipment, simply requires a good colour duplex ultrasoundmachine and a competent vascular technologist/sonographer. However, the technique isnot as widely applicable as conventional techniques.

In some patients, use of iodinated contrast media confers higher than usual risks, for example, in patients who have had severe contrast reactions or those with incipient renalfailure. In such circumstances, available choices for patients requiring intervention forperipheral vascular disease are:

• conventional techniques accepting the higher risks; • CO2 as a contrast agent for angiography and intervention; • magnetic resonance angiography (MRA) for diagnosis (and in the future probably for

intervention); or • colour duplex ultrasound in place of angiography and to guide intervention.

CO2 is a useful alternative to iodinated contrast media,1 but delivery systems are expensive and in centres where the facility is not available colour duplex ultrasoundoffers another alternative. Several articles have been published in recent years confirmingthe accuracy and outlining the limitations of duplex ultrasound for diagnosis in peripheralvascular disease.2–11 Manycentres, including ourown (Leicester Royal Infirmary) nowrarely perform diagnostic angiography. More recently descriptions of techniques andreports of the use of duplex ultrasound to guide angioplasty, rather than just as adiagnostic tool, have appeared from several centres.12–15

Cluley12, 13 and Ramaswami14 both describe a technique utilizing a balloon catheter called the Echo-Mark system. This is a standard angioplasty balloon catheter, which has apiezo-electric transducer in the mid-balloon region. This acts as an omnidirectionalreceiver. When integrated with a duplex ultrasound system by an interface it allowsvisualization of the position of the catheter by superimposing a mark on the B-mode image, even where the catheter itself is not directly visible on the image.

Our own technique and a similar technique described by Katzenschlager15 utilizes ordinary wires and balloon catheters similar to those stocked in all interventional suites. Itis not applicable to all lesions, since they must be visible on ultrasound. Obesity, bowelgas and heavy arterial wall calcification limit its application in iliac lesions, and heavycalcification in the artery wall can also be limiting in the femoropopliteal segment. Wherea lesion is visible, however, it is usually straightforward to carry out angioplasty, guided

only by ultrasound. Applying the method to stenoses in the crural vessels is more difficultbecause they can be difficult to scan in a supine patient. However, it is still possible toscan behind the upper calf with knee flexed and to manipulate wires and catheters underultrasound guidance.

Technique

The ultrasound machine we use is an ATL Ultramark 9 HDI with 3.5MHz and 5MHzbroad frequency probes. Patients have an arterial ‘map’ produced, marking lesion sites and severity (Figure 4.1) when they are seen initially. Immediately prior to treatmentlesions are rescanned (Figure 4.2a, b) to ensure that there has been no change since initialscanning. The ankle-brachial pressure index (ABPI) is measured for follow-up purposes and patency or otherwise of run off vessels confirmed, since during the procedure thiswill determine whether or not significant embolic complications have occurred. With thepatient supine the groin is scanned to assess the common femoral artery bifurcation andits level. The site of the lesion(s) to be treated is marked on the patient’s skin to aid rapid identification of the site(s) during the proce-dure (Figure 4.3a). The diameter of the normal artery proximal to the lesion is measured to determine appropriate balloon size.The groin is cleaned and draped and a sterile probe cover applied to the ultrasound probe(Figure 4.3b).

We tend to clean the skin to below the puncture site and drape the patient completely,except for the leg to be treated. The leg below the puncture site is regarded as a ‘dirty’ area and all catheter manipulations are performed on the draped area above the puncturesite. For treating iliac lesions, the reverse applies.

The puncture technique is a standard single-wall punc-ture with a one-part needle. This is not usually directed by ultrasound (in the author’s personal preference), but once the artery has been punctured the sterile cover on the probe is useful so that for antegradepunctures manipulations of the guidewire into the superficial femoral artery (SFA) can beobserved and directed. A straight tip 0.035" guidewire and appropriately sized arterialsheath are directed into the artery. The wire and a tapered-tip predilating catheter are then directed across the lesion under ultrasound guidance. The wire is clearly visible withinthe artery (Figure 4.4a). The predilating catheter is less so while it has the wire within it (Figure 4.4b), although if the wire is withdrawn it becomes clearly seen (Figure 4.4c). Since the wire becomes less easy to observe as it is covered by the catheter, it isimportant to keep the wire tip visible ahead of the catheter. The coordination ofinterventionist manipulating and sonographer following those manipulations to keep thewire tip in view is the most difficult aspect of the procedure initially, but with practicebecomes very straightforward. Once across the lesion, 5000 units of heparin are given viathe sheath or catheter and then, with the wire across the lesion and held fixed, anappropriately sized balloon catheter can be positioned in the lesion. We have used the MSClassique [Meadox, UK (Boston Scientific, UK)] and more recently the Schneider Smash[Schneider, UK (Boston Scientific, UK)] balloons. The radio-opaque markers on both these balloons have proved to be clearly visible to ultrasound, allowing accurateplacement of the balloon. The balloon is clearly seen as it is inflated and deflated with


saline (Figure 4.4d). After angioplasty the balloon is removed from the artery, leaving thewire in position. The flow velocities in the treated segment and adjacent segments arethen measured to assess the adequacy of the treatment (Figure 4.2c, d). Once angioplasty is judged satisfactory on haemodynamic criteria, the run-off vessels are checked for patency and adequate flow and the wire and sheath can be withdrawn from the artery andhaemostasis achieved by pressure on the puncture site.

Figure 4.1 After initial consultation, patients have a diagnostic duplex ultrasound assessment, not angiography. Findings are summarized on an arterial ‘map’, along with any relevant comments.

Ultrasound-guided angioplasty 101

Figure 4.2 Colour-flow images and doppler traces at the superficial femoral artery/lesion demonstrated in Figure 4.1. (a) (a) The proximal end of the occlusion, with a collateral vessel arising posteriorly; (b) the damped doppler waveform just proximal to the occlusion; (c) after angioplasty the lumen is restored, with no obvious turbulence; (d) the normal pattern three-phase waveform is restored.


Figure 4.3 Patient preparation. (a) The common femoral artery bifurcation is viewed for its location after marking the lesion site on the skin and measuring vessel diameter for (b) A sterile probe cover is used so that the probe can be brought close to the puncture site for catheter manipulation, but the leg distal to the puncture is not draped for ease of access of the sonographer and is regarded as a ‘dirty’ area. All catheter exchanges and manipulations are performed on the sterile drapes above the puncture site.

When assessing the result of an angioplasty, visual criteria based on angiography areused to determine a satisfactory result. When the procedure is ultrasound guided, the end-point has to be based on velocity ratios. What constitutes a satisfactory result based onpeak systolic velocity (PSV) ratios is not proven. We selected a PSV ratio of 1.5 or lessas a satisfactory immediate result. Mewissen16 showed that after conventional percutaneous transluminal angioplasty (PTA) a ‘satisfactory’ angiographic result can, in fact, hide a significant residual flow abnormality with PSV ratios greater than 2.0(equating to approximately 50% area stenosis17 though this approximation is questionedimmediately post-angioplasty).18 Mewissen16 also demonstrated that such a residual flow disturbance correlates with greater than 80% PTA failure within 1 year. However their‘immediate’ PSV ratio was actually measured 24 h postprocedure. Several studies have since looked at the value of ultrasound predicting durability of PTA up to 1 year. Mosthave looked at other factors in addition to post-angioplasty PSV ratios. The majority19–22

concur with the finding thata significant residual flow disturbance with a PSV ratiogreater than 2.0 correlates with higher rates of early failure. There are, however,conflicting studies,15, 23 although doubt has been cast on their validity.24 Also, in only one of all of these studies were PSV ratios actually measured at the time of angioplasty.In the others, ‘immediate’ measurements are actually 12–48 h post-procedure.


Figure 4.4 The same case as the previous figures (4 cm mid superficial femoral artery occlusion). (a) The tip of the guidewire is clearly seen in the lumen just proximal to the occlusion. (b) The wire tip is curled against the occlusion, but it is less visible behind the tip, where it is within the predilating catheter. (c) The predilating catheter without the wire is seen adjacent to the anterior wall of the superficial femoral artery. (d) The proximal end of the balloon is seen inflated by sterile saline in the occlusion. Inflation and deflation are very easily observed in real-time imaging.

In the absence of definite evidence, it seems reasonable to conclude that a residual stenosis after PTA predicts a likelihood of early failure but a good duplex result does notguarantee long-term success, and to reduce the number of early failures restoration of thePSV ratio towards 1.0 is likely to be desirable. This is supported by a study looking at thenatural progression of untreated lesions,25 which shows that the lower the PSV ratio themore likely it is that a lesion will be static or only slowly progressive, whereas once thePSV ratio is greater than 3.0 progression to occlusion is likely to be rapid, althoughmechanisms of progression may be different in untreated lesions.


So, although we set a PSV ratio of less than 1.5 as an end-point, this is set somewhat empirically but based on the available evidence. Our own data (see below) support thefindings of other studies22,26–28 that there are complex changes in the 30 days after angioplasty and the immediate haemodynamic changes will alter in the weeks followingangioplasty in a manner that is not predictable.

Evaluation of the technique

To evaluate the technique we selected lesions in 50 limbs (45 patients, 55 lesions). Mostof these initial cases were short, isolated stenoses in the superficial femoral artery (SFA)or popliteal artery in claudicants, but included four iliac artery lesions, threeasymptomatic vein graft stenoses and one posterior tibial artery lesion. Two lesions wereshort occlusions and three patients had critical ischaemia. The claudicants in the grouprepresented 58% of claudicants with stenotic disease who presented for angioplastyduring the study period. Since the study, we have treated more occlusions by bothluminal and subintimal angioplasty using ultrasound guidance. The longest occlusion wehave treated is 15 cm in an SFA (ultrasound guided, subintimal).

Patients had pre-procedure, immediate post-procedure and 30-day follow-up ABPI and PSV ratios measured. The results for the study group based on these figures aresummarized in Figures 4.5 and 4.6. An immediate improvement in ABPI from a medianvalue of 0.86 (range 0.52–1.10) to 1.00 (range 0.85–1.30) is demonstrated, and this had further improved to 1.1 (range 0.8–1.4) at follow-up. The median PSV ratio prior to dilatation was 4.2 (range 2.0–10.0) and fell to 1.1 (range 1.0–3.2) immediately post dilatation. Although the ABPI showed further improvement at followup, the median PSVratio had slightly increased again to 1.2 (range 1.0–3.0). Interestingly, of 36 limbs in which there was further increase in the ABPI at follow-up compared with the immediate post-dilatation measure, 10 (28%) showed a paradoxical rise in the PSV ratio.

During the study, we also noted that 85% of lesions require only one or two (usuallytwo) inflations of the balloon to restore the PSV ratio at the lesion site to <1.5. In theremaining 15%, five inflations were required and in one case it was not possible toimprove the PSV ratio to better than 3.2, despite repeated inflations. Interestingly, in thispatient at the 30-day follow-up the PSV ratio had improved to 1.7, and at 4 years he hasnot represented with symptoms.


Figure 4.5 Graphic summary of the changes and trend of ankle-brachial pressure index for measurements pre—angioplasty, immediately post-angioplasty and at 30-day follow-up.


Figure 4.6 Graphic summary of peak systolic velocity ratio changes and trend for measurements pre-angioplasty, immediately post-angioplasty and at 30-day follow-up.

To date, we have not had to deal with any complications during ultrasound-guided procedures. This probably reflects the patient selection more than anything else.Although the majority of these procedures has been performed in a day-case operating theatre rather than an X-ray screening room, a mobile C-arm with digital subtraction has been available, although so far it has not been required. It is now 4 years since the studyand only three limbs (6%) have required further intervention for symptomatic recurrence.


Keypoints

1. Lesions must be visible on ultrasound. 2. They must remain visible with the patient positioned for treatment. 3. Operator and sonographer must develop a mutual understanding/coordination.

The technique of ultrasound-guided angioplasty is straightforward but not applicable in all cases. For anyone attempting it, like any new technique it seems quite alien at first butrapidly becomes familiar. Careful case selection is important for the first few cases performed. It is a very useful technique for treating patients with deteriorating renalfunction or previous contrast reactions. Whether the haemodynamic information availablefrom duplex ultrasound at the time of the procedure can be used to predict outcome is stillopen to debate.

References

1. Back MR. Angiography with carbon dioxide (CO2). Review. Surg Clin North Am 1998; 4:575–91.

2. Edwards JM, Coldwell DM, Goldman ML, Strandness DE. The role of duplex scanning in the selection of patients for transluminal angioplasty. J Vasc Surg 1991; 13:69–4

3. Van der Heijden FHWM, Legemate DA, Van Leeuwen MS et al. Value of duplex scanning in selection of patients for percutaneous transluminal angioplasty. Eur J Vasc Surg 1993; 7:71–6.

4. Vashisht R, Ellis MR, Skidmore C et al. Colour coded duplex ultrasonography in the selection of patients for endovascular surgery. Br J Surg 1992; 79:1030–1.

5. Davis AH, Magee TR, Parry R. Duplex ultrasonography and pulse generated run-off in selecting claudicants for femoropopliteal angioplasty. Br J Surg 1992; 79:894–6.

6. Collier P, Wilcox G, Brooks D et al. Improved patient selection for angioplasty utilising colour doppler imaging. Am J Surg 1990; 160: 171–4.

7. de Smet AAEA, Vissier K, Kitslar PJEHM. Duplex scanning for grading aorto-iliac obstructive disease and guiding treatment. Eur J Vasc Surg 1994; 8:711–15.

8. Aly S, Sommerville K, Adiseshiah M et al. Comparison of duplex imaging and arteiography in the evaluation of lower limb arteries. Br J Surg 1998; 85:1009–12.

9. Sensier Y, Hartshorne T, Thrush A, Nydahl S, Boia A, London NJM. A prospective comparison of lower limb colour coded duplex scanning with arteriography. Eur J Vasc Surg 1996; 11:170–5.

10. Pemberton M, Nydahl S, Hartshorne T, Naylor ARN, Bell PRF, London NJM. Can lower limb vascular reconstruction be based on colour duplex imaging alone. Eur J Vasc. Surg 1996; 12:452–4.

11. Pemberton M, Nydahl S, Hartshorne T, Naylor ARN, Bell PRF, London NJM. Colour coded duplex imaging can safely replace diagnostic arteriography in patients with lower limb arterial disease. Br J Surg 1996; 83:1725–8.

12. Cluley SR, Brener BJ, Hollier LM et al. Ultrasound-guided balloon angioplasty is a new technique for vascular surgeons. Am J Surg 1991; 161:117–21.


13. Cluley SR, Brener BJ, Hollier LH et al. Transcutaneous ultrasonography can be used to guide and monitor balloon angioplasty. J Vasc Surg 1993; 17:23–31.

14. Ramaswami G, Al-kotoubi A, Nicolaides AN et al. Duplex controlled angioplasty. Eur J Vasc Surg 1994; 8:457–63.

15. Katzenschlagen R, AhmadiA, Minar E et al. Femeropopliteal artery: initial and 6 month results of colour duplex US-guided percutaneous transluminal angioplasty. Radiology 1996; 199:331–4.

16. Mewissen MW, Kinney EV, Bandyk DF et al. The role of duplex scanning versus angiography in predicting the outcome after balloon angioplasty in the femoropopliteal artery. J Vasc Surg 1992; 15: 860–6.

17. Ranke C, Creutzig A, Alexander K. Duplex scanning of the peripheral arteries: correlation of the peak velocity ratio with angiographic diameter reduction. Ultrasound Med Biol 1992; 18:433–40.

18. Pasterkamp G, Spijkerboer AM, Mali WPTMM. Residual stenosis determined by intravascular ultrasound and duplex ultrasound after balloon angioplasty of the superficial femoral artery. Ultrasound Med Biol 1996; 22:801–6.

19. Spijkerboer AM, Nass PC, de Valois JC et al. Evaluation of femoropopliteal arteries with duplex ultrasound after angioplasty. Can we predict results at 1 year? Eur J Vasc Endovasc Surg 1996; 12: 418–23.

20. Nayamekye I, Sommerville K, Raphael M et al. Non invasive/ assessment of arterial stenoses in angioplasty surveillence: a comparison with angiography. Eur J Vasc Endovasc Surg 1996; 12: 471–81.

21. Voght KC, Just S, Rasmussen JG, Schroeder TV. Prediction of outcome after femoropopliteal balloon angioplasty by intravascular ultrasound. Eur J Vasc Endovasc Surg 1997; 13:563–8.

22. van der Lugt A, Gussenhoven EJ, Pasterkamp G et al. Intravascular ultrasound predictors of restenosis after balloon angioplasty of the femeropopliteal artery. Eur J Vasc Endovasc Surg 1998; 16:110–19.

23. Sacks D, Robinson ML, Summers TA, Marinelli DL. The value of duplex sonography after periphal artery angioplasty in predicting subacute restenosis. AJR 1994; 162:179–83.

24. Yucel E. Femoropopliteal angioplasty: can we predict success with duplex sonography? AJR 1994; 162:184–6.

25. Whyman MR, Ruckley CV, Fowkes FGR. A prospective study of the natural history of femoropopliteal artery stenosis using duplex ultrasound. Eur J Vasc Surg 1993; 7:444–7.

26. Karanya ND, Loosemore TM, Ray SA et al. The differences in early haemodynamic between surgery and angioplasty after successful reopening of the superficial femoral artery. Eur J Vasc Surg 1993; 7: 717–19.

27. Henderson J, Chambers J, Jeddy TA et al. Serial investigation of balloon angioplasty induced changes in the superficial femoral artery using colour duplex ultrasonography. Brit J Radiology 1994; 67: 546–51.

28. Ramaswami G, Dhanjil S, Nicolaides AN et al. Restenosis after percutaneous transluminal angioplasty. Am JSurgery 1998; 176: 102–9.


Endoluminal approaches in limb revascularization: techniques and strategies

5 FRANK J.CRIADO, ERIC WELLONS, NADEEM A.PAROYA, OMRAN

ABUL-KHOUDOUD AND JOAO A.LOPES

Catheter-based endoluminal techniques are important components of the therapeutic armamentarium to revascularize ischaemic limbs. They are especially useful in thetreatment of focal disease of proximal inflow arteries that tend to respond quite well toendoluminal recanalization. More distal, multilevel occlusion continues to requiresurgical bypass grafting for optimal revascularization and limb salvage.

Indications and techniques strategies

Upper limbs

Percutaneous endovascular intervention is highly successful (and durable) in thetreatment of focal lesions of the subclavian arteries where atherosclerotic stenoses andshort occlusions often develop.1 The left subclavian artery is affected more commonly than the right. Indications for revascularization are well established (Table 5.1); prophylactic repair is a newly proposed but not yet validated indication.

Endoluminal approaches and strategies

Stenosis

Stenosis of the proximal segment of the subclavian artery can be approached bytransfemoral antegrade or retrograde transbrachial intervention. The latter is quite simpleand effective, and our choice whenever feasible.

Interventional techniques

• Retrograde transbrachial (Figures 5.1 and 5.2):

– percutaneous puncture of the brachial artery at the antecubital fossa; – over-the-wire insertion of 6–7 F radiopaque-tip long sheath; – retrograde (reflux) angiography; – wire crossing of lesion into the aortic arch;

– percutaneous transluminal angioplasty (PTA)/stent placement.

Knowledge of the precise anatomical origin of the subclavian artery off the aortic arch isvery important for accu-rate placement, but frequently difficult to determine. Combinedfemoral access for arch aortography and, par-ticularly, intravascular ultrasound imagingare helpful in this regard.

Anticoagulation with small doses of 2000–3000 units of heparin are used during theintervention; more aggressive

Table 5.1 Indications for revascularization

Subclavian arteries

Occlusions/stenosis causing:

● Arm claudication

● Digital embolization

● Symptoms of VBI

● In preparation for LIMA procedure (or to-correct coronary-subclavian steal)

● Prophylactic to preserve IMA (controversial)

– previous CABG

– severe CAD

Innominate and common carotid

Haemodynamically critical lesions (>75%)

Symptomatic lesions:

● TIA

● Amaurosis fugax

● Prior stroke without major sequelae

CABG: coronary artery bypass graft; CAD:coronary artery disease; VBI; vertebral-basilar insufficiency; LIMA: coronary bypass using left internal mammary artery; TIA: transient ischaemic attack.

Endoluminal approaches in limb revascularization: techniques and strategies 111

Figure 5.1 Percutaneous puncture of left brachial artery in the antecubital fossa with insertion of introducer sheath over a guidewire (a). A long 5–7 F sheath is placed retrograde to the level of the mid-subclavian artery, where it is used for angiography to delineate the proximal portion of the vessel and target lesion (b).

anticoagulation is unnecessary and increases the risk ofcomplications. • Antegrade transfemoral approach (Figure 5.3):

– aortography with 5 F pigtail catheter is the initial step; – a 90 cm long 7 F Flexor (Cook) sheath is introduced over the wire to the aortic arch; – selective catheterization of the target vessel may be simply done with an appropriate,

steerable 0.035 guidewire (i.e. Storq or Wholey guidewire). However, a preshaped selective catheter is often necessary for this purpose; our favourite is the JB-1 catheter;

– the catheter is advanced into the vessel over the wire; – the Flexor sheath is then advanced into the proximal subclavian (or

innominate/common) carotid, preferably over the selective catheter that is used as guide and support;

– antegrade guidewire crossing, PTA and stent placement proceed in standard fashion.

The decision to opt for the antegrade approach for treatment of subclavian artery stenosisis a matter of personal choice, except for truly ostial lesions, where the retrogradeapproach is far better. Use of an interventional sheath (or guiding catheter) is extremelyhelpful to secure stable access to the target vessel, permit repeated angiographicinjections as needed, and provide a protective conduit for delivery and deployment of


stent devices.

Figure 5.2 Retrograde giudewire crossing of the stenotic lesion (a), is followed by preliminary balloon dilatation (b) that precedes advancement of sheath across the stenosis (inset, c). A balloon-mounted Palmaz stent is advanced through the ‘protective conduit’ of the sheath to the desired location (c), with deployment effected by balloon inflation following retraction of the sheath (d).

Total occlusions

Total occlusions of the subclavian artery are more difficult lesions for endovasculartreatment. We still attempt retrograde access and recanalization whenever feasible, butfind that approximately 30% of occlusions are not amenable to retrograde traversal by


guidewire; antegrade recanalization thus becomes the only available option. Therefore, itis paramount that re-entry of the true lumen beyond the lesion is verified by injection of a small amount of contrast material through a straight 5 F flush catheter passed over thewire (Figure 5.3d, inset).

Figure 5.3 A long (90cm) 7F interventional sheath has been placed antegrade transfernorally, and a 5 F pigtail catheter introduced to the top of the aortic arch to obtain detailed angiography (a). The Vitek catheter is used to facilitate selective vessel cannulation (b). The guidewire is advanced through the occlusive lesion (c), with confirmation of luminal re-entry by transcatheter injection of contrast (inset, d).


Figure 5.4 ‘Standard technique’ of iliac stent placement via ipsilateral retrograde approach. (a) Balloon predilatation; (b) long sheath crossing into aortic lumen to protect stent on balloon; (inset, c) deployment by balloon inflation after retraction of the sheath.

Lower limbs

Percutaneous endovascular intervention is an appropriate and clinically successfultherapeutic approach for focal disease, especially that involving the proximal inflowarteries. For the infrainguinal vasculature, and especially with extensive multilevelocclusions, surgical revascularization with vein-graft distal bypass retains a very important clinical role, providing the best hope for limb salvage.2, 3

Inflow aortoiliac disease

Endovascular intervention has become the standard treatment of focal lesions affectingthe iliac arteries. Distal aortic stenoses are also amenable to catheter intervention, butpublished information is relatively scarce.4, 5

Basic techniques and strategies Isolated iliac artery disease can be treated quite effectively when focal lesions are present.Percutaneous translumi-nal angioplasty and stent placement produce excellent results.6Endovascular techniques are well defined, and relatively simple to perform (Figure 5.4). PTA alone, without stenting, may be optimal in a large number of cases; nevertheless, we(and many others) almost always place stents in iliac PTA procedures, in view of thepredictably good results that can be achieved (Table 5.2).


Total iliac artery occlusion is more technically challenging. Contralateral access for recanalization is a valuable option (Figure 5.5).

Aortic bifurcation lesions often ‘spill over’ into the CIAs. ‘Kissing’ stent placement is a highly successful intervention for this pattern of disease (Figure 5.6).

Diffuse disease involving various lengths of the infrarenal abdominal aorta and thecommon and external iliac arteries does not lend itself well to endoluminal therapy. PTAand multiple stents can technically be performed, but

Table 5.2 Rationale for routine stenting

● Predictable

● Universally successful

● Decreases:

– need for repeat angiography ;

– amount of contrast used

– procedure time

● Enhances:

– technical success

– rationale and safety of outpatient intervention


Figure 5.5 Sequential steps illustrate contralateral access for recanalization of total occlusion in the common iliac artery. Use of a preshaped curved catheter (a), with subsequent antegrade guidewire crossing of the occlusion is followed by capture of the wire with a ‘gooseneck’ snare device (b) that will facilitate conversion to a through-and-through


transluminal access. Conversion to ipsilateral retrograde approach by transiliac retraction of the wire (c), and subsequent through-catheter exchange for a stiffer guidewire (d).

Figure 5.6 Kissing stents. Note intra-aortic protrusion of 1–2 mm.

results are less than optimal, and costs become prohibitive with the number of devicesrequired. Endovascular grafting (Figure 5.7) may constitute a better endoluminalalternative, but further confirmation of initial reports7 will be necessary before it can be embraced more enthusiastically. Conventional bypass procedures continue to have animportant role for patients who are medically fit for major surgery.

Femoropopliteal superficial femoral artery territory

The superficial femoral artery (SFA) is the interventionist’s worst nightmare! While true that technically successful endoluminal therapy can be achieved in many cases(longsegment occlusions included), restenosis/reocclusion is likely to occur in more than50% of instances within a short time.8 Adding to the practical difficulties is the fact that those lesions that do respond reasonably well to PTA (i.e. focal stenoses) are unlikely tocause symptoms severe enough to warrant invasive therapy. It is for these reasons that wecurrently restrict endoluminal treatment to symptomatic focal disease, and tend to usestents only sparingly, such as when the results of angioplasty are less than optimal. Newon the horizon are endovascular grafts that promise to enhance catheter-based capabilities for treatment of more extensive lesions through ‘internal bypass’. Many such devices and


approaches are currently under investigation; general clinical application is not yetwarranted.

Beyond biomechanics, radiation therapy and pharmacologic adjuncts—among others—may represent real hope for improved results with endoluminal therapy in the femoropopliteal territory.

Figure 5.7 Concept of ‘intraluminal bypass’ with endovascular graft to recanalize extensive occlusive lesions. Note potential for coverage/occlusion of important branches.


Figure 5.8 Alternative access techniques for intraluminal intervention in the superficial femoral artery. (a) Ipsilateral antegrade access is used in the vast majority of instances. (b) Antegrade access by contralateral approach or (c) transbrachial catheterization is occasionally resorted to. (d) The retrograde popliteal puncture technique is useful for intervention in common femoral and proximal superficial femoral artery lesions.


Techniques and strategies

Endoluminal approaches to the SFA and popliteal arteries are straightforward. Antegradeipsilateral femoral access is preferred in most situations. Contralateral femoral andretrograde popliteal approaches are useful in some cases (Figure 5.8).

Below-knee arteries

The tibioperoneal arteries have not traditionally been considered within the domain ofinterventional therapy. More recent information, however, indicates that a significantnumber of patients may indeed benefit from below-knee PTA.9 As elsewhere in the vasculature, focal lesions tend to respond much better than extensive occlusions.9

The majority of patients who present with critical ischaemia continue to require distal bypass grafting as they often have extensive, multilevel occlusions.

Techniques and strategies Best-case scenario for endoluminal therapy is that of patients with unimpeded flow to thebelow-knee popliteal, focal disease in a single-patent infrapopliteal artery, and ‘need for short-term revascularization’ to enable minor foot amputation, or healing of an openlesion or pedal amputation site. The great majority of such patients is diabetic. Thetechniques (Figures 5.9–5.11) involve antegrade percutaneous femoral access, selective below-knee angiography, and angio plasty utilizing 0.018" small-vessel systems. Clinical success rates (and limb salvage) in the 60–80% range are achievable with selected patients.9 More importantly, a failed attempt at below-knee PTA will not impede or compromise subsequent surgical bypass grafting.9 Subintimal angioplasty, championed by Bolia et al., 10 may represent an opportunity to expand the indications for PTA in extensive occlusions.

Combined endoluminal/surgical approaches

Combined therapy is appropriate for multisegment tandem lesions, especially on patientswho need infrainguinal bypass grafting and have a severe inflow iliac lesion on the sameside. A simultaneous, single-stage approach is most appropriate. Management of the reverse situation, that is, endoluminal treatment of a distal lesion at the time of a moreproximal bypass, is less clear. It is our opinion that ‘compromise’ of the likely optimal long-term result of a vein-graft bypass by a less durable below-knee PTA is not reasonable, unless the available high-quality saphenous vein is not long enough toencompass the entire segment/s of disease.

Endoluminal approaches to treatment of vein graft stenosis

Techniques of angioplasty of vein graft lesions are not fundamentally different from PTAintervention in any other vascular territory. However, these lesions tend to be quitefibrotic and somewhat difficult to dilate; high-pressure bal loons, and prolonged inflationtimes are frequently necessary for optimal results.


There are several choices for percutaneous endoluminal access of lower extremity vein-graft bypasses (Figure 5.12):

Direct puncture of vein graft with antegrade placement of a 5 F percutaneous sheath isthe first option. This technique is particularly appealing for patients who have in situ vein grafts. At times, surgical cutdown is advisable.

Antegrade femoral artery access is also a good option, similar in every way to theantegrade approach for nativevessel infra-inguinal PTA. Selective catheterization of the vein graft can be difficult at times; grafts that originate in the mid or distal SFA or at thepopliteal artery level are easy to access with this strategy, whereas bypasses that originatehigh in the groin are better approached with a direct puncture technique, as described(Figure 5.13).

Figure 5.9 Selective angiography of below-knee vessels by placement of straight angiographic catheter to the distal popliteal artery.


Figure 5.10 Endoluminal technique for percutaneous transluminal angioplasty of tibial/peroneal stenosis requires use of a 0.0l8´´ guidewire. A straight catheter may be of help by stabilizing the wire.


Figure 5.11 Endoluminal technique for percutaneous transluminal angioplasty (PTA) of occlusive lesion. Initial crossing of the lesion is preferably performed using a hydrophilic guidewire, that is later exchanged (through a catheter) for a small-vessel 0.018′′ wire over which PTA is performed.


Figure 5.12 Techniques of endoluminal access for vein graft intervention.


Figure 5.13 Contralateral approach.

Contralateral access is another available option. It seems to work quite well in thehands of some interventionists, but it is not our preferred approach for distal-limb intervention.

Overall, endovascular treatment is selected for only 30–40% of lower extremity vein-graft lesions, especially those that are non-anastomotic in location. The majority continue to be treated by surgical revision.

References

1. Criado FJ, Queral LA, Twena M. Is endovascular intervention justified for disease of the supra-aortic trunks? In: RM Greenhalgh, FGR Fowkes (eds) Trials and tribulations of vascular surgery. London; WB Saunders, 1996, 131–50.

2. Londrey LG, Ramsey DE, Hodgson KJ et al. Infrapopliteal bypass for severe ischaemia: comparison of autologous vein, composite and prosthetic grafts. Vasc Surg 1991; 13:631–6.

3. Budd JS, Brennan J, Warren H et al. Infrainguinal bypass surgery: factors determining


late graft patency. Br J Surg 1990; 77:1382–7. 4. Henry M, Amor J, Ethevenot G et al. Palmaz stent placement in iliac and

femoropopliteal arteries: primary and secondary patency in 310 patients with 2–4-year follow-up. Radiol 1995; 197: 167–74.

5. Diethrich EB. Endovascular treatment of abdominal aortic occlusive disease: the impact of stents and intravascular ultrasound imaging. Eur J Vasc Surg 1993; 7:228–36.

6. Palmaz JC, Laborde JC, Rivera FJ et al. Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovasc Intervent Radiol 1992; 15:291–7.

7. Sanchez LA, Veith FJ, Ohki T. Endovascular grafts for the treatment of aortoiliac disease associated with severe limb-threatening ischaemia. Perspect Vasc Surg 1998; 9:71–7.

8. Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty: factors influencing long-term success. Circulation 1991; 83(Suppl. 1): I-70–80.

9. Criado FJ, Twena M, Abdul-Khoudoud O et al. Below-knee angioplasty: misguided aggressiveness or reasonable opportunity? J Inv Cardiol 1998; 10:415–24.

10. Bolia A, Bell PRF. Femoropopliteal and crural artery recanalization using subintimal angioplasty. Semin Vasc Surg 1995; 8:253–64.


Angioplasty and stent application for carotid atherosclerosis

6 PATRICE BERGERON AND JÉRÔME MASSONNAT

Introduction

Endoluminal vascular techniques were first introduced by Dotter1 and Grüntzig,2 both radiologists, and have henceforth complemented the armementarium available to vascularsurgeons and radiologists. Angioplasty of carotid arteries is recent and still remainshighly controversial,3–9 in the absence of long-term comparative results. However there are a number of elective indications that can be used for carotid angioplasty.

Atheromatous stenoses are conventionally treated surgically; however, some locationscan be treated in an endoluminal way when surgery is difficult or if the health status ofthe patient requires a less invasive technique.

Carotid endoluminal treatment is based on the principle of percutaneous balloonangioplasty.10–12 Variantsexistas to the access or the type of stent used. Here, we describethe treatment of internal carotid stenoses. Extension of this technique to other lesionsfollows the same principles.

Patient set-up

Preoperative period

Recent and complete radiological data are needed, e.g. arte-riograms including supra-aortic trunks and anteroposterior (AP) and lateral intracranial vessels (Figure 6.1). The brain computed tomography (CT) scan can be completed by an aortic arch CT in order todetect atheromatous debris or thrombus that might be a contraindication to archcatheterization (Figure 6.2).

Haemodynamic examination by means of transcranial Doppler helps to analyse thecircle of Willis and a duplex scan of neck vessels helps to identify the morphology of theplaque. The site of carotid bifurcation in cervical extension is traced by subsequentlandmarks on the patient’s skin, so as to facilitate direct puncture if the cervical approach is preferred. Alternatively, the femoral approach can be used. The patient should beevaluated clinically by a neurologist and an ophthalmologist. This examination will berepeated postoperatively.

The patient needs to be prepared in the same way as for conventional surgery, since conversion may be required. The patient’s groin and neck need to be shaved and

prepared. The patient’s biological findings (haemostatis and renal functions) and cardiacstatus, along with the pre-anaesthesic examination, will help the final decision concerning the procedure. Informed consent is required.

Figure 6.1 Different steps of an intracerebral angiogram.

Contraindications to angioplasty

A suspected endoluminal thrombus is a strict contraindication because of the risk of brainembolism. There are also relative contraindications, e.g. some lesions of the bifurcationfor which current state-of-the-art stents do not fit. Finally, highly calcified lesions (above 50% of the circumference and/or over 2 cm in length) are also contraindications.

Medications

In our practice, antiplatelet medication (250 mg aspirin and 250 mg ticlopidin or 75 mgplavix) is administered 24 h beforehand and continued for a minimum period of 1 monthpostoperatively.

Angioplasty and stent application for carotid atherosclerosis 129

Figure 6.2 Macroscopic examination of an aortic arch in correlation with a computed tomography scan.


The operating room

Description

Top quality radiological equipment should be available, whether in a radiological roomadjacent to the operating theatre, or in the operating theatre itself using mobile equipmentfitted with digital substraction and roadmapping facilities. Collaboration between thevascular surgeon and the radiologist for a better interpretation of intracranial angiographycan be beneficial.

Monitoring equipment

Electrocardiogram (EKG) and arterial blood pressure monitoring are aimed at detectinghypotension or arrythmia. Bradycardia observed in the course of angioplasty usuallyresponds to intravenous injection of 1 mg atropine; however, a temporary pacemaker isoccasionally indicated. Neurological monitoring is at best obtained by a local anaesthesia.In case of general anaesthesia, transcranial Doppler is used to monitor the intracranialflow and to detect potential brain embolism.

Set-up

In the event of direct cervical access, the patient is placed supine, and the head rotated tothe contralateral side, thus offering exposure of the lesion to be treated. A cushion underthe patient’s shoulder is helpful. Anaesthesia can be either local or general. The femoralapproach can be used with local anaesthesia, whereas the cervical approach often requiresgeneral anaesthesia with intubation.

Checking revascularization

Angiography offers continuous monitoring during the procedure, assessment of the finalresult and of possible com-plications. A pressure gradient record is not necessary if the puncture site is located below the lesion, since measurement would involve passingthrough the lesion; it can, however, be useful in the case of a retrograde cervical punctureabove a stenosis of the supra-aortic trunks. Angioscopy is useless and hazardous.

Intravascular ultrasound accurately quantifies the diameter of the carotid and its stenoses, and confirms the correct application of the stent on the arterial wall. However,this investigation is expensive and involves a potential risk of embolism, and shouldtherefore not be performed routinely. No additional benefit of intravascularultrasonography has been demonstrated over the use of angiography alone.


Carotid angioplasty

The various techniques of carotid angioplasty

Arterial approach

Three approaches can be used: femoral, cervical and brachial.

Retrograde femoral approach (Figures 6.3–6.6) This is the most popular approach, is similar to diagnostic catheterization and follows thesame major steps:

• A J 0.35 hydrophilic guide-wire (Terumo) up to the aortic arch or a stiff hydrophylic guide-wire with distal soft tip is introduced.

• A long (100 cm) 7 F sheath is introduced and an injection of 5000 units of heparin placed in the descending aorta.

• Catheterization of the left common carotid artery or the inominate artery in undertaken. Several types of 5 F catheters can be pushed over the hydrophilic guidewire; the partial withdrawal of the latter releases the kink of the catheter so that it spontaneously fits with the ostium of both vessels. Several catheters can be used, depending on the morphology of the aortic arch. We often use a BENTSON JB2 catheter (Schneider, Cordis) for the left common carotid artery and a SIMMONS 2 or 3 for the right common carotid artery, according to the width of the aorta. We also recommend the VITEK catheter in both cases.

Some authors prefers the headhunter, mani, multipurpose, Bentson JB1 or JB3 catheters(Figure 6.7). In fact, with training any catheter that can cannulate the inominate or left common carotid artery and allow a stiff Terumo or Amplatz guide-wire to be passed, can be used.

• After angiography and roadmapping of the carotid bifurcation, the guide-wire is further pushed into the common carotid and the external carotid artery.

• The guide-wire is then swapped for a rigid 260cm Amplatz Super Stiff (Cook or Boston Scientific, USA) and the catheter is removed.

• The long 7 F sheath over its mandrel is advanced in the common carotid artery immediately below the carotid bifurcation. Angiography of the bifurcation can then enable the best incidence so as to free the lesion, but it also enables intracerebral circulation to be checked laterally and frontally, which serves as a reference prior to angioplasty.


Figure 6.3 Different steps of carotid catheterization via femoral access. The hydrophylic J-guide is positioned in the external carotid artery.


Figure 6.4 The 5 F catheter (here JB2) is pushed into the external carotid artery and the guide is changed for a stiff guide (0.35 or 0.18).

Angioplasty is then performed. This step remains identical whatever the approach, usingprotective devices.

Advantages and drawbacks. The femoral route, which is a conventional approach fordiagnostic investigations, can also be used to treat all lesions of the supra-aortic trunks, the common carotids and of the intracerebral vessels. Retrograde puncture is easy if theiliac flow is high enough. Its main advantage lies in local anaesthesia, which enables acontinuous monitoring of the patient’s state of consciousness.

In case of embolus migration, thrombolytic treatment can be given with little increased


risk of local haematoma. Among the drawbacks is the fact that the distance between the groin and the cervical

vessels requires long instruments (catheters, balloons, etc.). This long and tortuous routedemands flexible materials, but prohibits the use of rigid stents, which could becomeblocked in tinted vessels. It requires a certain degree of expertise (5% failure rate) andexperience with supra-aortic trunk catherization.

Figure 6.5 After the retreat of the 5 F catheter, the long 7 F sheath. is pushed with its mandrel into the common carotid artery.


Figure 6.6 Now the internal carotid artery (ICA) can be catheterized safely with a soft-angled guide-wire (0.18, 0.14, 0.35).

These manoeuvres can damage diseased aortic arches and cause brain embolism morefrequently than diagnostic catherization, because of the larger size of the sheath used. Thetechnique can be difficult in the presence of an important kinking at iliac, commoncarotids or inominate artery levels (Figure 6.8), an ectopic emergence of the left commoncarotid artery from the inominate artery (Figure 6.9a), or an acute aortic arch with a low origin of the inominate artery (Figure 6.9b). These manoeuvres are said to be morehazardous in the presence of an aneurysmal abdominal aorta with thrombus present. Also,a time limit should be decided in the event that selective catheterization takes too long.


Antegrade cervical access (Figures 6.10–6.13) The so-called ‘direct puncture’ consists of puncturing the common carotid artery at thebase of the neck. Needle is guided by touch, sometimes by ultrasonography, or by meansof a needle combined with Doppler imaging (‘smart needle’ from cardiovascular dynamics).

This access is time saving but the technique requires a high degree of accuracy, as explained opposite.

• The common carotid artery is punctured 2 cm above the clavicle following a 45° maximum oblique axis, so as to avoid folding the sheath. Skin landmarks identifying the bifurcation site need to be checked in order to puncture down below these landmarks. Puncture needs to be frank, as the artery tends to roll easily. It may be useful to identify the artery by means of a fine needle which can be left in place during puncture.

• A few millilitres of contrast medium are then injected to check the site of puncture with respect to the carotid bifurcation and to perform roadmapping before placing the guide in the external carotid artery. If the puncture is too close to the bifurcation, it has to be repeated. In this case, before removing the needle, angiography and roadmapping can be used to guide the new puncture. Should the cervical access be used after failed femoral procedure, roadmapping is obtained before removing the femoral catheter.

• A short 5 or 6 F sheath, which does not exceed 5.5 cm in length (Cordis SM 6836), fitted with a distal bright tip, is located below the bifurcation and fixed to the skin (Figure 6.14). Moderate heparinization (2000 units) is used, as procedure time is short.

Advantages and drawbacks. Cervical access is used in case of failure of the femoral route(5% of cases). It is simple and fast. A small incision at the base of the neck can helpaccess to the carotid when the patient is given high dose rates of antiplatelet medication.Endoaortic manoeuvres can thus be reduced to limit the risk of brain embolism. There isa theoretical risk of cervical haematoma at the site of puncture.

The main drawback is the discomfort for both the patient and the operator when the procedure is performed with local or locoregional anaesthesia. It is therefore desirable toadminister a general anaesthesic. In this case, the control of intracerebral circulation witha transcranial Doppler allows continuous monitoring to detect possible brain embolism.

Retrograde carotid approach This route is used for lesions of the common proximal carotid by cervical approach, as analternative to femoral access (Figure 6.15).


Figure 6.7 Different catheters used during femoral approaches (upper: our choice, lower: others’ choice).

Brachial route This approach requires an arterial diameter large enough; it is rarely used with femalepatients. It was recently suggested as a possible alternative to carotid puncture but itreduces passage through the aortic arch and therefore increases the risk of embolism. Thehumeral approach is the preferred access to catheterize the contralateral artery; however,spasm remains a major concern with this approach. A simmons 2 or 3 catheter can beused in this procedure.

Assessment of the lesion

This is an essential stage, as it defines the materials that will be used. Assessment can bemade along with preoperative


Figure 6.8 Carotid king—king not suitable for femoral approach.

Figure 6.9 (a) Configuration not suitable for femoral approach; ectopic emergence of the left common carotid artery. (b) Acute aortic arch with a low origin of the inominate artery.


Figure 6.10 Different steps of the carotid catheterization via cervical approach. When it is too narrow we predilate with a little balloon (2 atm). An occlusive balloon is placed upon the lesion when possible.

examination, i.e. measurement of the diameter and length of the vessels. It is necessary tohave a scale of reference, the ideal being a graduated guide-wire placed in the carotid lumen. Alternatively, a graduated rule can be projected on the screen as a reference. Thediameter and length of both balloon and stent can then be estimated (Figure 6.16).


Figure 6.11 Primary stenting.


The angioplasty

Protective device set-up Special techniques are required, according to different models.

Predilation Angioplasty of very tight stenoses, with approximately 90% occlusion and with a patentlumen of less than 2 mm does not permit primary stenting because of the potential risk ofstent displacement or of detaching embolic particles. Predilation is necessary in suchcases. Two possibilities are available:

1. The first one consists of using a low-profile small-diameter balloon (3 mm) designed for coronary vessels and inflated at a high pressure.

2. The second, which we like best, consists of using a balloon of the same size as the carotid, inflated at a low pressure (2–3 atm) so as to widen the lumen and preserve the plaque.

In tight and irregular stenoses, 0.018 or even 0.014 coronary guides can be used, along with dilatation using a lowprofile coronary balloon. At present, there is a tendency to work with these types of materials routinely.

Implanting the stent It is now generally accepted that the deployment of a stent is helpful for any carotid atheromatous lesion, including restenoses, if one wishes first to obtain a good anatomical result. It may also help prevent embolism, as balloon angioplasty alone entails greater arterial dissection.

The stent is pushed along its deployment system, which can be either a balloon or a delivery system if the stent is self-expandable. Positioning the stent requires great accuracy, particularly if one wishes to open the internal carotid adjacent to the ostium and still avoid damaging the external carotid. Two techniques are possible:

1. Under general anaesthesia, roadmapping before implantation allows an accurate positioning on the mask.

2. Under local anaesthesia, the patient’s deglutition movements require repeated injections of contrast medium during positioning.


Figure 6.12 An aspiration catheter is used to collect the debris.


Figure 6.13 The aspiration catheter is pushed across the stent to wash and the occlusive balloon is deflated.


Figure 6.14 Short 6 F sheath (cordis).

Figure 6.15 Treatment of the common carotid artery by retrograde approach.

Figure 6.16 Approximate estimation of the length of the stenose using the projection of the balloon over the road mapping lesion.


Deploying the stent (Figure 6.17) We prefer to deploy a stent with a balloon. We generally use a 5 or 6mm diameterballoon, which is deflated and removed as soon as the stent is deployed. The result ischecked by means of angiography. A second balloon dilatation can be required,sometimes with a larger diameter balloon. We usually use Palmaz stents (Johnson &Johnson) (Figure 6.18) because of their good radial force and good radio-opacity, which

Figure 6.17 Stent deploying.

Figure 6.18 Example of Palmaz stenting.


allows optimum positioning. We use the shortest possible stents (P104, P154, or P204).Their simplicity of use is excellent in the cervical route. There is a potential risk ofextrinsic compression in case of cervical trauma. This occurs in less than 2%, but is still aproblem.

Many practitioners prefer to use the self-expandable Wallstent, but it is more difficultto position it accurately; the stent needs to be longer and it seems necessary to cover thebifurcation. The risk of external carotid thrombosis is real. We use the Wallstent for longor double internal carotid stenoses (Figures 6.19–6.20). The Wallstents flexibility in most cases allows it to be inserted by the femoral route.

These is no doubt that the new nitinol dedicated carotid stents are preferable (Cordis Smart, Guidant, Boston Scientific).

Intracerebral vessels inspection Intracerebral angiography is indispensable. AP and lateral views showing all the centraland cortical arterial branches are necessary. One has to observe whether the contrastmedium velocity is evenly distributed without any delay, and a delayed angiogram or‘parenchymography’ can possibly identify circulatory interruptions. These views have tobe compared with previous ones. In case of problems, in situ thrombolysis should be performed. The femoral route appears to be far less hazardous.

Withdrawing the sheath When the femoral route is chosen, withdrawal can be postponed and performed in themonitoring room with compression maintained for 10–15min and subsequent application of a compression bandage or sealing device.

With the cervical route, the carrier is withdrawn immediately at the end of theprocedure: mild compression over 10–15 min is enough and a compression bandage is not used. Heparin will not be neutralized. Extravascular sealing devices can be used.


Figure 6.19 Three-dimensional CT scan of Wallstent carotid stenting.


Figure 6.20 Wallstent indication: double internal carotid artery stenoses.

The issue of cerebral protection

The risk of brain embolism is unavoidable with this operative technique because of thepossible rupture of atheromatous plaques due to the various manoeuvres performed onthe aortic arch or the carotid vessels. Our early studies and others13 had shown the hazardous nature of balloon angioplasties; however, the results obtained with primarystenting have undoubtedly offered greater safety. This technique still remains risky, asevidenced by different studies, and the use of a protective device may be helpful.

Two systems are currently under development: filters and balloons. The concept of protective balloons was developed by Theron.14 In his experience, this technique reducedthe risk of brain embolism from 8% to none. This device is now available on the marketand we believe it should be used routinely. It allows the treated zone to be aspirated andflushed into the external carotid artery (Figures 6.21 and 6.22). Kachel15 suggests the use of an occlusive balloon in the common carotid, and Wholey16 and Roubin have developed a filter system. These filters spontaneously deploy above the treated site, andcan retrieve emboli, allowing blood flow preservations.

Occlusive balloons remain a problem when occlusion is not tolerated. As for coronaryangioplasty, perfusion balloons may help in this case. We have recently started using thePercursurge system (Figure 6.23), which is a small balloon mounted on a 0.14 guide andwhich we believe is promising, and may prove to be extremely useful.


Figure 6.21 Collection of debris after aspiration.

Figure 6.22 Procedure with the protective balloon.

Results

Several individual studies have been published and report a rate of neurologicalcomplications of around 10%.17–19 More recent series with primary stent implantation without predilation have offered improved results with a 5% major complication rate.20, 21 An international registry coordinated by Wholey22 has recorded 5% major complications in 2500 cases.

Among multicentric studies, the CAST study23, 24 is a tolerance study that includes 100 highly selected patients treated in seven different surgical centres; no serious stroke wasreported and a 4% incidence of transient ischaemic attack is mentioned. The CAVATASstudy25 is the only randomized study currently completed. The results do not show any


superior benefit for surgery or angioplasty, but the stroke—death complication rate remains high in both groups

Figure 6.23 Percursurge system.

(10%). No protective devices have been used in these trials. Several large, randomizedtrials are currently in progress: notably CREST26 and CASET.27

Indications

As comparative data with surgery are missing, indications concern selected symptomaticpatients only.

Reasonable indications28, 29

Until further studies are available, angioplasty should be reserved for symptomaticpatients only. In particular, the endovascular route is preferred in patients in whomsurgery is contraindicated or difficult. This includes recurrent stenoses after surgicalendarterectomies, radiotherapyinduced stenoses, very distal lesions at the basis of theskull and proximal lesions on the common carotid or the inominate artery, in order toavoid a sternotomy.

More controversial indications

Not all lesions can be submitted to endovascular treatment. In particular, lesions affectingthe carotid bifurcation are very difficult. Currently available stents are not adapted to alltypes of lesions; bevelled stents will be better adapted to lesions adjacent to thebifurcation. The indications will probably be modified with the use of reliable protectivedevices.


Conclusions

Results after surgical treatment are excellent in atheromatous lesions of the carotidbifurcation. However, the search for a better treatment, which should be as simple aspossible, is fully justified for patients at high risk, whether due to their general condition(old age, acquired or iatrogenic haemostatic disorders, unstable respiratory or cardiacstatus) or due to associated lesions (cerebral infarction, occlusion of other cerebraltrunks). Results from major randomized trials are still needed before drawing concreteconclusions.

In practice

Many practitioners have opted for the femoral route on a routine basis. They use localanaesthesia and preferably flexible stents, such as the Wallstent™ or the new nitinol stent, and less commonly the short Palmaz™ stents (less than 2 cm). It is only when femoral access is impossible that they use the cervical approach.

Others consider carotid stenting as an additional treatment method, just asendarterectomy or carotid bypass grafting, and therefore use the same managementprinciples. They decide about anaesthesia as a function of the patient’s condition. As for any other surgical operation, general anaesthesia is for patients with good generalcondition, and the cervical route is preferred. Patients with poorer condition or with aspecific risk are treated with local anaesthesia. In these cases, it is better to use thefemoral approach for reasons of comfort and better accuracy. Flexible stents are alsorecommended for these patients.

Carotid angioplasty offers a less aggressive alternative treatment than surgery forcertain lesions affecting carotid arteries. Angioplasty still needs to be assessed as analternative treatment of carotid bifurcation stenoses, but it can already palliate somespecific lesions that are difficult to treat surgically, such as distal lesions of the internalcarotid, radio-induced stenoses or restenoses following endarterectomy, and proximal stenoses of supra-aortic trunks.

Since the writing of this chapter, the authors treated over 60 patients by protected carotid angioplasty and stenting with a decrease in ispsilateral embolic complication ratedown to 2% (1 TIA). The ispsilateral/death rate was 0%, although one patient died from anon-embolic cause (intracerebral haemorrage).

References

1. Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction: description of a new technique and a preliminary report of its application. Circulation 1954; 30:554–670.

2. Gruntzig A, Hoptt H. Perkutane rekanalisation chronischer arterieller verschiuesse mit einem neuen dilatations—Katheter. Disch Med Wochenschr 1974; 99:2502–5.

3. Agence nationale pour le développement de l'évaluation médicale. Sténose de l’origine


de la carotide interne cervicale et de la bifurcation carotidienne: chirurgie, angioplastie. In: Recommandations et references médicales. ANAES, 1997, 115–37.

4. Baker W. OREST a moral and ethical conundrum. Cardiovasc Surg 1997; 5:461–2. 5. Bergeron P, Chambran P, Benichou H et al. Recurrent carotid disease: will stents be an

alternative to surgery? J Endovasc Surg 1996; 3:76–9. 6. Bergeron P, Chambran P, Blanca S, Benichou H, Masson J. Traitement endovasculaire

des artères a destinée cérébrale: échecs et limites. J Mal Vasc 1996; 21(suppl. A): 123–31.

7. Bergeron P, Chambran P, Hartung O, Blanca S. Cervical carotid artery stenosis: which technique balloon angioplasty or surgery? J Cardiovasc Surg 1996; 37(Suppl. 1): 73–5.

8. Jordan WD, Schroeder PT, Flascher WS et al. A comparison of angioplasty with stenting versus endarteriectomy for the treatment of carotid artery stenoses. Ann Vasc Surg 1997; 11:2–9.

9. Thompson JE. Carotid angioplasty—a reserved position. Cardiovasc Surg 1997; 5:459–60.

10. Bergeron P. Endovasclar treatment of brachocephalic lesions. In: LR Caplan, EG Shifrin, AN Nicolaides, WS Moore (eds) Cerebrovascular ischemia investigation and management, London: MedOrion, 1996, 479–90.

11. Bergeron P. Stenting of carotid and arch vessels. In: U Sigwart (ed.) Endoluminal stenting. London: WB Saunders, 1996, 467–93.

12. Dietrich EB, Marx P, Wrasper R, Reid DB. Percutaneous techniques for endoluminal carotid interventions. J Endovasc Surg 1996; 3: 182–202.

13. Theron J, Courtheaux P, Alachkar F et al. New triple coaxial catheter system for angioplasty with cerebral protection. ANJR 1990; 11:859.

14. Ohki T, Marin M, Lyon R et al. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg 1996; 27:463–71.

15. Kachel R. Results of balloon angioplasty in carotid arteries. J Endovasc 1996; 3:22–30.

16. Wholey MH, Wholey M, Jarmoliwski CR et al. Endovascular stents for carotid occlusive disease. J Endovasc Surg 1997; 4:326–38.

17. Dietrich EB, Ndlaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 1996; 3:42–62.

18. Gil-Peraita A, Mayol A, Marcos JR et al. Percutaneous transluminal angioplasty of symptomatic atherosclerotic carotid arteries. Results, complications and follow-up. Stroke 1996; 27:2271–3.

19. Yadav JS, Roubin GS, Lyers S. Elective stenting of extracranial carotid arteries: Immediate and late become. Circulation 1997; 95:376–81.

20. Mathias KD, Jaeger MJ, Sahl H. Internal carotid stents PTA: 7 years’ experience. Cardiovasc Interv Radio 1997; 20(Suppl. 1): 146.

21. Theron J, Payelle G, Coskun O et al, Carotid arteriel stenoses treatment with protected balloon angioplasty and stent placement. Radiology 1996; 201:627–36.

22. Wholey MH, Wholey M, Bergeron P et al. Current global status of carotid artery stent placement. Cath Cardiovasc Diagn 1996; 44:1–6.

23. Bergeron P, Alessandrescu V, N’Guyen CM, Amichot A. Angioplastie percutanée de l’artère carotide interne; l'étude CAST 1. In: A Branchereau, M Jacibs (eds) Nouveautés en pathologie carotidienne. Amonk: Futura Media Services, 1998, 269–300.


24. CAST’investigators. The carotid artery stent trial. J Endovasc Surg 1999 May; 6(2): 155–9.

25. Sivaguru A, Venables GS, Beard JD et al. European carotid angioplasty trial. J Endovasc Surg 1996; 3:16–20.

26. Hobson RW, Brott T, Fergusson R et al. Carotid revascularization endarteriectomy versus stent trial. Cardiovasc Surg 1997; 5:457–8.

27. Clagett GP, Barnett HJ, Easton JD. The carotid artery stenting versus endarteriectomy trial (CASET). Cardiovasc Surg 1997; 5: 454–8.

28. Bergeron P, Rudondy Ph, Benichou H et al. Transluminal angioplasty for recurrent stenosis after carotid endarteriectomy. Int Angiol 1993; 12:256–9.

29. Dietrich EB. Indications for carotid artery stenting: a preview of the potential derived from early clinical experience. J Endovasc Surg 1996; 3:132–9.


Thrombolysis techniques and devices

7 MEENA NARAYANSWAMY AND KRISHNA KANDARPA

Introduction

Obstruction of arteries or veins by thrombus develops secondary to a wide variety ofpathological disorders. Predisposing factors include primary arterial pathology as inobstructive atherosclerosis and altered haemodynamics, as in deep venous thrombosisand hypercoagulable conditions. Other clinical presentations involve the distalmanifestation of thrombi, remote to their site of origin, as in embolic occlusion of arterialbeds from cardiac mural thrombi. The management of arterial thrombi hinges on therapid restoration of blood flow in the obstructed vessel and thereby in the prevention offurther ischaemia in the distal bed. On the venous side, the goal is to prevent distalembolism and chronic damage to the occluded veins. In both situations, localthrombolytic therapy is currently frequently used for treatment.

Traditional forms of therapy included systemic anticoagulation and/or surgery. Both modalities had their limitations. Anticoagulant therapy (heparin sodium, coumadin, etc.)limits the further development of thrombosis but has no direct lytic effect on thethrombus and thus relies on the endogenous lytic system to relieve the obstruction.1, 2

Surgical techniques (despite improvement in surgical practice in recent years) presenthigh morbidity and mortality rates. In what was the prevailing climate of limitedtherapeutic alternatives, the first successful clinical investigations of the thrombolyticagent streptokinase (sk) conducted by Johnson and McCarty3 in 1959, set the stage for a revolution in the management of thromboembolic disease. Early studies with intravenousstreptokinase,4, 5 among them one study published by Dotter and colleagues2 in 1972, indicated that the efficacy of lysis, apart from being related to the agent employed, couldalso be affected by the age of the clot. This study also made two further observations: (a)that the catheter could be used for intra-arterial delivery of the thrombolytic agent; and(b) that such a technique would reduce the dose, the lysis time, as well as the systemiccomplications associated with the intravenous route. With the development of intra-arterial techniques in the late 1970s and their increasing use in the early 1980s, mostfurther studies focused on the application of these techniques and agents to a variety ofclinical situations.

Indications and contraindications for pharmacological lysis

Transcatheter thrombolytic therapy is the primary treatment modality in the

interventional radiologist’s domain of thromboembolic disease of the extremity arteriesand veins, embolic stroke and thrombosis of haemodialysis access grafts. More recently,there has been a revival in the use of these techniques in pulmonary thromboembolism,The procedure has been applied successfully but far less frequently to the visceralarteries. Proper selection of patients for safe, successful lysis is important. All currentlyavailable thrombolytic agents create some degree of a systemic lytic state in the patient,with the potential danger of haemorrhage, and contraindications have been defined inanticipation of this.6 Reperfusion injury of a severely ischaemic limb (SVS/ISCVS III)with consequent metabolic complications of acidosis, hyperkalaemia and renal failure,occurs in less than 1% post thrombolysis, but is serious enough to warrant consideringsuch patients as an absolute contraindication to lytic therapy.7, 8 The presence of a mobile left cardiac thrombus carries the risk of distal embolizations from this source.9, 10 Thus, absolute contraindications to the procedure include: (a) active internal bleeding; (b)irreversible limb ischaemia (SVS/ISCVS Grade III); (c) stroke within 1 year or transientischaemic attack (TIA) within 2 months; (d) intracranial neoplasm or a recentcraniotomy; and (e) a suspected or known protruding, mobile left heart thrombus.Relative contraindications also centre around bleeding complications and includegastrointestinal haemorrhage, recent major surgery or biopsy within 2 weeks, severeuncontrolled hypertension and recent trauma.

Thrombolytic drugs

Streptokinase (SK) was isolated from streptococci by Tillett and Garner11 in 1933, and was found to have fibrinolytic properties. However, the initial agent was too toxic forhuman use and it was a couple of decades before a purified form of the drug (Streptase,Hoechst) was available for clinical use. Though it resulted in efficient clot lysis, andtherefore presented a potential benefit over anticoagulants, its use was associated withseveral complications.4, 5 SK being of bacterial origin, is antigenic and causes a wide variety of allergic symptoms. It must first bind with plasminogen to achieve lysis andtherefore causes a depletion of both circulating and fibrin-bound plasminogen, as well as of other clotting factors (e.g. fibrinogen), thus predisposing to a systemic lytic state withpotential haemorrhagic complications. Also, initial studies reported long intravenousinfusion times for SK, ranging from 18 to 34 h for clot lysis to take place.2, 4, 5 Urokinase (UK), first isolated from human urine by Macfarlane and Pilling in 1952,12 has since been isolated from foetal kidney cells (Abbokinase, Abbot Laboratories) and is currentlybeing produced through recombinant DNA technology (r-UK, Abbott Laboratories). It was first used clinically in 1959 by Sherry and coworkers.13 The mechanism of thrombolysis is different, in that UK is a direct plasminogen activator and does not needto complex with plasminogen as SK does. Initial trials with intravenous UK reportedequivocal findings with marginal benefits for this drug as compared to SK.14, 15 In the light of this and of its high cost, UK was not popular in clinical thrombolysis until intra-arterial techniques of drug delivery evolved. The earliest comparative randomized trialsto evaluate the advantages of UK and SK over anticoagulant heparin sodium were theUPET trial in 1970 (Urokinase Pulmonary Embolism Trial)14 and the USPET trial in


1974 (Urokinase Streptokinase Pulmonary Embolism Trial).15 These studies of thrombolytic therapy for pulmonary emboli observed that: (a) both SK and UK weresuperior to heparin therapy with regard to clot lysis; (b) there was no added benefit froma 24-h infusion of UK, as compared with a 12-h infusion; (c) there were equivocalfindings regarding the superiority of UK in clot lysis, except that it was more efficient incausing lysis by achieving the same amount of lysis in a shorter time (12 h). The overallincidence of complications was comparable for the two drugs. The high incidence ofsystemic haemorrhagic complications with the intravenous use of these drugs, ledinvestigators to consider alternative methods of drug delivery with intent to avoid thisinduced systemic lytic state. Thrombolytic research since the 1980s, has been two-pronged: First, towards the development of an agent capable of rapid, complete andstable clot lysis with fewer complication, and secondly, towards more efficient methodsof delivery of the thrombolytic drug. More recently, there has been increasing interest inthe use of thrombectomy devices, either alone or in combination with lytic drugs. Thischapter discusses these techniques and devices.

Newer agents

The shortcomings of the first generation thrombolytics SK and UK prompted thecontinuing search for a more fibrinspecific agent which, by targeting only fibrin-bound plasminogen, would spare the circulating levels, with the consequent advantage of fewerbleeding complications. An equimolar complex of SK and acylated human plasminogen,termed anisoylated plasminogen streptokinase activator complex (APSAC), wassynthesized to improve upon the deficiencies of SK.16 This agent has a longer half-life and can thus be administered as an intravenous bolus. Though APSAC is significantlymore fibrin specific and yields shorter lysis times, its inherent antigenicity is an importantlimiting factor in its use.17 The second generation of thrombolytics, tissue plasminogen activator (t-PA) and single chain urokinase type plasminogen activator (scu-PA or prourokinase) were then developed, with the continued intent of greater fibrin specificity.t-PA (Alteplase),18 which physiologically is the prime activator of plasminogen, is isolated from tissue culture supernate and can also be cloned from E. coli by recombinant DNA techniques (rt-PA, Activase (Genentech)19 and a newer mutant form of rt-PA, Reteplase).20 t-PA has a high affinity for fibrin and demonstrates increased affinity forplasminogen in the presence of fibrin. The clinical benefit of thrombolytic agents variesaccording to the involved vascular bed. The coronary arteries have been the subject of themajority of large clinical trials with these drugs, owing to the high prevalence andmortality of acute myocardial infarction (AMI). Although it was anticipated that thegreater fibrin specificity of t-PA would result in a lesser degree of haemorrhagiccomplica-tions, the incidence was actually equal to or more than that of SK in the initial trials.21–23 A systemic lytic state does occur with its use, albeit in a minority of patients.The 1993 GUSTO trial with t-PA and SK in acute myocardial AMI demonstrated the superiority of t-PA, as compared to other thrombolytic regimens in effecting both reperfusion and reduced mortality.24 Comparative studies of rt-PA with SK and /or UK have generally concurred on the rapidity of action of rt-PA, with equivalent clinical outcomes for both rt-PA and UK.25–29 Meyerovitz and colleagues, conducted a

Thrombolysis techniques and devices 157

prospective, randomized trial of rt-PA and UK and observed that: (a) rt-PA causes more rapid lysis than urokinase, although the rates were similar at 24 h; (b) bleedingcomplications were more in the rt-PA group, although this was not statisticallysignificant; and (c) both groups had similar clinical outcomes.29 It is now generally accepted that intra-arterial UK and rt-PA effect more rapid and successful lysis than SK,with fewer complications in peripheral arterial occlusions.25, 28, 30, 31 Though rt-PA is known to cause greater initial clot lysis, the slightly increased risk of bleedingcomplications and the greater cost could be determining factors in its use.

The above described four drugs—SK, UK, APSAC, and t-PA—are the only commercially available lytic agents in the USA. Newer drugs are still being investigatedto develop more efficient lysis and some of the more common ones are:

1. Reteplase 2. TNK-tPA 3. Pro-urokinase 4. Recombinant urokinase (r-Urokinase) 5. Recombinant glycosylated pro-urokinase 6. Recombinant staphylokinase 7. Bat plasminogen activator 8. Antibody-targeted thrombolysis 9. Chimeric plasminogen activators 10. Fibrolase.

Of the above, recombinant glycosylated pro-UK, recombinant UK and recombinant SKhave been evaluated in peripheral arterial occlusions.31–34 None of these are as yet approved for clinical use; they are still investigational, at different stages of clinical trials.

Infusion techniques

Intravenous infusion of thrombolytic drugs has been largely replaced by local, intra-arterial delivery using percuta neous catheter techniques. As many as nine studies using alocal, intra-arterial drug delivery were published prior to the first large series published by Dotter and colleagues in 1974,35 who described the technique of intra-arterial lowdose streptokinase in 17 patients. Following diagnostic angiography, a ±5F end-hole catheter was advanced to the site of the thrombus and positioned immediately adjacent tothe thrombus, or with the tip embedded just within the actual substance. SK was infusedthrough the catheter at a dose of 10000U/h and infusion was continued until: (a) lysis wasachieved; (b) no lysis was seen even after 3 days; or (c) the development of bleeding orother complications forced discontinuation of infusion. Over two-thirds of the patients in this study demonstrated at least partial lysis, the majority of which occurred under 20 hand significant complications were noticed in three patients. The authors also observedthat patient selection is an important criterion for thrombolytic success and suggested thepossibility of treating the underlying causative pathology once the thrombus was lysed.

Innovations in catheter-based techniques may also have been spurred by the increasing awareness of the limitations of the Fogarty balloon thrombectomy, which include high


incidences of both residual thrombus and intimal or medical hyperplasia.36, 37 Intra-arterial low-dose SK was used by Katzen and colleagues38 in 12 patients with acute arterial thromboses. The technique was the same as that described by Dotter;35 however, the dose was reduced even further to 5000 U/h and the duration of infusion ranged from 5to 16h. Effective clot lysis was achieved in 92% and no significant complications werereported. This extremely encouraging outcome prompted further studies with the sametechnique of lytic agent delivery,39–41 all of which reported similar results.

To further shorten both the procedure time and the amount of drug infused, is 1981 Hess and colleagues42 developed the intrathrombic stepped infusion technique, which involved initial placement of the catheter about 1 cm into the substance of the thrombus,following which 1–3 ml SK solution in saline with a concentration of 1000 U/ml wasinfused directly into the substance of the thrombus. After 5–15 min, the catheter was advanced fluoroscopically further into the substance of the thrombus and infusionresumed. The thrombus was thus infiltrated with the drug along its entire length in asystematic fashion with the gradual, distal, step-by-step advancement of the catheter as and when lysis of the more proximal portions took place. This was continued until the catheter tip entered clot-free lumen and antegrade flow was observed. The duration oflysis was between 1 and 5 h. The infusion was stopped when complete lysis was observedand when antegrade flow was noticed for at least 10min. The difference between thisstudy and the previous two35, 39 involved not just technique, but that study subjects hereincluded both acute and chronic thrombi. The advantages reported were a more efficientclot lysis with shorter infusion times, a lower incidence of bleeding complications and theability to monitor the procedure fluoroscopically. However, this technique consumessignificant operator time. Using the same method, Lammer and colleagues43 confirmed the usefulness of the intrathrombic catheter position for lysis of chronic clots. Therationale behind this is explained by the presence of highflow collaterals at both theproximal and distal end of the chronically thrombosed segment, which effect a rapid stealof the drug, if the catheter is placed in a parathrombic situation, whereas theintrathrombic position enables the drug to remain in prolonged contact with the clot andeffect effi-cient lysis. It was also suggested (in what remains one of the earliest mentions of the advantages of mechanical disruption of clot) that the intrathrombic position of thecatheter resulted in the breaking up of the clot, thus increasing the surface area of thethrombus that is exposed to the thrombolytic agent, which also allows for more efficientlysis. The complications with this technique included intramural passage of the catheter(19%) and peripheral embolism of lysed fragments (all of which were, however, treatedby continued infusion) in 13%. A comparison of this technique with the original methoddescribed by Dotter and colleagues,35 revealed significant improvements over the latter,as regards the success rate, the mean total dose of SK used, and the incidence of bleedingcomplications. The intrathrombic technique was further refined by Mori andcolleagues,44 who introduced a guide-wire into the thrombus and passed a multiple-hole catheter over the guide-wire into the substance of the thrombus. This techniques resulted in lower percentage of transmural injections, which was noted to be a complication withthe original technique described by Hess and colleagues.42

Most intra-arterial thrombolytic studies between 1981 and 1985 were conducted usingSK. The low-dose SK regimen, though more effective than systemic infusions,


demonstrated a variable and unpredictable response in different studies, prolongedinfusion times and adverse reactions, at least some of which could be attributed to theinherent anti genecity of the drug. UK, though non-antigenic, was not as extensively studied due to both its higher cost (approximately three times that of SK) and preliminaryinvestigations, which reported success rates of 25% and 40% with the intraarterial use ofone-twentieth and one-tenth the systemic dose.39, 45 A randomized, double-blind study to assess the efficacy of intracoronary UK versus that of intracoronary SK was conducted in1984 by Tennant and colleagues,46 who elaborated the benefits of UK when used in a short-term high-dose of 6000 U/h over that of SK. Though this study showed an equivalent efficacy of lysis with both UK (60%) and SK (57%), the incidence of systemicfibrinogenolysis and thus of bleeding complications were significantly higher with SK(29%), as compared with UK (11%). This study prompted the trial of UK by McNamaraand colleagues47 in a landmark study of peripheral intra-arterial thrombolytic therapy in 1985, and established the technique of intrathrombic high-dose urokinase by graded infusion. This technique, or a modified version, is what is now standard procedure forintra-arterial thrombolysis. The procedure involves passing a guide-wire either well into or through the entire length of the thrombus, over which a catheter (a 5F end-hole catheter) is advanced. UK is infused into the thin channel created by the guide-wire at a rate of 4000U/min until luminal patency is established. At this stage, the catheter isrepositioned to dissolve remaining clot and infusion restarted at a reduced dose of 1000U/min. When repeat angiography shows complete dissolution of the thrombus, theunderlying causative lesion, if any, is treated. To compare their results with the low-dose SK regimen, the authors48 analysed five series that used this latter technique and reporteda combined average of 45% for complete lysis, 41 h for infusion duration, and 13% formajor bleeding. Average figures of 75%, 18 h and 4%, respectively, were reported withthe high-dose UK regimen. These results established that the high-dose intra-arterial infusion of UK is effective and safe. It was suggested that the decreased cost of a shorterinfusion time and a reduced hospital stay would offset the drug cost. Subsequentcomparative series and studies conducted with UK alone were in agreement on this48–53

and established the superiority of UK over SK. McNamara’s study47 also introduced the guide-wire traversal test (Figure 7.1b). It was observed that the ability of the guide wireto traverse the clot was the single best predictor of successful recanalization.

McNamara’s technique has been modified by altering the dosing regimens or by theuse of newer infusion catheter systems, or both. Low-dose intrathrombic UK therapy has been attempted in the hope of further reducing haemorrhagic complications, using dosesranging from 50 000 U/h to 100000U/h as against the high-dose technique, which employs 240000U/h of UK.54–56 Comparative studies of the low-dose versus the high-dose UK regimen have revealed conflicting reports. The largest such series by Cragg andcoworkers56 reports that the percentage of successful recanalizations, as well as bleeding complications, is equivalent in both groups.


Figure 7.1 Stages of intraarterial thrombolysis. (a) An occluded segment of vessel is demonstrated arteriographically. (b) A coaxial catheter is advanced through the interarterial sheath and advanced into the proximal thrombus; a guide-wire is then advanced to the distal end of the thrombus (GW traversal test). (c) A tip-occluded multiside-orifice catheter is advanced into the entire thrombus, which is saturated with a bolus dose of lytic agent deposited by rapid pulse-spray infusion. (Alternatively, an end-hole catheter or a catheter with fewer distal side holes is advanced distally and then retracted proximally, while depositing small doses of lytic agent at each station). (d) Continuous infusion is administered with an end-hole catheter with its tip in the proximal thrombus and a smaller side-hole catheter, which is advanced much farther into the clot. (A distal untreated segment is shown here, but a side-hole catheter with its tip occluded, may be advanced so as to bathe the thrombus with lytic agent throughout it length.) (e) As thrombolysis progresses, both catheters may be advanced, but with this configuration the inner catheter alone may be advanced into the receding thrombus front. This is continued until the entire thrombus is dissolved and an underlying obstructing lesion is uncovered for treatment by angioplasty or surgery. (Courtesy of Lippincott-Raven Publishers.)


In a study of 44 patients with femoropopliteal graft occlusions in 1986 Gardiner and colleagues, described the use of an intrathrombic bolusing, prior to infusion with either lowdose SK or high-dose UK (Figure 6.1c). An intrathrombic lacing of 25 000–250 000 U for the SK group and 30 000–60 000 U for the UK group was employed, followed byinfusions of 5000 U/h for SK and the modified graded schedule similar to that describedby Traughber et al. for UK.49 The study agreed with then current reports of UK as the more efficacious lytic agent, and though a more rapid lysis was observed with the use ofthe initial lacing, the difference was not statistically significant. Results confirming thebenefits of an intrathrombic lacing were reported by Sullivan and colleagues,58 who observed more rapid lysis with a net lowered dose of UK following lacing with largedoses (120 000–150 000 U) prior to infusion. The technique, best referred to as ‘intrathrombic lacing’ rather than ‘intrathrombic bolusing’, involves positioning of a catheter (either end-hole or multiple side holes) directly in the thrombus, with the catheter tip at the distal most part of the thrombus. As the agent is injected, the catheter is slowlywithdrawn over the clot, thus lacing its entire length with the drug. A more recentprospective study using the same technique with t-PA, has observed improved results with the combination of the high dose lacing followed by slow infusion, as compared toinfusion alone.59 Current dosing regiments for UK involve infusion of 4000 U/min for the first 2h, followed by 2000U/min for the next 2h, and finally 1000U/min untilcomplete lysis (Figure 7.2).

The advantages of mechanical disruption of the clot using a guide wire or a catheter had already been described.41, 51 Although the rate of diffusion of drug into the thrombus is yet to be determined, slow diffusion may constitute an important limiting factor. Bybreaking up a clot, the surface area exposed to the lytic agent increases, making for moreeffective lysis. In a 1985 paper titled ‘Accelerated thrombolysis’, Bookstein and coauthors60 confirmed the advantage of clot disruption. This hypothesis led to successfulattempts at creating a more homogenous and accelerated thrombolysis by forced pulsatileintrathrombic injection of thrombolytic agents in both in vitro61 and in vivo animal studies.62 Initial clinical results using this new technique, called pulse-spray pharmacomechanical thrombolysis (PSPMT), were published in 1989, by Bookstein and coauthors.63 The study used modified catheters, highly concentrated UK and pulse-spray injection, to treat patients with lower arterial occlusions. Pulse-spray catheter designs incorporate multiple side orifices over defined distances on the distal end, called theactive length of the catheter. Commercially available catheters are manufactured indifferent sizes of the active length to correspond to the length of the thrombus. Thethrombus is traversed with a guide wire and a special pulse-spray catheter is advanced over it and positioned in the thrombus in such a way that the active length of the catheteris located within the thrombus and a small distal portion of the thrombus is free of the


Figure 7.2 Case 1. (a) 1-month-old occlusion of a Femoroposterior tibial graft. (b) Distal occlusion of the posterior tibial with reformation by collaterals. (c) 5F sheath passed over the bifurcation from right to the left side using a crossover technique. (d) 20cm Cordis infusion catheter with radio-opaque marker denoting the active length of the catheter. (e, f, g) Progressive thrombolysis with urokinase using the Pulse-spray technique. (h) Successful thrombolysis with demonstration of re-established blood flow to the foot.

catheter to prevent distal embolization. This portion is subsequently treated as lysis progresses. The end hole is occluded with a tip-occluding wire and the lytic agent


(usually UK) is forcibly injected through the thrombus using a pulse-spray injector or by forceful manual injections with a tuberculin syringe. We conducted a prospective,randomized trial of forced periodic infusion and continuous slow infusion, using similartechniques and doses, with the addition of an initial intrathrombic UK lacing in patientswith acute lower limb arterial occlusions.64 Our study did not reproduce the lysis timesreported by Bookstein and colleagues63, 64 and our findings did not demonstrate a significant difference between the forced infusion and the continuous infusion withregard to rapidity of lysis or 30-day clinical outcome. However, overall total lysis timeswere reduced to 24 h, compared with our previous longer treatment times.

Tissue plasminogen activator (t-PA), and its recombinant form(rt-PA) have also been extensively studied in thrombolysis of peripheral arterial occlusions. The tech niquesinvolved in their use are the same as above. Dosage schemes range from 0.5 mg/kg/h to10mg/kg/h.64 The current consensus of thrombolytic agents is that t-PA and UK effect equivalent clinical outcomes and are superior to SK.25–31, 65–58 Although cost effectiveness of UK compared with SK has been established, as yet, similar comparisonsbetween UK and rt-PA are unavailable. Comparison of percutaneous intra-arterial thrombolysis with surgery has yielded contrasting results and has been the subject ofmuch unnecessary controversy, since these procedures are complementary and notcompetitive.66–73 We conducted a recent review of the risks and benefits of both procedures by analysing the results of six large, retrospective studies and of twoprospective, randomized trials that compared the two procedures in the management ofacute lower limb ischaemia (ALLI).73 Combined percentages indicated a substantially better limb salvage rate of 93% for thrombolytic therapy, as against 85.5% for surgery.Mortality rates were 4% and 16%, respectively, in these patients. Our findings concurwith prior studies, which suggest that intraarterial thrombolysis should be the initialtreatment for patients with acute lower limb ischaemia.

Infusion catheters (Table 7.1)

Commercially available catheters used for infusion thrombolysis include standard end-hole catheters, coaxial systems for split-level infusion of the drug, multiple side-hole catheters with tip-occluding wires and the newer pulsespray catheters. Many of theavailable infusion systems can be used for both conventional slow infusion and pulsedspray infusion. End-hole catheters are primarily used for slow, continuous infusion.Small, French-size catheters are available, which permit more easy negotiation of tortuous and distal vessels. Multiple side-hole catheters have, as the name suggests, side-holes over a variable length on the distal end of the catheter, called the active length.These catheters are commonly used with a tip-occluding wire and the lytic agent is evenly dispersed into the substance of the thrombus through the side-holes. A catheter with pressure responsive side slits, which is especially effective for pulsespray infusion,is available (Angiodynamics, Glen Falls, NY, USA) (Figure 7.3). Coaxial inner and outer catheter systems are utilized for the simultaneous lysis of both the proximal and the distalends of especially long thrombi, thereby avoiding catheter exchanges (Figure 7.1d). The McNamara coaxial catheter infusion set (Cook Inc., Indianapolis, IN,


Table 7.1 Commonly used infusion catheters

Application Name Comment

Slow infusion (end-hole only)

* Sos-wirea 0.03522′′ or 0.0382c'' OD, teflon catheter;

0,018'' or 0.021'' inner wire for co-axial introduction

* Cragg convertible wireh

0.038'' OD (accommodates inner 0.025" wire); 145 or 170cm long; removable hub .

Teflon jacket, 12cm distal floppy tip

Cragg FX (fixed hub) for microembolization

* Fast-Trackerc 3F end-hole catheter with clear radiopaque distal marker

Designed to track easily thorough small, tortuous arteries

Excellent for microembolization

* Micro-Soft Streamd

3F small vessel catheter with distal marker

Pulse-spray and slow infusion sion

* PRO pressure-responsive side slitse

4 or 5F; 90 or 135 cm long; 10 or 20 cm, infusion length

0.035'' tip-occluder wire for pulse-spray

Slow infusion without the wire , :

* Mewissen infusion catheterb

5F; 35, 65, 100 cm long; 5, 10 or 15 cm infusion length; can be used with the Katzen wire

* Katzen infusion wireb

0.035'' OD; 145 cm; removable hub; 3, 6, 9, or 12 cm infusion length with side holes; Teflon coated

* Multi-sideport infusion catheterf

5F; 65 or 100 cm long; 0.035'' or 0.038'' guide wire 4, 7, 11 or or 15 cm infusion lengths

* McNamara coaxial catheter infusion setf

Outer 5.5F catheter with coaxial inner 3F multi-sidehole catheter; advantage: infusion length can be adjusted to to match the thrombus length without catheter exchanges

OD=outer diameter; GW=guide wire diameter, Consult package inserts and manufacturer for available French sizes (guidewire accommodation), lengths, and possible flow rates, a: USCI Bard, Billerica, MA, USA. b: Medi-Tech, Watertown, MA, USA. c: Target Therapeutics, Freemont, CA, USA. d: Medtronic MIS, Sunnyvale, CA, USA. e: Angiodynamics, Glen Falls, NY, USA. f: Cook, Inc., Bloomington, IN, USA.


USA) (Figure 7.4) is one such system, which allows the infusion length to be varied asthrombolysis progresses. The Mewissen multiside-hole, over-the-wire infusion catheter (Figure 7.5) can be used alone or in combination with a coaxially placed Katzen infusionwire (both by Medi-Tech/ Boston Scientific, Watertown, MA, USA). Infusion catheter systems facilitate the process of intra-arterial

Figure 7.3 Angiodynamics pulse-spray infusion catheter. (Courtesy of Angiodynamics, Geln Falls, NY, USA.)

thrombolysis and, more importantly, aid the achievement of a more homogenousthrombolysis.74

Adjunctive anticoagulation

The use of adjunctive heparin has been a source of controversy; some investigatorsbelieve that concomitant

Figure 7.4 Multi-sideport infusion catheter. (Courtesy of Cook, Inc. Bloomington, IN, USA.)


Figure 7.5 Mewissen infusion catheter with an inner, coaxial, Katzen wire. (Courtesy of Medi-Tech/Bostan Scientific Corporation, Watertown, MA, USA.)

anticoagulation will increase the risk of bleeding38, 45 and other series have reported equivalent success rates when no heparin or low-dose heparin was given.54 Rethrombosis occurring during thrombolytic is multifactorial. Thrombolytic agent themselves produceprocoagulant effects and a low blood flow and the inherent thrombogenecity of thecatheters also contribute. The benefits of anticoagulant therapy in reducing reocclusionsand pericatheter thrombosis has been established in numerous studies.47, 57, 75–77 The incidence of rethrombosis with concomittant heparin approaches 3%.47, 57 Dosages commonly used are an intravenous bolus of 70 U/kg followed by continuous i.v. infusionat 600–1200 U/h. The dosage of heparin is adjusted to maintain the PTT at 1.5–2 times


the control, during lytic therapy. It has been suggested that the injection of heparinthrough the intra-arterial sheath in smaller doses might be sufficient to prevent the development of pericatheter thrombosis.77 Research is underway with a wide range ofnewer anticoagulants. These include the direct thrombin inhibitors hirudin and hirulog,the low molecular weight heparins, direct factor Xa inhibitors, tissue factor pathwayinhibitor and activated protein C, all of which are currently undergoing trials. Thedevelopment of these agents and their use change the current methods of anticoagulationin the future.

Mechanical thrombectomy

Mechanical thrombectomy refers to the bulk removal of the offending thrombus orembolus, and comprises two primary modalities: (a) the surgical approach—involving an arteriotomy and the subsequent use of the Fogarty balloon for thrombus removal; and (b)the percutaneous approach—involving percutaneously placed catheters or devices used to remove the thrombus. The following discussion focuses on the percutaneous techniques,their development and use.

There are two methods for percutaneous removal of thrombus: (1) percutaneous aspiration thromboembolectomy (PAT) which, as the name implies, entails aspiration ofthe clot by the application of suction through the catheter; and (2) percutaneousmechanical thrombectomy (PMT), involving the mechanical disruption of the clot intosmaller fragments, which then may or may not be aspirated, depending on the fragmentsize. The 1990s saw rapid advances in mechanical methods of thrombus removal. Theuse of endovascular mechanical devices is still currently limited, primarily due to thesuccess of thrombolytic agents and also because of persistent worries regarding theirpotential to cause distal embolization and vascular injury. The major advantage ofmechanical thrombectomy is the rapidity with which luminal recanalization can beestablished and the absence of overt systemic side-effects with their use. The main indications for their application lie in situations where thrombolytic therapy iscontraindicated, where smaller doses of thrombolytic agents may be preferred, whereinthe clinical condition demands rapid lysis and in acute postangioplasty embolism. Theprincipal disadvantages with the use of these devices are postprocedural residualthrombosis and the injury to the vascular wall.

Percutaneous aspiration thromboembolectomy (PAT) (Table 7.2)

This technique was first described in 1961 by Dale and colleagues,78 who aspirated thrombi through catheters of different sizes that were introduced coaxially through thevascular lumen. In 1969, Greenfield and coworkers,79 described the aspiration of a pulmonary embolus using a balloon catheter with a cup at the distal end. The catheter wasadvanced into the artery until the cup abutted the embolus. The balloon was then dilatedto isolate the occluded segment and the embolus was aspirated into the cup using suction.The balloon was deflated and the embolus removed, trapped within the cup. Apart from areference to the use of percutaneous aspiration to remove an iatrogenic embolus that


occurred following angiography of the renal artery,80 no studies were conducted in the 1970s utilizing this technique. In their discussion on complications of angioplasty,Horvath and colleagues81 suggested that emboli resulting from the procedure could be aspirated with a catheter, although they did not cite any clinical experience. In 1984,Sniderman and colleagues82 described the use of the PAT in six patients who developed distal emboli post angioplasty. The procedure was successful in all but one case.Following preliminary angiography, an 8F sheath (to help minimize arterial wall injuryduring catheter exchanges and protect branches and collateral vessels from ‘drop’ emboli) is intro-

Table 7.2 Major PAT Series

Study Number Site of occlusion

Acute/chronic Type of occlusion

Adjuvant therapy

E T

1, Wagner et al., 199285

n=102 Lower limb arteries

71.6%−<3days 100% 12.7%–RAT

20.6–4–30 days

7.8%—>30 days

2. Turnipseed et al., 198686

n =42 (44 procedures)

Lower limb arteries

All acute 75% 25% 64%–(PAT; lysis)

(Acuteness NS)

(Acuteness NS)

3. Starck et al., 198583

n=41 (45limbs)

Lower limb arteries

N.S. 80% 20% 69%–(PAT; lysis)

−43

Visceral arteries,

−2

4. Turmel-rodrigues et al., 199787

n=59 Hemodialysis grafts

All acute All 5%–(stents)

PTFE–73% (Acuteness NS) 3.2%–(stents for reintervention) NF–27%

Technical success

Clinical success/patency rates

Complication Procedure/thrombectomy time

93.1% Clinical success; 8.8% Ave procedure time;

(time period NS): = 150 min


duced. A bolus of 5000 U of heparin is administered after placement of the guide-wire. The guide wire is advanced through the length of the thrombus.† Following passage through the thrombus, the guide-wire is withdrawn into the clot-free lumen and the aspiration catheter is advanced over it, until its tip is embedded within the substance ofthe clot and no backbleeding is evident on suction—an indication that the catheter lumen is blocked by the clot. The catheter, with the clot sucked into its distal end, is withdrawnunder continuous suction. A number of catheter passes can be made until successfulaspiration of the offending clot.

Numerous varieties of aspiration catheters are available on the market; the basic designincludes a mildly tapered end in different French sizes (the most effective aspiration isachieved when the catheter size corresponds directly to the arterial lumen diameter). Thestudy by Sniderman and colleagues82 observed that the incidence of emboli was higher following angioplasty for occlusions (11%) than that for stenoses (2.2%). They alsosuggested that sheath removal should be accompanied by continued suction andaspiration to prevent re-embolization from trapped thrombi or debris within the sheath.

In a comparatively larger series in 1985, Starck and colleagues,83 reported the use of PAT in 41 patients who had acute emboli from either angioplasty, lytic therapy(residual)or a cardiogenic source. The procedures employed included, PAT alone or incombination with local lysis and balloon dilatation. Angiographic success, defined as

87.3%

95.0% NS 17.0%,(8/42) NS

Haematomas−n=7

Pseudoaneurysm−n=1

97% Clinical success; 19.5% (8/41) NS

(Follow -up week—2 years); 93%;

Haematomas−n=6

Embolisation−n=1

Paresthaesia-n=1

PTFE–100% PTFE: NF:

NF–81% Immediate: PTFE−119 min

100% 81% ±29

1 month; NF−151 min

85±5% 81±10% ±56

6 months:

33±8% 74±14%

Ave; average; E= emboli; NF: native fistulas; NS: not specified; PAT: percutaneous aspiration thrombectomy; PTA: percutaneous transluminal angioplasty; PTFE: polytetrafluoroethylene; RAT: rotatory aspiration thrombectomy.


improved lumen patency was seen in 97%, whereas clinical success, described as animprovement of one Fontaine stage or improvement within the same stage, was 93%.These figures, however, apply to the combination of the procedures employed andindividual figures were not reported. The authors suggested using PAT forthromboembolic conditions below the iliacs and observed that the Fogarty technique maybe of better use in the aorto-iliac region, due to the inherent large volume of the thrombus in these areas, which would make retrieval by the percutaneous technique difficult. Thestudy went on to define

†If there is strong resistance to the passage of the guide-wire, the clot may be organized, chronic and adherent to the wall. At this time, a trial run of lytic therapy may be tried, to soften the clot and allow the smooth passage of the guide-wire and the aspiration catheter. In this way, the two procedures, i.e. lytic therapy using intra-arterial infusion of thrombolytic agent, and PAT, can be mutually beneficial, with the ultimate advantage of a reduction in both procedure and lysis times.

advantages of PAT over the Fogarty procedure, which included comparable limb salvagerates, a lower mortality rate, less injury to the vessel wall and the use of fluoroscopy,affording a high degree of control over the procedure. In 1988, Starck and McDermott84

improved the technique by incorporating an 8F double-lumen aspiration catheter, which allowed both aspiration and injection of contrast or lytic agent. They also described aspiral-tipped, roundended, stiff, guide-wire and a 5–8F rotating basket as accessory aids to thrombus removal by aspiration. These additions to the technique were incorporated inthe largest series of PAT, comprising 102 patients with acute embolic occlusions of theinfra-inguinal arteries.85 The 5F catheter used here was specially developed with the distal 5 cm tapered to 4F and a Berenstein configuration of the tip. Aspirationthrombectomy was employed, as previously. However, when a chronic, organized clotoffering resistance to the guide-wire was encountered, the spiral (in smaller vessels) andthe basket, which on slow rotation detaches the clot from the walls, (in larger vessels)were used to assist in removing the thrombus. Both devices caused minimal damage tothe intima and were used only as adjuncts to the primary Pat procedure when the latterwas not successful. Angiographic success was reported in 93%, clinical success in 87%and limb salvage in 94%. The authors concluded by suggesting that all suspected embolicocclusions distal to the inguinal ligament should have a primary PAT procedure, with theabove adjunctive devices used as needed. Similar rates of success have been proved byother studies.86–89 Long-term results of PAT have been reported over a 5-year period, in the treatment of acute embolic occlusions of the infra-inguinal arteries.90 The primary patency rate at the end of 1 year was 88% and at the end of 4 years was 86%. Further, adecrease in mortality rates and an increase in patency rates with the concomitant use ofthe anticoagulant coumadin was observed.


Percutaneous mechanical thrombectomy (PMT) (Tables 7.3 and 7.4)

As opposed to PAT, which is a relatively simple procedure utilizing simple manualsuction to aspirate the clot out of the lumen, PMT employs a wide array of devices, whichmechanically disintegrate and fragment the clot, using aspiration as an adjunctive finalstep if necessary. The thrombus is fragmented, in contradistinction to the slow

Table 7.3 Major PMT series—hydrodynamic mechanical thrombectomy (ATD)



Adjuvant therapy

E T

5. Rillinger et al., 1997106

n =40 Lower limb arteries

All acute: ave–2 days.

80% 20% 20%–(lysis, PTA, atherectomy) Native–78% range−(3h-8

days)

Graft–22%

6. Uflacker et al., 1996107 (randomized)

n=37 Hemodialysis All Acute < 1 week

MT–100%(PTA; lysis)

MT–19 grafts (PTFE) ATD–ave 3.3 days

All

ST–18 ST–ave 3.4 days ST–none

Technical success Clinical success/patency rates


95% Clinical success; 95% at 1 week

10% Thrombectomy time;

—complete success:

Haematoma—1 complete success—75 s

75% Mechanical failure—3

partial success—90s

—partial success: 25%

1 month: Ave thrombectomy time (MT):

MT–89% MT–47%

MT − Haemolysis—63%

4 min 6s


dissolution that occurs with infusional lytic therapy, with the obvious advantage being therapidity of the process effecting early re-establishment of antegrade flow. Theeffectiveness of the PMT device depends upon the volume of thrombus fragmented bythe device into sufficiently small particles.91 The maximum acceptable particle orfragment size depends on the size of the vessel and sizes of 500–1000 µm are considered significant in the pulmonary tree and in peripheral systemic arteries.92 Though some of the initial designs are no longer in vogue, they have been an important process in theevolution of the concept. This technique is not yet widely practiced and most of thesedevices have not been put through large clinical trials. The following paragraphs containa description of some of these devices.

The earliest form of mechanical thrombectomy is the rotational thrombectomy system. The initial, technically simple designs functioned on the principle of motor-driven rotation of the distal end of either a catheter or a wire, which lysed the clot by literallydrilling through it. The midto late 1980s witnessed the development of a number ofdevices based on the same principle. The first device that employed this principle wasdesigned by Hawkins and colleagues in 1985.93 It used both a rotation and oscillating spiral for clot transportation. In 1986, Ritchie and colleagues,94 described a catheter system that consists of a 4F inner catheter, an 8F guiding catheter and a rotating flexiblesteel wire with a rounded platinum tip, which is motor driven at 4000 rpm. Oncepositioned in the thrombus, the wire was rotated and the thrombus lysed, with its fibrinmatrix entangled around the wire and its cellular elements loosened free into the flow. In1988, Starck and coworkers,84 working on the same principle, designed a rotating spiral-tipped wire to be used as an adjunctive device with percutaneous aspirationthrombectomy.

The next generation of rotational thrombectomy devices incorporated design modifications of the same rotating mechanism, primarily those of the additions of acutting tip and/or alteration in the speed of rotation. Most of these devices differ in thetype of cutting implement added and on the rotational speed. Ritchie’s original design was modified by Hansen and colleagues in 1987,95 by adding a cutting abrasive head (made of minute diamond particles embedded in nickel) to the wire and by increas-

ST–83% ST–77% ,

—(Haematoma, Ps. aneurysm)–15%

—Mechanical failure–10%

ST—28%

ATD: Amplatz Thrombectomy device; Ave: average; MT: mechanical thrombectomy; E: emboli; NF: native fistulas; NS; not specified; PAT: percutaneous aspiration thrombectomy; PTA; percutaneous transluminal angioplasty; PTFE: poly tetra fluoro ethylene; ST: surgical thrombectomy; T: thrombi; Complete success; ATD alone, no ancillary procedures; Partial success; ATD with adjuvant therapy; Ps. aneurysm: pseudoaneurysm.


Table 7.4 Major PMT series—hydraulic mechanical thrombectomy

A AngioJet



Adjuvant therapy

E T

A AngioJet

1. Wagner et al., 1997112

n=50 Lower limb arteries

All acute (5 days ± 5)

NS 100%–(PTA; lysis; stent, PAT)

Native–78%

Grafts—22%

2. Stainken et al., 1993113

n= 16 Heterogenous: native

All acute NS 50% – (lysis)

(18 procedures)

artery—2; prosthetic

(acuteness NS)

conduit—9; native

vein—2; vein

bypass—5.

3. Ramee et al., 1994111

n =11 (17 procedures)

Hemodialysis grafts (PTFE)

NS All 100%–(PTA; lysis, atherectomy. stent)

Technical success



90% Immediate; 82% 22% Mean device activation time: 7 rain 28 s

1 month: 76% Embolization—6%

6 months; 72% Dissection—6%

Perforation—4%

Haematoma—4%

Retroperitoneal bleed -2%

78% NS 22% NS


100% At 4.2 months None Mean device activation time: 8.2 ± 4.2 min

B Hydrolyser

Study Number Site of occlusion Acute/chronic Type of occlusion

Adjuvant therapy

E T

1. Henry et al., 1996118

n=50 Heterogenous; predominantly native arteries—70%

All acute (mean 8.2 days ± 7.3) range –1–30 days

All 100%-(PTA; lysis; PAT)

2. Reekers et al., 1996120

n= 28 Lower limb: Mean thrombus age

Native arteries—11

- 12days 4% 96% 100%-(PTA; lysis; stent) Bypass grafts -17 (range: 1–63)

3. Overbosch et al., 1996119

n= 49 (65 procedures)

Haemodialysis grafts: PTFE-28%

All acute (0.5–2.0 days)

All 88%-(PTA; lysis; stent)

B-CF-37%

Vein loop—35%

Technical success



82% Immediate: 82% 1/41—distal embolization treated with PAT

NS

1 month: 74%

93% 1 month: 50% 41% (distal embolization) - only with grafts

NS

Native arteries—73%

-73%

Grafts-35% −35%

89% Immediate: 80% 15% Average procedure time: 60–90 min

PTFE-100% Median primary patency for all –14 weeks

Haematoma−n=7

B-CF-83% Embolization−n= 3

Vein loop-87%

Median assisted patency:

PTFE-52 weeks


ing the speed of rotation to 40 000 rpm. This newer version, though more effective inlysis, had the serious disadvantage of arterial injury. In the latest version of this device,redesigned in 1993, the tip is back to a non-cutting one and the speed is down to 5000rpm.96 The Kensey dynamic angioplasty catheter (KDAC), designed in 1987, was initially used as an atherectomy device; its use has since been extended to thromboticocclusions of peripheral vessels.97 This device, later called the Trac-Wright catheter, was the trendsetter in the use of the hydrodynamic, rheolytic principle for thrombectomy. Arotating cam at the distal tip of a polyurethane wire is driven at speeds of 100 000 rpm byan electrically driven internal torsion guide-wire. The catheter also contains a continuous channel through which fluid flows under pressure and exits at the base of the cam in finejets directed laterally against the vascular wall. These jets cool and lubricate the cam. Thecombination of the rapidly exiting fluid perfusate and the rotating tip creates a low-pressure vortex ahead of the tip, which aspirates intral-arterial debris toward the cam. Studies with this device have revealed successful recanalization in all arteries. However,a significant amount of intimal and medial injury, as well as evidence of distal emboli tothe brain and kidneys, have been reported.98–100 The clinical use of the KDAC in a small series also demonstrated distal embolization and rethrombosis.98, 101 The device design, which has the nonrecessed propeller tip/cam extending beyond the catheter into thelumen and the fluid jets that impact directly on the wall, has been implicated in vessel-wall injury.

The Bildsoe mechanical thrombectomy device, designed in 1989, uses a catheter with asmall, distal, high-speed propeller recessed in a special housing.102 The 8F polyurethane catheter has a 1 cm long open-ended metal cylinder with two side holes, into which asmall propeller is recessed and protectively housed. This propeller is attached by a drivenshaft to high-speed motor capable of achieving rotational speeds of up to 100000rpm.Saline or lytic agents can be infused through the catheter, both of which will lubricate andcool the drive shaft. The initial in vivo experiments using different speeds of rotationsuggested that the efficiency of lysis was related directly to the speed and duration of therotation.102 At 80000 rpm, 97% dissolution of the clot was achieved in 10s, withinsignificant haemolysis. This device was expected to be safer than the KDAC, due to therecessed rotating blades, and it was thought that the forceful retrograde flow produced bythe device would lyse the thrombus from proximal to distal end, thus reduc ing thechance of embolization. Lack of effective steerability was a limitation. The study stressedthe potential advantages of PMT over surgical thrombectomy and local lysis, especiallyin acute emboli in haemodialysis grafts.

The Gunther catheter was designed in 1990 and combined mechanical and aspirationtechniques to effect thrombectomy.103 The system consists of 7F teflon catheter with a co-axial, 0.4 mm propeller-tipped wire, which is motor driven to 500–1000 rpm.

Others—34 weeks

Ave; average; B-CF: Brescia-cimino fistulas; E: emboli; NF; native fistulas; NS; not specified; PAT: percutaneous aspiration thrombectomy; PMT: percutaneous mechanical thrombectomy; PTA: percutaneous transluminal angioplasty; PTFE: polytetrafluoroethylene; ST: surgical thrombectomy; T: thrombus.


Continuous suction of disintegrating clot material was achieved by a roller pump, througha suction tube attached to as side-arm adaptor. An additional side arm allows forinfusions. The system is introduced through a 7F vascular sheath. Initial case reports ofits use in three patients (two occlusions of the superficial femoral artery and one occludedpolytetrafluoroethylene [PTFE] haemodialysis graft), described effective, rapid lysis andearly restoration of flow.103 Because of the size of the propeller, the catheter tip is not rigid, which allows it to enter smaller vessels. Another advantage with this device is thatthe propeller (as in the Bildsoe catheter) is recessed into the lumen of the catheter, andwith this design vessel injury has not been reported. With the rapid development yet scantclinical experience with these thrombectomy devices, Schmitz-Rode and colleagues100

conducted an in vitro comparative analysis of the above-described three catheters, along with two modified aspiration catheters on both femoral arterial (adherent) and pulmonaryartery (free-floating) thrombi. The devices studied were the Kensey catheter, the Bildsoecatheter, the Gunther catheter, a prototype propeller aspiration catheter (propellerdimension similar to the Bildsoe, attached to a drive-wire rotating at 80 000 rpm in the distal end of a large bore catheter) and a prototype loop aspiration catheter (a wire-driven loop made of flat profile spring steel, rotating in the distal end of the catheter). The studydrew the following conclusions:

• all tested catheter systems were effective in recanalization of the adherent thrombi in the femoral flow model;

• the apposition of fibrin filaments to the catheter surface after removal of free floating thrombi was less marked with the Gunther catheter;

• fragmentation of large thrombi with the Bildsoe was impaired by fast fibrinous obstruction of the metal housing; and

• the Kensey catheter yielded the best results in lysis of large thrombi.

Two important and relevant criteria—that of vascular damage and device steerability—were not addressed, due to the in vitro nature of the study.

Three new systems based on ‘vortex’ generation have been introduced in recent years. These are the Amplatz thrombectomy device, the AngioJet catheter and the hydrolyser.The recirculation concept revolves around the development of a ‘low-pressure vortex’ at the distal end of the catheter. This vortex develops under two conditions: hydrodynamicand hydraulic. A hydrodynamic vortex develops when high-speed rotation of an impeller creates a rotational flow region with a central low-pressure zone (Venturi effect); which has an apex directed towards the source of rotation. This region of low pressure aspiratesany material in its path (in this case, thrombus) towards it, akin to a whirlpool. Regardlessof the position of the rotatory cutting up tip with regard to the catheter (i.e. eitherrecessed or not), the vortex aspirates more clot towards the rotating device, where it getspulverized into fragments. An effective vortex is only created when the speed of rotationis very high. The earlier devices by Hawkins, Beck, etc. used rotatory ends with relativelylow speeds (4000–40000 rpm). The Kensey catheter employs a speed of 100000 rpm andthe Amplatz thrombectomy device (ATD) uses 150 000 rpm. A useful vortex is generatedonly under such high-speed conditions. Whereas mechanical rotation is used to createhydrodynamic vortices, hydraulic vortices are generated using retrograde (towards thelumen of the catheter) high-speed saline jets, which create a low-pressure zone that traps


and aspirates the thrombus into it. The primary complications with the use of thesedevices are haemolysis and vascular injury. The first description of the use of saline jetsto create a rheolytic, hydrodynamic vortex in a thrombectomy device was made byKensey in 1987.97

Amplatz thrombectomy device (ATD) (Microvena Corporation, White Bear Lake,MN, USA) (Figures 7.6 and 7.7). This device is a modified version of the Bildsoecatheter and is designed by the same group. The device consists of an 8F polyurethanecatheter with an impeller mounted on a drive shaft recessed into a 1 cm long openendedmetal cylinder, with two side holes. The impeller and shaft are driven by an air motor at150000rpm. A Y-connector at the proximal end of the catheter permits infusion of saline or lytic agents, which serve to lubricate and cool the device. The device does not have acentral channel and cannot be threaded over a guide-wire. Once positioned at

Figure 7.6 Amplatz thrombectomy device—ATD. (Courtesy of Microvena Corp., White Bear Lake, MN, USA.)

the target site of occlusion, the ATD is activated with a foot switch and is advancedslowly through the thrombus from the proximal to the distal end using a slow to-and-fro motion. The ATD has been studied in arterial, venous and haemodialysis graft occlusionsin the USA and is approved by the Food and Drug Administration (FDA). Initial clinicalevaluation of the ATD by Coleman and colleagues104 in five patients with acutely occluded lower limb arteries or grafts reported complete lysis in three and partial lysis intwo patients. A blood pressure cuff was inflated over the proximal calf prior to activationof the device


Figure 7.7 Close-up of the Amplatz thrombectomy device. Note the impeller recessed within the metal housing and the side holes. (Courtesy of Microvena Corp., White Bear Lake, MN, USA.)

(to prevent particulate embolization), and on visualization of homogeneous lysis thedevice was exchanged for an 8F guiding catheter, through which the macerated clot wasaspirated. Complete lysis was effected in 138s, a marked reduction in lysis timecompared to any other current technique. Mechanical failure caused by a broken shaftresulted in partial lysis in two patients, in whom the aspirate revealed more organizedclot. Tadavarthy and colleagues105 described the use of the ATD in 14 patients with acuteor subacute thrombosis, the majority of which were in PTFE graft. Complete success,defined as complete clinical improvement by complete clearing of thrombotic material inthe treated arterial segment without the need for adjunctive interventional or surgicalprocedures, was reported in 71% of patients. Partial success, defined as incompleteclearing of thrombus, necessitating adjunctive interventional or surgical procedures toachieve complete clearing of the artery, was reported in 14% or patients. Failure, definedas those cases in whom the device did not contribute to or shorten time towards completeresolution of the clot, was reported in a further 14%.

Mean thrombectomy time was 2 min 45 s, and the procedure entailed between one andthree passes of the device for successful lysis. Complications were noted in 28% transienthaemolysis occurred in all patients and distal embolization requiring further use of thedevice was seen in two patients. A more recent study involving the use of the ATD in 40patients (the largest series to date), with acute (mean 2 days) occlusion of the lower limbarteries (the majority of which were embolic), reported complete success in 75%, with amean thrombectomy time of 75 s.106 Partial success was achieved in 20%, with a mean device activation time of 90 s. These latter patients had an average total treatment time(inclusive of local lysis and or adjunctive procedures) of 12 h. The total limb salvage ratewas 95%. Complications were observed in four patients (10%), three of which were dueto mechanical failure of the device, resulting from breakage of the drive shaft. In all three


cases, complete recanalization was obtained with adjunctive local lytic therapy andadditional angioplasty. Mechanical thrombectomy was commenced at the proximal sideof the thrombus and a primary passage through the thrombus was avoided. In addition,the technical design of the device allowed the clot to be dissolved from its proximalextent to its distal extent without to tendency to push or expel significant debris distally.No clinically relevant distal embolizations were noted and the authors felt that this had todo with their technique. Regarding particle size, the findings of an in vitro study reported that 98% of the fragmented clot material is small enough to pass through the capillarybed, that the number of larger particles decreased as the activation time increased, andthat the age of the thrombus had little influence on the results.92 Similar success rates have been described with the ATD, and most reports also concur on thedisadvantages.104–107 The ATD is not steerable, is ineffective in the treatment of chronic clots and its size precludes its use in smaller arteries. Device modifications include asmaller (6F) size108 and an ATD with three side holes (one smaller than the other two) on the distal end of the catheter.109 This latter design allows lateral deflection of the cathetertip during device activation and provides a steering mechanism.

The Rheolytic thrombectomy catheter (RTC) or the ‘AngioJet’ (Possis Medical, Minneapolis, MN, USA) (Figures 7.8 and 7.9) catheter system was first described in1992.110 The system is made up of a disposable catheter and a pump set with a reusablepump drive system. The 6F catheters have a high-pressure stainless steel tubing to supply the jets. The larger lumen can be used for tracking over a wire and for the removal ofdebris. The distal end of the stainless steel tube projects beyond the catheter tip andcontains between four and eight high-speed jet orifices oriented at a retrograde angle toavoid direct contact with the vessel wall. In the gap between the jets and the end hole ofthe catheter a low-pressure zone is created by the retrogradely exiting high-speed jets, resulting in a vortex that pulverizes and aspirates the obstructing thrombus. A disposablepump supplies pressurized saline to the catheter (at up to 30 000 psi) and is activated by afoot switch. Tubing attached to the catheter exhaust port is passed through a roller pumpso that the rate of exhaust equals that of saline infusion. The RTC is advanced into thevessel over a guidewire to the thrombus site. The jets are activated and the RTC isadvanced throughout the thrombus with the jets activated. Slurry and debris of lysed clotis continuously removed through the exhaust lumen by the roller pump. Initial in vitroand in vivo animal studies were reported in 1992,110 and technical success in acute thrombus was confirmed. Treatment of an entire occlusion may be achieved with a singlepass, thus avoiding the tenuous repeated withdrawals and insertions with most otherdevices. Removal of thrombotic debris, rather than fragmentation of thrombi into thedistal circulation, is another advantage, reducing the possibility of embolizations.Furthermore, contrast


Figure 7.8 Case 2. (a) Contrast lining thrombus occluding a haemodialysis graft. (b) AngioJet seen positioned within the thrombus in the graft. (c) Complete lysis of the thrombus, with re-establishment patency. (Courtesy of Drs M.F. Meyerovitz and S. Bravo, Cardiovascular and Interventional Radiology, Brigham and Women’s Hospital, Boston, MA, USA.)

medium can be easily injected through the exhaust lumen and allows simultaneousassessment of the procedure. It was observed that spacing of jets close together resultedin fewer passes with the device, and that jets that direct the flow radially without an axialcomponent tend to restrict any axial particulate embolization proximal to the catheter tip.This device has potential for use in both pulmonary and coronary arteries.

Early studies on both arteries and haemodialysis grafts observed a greater percentage of success in grafts; the larger number of failures in the native arteries could be related tothe age of the clot (thrombi in grafts and emboli being generally recognized as moreacute nature.110–113 Haemolysis produced by the device; even at longer runs, wastransient and mild. A newer version with six jets has been designed and a preclinicalstudy on its safety has been published.114 Three high-pressure jets (1–2 psi) are aimed retrogradely towards the evacuation lumen. Three additional jets at low pressure (1000psi) that are directed radially, optimize the recirculation vortex. An animal study thismodified version was analysed and observed, indicating insignificant direct trauma to thevessel wall or target vessels, transient systemic haemolytic effect, limited number andsmall size of the particulate debris, absence of retrograde reflux of released particles andabsence of tissue necrotic effect from the released particles.114 Technical


Figure 7.9 Rheolytic thrombectomy catheter—AngioJet. The illustration shows both non-functioning and functioning (activated) jets. (Courtesy of Possis Medical Minneapolis, MN, USA.)

advantages of the device are the ability to advance the device over a guide-wire and greater flexibility. The report ends on a note of caution, suggesting that significanthaemolysis could occur with prolonged activation, which might therefore be a possiblelimitation of its use in patients with volume or renal compromise.

The Hydrolyser (Cordis Europa, Roden, The Netherlands) (Figures 7.10 and 7.11)

This device was first described in 1993 and works on the same principle as theAngioJet.115 It uses a 7F doublelumen (catheter a narrow-injection lumen and a wider exhaust lumen) with an oval side hole measuring 6 mm at its distal end. The injectionlumen bends 180 degrees at its tip. Saline is injected into this narrow lumen at a pressureof 750 psi, provided by a conventional contrast medium injector. The high-velocity saline jet is directed over the side hole, creating a low pressure locally in the region of the sidehole. The negative pressure aspirates the thrombus into the side hole, where it getsfragmented into smaller particles, which are then discarded through the exhaust lumen. A6F version has been developed and studied in aortocoronary bypass grafts.116 The Hydrokyser is not yet approved for use in the USA. Thrombolytic success with theHydrolyser has been reported in several European studies in different vascular territoriesincluding the coronaries, with procedure times ranging from 45 to 90 min.115–122 In a large, retrospective series of 45 patients with occluded haemodialysis access shunts,primary success with the Hydrolyser was seen in 89% and minor complications in15%.123 The authors observed that the rates of technical success, complications andprimary patency are similar to that of alternative radiological techniques, with the addedadvantages of ease of use and reduced procedure time at comparative cost. Regardingvessel wall trauma and reac


Figure 7.10 Hydrolyser with guide wire in larger exhaust lumen. Note the projecting nozzle in the oval side hole, through which the saline jet emerges. (Courtesy of Cordis Corp. Warren, NJ. USA.)

tion, it has been reported that a single passage of surgical thrombectomy ballon issignificantly more traumatic than the Hydrolyser and that there is no difference in arterialinjury between a functioning (activated) device and a nonfunctioning device.119, 122

A comparative in vitro study of the two systems—the AngioJet and the Hydrolyser—was conducted by Bucker and colleagues in 1996,124 employing both an arterial adherent thrombus model and a venous, free-floating thrombus model. The AngioJet embolized significantly less than the Hydrolyser. In both the venous flow and the arterial flowmodels, both systems could achieve acceptable clot removal rates when employed with aguiding catheter. Under these conditions, results were comparable in the venous flowmodel, but the AngioJet showed a significantly higher rate of thrombus removal in thearterial model. Both systems removed fresh thrombus from vessels as large as 20 mm,though more effectively when used with a guiding catheter. Another device employingthe same rheolytic principle is the Saline jet aspiration catheter. This device, which was first described and tested successfully in a patient with an IVC thrombus in 1993,123, 125

consists of an inner 4F nylon tube with a 180-degree curved nozzle 2 mm proximal to thecatheter tip, and an outer nylon tube with an outer diameter of 4 mm. The saline flow


provided by an angiographic power injector is pumped from the inner to the outer tube,thereby creating a negative pressure region at the distal end of the catheter, into which thethrombus is evacuated and fragmented.

Figure 7.11 Schematic representation of the hydrodynamic vortex produced by the hydrolyser. The arrows pointing backwards (to the right of the figure) represent the retrogradely directed saline jets. P depicts the low-pressure zone created by the Venturi effect. All other arrows indicate the sucking in of the thrombus towards the low-pressure zone, the fragmentation of the thrombus, and recirculation. (Courtesy of Cordis Corp., Warren, NJ, USA.)

Other design innovations using rotating baskets at the catheter end instead of impellersentered the thrombecto-my device market in the early 1990s. The filaments of the baskets have a smooth and atraumatic contour to minimize the injury to the arterial wall and arevery effective in the removal of adherent thrombi. The earliest description of such adevice was by Starck and colleagues,84 who added a basket as an adjunctive device to their percutaneous aspiration catheter. Two such devices that effect thrombectomy byemploying a ‘pull-back’ approach similar to the Fogarty ballon are the ‘mini basket’ and the CTD. The mini basket, described by Gunther and colleagues in 1991,126 is a helical Dormia basket made from eight ultra-thin stainless steel wires, soldered at one end to guide-wire and at the other to a 2cm long floppy tip. This wire, with the restrained basket,is inserted through a 3F teflon catheter and the assembly is then introduced into the vesselthrough an 8F sheath with a haemostatic valve. The catheter with the indwelling guide-wire is passed through the thrombus or embolus targeted to be captured and positioned sothat the basket is distal or beyond the embolus. The position can be easily confirmed bythe radio-opaque soldered ends. The outer catheter is now withdrawn, allowing the basket to expand to its unconstrained shape (diameter 6mm; length 14 mm), and the basket iscarefully withdrawn, entrapping the clot. The basket with enmeshed clot is then pulledback through the sheath. The above study described its use in six clinical cases, all ofwhich proved successful. The advantages of the basket over the Fogarty balloon are itscapacity to adapt smoothly to the sheath when retracted and the absence of overdilationor injury to the wall. However, fragments of clot tend to shear off, causing distalembolization.


The Ponomar transjugular clot trapping device (CTD)

This was described in 1991 in the specific clinical situation of an inferior vena cavalthrombus.127 The device requires the adjunctive use of the ATD for fragmentation of the clot after the clot is trapped in the Ponomar basket. In this way, the Ponomar is only atrapping device and does not in itself effect a thrombectomy. The device consists of a 12Fdouble-lumen catheter; the smaller lumen houses a stainless steel wire whose distal end emerges as spring loop at a 90degree angle to the shaft, to which is attached the distal endof a 15 cm long, funnel-shaped polyvinyl bag. The proximal end of the bag is connectedto the primary lumen of the catheter, the proximal end of which is then attached to acoaxial introducer with a check-flow valve and side-arm flushing port. The bag can be opened or closed by advancing or retracting the wire. The device is introduced over astiffening wire through a sheath placed in the right internal jugular vein, and positioned inthe inferior vena cava, below the level of the renal veins. Once the bag is opened in theinferior vena cava, the flow of blood through the bag and out of the two side holes in thesides of the primary lumen allows for the maintenance of blood flow in the vena cava. Anocclusion ballon can be passed through the checkflow value and advanced over a guide-wire into the vena cava, beyond the site of the thrombus. Using this inflated balloon, in amanoeuvre similar to the Fogarty technique, the thrombus is dragged back into the bag.Once the thrombus is within the bag, the balloon is deflated and withdrawn, and the bagis closed, trapping the thrombus. An ATD is now passed through the primary lumen intothe bag and activated, thereby macerating the thrombus trapped in the bag. The slurry offragmented clot is thus confined to the bag and minimizes any chance of embolization.The slurry can be aspirated after removal of the ATD through the side-arm flushing port. The in vivo animal studies conducted with the CTD report successful trapping of the clotin all animals, no pulmonary embolizations and no endothelial desquamation or directvessel wall injury.127 This device, although useful in the entrapment and subsequent fragmentation of large caval thrombi, is cumbersome to use and needs the ancillarysupport of a mechanical thrombectomy device to fragment the clot.

Basket-shaped devices whose mechanism of action include, in addition to pull-back thrombectomy, mechanical rotation with or without PAT include the impeller basket andthe arrow device. The impeller basket was designed in 1991 by Schmitz-Rode and colleagues128 for use in the fragmentation of pulmonary emboli. The device consists of a 7F flexible catheter, to the distal end of which is attached a self-expandable basket made up of four spiral-shaped wires (unconstrained diameter 17 mm; length 38 mm). Animpeller (diameter 7F; length 2.5mm; rotation speed 100 000 rpm) is mounted on tworevolving bearings in the centre of the basket and is connected proximally to an externalportable drive system by a coaxial, flexible 0.5 mm torsion drive-wire placed through a 9F introducer sheath. The catheter is then introduced and the basket is opened, distal toand beyond the embolus fixing it. The impeller is rotated for several seconds at100000rpm and the hydrodynamic vortex thus created effectively fragments the clot. Theparticulate material is not aspirated and is allowed to wash away with the antegrade bloodflow. The in vitro experiments conducted observed that more than 90% of the resulting fragments have a diameter smaller than 10 µm.128 The device is steerable and can be positioned easily in the pulmonary tree.


The arrow device consists of a motor-driven fragmentation cage, at one end of a stainless steel drive cable housed inside a 5F catheter and introduced through a 5Fsheath.129, 130 The device is rotated using a hand-held motor at low speeds of 3000–4500 rpm. The restrained cage and its catheter assembly are introduced into the thrombosedvessel and positioned to that the cage lies distal to the thrombus. After withdrawal of therestraining catheter, the now expanded cage is rotated and pulled gently back through thethrombus fragmenting it into particles, 3 mm in size or less, which are aspirated throughthe side port of the sheath. This device has been used in venous thromboemboli, and inclotted haemodialysis grafts. In a comparative study of the device with pulse-spray pharmacomechanical thrombolysis of clotted haemodialysis grafts, it was shown that thisdevice is at least as safe and effective as pulse-spray pharmacomechanical thrombolysis.The device and pulse-spray thrombolysis had comparable immediate technical patency rates (95%), 3-month patency rates (39–40%) and a similar incidence of complications (8–9%). The Trerotola device, however, had shorter procedure times—75 min as compared to 85 min with pulse-spray thrombolysis.130 However, in treating venous thromboemboli, the device has demonstrated endothelial injury equivalent to that of theFogarty balloon.129 This, and the large size of the particulate debris, are disadvantages of this device.

Devices like the Gunther mini basket and the Ponomar, that use a pull-back thrombectomy approach similar to the Fogarty procedure suffer from disadvantages ofincomplete thrombectomy and fragment embolization, which largely result from sizediscrepancies between the thrombi and the sheath or bag into which they are retracted. Toovercome this, designs that allow for temporary expansion of the distal end of the sheathto enable a better fit for the trapped thrombus were incorporated into mechanicalthrombectomy systems. One of these is the ‘Tulip sheath’, which was described by Vorwerk and Gunther in 1992.131–132 A self expandable stent (Wallstent, Schneider) isfixed mechanically on an inner 5F polymer catheter and the distal, free, tulip-shaped end is closed by advancing an outer catheter over it. Once in position, withdrawal of the outercatheter allows the tulip sheath to expand and adapt itself to the vessel lumen. Pull-back thrombectomy is effected by dragging the thrombus into the expanded tulip using either aFogarty ballon or a Dormia basket. In vivo experiments conducted with the Tulip sheath proved extremely successful, with distal embolization less than 1%.131 Design modifications include silicone coating of the Tulip and a smaller 7F version. However,the coated sheath seems to be less efficient in entrapment, since the fluid parts of thethrombus cannot escape through the otherwise open interstices, with consequent poorcompression of the clot substance against the Tulip walls.

Another device that uses a similar technique is the ‘Expandable vascular sheath (EVS) system.133 This system can be inserted over a guide-wire and consists of an outer 9F sheath assembly and an inner obturator assembly. The distal end of the sheath assemblyhas a collapsible funnel made of polyester coated with silicone, and the obturatorassembly has a polyester, umbrella-shaped distal tip that has a maximum diameter of 7mm. The umbrella is deployed by an activating button that is present on the proximalhandle of the assembly. In turn, the open umbrella can both open and close the funnel atthe distal end of the sheath. To effect thrombectomy, the umbrella is opened to its fulldiameter and withdrawn into the distal end of the sheath. This manoeuvre opens the


funnel and the thrombus is thus withdrawn into the funnel and extracted. Preliminary invivo results with this device in rabbits report device limitations in older, more organizedclots and vascular injury comparable to balloon embolectomy.133

Wall adherent thrombi, especially in old organized clots, have always been a problemto lyse, even with most mechanical thrombectomy devices. A new device developed toaddress this problem was tested successfully in both in vitro models, as well as clinical thrombosed haemodialysis grafts. The mesh basket was designed by folding both ends of a selfexpandable Wallstent (Schneider) and mechanically fixing them into sleeves.134 The proximal sleeve is mounted on a 0.035′′ guide-wire and the distal sleeve is attached to thefloppy tip of a 0.035′′ guide-wire. The wire with the closed basket is coaxially inserted into an outer introducer catheter, the withdrawal of which results in the opening of thebasket. By gently retracting the open basket, the adherent thrombi are scraped off thewalls by the protrusions on the surface of the basket. The action is brush-like. Devices developed with a similar intent of clearing wall-adherent thrombi were described as earlyas the late 1980s by Crispin and colleagues who used endovascular brushes as adjuncts tothe Fogarty balloon with effective results.135 A similar device called the Cragg thrombolytic brush catheter (Micro Therapeutics, Aliso Viejo, CA, USA), which can beintroduced percutaneously, was developed in 1994.136 This consists of a 6F infusion catheter housing a coaxial atraumatic nylon brush (diameter 6mm; length 10mm), whichis rotated at low speed by a hand-held electric unit. Thrombolysis with this device includes the concomitant infusion of low-dose UK through the infusion catheter and thus combines mechanical thrombectomy with drug-induced lysis. The device has been tested in an animal study of 12 implanted thrombosed femoral loop grafts, which reportedsuccessful lysis in all grafts with a treatment time of between 8 and 12 min and nosignificant endothelial or other vascular injury.136

Three devices that use the catheter itself as the rotating device are the thrombolizer, the modified impeller catheter and the pigtail catheter. The pigtail catheter is a 5F hightorque, 110 cm long catheter with 10 side ports for contrast injection.137 The outer aspect of the pigtail loop contains a side hold, through which a guide-wire can be passed, which then serves as the axis around which the catheter rotates and fragments the clot. Rotationcan be motor driven or manual. The pigtail catheter has been primarily used in thepulmonary tree, where its advantage lies in its easy manoeuvrability. The thrombolizer(Cordis, Roden, The Netherlands), consists of an 8F sheath and an inner 5F rotatingcatheter, which protrudes 7 cm from the tip of the sheath.138 In the tip region, this inner catheter has four longitudinal slits 15 mm long. The resulting four struts, which are flatwhen the device is not rotating, open during rotation into a basket-like shape, to a diameter which is dependent on the rotational speed. The modified impeller basket catheter is an over-the-wire version of the previously described impeller basket.128 The outer 8F Teflon catheter has an inner 5F rotating catheter and tracks over a 0.035" guide-wire. As in the original design, the outer catheter has a static protection basket; therotating inner impeller is also shape like a basket, the diameter of which depends on therotational speed. Both the thrombolizer and the modified impeller basket, employ high-speed rotation. In a comparative study of both catheters by Schmitz-Rode, in pulmonary emboli, the Impeller catheter provided more effective embolus fragmentation, andconsiderably less vessel trauma than the Thrombolizer.138


Sonic thrombolysis

Ultrasound can be used to treat thrombi by either effecting mechanical thrombectomywith an oscillating ultrasound probe (with or without aspiration) or byultrasoundaugmented pharmacological thrombolysis. The earliest description of the useof mechanical sonic thrombectomy was in 1976 by Trubestein.139 Since then, the capacity of ultrasound to lyse both thrombus and atherosclerotic plaque has been welldocumented.140–145 The underlying mechanism is thought to be acoustic cavitation.Technical difficulties include the high temperatures generated for which additionalcooling mechanisms have to be incorporated, poor flexibility and limited steerability. Amore recent design modification, employing a direct endovascular probe, consists of a 9Fcatheter with a tip-mounted transducer.144 Ultrasound also augments the effect of thrombolytic agents, thus reducing the procedure time and increasing the efficacy ofpharmacological thrombolysis.141–145 Catheter-directed ultrasound thrombolysis is described by Tachibana,143 in a study that demonstrates the in vitro enhancement of fibrinolysis. It was observed that ultrasound by itself does not cause fibrinolysis, butincreases the lytic potential of UK by enhancing penetration through the thrombus. Thisenhancement of lysis was maximal in the early stages of lysis. With this procedure, theconcentration of UK could be reduced to almost one-tenth the original dose and still achieve equal fibrinolysis. The same principle has been tested in vivo in rabbits using percutaneous ultrasound, and the study has confirmed the acceleration of thrombolysiswhen used in tandem with the thrombolytic agent.145 Initial results with sonic thrombolysis appear promising; however, as with most mechanical thrombectomydevices, larger clinical trials and long-term evaluations of their use will be needed.

In conclusion, these advances in the management of thromboembolism allow the utilization of more than one technique when required to effect more completethrombolysis. In their current stage of development, pharmacological thrombolysis andthrombectomy are complementary techniques. The development of mechanicalthrombectomy systems has opened an exciting chapter in the management ofthromboembolic disease. Although they have not as yet been put through rigorousclinical trials, the early results are promising.

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Endoscopic thoracic sympathectomy

8 CATHAL J.KELLY, DAVID J.BOUCHIER-HAYES AND AUSTIN

L.LEAHY

Introduction

Kotzareff first described upper thoracic sympathectomy for hyperhydrosis, using an opensurgical technique, in 1920.1 In the 1930s, several surgical techniques were developed,including the dorsal paravertebral and supraclavicular approaches.2 In 1954, Atkins first described the open transaxillary approach.3 However, the morbidity and mortality of a thoracotomy, for benign conditions such as hyperhydrosis, have stimulated a search forless invasive methods to ablate the upper thoracic sympathetic ganglia.4 Percutaneous destruction of T2-T3 ganglia by radiofrequency, by phenol or by stereotacticthermocoagulation have all been described, but the overall results have beenunsatisfactory.5–7 The first proponent of endoscopic procedures of the sympathetic chainwas Kux, who published his extensive experience of thoracoscopic neurotomies in 1951.8This technique did not gain rapid acceptance despite several series demonstrating itsefficacy in the 1970s and 1980s.9,10 However, with the general move to minimallyinvasive surgery and a marked improvement in endoscopic equipment, there has been anupsurge in endoscopic procedures of the upper thoracic sympathetic chain.11–12

Indications

Hyperhydrosis

Primary hyperhydrosis has an impact on professional and social life and may lead toemotional problems.2 Axillary hyperhydrosis causes wetness and staining of clothes, causing social embarrassment Palmar hyperhydrosis has a social impact: patients arereluctant to shake or hold hands and may become socially withdrawn. Professionally,patients may have difficulties grasping objects, papers become wet, and ink runs.13 The sweat is secreted by eccrine glands, innervated by cholinergic fibres from the sympatheticnervous system. Mental stimuli, rather than heat or exercise, induce excessiveperspiration. There is no evidence that these patients are unduly anxious or neurotic.14

Studies suggest that the incidence in Europeans is between 0.6 and 1%.15 The incidence in a young oriental population was reported as 0.3%, with a family history of 12.5%.16

Causalgia

Reflex sympathetic dystrophy, characterized by unexplained severe pain, oedema, skincolour and temperature changes, limited range of movement and trophic changes in boneand muscle of the extremities, has been attributed to sympathetic nervous systemactivation by unknown factors that stimulate nocioceptive receptors.17, 18 There are three therapeutic approaches: psychological therapy, physical therapy and sympatholyticprocedures and drugs. The benefit of psychological therapy is controversial.19 Physical therapy is reported to be of benefit, particularly in combination with some types ofsympatholytic procedure.20 A wide variety of sympatholytic procedures or adrenergic blocking agents have been used, including electrical nerve stimulation, perivascular orparaspinal surgical sympathectomy, local anaesthetic agents, regional intravascularinfusion with guanethidine, bretylium, reserpin or phentolamine or oral administration ofphenoxybenzamine and prazosin.21 Sympathetic ganglion blockade with local anaesthetic are sometimes effective for pain relief.22 However, there are case reports where stellate ganglion blockade is only partially effective, yet thoracoscopic electrocauterization of theright sympathetic ganglion at the level of T3 proved to be permanently effective.23 Open surgical sympathectomy has been performed for the management of reflex sympatheticdystrophy with good results in 59–74% of patients.24, 25 Drott et al. have reported two cases, one with causalgia pain induced by a crush injury to the forearm and the secondwith reflex dystrophic pain after first-rib resection.3 Both patients had temporary pain relief after sympathetic block using local anaesthetic and permanent pain relief afterendoscopic electrocautery of the second and third thoracic sympathetic segments.

Cardiac disease

The sympathetic system is important for the perception of anginal pain.26 Studies have previously demonstrated that sympathectomy of the thoracic portion of the sympatheticchain decreases the perception of angina.27 In addition to a direct analgesic effect,sympathetic blockade decreases myocardial oxygen consumption.28 Experimental studies demonstrate that thoracic epidural anaesthesia, blocking sympathetic afferent andefferents, reduces the major determinants of myocardial oxygen consumption, i.e. meanarterial pressure, heart rate and contractility.29 Wettervik et al. have reported the effects of endoscopic transthoracic sympathectomy on a group of patients with severe anginapectoris.30 The majority of patients had bilateral sympathectomies (92%) and 17% had all 10 sympathetic ganglia cauterized. They were able to demonstrate that sympathectomyresulted in a significant reduction in the frequency of anginal attacks and a reduction inST depression for maximum comparable workload. The work of Austoni and colleaguesindicates that sympathetic ablation of both sides or of the left side alone produces a β-adrenergic blockade, whereas ablation of the right side alone produces the oppositeeffect.31 In the authors’ experience of eight patients with intractable angina, aftercoronary artery bypass, ablation of T2-T4 sympathetic ganglia on the left side onlyresulted in good symptomatic relief in seven out of eight patients ,32

In addition to its anti-ischaemic effects, sympathectomy may also have anti-arrhythmic effects. Cardiac sympathetic denervation of the left side has been shown to reduce the


incidence of tachyarrhythmic syncope and the risk of sudden death.33 Endoscopic transthoracic sympathectomy has been reported to effectively treat congenital long-QT syndrome.34

Vascular disorders

There has been extensive experience of open sympathectomy for upper extremityvascular disorders since the 1930s. The results have not been as durable as they are forcausalgia or hyperhydrosis.24, 25, 35 The results for obliterative arterial disease seem more durable than those for vasospastic disease.36 Kux and coworkers, in a series of 34 casesof vasospastic disease of the upper extremity managed by endoscopic sympathectomy,found immediate good results in all patients; however, in the long term the procedure wasonly effective in around 50% of patients.37 Most authors do not recommendsympathectomy for Raynaud’s syndrome.

Surgical anatomy

The sympathetic chain passes over the neck of the first rib, beneath the parietal pleura. Itlies on the necks of the ribs in the upper third of the thoracic cavity. As the thoracicvertebra increase in size, it comes to lie on the costovertebral joints in the mid thorax andthen on the vertebral bodies in the lower third of the chest, passing under the medicalarcuate ligament as the lumbar chain. The first thoracic ganglia and the inferior cervicalganglion fuse to form the stellate ganglion, located on the neck of the first rib. In additionto the sympathetic chain, there are highly variable interganglionic connections runningparallel to the main trunk; fibres may also pass from the sympathetic chain (at the level ofthe second ganglion) to the brachial plexus. This connection, known as the nerve ofKuntz, is present in 10% of the population. Preganglionic sympathetic nerve fibres arisefrom the spinal segments as myelinated fibres and leave the spinal cord in thecorresponding spinal nerves. They join the sympathetic ganglia as white ramicommunicantes and synapse within the ganglia. Unmyelinated postganglionic fibresleave the sympathetic chain as grey rami communicantes to join the corresponding spinalnerve.

Surgical technique

A pre-operative chest X-ray should be performed to outrule pulmonary disease, whichmight preclude one-lung anaesthesia or prevent access to the sympathetic chain. The procedure is carried out under general anaesthetic using a double-lumen endotracheal tube. The patient may be placed supine or in the lateral position; a sandbag placed underthe shoulder will improve access to the axilla. The supine position allows bilateralsympathectomies to be performed. In the author’s unit, one side is done first to allow assessment of the patient’s response to the procedure before proceeding with the other side. The underlying lung is disconnected from the ventilator, allowing the lung to

Endoscopic thoracic sympathectomy 199

collapse. A 1 cm incision is made in the mid-axillary line, at the level of the fourth intercostal space. The pleural space is entered by blunt dissection with an artery forceps.A 10mm port is inserted and the thoracoscope introduced. Carbon dioxide is not routinelyinsufflated. This may be necessary to further collapse the lung, after first dividing any pleural adhesions. The line pressure should be maintained at <10mmHg.

A second port is inserted, under direct vision, in the third or fourth intercostal spaceadjacent to the 10mm port. The second port may also be placed in the mid-clavicular line to triangulate the instruments; however, this position does not diminish the cosmeticresult of the operation. Attention to haemostasis at this point is important, especially ifthe lateral position is used, as the blood will pool in the paravertebral gutter, obscuringthe sympathetic chain.

The upper thoracic sympathetic chain can be seen beneath the parietal pleura, running over the necks of the ribs. The position of the chain can be confirmed by running a probealong the surface of the rib and feeling the cablelike sympathetic chain runningunderneath. The stellate ganglia is obscured by a fat pad lying on the neck of the first rib.

The sympathetic chain is then interrupted by cautery ablation at the appropriate ganglia. Some surgeons divide the chain with scissors above the second thoracic ganglionprior to diathermy ablation, to avoid transmission of diathermy current to the stellateganglion and the risk of Horner’s syndrome. Excision of the sympathetic chain iscomparable to open surgical practice. This allows histological confirmation that theprocedure has been successful, but does involve a more extensive dissection andincreases the risk of troublesome bleeding from the posterior thoracic wall veins.

A third technique of sympathectomy has been proposed by Wittmoser. This involvesmeticulous exposure and division of the rami communicantes, while preserving the mainsympathetic trunk,38 the aim of this procedure being to reduce the risk of compensatoryhyperhydrosis. The extent of sympathectomy is debatable. In the authors’ experience, interruption of the chain at the level of the second and third ribs adequatelysympathectomizes the hand. Extending the sympathectomy to the fourth and fifth gangliais recommended for axillary hyperhydrosis. The increased risk of compensatoryhyperhydrosis and a failure rate of up to 40% has led many surgeons to abandon thisprocedure in favour of axillary skin excision. On comple-tion of sympathectomy, the lung is expanded under direct vision. The muscle layer at the port holes is closed with a 2/0absorbable suture and the skin incisions are closed with a subcuticular absorbable suture.A chest drain is not routinely inserted. A chest X-ray is taken in the recovery room.

The effect of the sympathectomy is usually immediate ly apparent, with the hand feeling warm and dry. Patients are warned that they may experience a transient return ofsweating on the third or fourth post-operative day and that this is transitory, usuallyresolving within 24 h.

In some units, this is carried out as a day-case procedure. There is a small risk of adelayed pneumothorax and in view of this, patients in the authors’ unit are detained overnight.


Complications

Pneumothorax

The incidence of pneumothorax after endoscopic transthoracic sympathectomy isreported at between 1 and 2% 12, 39 A significant pneumothorax can usually be aspirated. Insertion of a chest drain is rarely required.

Horner’s syndrome

The incidence is reported as being from 2 to 5%.40, 41 This is due to direct or transmitted electrocautery. In most cases, Horner’s syndrome after transthoracic sympathectomy is transient and resolves within 6 weeks. In addition to accurate identification of theanatomy, use of bipolar diathermy and/or division of the chain prior to cautery mayfurther decrease the incidence of this complication.

Post-operative chest or arm pain and parasthesia

Injury to the intercostal or intercostobrachial nerves can cause severe pain or parasthesiain their distribution. Cautery of the chain over the neck of the rib, avoiding the intercostalspace, reduces this complication. Severe postsympathectomy neuralgia can bedevastating, requiring brachial plexus nerve blocks and transcutaneous nerve stimulation.

Compensatory hyperhydrosis

This condition is characterized by increased sweating in other areas of the body,particularly the chest, abdomen and buttocks. It occurs to some extent in most patients,the reported incidence varying with the intensity of questioning. Andrews and colleaguesreported that it occurred in 36 of 42 patients (86%) after sympathectomy for palmarhyperhydrosis.42 Only rarely is this symptom of disabling severity (1.76%). This phenomenon is independent of technique used and may represent a physiologicalthermoregulatory response to the loss of sweat gland function. One strategy for reducingthis phenomenon may be to reduce the extent of the sympathectomy to one or two levels or to use the Wittmoser technique.38, 43 Informed consent should include discussion of Horner’s syndrome and compensatory hyperhydrosis.

Results of endoscopic thoracic sympathectomy

Objective assessment of the results of sympathectomy

It is impossible to measure sympathetic denervation objectively; however, these methodsare not commonly used in clinical practice, because most are complex, time consumingand often imprecise. 44 Finger sudometry, which is a sensitive measure of sudomotor


drive to the fingers, continuously measures the effect of stimuli on sweat produced by afinger and the results of sympathectomy.45 This test may have a role in the work-up of patients going for sympathectomy, particularly re-operation.46

Results of sympathectomy for hyperhydrosis

The results of endoscopic surgery on hyperhydrosis are excellent and durable, persistingfor more than 10 years in some studies.47 Kux reported complete relief of palmarhyperhydrosis in 63 patients, although 19% still had some axillary sweating.9 Fritsch and colleagues reported on 720 procedures performed for 367 patients. Five patients hadprimary failures and four had early recurrences.47 The reasons for failure were only partial diathermy of the sympathetic chain or possibly a failure to identify and coagulatethe nerve of Kunz. Byrne et al and Edmonson et al respectively, report 96 and 97% reliefof symptoms.11, 12 Compared with open surgery, endoscopic surgery results in lowmorbidity and reduced length of hospital stay. Patients are also more likely to acceptbilateral procedures. In contrast with open unilateral sympathectomies, about 20% ofpatients who have had a successful procedure will not agree to have the other sideoperated on because of the pain experienced after the initial operation.48 In a review of the surgical management of primary hyperhydrosis, Moran and Brady compared theresults of open surgery with endoscopic surgery.49 Success was achieved in 90% of 192patients from three series who were treated endoscopically, compared with 97% of 435patients from six series who underwent open cervical or transaxillary sympathectomy.Endoscopic sympathectomy was carried out by diathermy coagulation, which mayexplain the lower success rate compared with that achieved with excision of thesympathetic chain at open surgery.

The efficacy of endoscopic sympathectomy for relieving axillary hyperhydrosis is less clear cut and some authors reserve this procedure for palmar hyperhydrosis only.50

Diathermy coagulation of the sympathetic chain below the first thoracic ganglion to thesecond thoracic ganglion, to destroy the nerve of Kunz, will reliably stop palmarhyperhydrosis. The extent of further destruction of the caudal sympathetic chain toabolish axillary hyperhydrosis is not clear. Kux excised the second to sixth thoracicganglia, but still had axillary wetness in 19% of patients.9 Diathermy coagulation of the second, third and fourth ganglia, by Edmonson and colleagues, relieved palmarhyperhydrosis in 98% of patients, but only 77% of those with axillary hyperhydrosis wererelieved. With both palmar and axillary involvement, symptomatic relief was obtained in90% of patients.12 Transthoracic endoscopic sympathectomy with diathermy of thesecond, third and fourth thoracic ganglia, in a series of 26 patients with a median follow-up of 10 months, resulted in 100% relief of palmar hyperhydrosis. Complete relief wasobtained in 83% of patients treated for axillary hyperhydrosis alone and in 75% of limbstreated for combined axillary and palmar hyperhydrosis.51

Conclusion

Upper limb sympathectomy retains a useful place in modern vascular surgical practice to


treat hyperhydrosis and selective ischaemic and post-traumatic pain syndromes. Palmar hyperhydrosis, the most common and clear-cut indication for this procedure, is a benign condition and its treatment should combine safety with good cosmetic results and patientsatisfaction. Endoscopic transthoracic sympathectomy fulfils all of these criteria and isnow the treatment of choice for this condition.

References

1. Kotzareff A. Resection partielle de trone sympathetique cervical droit pour hyperhidrose unilaterale. Rev Med Suisse Romande 1920; 40: 111–13.

2. Atkins MBJ. Sympathectomy by the axillary approach. Lancet 1954; 1:538–9. 3. Drott C, Gothberg G, Claes G. Endoscopic procedures of the upperthoracic

sympathetic chain. Arch Surg 1993; 128:237–41. 4. Palumbo LT, Lulu DJ. Anterior transthoracic upper dorsal sympathectomy: current

results. Arch Surg 1966; 92:247–57. 5. Wilkinson HA. Percutaneous radiofrequency upper thoracic sympathectomy: a new

technique. Neurosurgery 1984; 15:811–14. 6. Adler OB, Engel A, Rosenberger A, Dondelinger R. Palmar hyperhydrosis CT guided

chemical percutaneous thoracic sympathectomy. Fortsch Rontgenstr 1990; 153:400–3. 7. Chuang KS, Liou NH, Liu JC. New stereotactic technique for percutaneous

thermocoagulation of upper thoracic ganglionectomy in cases of palmar hyperhydrosis. Neurosurgery 1988; 22:600–4.

8. Kux E. The endoscopic approach to the vegetative nervous system and its therapeutic possibilities. Dis Chest 1951; 20:139–47.

9. Kux M. Thoracic endoscopic sympathectomy in palmar and axillary hyperhydrosis. Arch Surg 1978; 113:264–6.

10. Horgan K, O’Flanagan S, Duignan PJ, Hederman W. Palmar and axillary hyperhydrosis treated with sympathectomy by transthoracic endoscopic electrocoagulation. Br J Surg 1984; 71:1002.

11. Byrne J, Walsh TN, Hederman WP. Endoscopic transthoracic electrocautery of the sympathetic chain for palmar and axillary hyperhydrosis. Br J Surg 1990; 77:1046–9.

12. Edmonson RA, Banerjee AK, Rennie JA. Endoscopic transthoracic sympathectomy in the treatment of hyperhydrosis. Ann Surg 1992; 215:289–93.

13. White JW. Treatment of primary hyperhydrosis. Mayo Clin Proc 1986; 61:951–6. 14. Lerer B, Jacobwitz J, Wahba A. Personality features in essential hyperhydrosis. Int J

Psychiatry Med 1980–1981; 10:59–67. 15. Adar R, Kurchin A, Zweig A, Mozes M. Palmar hyperhydrosis and its surgical

treatment: a report of 100 cases. Ann Surg 1977; 186: 34–41. 16. Kao MC, Lin JY, Chen YL, Hsieh CS, Cheng LCJ, Huang SJ. Minimally invasive

surgery: video endoscopic thoracic sympathectomy for palmar hyperhydrosis. Ann Acad Med Singapore 1996; 25:673–8.

17. Veldman PHJM, Reynen HM, Arntz IE, Goris RJA. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet 1993; 342:1012–6.

18. Kurvers HA, Jacobs MJ, Beuk RJ et al. Reflex sympathetic dystrophy: evolution of microcirculatory disturbances in time. Pain 1995; 60: 334–40.

19. Lynch ME. Psychological aspects of reflex sympathetic dystrophy: a review of the adult and paediatric literature. Pain 1992:49:337–47.


20. Lloyd-Thomas AR, Lauder G. Reflex sympathetic dystrophy in children. Br Med J 1995; 310:1648–9.

21. Paice E. Fortnightly review: reflex sympathetic dystrophy. Br Med J 1995; 310:1645–8.

22. Murray P, Floor K, Atkinson RE. Continuous axillary brachial plexus blockade for reflex sympathetic dystrophy. Anaesthesia 1995; 50: 633–5.

23. Honjyo K, Hamasaki Y, Kita M et al. An 11 year old girl with reflex sympathetic dystrophy successfully treated by thoracoscopic sympathectomy. Acta Paediatr 1997; 86:903–5.

24. Mockus B, Rutherford RB, Rosales C, Pearce WH. Sympathectomy for causalgia. Arch Surg 1987; 122:668–72.

25. Olcott C, Eltherington LG, Wilcosky BR et al. Reflex sympathetic dystrophy: the surgeon’s role in management. J Vasc Surg 1991; 14: 488–95.

26. Maseri A, Crea F, Kaski JC, Davies G. Mechanism and significance of cardiac ischaemic pain. Prog Cardiovasc Dis 1992; 35:1–8.

27. Lindgren I. Angina pectoris, a clinical study with special reference to neurosurgical treatment. Acta Med Scand 1950; 1–141.

28. Kock M, Blomberg S, Emanuelsson H et al. Thoracic epidural anaesthesia improves global and regional left ventricular function during stress-induced myocardial ischaemia in patients with coronary artery disease. Anaesth Analg 1992; 71:625–30.

29. Davis RF, DeBoer LWV, Maroko PR. Thoracic epidural anaesthesia reduces myocardial infarct size after coronary artery occlusion in dogs. Anaesth Analg 1986; 65:711–7.

30. Wettervik C, Claes G, Drott C et al. Endoscopic transthoracic sympathectomy for severe angina. Lancet 1995; 345:97–9.

31. Austoni P, Rosati R, Gregorini L et al. Stellectomy and exercise in man. Am J Cardio 1979; 43:399.

32. Kelly CJ, David S, O’Callaghan DM, Browne G, Horgan JH, Leahy A. Endoscopic transthoracic sympathectomy in angina AESGBI [abstract].

33. Bhandari AK, Scheinman MM, Morady F et al. Efficacy of left cardiac sympathectomy in the treatment of patients with long QT syndrome. Circulation 1984; 70:1018–23.

34. Wong CW, Wang CH, Wen MS et al. Effective therapy with transthoracic video-assisted endoscopic coagulation of the left stellate ganglion and upper sympathetic trunk in congenital long QT syndrome. American H J 1996; 132:1060–3.

35. Manart FD, Sadler TR, Schmitt EA, Rainer GW. Upper dorsal sympathectomy. Am J Surg 1985; 150:762–6.

36. Van de Wal HJCM, Skotnicki SH, Wijn PFF, Lacquet LK. Thoracic sympathectomy as therapy for upper extremity ischaemia: a longterm follow-up study. Thorac Cardiovasc Surg 1985; 33:181–3.

37. Kux M, Fritsch A, Kokoschka R, Muller M. Endoscopic thoracic sympathectomy for the treatment of Raynaud’s phenomenon and disease. Eur Surg Res 1976; 8:32–3.

38. Wittmoser R. Thoracoscopic sympathectomy and vagotomy. In: A Cuschieri, G Buess, J Perissat (eds) Operative manual of endoscopic surgery. New York: Springer 1992, 110–33.

39. Claes G, Gotheberg G, Drott C. Endoscopic electrocautery of thoracic sympathetic chain: a minimal invasive method to treat palmar hyperhydrosis. Scand J Plast Reconstruch Hand Surg 1993; 27:29–33.

40. Johnson ENM, Summerly R, Birnotingl M. Prognosis in Raynaud’s phenomenon


after sympathectomy. Br Med J 1965; 1:962–4 41. Tygesea H, Claes G, Drott C et al. Effect of transthoracic sympathectomy on heart

rate variability in severe angina pectoris. Am J Cardiol 1997:79:1447–52. 42. Andrews BT, Rennie JA. Predicting changes in the distribution of sweating following

thoracoscopic sympathectomy. Br J Surg 1997; 84: 1702–4. 43. O’Riordain DS, Maher M, Waldron DJ, O’Donovan B, Brady MP. Limiting the

anatomical extent of upper thoracic sympathectomy for primary palmar hyperhydrosis. Surg Gynae Obstet 1993; 176: 151–4

44. Harris JP, Satchell PM, May J. Upper extremity sympathectomy. In: RB Rutherford (ed.) Vascular surgery. 4th edition. New York: W.B Saunders 1995; 2:1008–16.

45. Satchell PM, Ware S, Barron J, Tuck R. Finger sudometry and assessment of sudomotor drive. J Neurosci Meth 1994; 53:217–23.

46. van Rhede van der Kloot EJ, Jorning PJ. Resympathectomy of the upper extremity. Br J Surg 1990; 77:1043–5.

47. Fritsch A, Kokoschka R, Mach K. Ergebnisse der thorakoskopischer sympathectomie bei hyperhydrosis der oberen extremitat. Wien Klin Wochenschr 1975; 87:548–50.

48. Sternberg A, Brickman S, Kott I et al. Transaxillary thoracic sympathectomy for primary hyperhydrosis of the upper limbs. World J Surg 1982; 6:458.

49. Moran KT, Brady MP. Surgical management of primary hyperhydrosis. Br J Surg 1991; 78:279.

50. Gordon A, Collin J. Treating hyperhydrosis. Br Med J 1993; 306: 1752. 51. Sayeed RA, Ghauri ASK, Nyamekye I, Poskitt KR. Assessment of outcome after

thoracoscopic sympathectomy for hyperhydrosis in a specialised unit [letter] J R Coll Surg Edin 1997; 42:287–8.


Retroperitoneoscopic lumbar sympathectomy

9 YUK-MAN KAN, A.W. DARZI AND N.J. CHESHIRE

Introduction

History

Lumbar sympathectomy was first performed and described in 1923 by Dr D.Royal in theLewisham Hospital, Sidney to treat spastic paralysis secondary to a cerebral corticalbullet injury in a 30-year old man.1 The result was dramatic with respect to the spasticity, but it was also noted that the treated limb became much warmer and developed capillarydilatation. In subsequent years, an increasing body of surgeons documented the vascularchanges associated with sympathetic denervation and use of the procedure was extendedto treat conditions such as atherosclerotic occlusions, Raynaud’s phenomenon, and thromboangiitis obliterans.2, 3

Surgical sympathectomy remained the mainstay of the treatment of lower limb occlusive disease until open vascular reconstruction became possible in the early 1950s,after which its use steadily declined. This has become even more apparent over the past20 years, as reconstructive surgery has developed and the role of endoluminal therapy hasadvanced. Despite this, there are still some clinical situations in which sympatheticdenervation remains a valuable treatment option; these include lower extremity causalgicpain4–6 hyperhydrosis,7 distal arterial occlusive disease not amenable to direct surgical attack and selected patients with vasospastic disorder.8–10

Functions of the sympathetic nervous system

The primary functions of the sympathetic nervous system are to prevent heat loss,through reduction of superficial extremity blood flow, and to modify basal organfunction. Resting sympathetic activity primarily antagonizes the vasodilating influence ofthe parasympathetic nervous system on arteriolar resistance vessels, cutaneousprecapillary sphincters and capacitance vessels. Local increase in sym pathetic outflowcauses decreased skin blood flow, piloerection and sweating. These responses aremediated by the constricting influence of norephinephrine on vascular smooth muscle.Abolition or opposition of sympathetic efferents leaves the parasympathetic nervoussystem unopposed and leads to theoretical increases in cutaneous blood flow as great as40–100%.11 Controversy remains about the precise mechanisms of flow improvement, if any, in chronically ischaemic extremities and there are wide variations in the degree ofclinical improvement observed by different authors. Both clinical and experimental

studies indicate that the major circulatory effect of sympathectomy is increased skinblood flow caused by shunting of blood through cutaneous arteriovenous anastomoses,11

without alteration in overall limb perfusion. The mechanism(s) by which sympathectomy relieves pain in causalgia is similarly

uncertain. Some authors believe that symptoms are due to ischaemic changes inperipheral nerves and suggest that shunting of blood may improve this and thus providerelief. Others believe that benefits are brought about by the attenuating effects ofsympathectomy on pain perception through the division of the afferent pathway.

Surgical methods

Traditionally, surgical lumbar sympathectomy is carried out extraperitoneally, through anoblique incision in the iliac fossa, extending medially. In expert hands, this incision splitsrather than cuts most of the abdominal musculature and pro-vides excellent exposure for excision of the sympathetic chain between the lower pole of the kidney and the pelvicbrim. In addition, a specimen of the chain is obtained for histological confirmation ofsympathectomy. On the other hand, such incisions are painful, often require parenteralopiate analgesia and thus necessitate overnight stay in hospital.

During the past 20 years, the role of open sympathectomy has been challenged by percutaneous chemical ablation with phenol or alcohol solutions introduced usingradiographic localization. A common technique utilizes CT scanning to accurately guidethe needle tip to the sympathetic chain alongside the lumbar vertebral bodies before aphenol solution is injected. As with open surgery, in skilled hands the technique is quickand simple and has the advantage of being relatively painless. Hospitalization is notalways required. Against this, the uncontrolled nature of the intervention means thatinjury to other retroperitoneal structures can occur and lysis of somatic nerves, the caudaequina and ureters have all been described.12–14 In addition, chemical sympathectomydoes not provide a specimen for confirmation of completeness, leaving cliniciansuncertain if the intervention fails to improve the clinical problem.

The introduction of the endoscope to general surgical practice and the development of affordable imaging technology have allowed the development of a new approach tolumbar sympathectomy using retroperitoneoscopy.15, 16 The technique utilizes a balloon dissector to create space in the retroperitoneum and then allows sympathectomy to beperformed under direct vision using three small port incisions. The technique has gainedfavour with some vascular surgeons as it may provide the accuracy and completeness ofsympathectomy associated with open surgery, while avoiding the painful wound and in-hospital stay.


Technique of retroperitoneoscopic sympathectomy

The following is a description of the technique as we perform it at St Mary’s Hospital, London. Subtle variations are found in the literature.

Under general anaesthetic with muscle relaxation, the patient is placed in a semilateralposition with the operating table broken at the level of the umbilicus (L3–4) to 30degrees. A 12 mm incision is made laterally in the flank (Figure 9.1). This permits finger dissection into the extraperitoneal plane posteriorly. A 12 mm balloon dissecting port(Origin Medisystem, San Francisco, CA, USA) is inserted through the incision and theretroperitoneal space developed by hand insufflation with air. Figure 9.2 shows a view of the retroperitoneal balloon, as seen through a laparoscope introduced through theumbilicus. Transperitoneal observation of balloon dissection is useful but not essentialand we have now abandoned it for routine procedures, as visu

Figure 9.1 Left retroperitoneoscopic lumbar sympathectomy. The patient is placed in a semilateral position with the table broken to open the space between costal margin and iliac crest. A 12 mm incision is made in the flank halfway between the bony landmarks and the retroperitoneal space developed. In this example, an umbilical, laparoscopic port is already in place to observe the retroperitoneal dissection. We have now stopped this as a routine procedure.

alization with a camera inside the dissecting balloon can also be used to observe progressof the dissection.

Depending on the size of the patient, approximately 1–1.5 litres of air is insufflated into the balloon to a maximum pressure of 15 mmHg. Once complete, the balloon isremoved and a self-sealing port inserted into the incision, followed by insufflation withCO2 to a pressure of 15 mmHg.

A 10 mm port is inserted in the anterior axillary line under vision just above the iliac

Retroperitoneoscopic lumbar sympathectomy 209

crest. The operative field

Figure 9.2 Transperitoneal, laparoscopic view of the left retroperitoneal balloon dissection. The ureter can be seen elevated an the undersurface of the posterior peritoneum. Laparoscopic observation is not essential for retroperitoneal balloon dissection.

Figure 9.3 The broad nosed, blunt ‘finger dissector’ being used to devel op the retroperitoneal plane under direct vision.


Figure 9.4 The gonadal vessels (arrowed) on the superior surface of the prepared operating space during left retroperitoneoscopic lumbar sympathectomy.

is advanced medially and proximally, using blunt dissection. We find the use of a broad-nosed ‘finger dissector’ particularly useful for this manoeuvre (Figure 9.3). When the dissection allows, a 5 mm subcostal port is inserted in the mid-axillary line, again under direct vision. This port allows the introduction of scissors and grasping forceps. At thisstage, the ureter and gonadal vessels should be identified on the undersurface of theperitoneal roof of the operating space (Figure 9.4).

The lumbar sympathetic chain is identified in a longitu-dinal leash of fibrofatty tissue lying alongside the lumbar vertebral bodies, in the groove formed by the medialattachment of the psoas major muscle (Figure 9.5). On the left it is overlapped by theaorta and on the right by the inferior vena cava. Adequate exposure of the sympatheticchain requires excision of the lateral peritoneal attachment of the right or left colon fromthe hepatic or splenic flexure down to the pelvic brim. The medial border of the psoasmuscle caudally can act as a guide towards the location of the sympathetic chain. Thelower pole of the kidney and its perirenal fat should be dissected from theretroperitoneum and rotated medially. At this site, the renal pedicle forms the landmarkof the second lumbar ganglion, while inferiorly the iliac arteries locate the level of thefourth lumbar ganglion. Care at this stage is essential on the right side, to avoid thelumbar veins, which lie anterior to the sympathetic chain (Figure 9.6). Once the appropriate ganglia of


Figure 9.5 The lumbar sympathetic chain identified during left retroperitoneoscopic lumbar sympathectomy. The chain lies in fibrofatty material running alongside the lumbar vertebral bodies.

Figure 9.6 Lumbar veins running over the area to be dissected for right retroperitoneal lumbar sympathectomy.


Figure 9.7 Breach of the peritoneum at the superiomedial limit of left retroperitoneoscopic lumbar sympathectomy. A suture is being used to close the defect after decompression of the peritoneal cavity with a Veress needle.

L2, L3 and L4 are identified, they are then excised and the specimen removed forhistological confirmation. Drainage of the retroperitoneal space is not necessary and thewounds are closed with single sutures to the fascia, the rectus sheath and the skin.

If pneumoperitoneum occurs through inadvertent puncture of the overlying peritoneum (usually at its medial limit) it can render the exposure difficult. This can usually beminimized by the introduction of a Veress needle into the general peritoneal cavity at thelevel of the umbilicus and by clipping or sewing of the breach in the peritoneum (Figure 9.7)

Discussion

Retroperitoneoscopic lumbar sympathectomy (RLS) is a relatively new technique thatmay offer the minimally invasive advantages of chemical sympathectomy with thesurgical control of open surgery. Reports of the procedure did not begin to appearregularly in the literature until 1996 and there are currently no large-scale series reporting either outcomes or complications, so that to date the method remains unvalidated. Ourown experience of over 30 lumbar sympathectomies performed in this manner suggeststhat complication rates are low (under 5%) and minor, but clearly more data is requiredbefore the vascular surgeon can begin to compare RLS with the current options ofchemical sympathectomy or open surgery. It is of value to consider the currentunderstanding of each of these techniques when considering RLS.

Proponents of percutaneous techniques point out the simplicity and speed of the method, but this is not always borne out by the data; mortality is low overall, but may riseas high as 10% in the elderly.12, 16 In addition, a number of significant complications


involving the ureters, spinal cord and lower limb nerves are well-recognized (see above). A lesser complication, although perhaps one of the most troublesome, ispostsympathectomy neuralgia. This has been reported in frequency ranging from 5 to40%15,16 and is one of the most frequent of patient complaints. In addition, outcomereports of the technique are plagued with inconsistent results, particularly concerning theduration of sympathetic block.10, 13, 14 This is a difficult point for supporters to argueagainst, given the absence of histological confirmation of sympathectomy.

Open sympathectomy allows safe and complete ganglionectomy at the expense ofgeneral anaesthesia and a painful muscle-cutting incision. Mortality rates range up to 12%, particularly when there is coexistent ischaemic heart disease,9, 19 but the incidence of injury to associated organs is small. The technique may be acceptable but it can bedifficult to justify the required hospitalization against a seemingly simpler radiologicalintervention.

The technique of RLS is relatively simple for surgeons with laparoscopic experience (particularly those with experience of extraperitoneal hernia repair or colposuspension)and is easily learned by those without. Evidence from the literature, and from the use ofretroperitoneoscopy for other procedures, suggests that the procedure is safe andassociated with fewer potential complications than laparoscopy. One of the drawbacks tothe method described above is the use of expensive disposable equipment such as theballoon dissector. At least two other techniques utilizing either laparoscopy or a no-insufflation technique20, 21 have been described in the literature. Although we have no experience, these techniques may be suitable for centres where disposable equipment isnot available.

We believe that RLS may have a role in modern vascular surgery. Incompletesympathectomy after percutaneous injection is arguably one of the reasons why theprocedure has fallen into further disrepute over the past 20 years. Obviously, moreevidence is required before we can accurately define the role of RLS; a randomized trialof the technique against chemical sympathectomy may answer some of the questions.However, if clinical outcome is used as the end-point, then the primary question willbecome lost in the difficult issue of the indications for sympathectomy in the modern era. The use of surrogate end-points to indicate the completeness of sympathectomy may be of scientific validity but will not satisfy the criticisms of those who believe that theoperation has little or no role in modern vascular surgery. Aggregation of data from thosecentres currently performing the operation is urgently needed.

References

1. Royle ND. A new operative procedure in the treatment of spastic paralysis and its experimental base. Med J Aust 1924; 1:77–86

2. Adson AW, Brown GE. Treatment of Raynaud disease by lumbar ramisection and ganglionectomy and perivascular sympathetic neurectomy of the common iliac. JAMA 1925; 84:1908–10

3. Diel J. Un nuevo metodo de simpatectomia periferica para el tratamiento de affecionas troficas y gangrenosas de los miembros. Bol Soc Cir Buenos Aires 1924; 8.

4. Mockus MB, Rutherford RB, Rosale SC, Pearce WH. Sympathectomy for causalgia—


patient selection and long term results. Arc Surg 1987; 22:668–72. 5. Cornelius O, Lorne G, Bernard RW. Reflex sympathetic dystrophy - the surgeons role

in management. J Vasc Surg 1991; 14: 488–95. 6. AbuRahma AF, Thaxton L, Robinson PA. Lumbar sympathectomy for causalgia

secondary to lumbar laminectomy. Am J Surg 1991; 171: 423–6. 7. Moran KT, Brady MP. Surgical management of primary hyperhydrosis. Br J Surg

1991; 78:279–83. 8. Kruse CA. Thirty-year experience with predictive lumbar sympathectomy. Am J Surg

1985; 150:232–6. 9. Norman PE, House AK. The early use of lumbar sympathectomy in peripheral vascular

disease. J Cardiovasc Surg 1998; 29:717–22. 10. Baker DM Lamerton AJ. Operative lumbar sympathectomy for severe lower limb

ischaemia: still a valuable treatment option Ann R Coll Surg Engl 1994; 76:50–3. 11. Cronenwett JL, Lindenauer SM. Haemodynamic effects of sympathectomy in

ischaemic canine hind limbs. Surgery 1980; 87: 417–24. 12. Kim GE, Ibrahim IM, Imperato AM. Lumbar sympathectomy in endstage arterial

occlusive disease. Ann Surg 1976; 183:157–60. 13. Trgaux JP, Decoene B, Van Beers B. Focal necrosis of the ureter following CT-

guided chemical sympathectomy. Cardiovasc Intervent Radiol 1992; 15:180–2. 14. Haynsworth RF, Noe CE. Percutaneous lumbar sympathectomy: A comparison of

radiofrequency denervation versus phenol neurolysis. Anaestheiology 1991; 74:459–63.

15. Cheshire NJ, Darzi AW. Retroperitoneoscopic lumbar sympathectomy. Br J J Surg 1991; 84:1094–5.

16. Hourlay P, Vangertruyden G, Verduyden F, Trimpeneers F, Hendricks J. Endoscopic extraperitoneal lumbar sympathectomy. Surg Endosc 1995; 9:530–3.

17. Cousins MJ, Reeves TS, Glynn JA, Walsh JA, Cherry DA. Neurolytic lumbar sympathetic blockade: duration and relief of rest pain. Anaesth Intensive Care 1979; 7:121–33.

18. Boas RA. Sympathetic block in clinical practice. Int Anaesthesiol Clin 1978; 16:149–80.

19. Blumenberg RM, Gelfand ML. Lumbar sympathectomy for limb salvage—a goal-line standard. Am J Surg 1979; 138:241–5.

20. Wronski J. Lumbar sympathectomy performed by means of videoscopy. Cardiovasc Surg 1998; 6(5): 453–6

21. Wattanasirichaigoon S, Hgaoruhgsri U, Wanishayathanakorn A, Hutachoke T, Chulakamontri T. Laparoscopic transperitoneal lumbar sympathectomy: a new approach. J Med Assoc Thailand 1997; 80(5): 275–81.

Further reading

Darzi A (ed.) Retroperitoneoscopy. Oxford: Isis Medical Media, 1996. Moore WS. Vascular surgery: a comprehensive review. London: W.B. Saunders, pp.

349–59. Alomare DF, Regina G, Lovreglio R, Memeo V. Acetylcholin e sweat test: an effective

way to select patients for lumbar sympathectomy. Lancet 1994; 344:976–8. Ellis H. Lumbar sympathectomy. Br J Hosp Med 1986; 124–5. Kathouda N, Wattanasirichaigoon S, Tang E, Yassini P, Ngaorungsi U. Laparoscopic


lumbar sympathectomy. Surg Endosc 1997; 11: 257–60. Cotton LT, Cross FW. Lumbar sympathectomy for arterial disease. Br J Surg 1985;

72:678–83.


Endovascular treatment of aortic aneurysms

10 JAMES MAY, GEOFFREY H.WHITE AND JOHN P.HARRIS

Introduction

Endovascular aneurysm repair involves the transluminal placement of a graft within theaneurysm from an accessible remote site. The purpose of this graft is to completelyexclude the sac from the general circulation. The graft is anchored in place by a balloonexpandable or self-expanding metal frame, which supports all or part of the graft in addition to providing a watertight seal proximal and distal to the dilated segment of theartery. Much of the morbidity and mortality of open repair of abdominal aortic aneurysm(AAA) is associated with the need for laparotomy, cross-clamping of the aorta and the obligatory blood loss associated with opening the aneurysm sac. Since the endoluminaltechnique eliminates all three, it has much to recommend it.

Despite the attractions, there are two areas of concern with the endovascular method.One is the unknown longterm outcome and the other is for those complications specific toendovascular repair. Manipulation of endovascular devices within an aneurysm hasresulted in massive microembolization, which has proved to be fatal.1 Despite improvements in technology and increasing experience, endoleak, a phenomenon uniqueto endovascular repair, remains a problem in up to 20% of patients.2, 3 This term refers to incomplete exclusion of the aneurysm sac, where a leakage remains within the confinesof the vessel but external to the endovascular graft. Aneurysms with this clinical courseusually continue to expand and may go on to rupture.

In attempting to determine the place of endovascular repair of aortic aneurysms relative to open repair, there are reports of historic comparison4 and concurrent comparison5 of the two methods, but no prospective randomized trials.

History

Endovascular treatment of aortic aneurysms is not new. As early as 1864, Moore iscredited by Keen with having attempted thrombosis of an aneurysm by the introductionof large masses of intraluminal wire.6 In pre-antibiotic days the majority of aneurysmswere syphilitic in origin and saccular in morphology. This made them more amenable totreatment by wiring than the fusiform variety seen today. In 1879, Corradi modified theprocess by passing an electric current along an insulated wire.7 Power described a device, credited to his house surgeon, Colt, that delivered a selfexpanding wire umbrella into theaneurysm via a trocar.8 The method encouraged thrombosis and met with limited success.

As late as 1938, Blakemore was reporting electrothermic coagulation of aorticaneurysms.9

Indications for treatment

It was in the high-risk group of patients who were unfit for conventional open repair thatendovascular repair first found a place in the management of aortic aneurysms. Whilemany high-risk patients were thus able to be treated, there were important implications ifthe endovascular technique failed and required conversion to open repair in patientsdenied conventional surgery due to medical comorbidities. The mortality in patients withthis clinical course proved to be very high.10 With improvements in technology andincreasing experience, however, the incidence of conversion from endovascular to openoperation is falling.11 High-risk patients may therefore continue to be considered forendovascular repair, provided the size of the aneurysm justifies intervention and thepatient understands the increased risk. Following the establishment of the feasibility andrelative safety of endovascular repair, the procedure has been offered to patients who are good risk and considered fit for conventional open repair. It is important, however, thatthese patients understand that the longterm outcome of these procedures is unknown andthat concurrent comparison of endovascular and open repair of AAA demonstrates asignificantly higher failure rate for the endovascular method in the mid-term.5 A compelling argument in favour of offering endovascular repair to this large group ofpatients is the low mortality rate. In the last 180 patients in this group treated by theauthors, there has been only one death. In the authors’ experience, this mortality (0.6%) compares very favourably with that for open repair (5.6%).5

With the evolution of modular prostheses, the endovascular method of repair hasbecome a feasibility for managing ruptured aneurysms. Provided the patient ishaemodynamically stable and monitored during computed tomography (CT)interrogation, ruptured aneurysms may be legitimately treated by this technique (Figure 10.1).

Criteria for endovascular treatment

Not all aneurysms are anatomically suitable for endovascular repair. The majordeterminant in deciding suitability is the size and morphological features of the proximalneck of the aneurysm. A collar of normal aorta between the renal arteries and theaneurysm of length 15 mm or greater and

Endovascular treatment of aortic aneurysms 219

Figure 10.1 Contrast computed tomography scan of a haemodynamically stable patient with ruptured abdominal aortic aneurysm successfully treated by endovascular repair.

diameter 28mm or less is required. The presence of heavy circumferential calcification,mural thrombus or inverted funnel shape are contraindications to the endovascularmethod.

Tortuosity is also important in determining suitability for endovascular repair. Since aneurysms expand longitudinally as well as transversely, the increase in sizelongitudinally may be accommodated by angulation in the neck, the aneurysm itself, theiliac arteries or any combination of the three. The recommended maximum angulation inthe neck is 120 degrees (180 degrees representing a straight course without angulation)and in the iliac arteries, it is 90 degrees.12

Since the endovascular method of aneurysm repair requires isolation of the aneurysm sac from the circulation, the presence of large patent collateral channels such as theinferior mesenteric artery and the internal iliac arteries communicating with the aortic oraorto-iliac sac is a relative contraindication. These may be occluded by coil embolizationpre-operatively or intra-operatively and need not necessarily preclude the use of the endovascular method (Figure 10.2).

Pre-operative imaging

Pre-operative imaging is very important, since patient selection and sizing of theendograft are dependent on it. Contrast-enhanced spiral CT is the preferred initial investigation. The dimensions of the proximal neck can be accurately determined and thepresence of calcification or mural thrombus noted. The size of the iliac arteries and thepresence of aneurysm disease and calcification can also be noted.


Although the anatomy of the iliac arteries and accessory renal arteries can bedemonstrated by spiral CT, most centres perform aortography when the patient has beenfound to be suitable for endovascular repair by CT. The aortogram should be performedwith a calibrated catheter to allow accurate measurements to be made withoutmagnification, which occurs with external calibration.

Endovascular prostheses

Tubular prostheses have been shown to be less successful than non-tubular prostheses in the treatment of AAA.13 Early bifurcated prostheses were one-piece rather than modular in construction and unsupported between the graft attachment devices. Problems withtwisting of one-piece

Figure 10.2 (a) Angiogram demonstrating intra-operative selective catheterization of the inferior mesenteric artery. (b) Hard copy of image intensifier demonstrating intra-operative coil embolization of a previously patent inferior mesenteric artery.

prostheses during deployment were reported,10, 14 together with thrombosis of the unsupported limbs.

The limitations of these devices became apparent and a second generation of prostheses were developed. In these, the fabric was supported throughout by a metallicframe to prevent kinking and add column strength. The modular method was used todeploy bifurcated grafts, with component parts being delivered from both groins. TheFrench size of the delivery system’s internal diameter was reduced from 24 to 21F and the flexibility increased.


Technique of endovascular repair

Endovascular repair is best performed in the operating room under general or regionalanaesthesia. The patient should be draped for open repair in the event of failedendovascular repair or occurrence of complications requiring open operation. Aradiolucent operating table, preferably carbon fibre and a C-arm to provide cine loop angiography with the capability for digital subtraction and frame-by-frame replay is required. The patient is positioned so that the C-arm can be placed beneath the abdomen and lower chest without obstruction from the table. A radio-opaque ruler is placed beneath the patient as a reference point during deployment.

The common femoral artery in the ipsilateral groin is exposed and the patient heparinized. A preprocedure aortogram is performed using the largest screen sizeavailable, a power injector and a calibrated pigtail catheter placed with the holesimmediately above the renal arteries. The positions of the renal arteries, aortic bifurcationand iliac bifurcations are noted relative to the ruler. The position of one of the digits onthe ruler is identified on the image intensifier screen by a piece of tape. This enables theimage intensifier to be moved inferiorly to monitor the introduction of the prosthesis andreturned to the same position without introducing errors of parallax. An angiographiccatheter is introduced percutaneously over a guide-wire into the contralateral femoral artery.

An extra stiff guide-wire is introduced through the pigtail catheter as far as thedescending thoracic aorta and the catheter removed. A transverse arteriotomy is made inthe ipsilateral common femoral artery in such a way that the guide-wire is situated within the arteriotomy. The catheter and prosthesis within it are introduced over the extra-stiff guide-wire after checking the orientation of the device under the image intensifier. Thecatheter is advanced under radiographic control until the superior end of the prosthesis isimmediately below the renal arteries. The image intensifier is moved superiorly to place the superior end of the prosthesis (and therefore the renal arteries) in the centre of thefield. The angiographic catheter is withdrawn to the point where contrast injected throughit will accurately locate the exact position of the renal arteries. These last manoeuvreseliminate parallax and avoid errors caused by the catheter, straightening an angled aortaand moving the renal arteries to a different level.

After ascertaining that the systolic blood pressure is less than 100mmHg, the trunk andipsilateral limb of the bifurcated prosthesis are deployed under radiographic control. Thedetailed technique of deployment for individual prostheses is beyond the scope of thischapter.

Following ipsilateral limb deployment, attention is directed to passing a guide-wire from the contralateral femoral artery through the stump of the prosthesis. This can usuallybe achieved from below using an angled guiding catheter. If difficulty is experienced, theguide-wire may be passed from the ipsilateral groin through the ipsilateral limb of theprosthesis and, again with the aid of a guiding catheter, inferiorly through thecontralateral stump into the aneurysm sac. From here, it may be retrieved by a snarepassed from the contralateral groin. An approach from the left brachial artery may also beused if the two previous methods fail. A guide-wire is passed from the left brachial artery


and directed down the descending thoracic aorta, either by a guiding catheter or ballooncatheter, which can be inflated in the aorta and carried distally by blood flow to reach theaneurysm sac via the contralateral stump. The brachial approach is also very useful incases of extreme tortuosity in the iliac arteries. After retrieval of the brachial guide-wire in the aneurysm sac by snare, tension can be applied from the brachial and femoral ends.This results in considerable straightening of the iliac arteries (Figure 10.3), allowing passage of the catheter.

Following cannulation of the contralateral stump, the contralateral limb, within its catheter, is delivered under radiographic control to a position within and overlapping thecontralateral stump. This position is identified by clearly visible radio-opaque markers on the stump and endograft limb. The limb is now deployed, again under radiographiccontrol. The pigtail catheter is re-introduced and a postprocedure digital subtraction aortogram is performed. The cine loop is examined on a number of occasions to look forextravasation of contrast suggesting an endoleak. Flow of contrast through the iliacarteries is also examined for any evidence of kinking or twisting.

Follow-up after endovascular repair

Since the long-term outcome of endovascular repair is unknown, careful and prolonged follow-up is required.

Figure 10.3 (a) Aartogram demonstrating abdominal aortic aneurysm (7 cm diameter) and extreme tortuosity of the left common iliac artery. (b) Contralateral sheath traversing the aorta and left iliac arteries in the patient from (a) appearance following traction on the brachial and femoral ends of the through-and-through guide-wire. Note the disappearance of the acute angle between the aneurysm and the left common iliac artery. (From Rutherford, 2000, Vascular Surgery, with permission)

Physical examination and contrast-enhanced CT within 1 week of operation, at 6, 12 and18 months after operation and annually thereafter, is recommended.


Complications

Complications have been divided into remote/systemic and local/vascular by the Ad hocCommittee of the Joint Societies of Vascular Surgery and North American Chapter of theInternational Society for Cardiovascular Surgery for uniform reporting standards. Theremote/systemic complications following endoluminal AAA repair do not vary greatlyfrom those following open aneurysm repair and will not be dealt with further in thischapter. The local/vascular complications, however, are important as many of them arespecific to the endoluminal method of aneurysm repair. A complete list of thesecomplications is presented in Table 10.1. Of these, endoleak is the single most common cause of failure in endoluminal AAA repair and will be considered in detail.

Endoleak

Endoleak is a condition associated with endoluminal vascular grafts, defined by thepersistence of blood flow outside the lumen of the endoluminal graft but within an

Table 10.1 Local/vascular complications following endoluminal repair

Injury to arteries of access

Iliac

Suprarenal arteries (if brachial approach is used)

Embolization

Microembolization/renal failure

Distal embolization/ischaemia

Endoleak

Type I (graft related)

Type II (collateral channel related)

Post-implant syndrome

Graft limb thrombosis

Groin wound complications

Conversion to open repair: current indications

Aortic rupture

Endograft migration obstructing iliac outflow

Persistent endoleak following unsuccessful secondary endoluminal repair

Endograft infection

After Rutherford, 2000, Vascular Surgery,


aneurysm sac or adjacent vascular segment being treated by the graft. Endoleak is due toincomplete sealing or exclusion of the aneurysm sac or vessel segment, as evidenced byimaging studies such as contrast-enhanced CT, ultrasonography or angiography.2

Figure 10.4 Contrast computed tomography scan demonstrating a type I endoleak resulting from dislocation of the contralateral limb of a modu-lar endograft (lying horizontally) from contralateral stump.

Figure 10.5 Contrast computed tomography scan demonstrating a type II endoleak from the inferior mesenteric artery.


Classification of endoleak

A clear distinction should be made between endoleak related to the graft device itself(Type I) (Figure 10.4)16 and endoleak associated with flow from collateral arterialbranches (Type II) (Figure 10.5).17

Endoleak may also be classified according to the time of occurrence.

Primary endoleak

This is an endoleak that is present from the time of the implantation procedure or initiallydiagnosed during the 30-day perioperative period.

Secondary endoleak (or late endoleak)

This is an endoleak occurring as a late event after successful endoluminal graftimplantation procedure. No endoleak is present at the time of implantation or during theperioperative period.

Recurrent endoleak

This is an endoleak that has been demonstrated to have sealed spontaneously, thenrecurred subsequently.

Outcome following endoleak

The incidence of endoleak has been variously reported at 44% by Moore andRutherford,18 27% by Marin et al.19 and 10% or less by Blum et al.,20 Parodil and May et al.21

Untreated, an endoleak leads to continued expansion of the AAA.22–26 The endoleak may sealspontaneously by thrombosis. This occurred in over half the cases of endoleakreported by Moore and Rutherford, leaving them with a permanent endoleak rate of 21%.Spontaneous sealing of the endoleak is accompanied by reduction in the diameter of theAAA. Conversely, the diameter of the AAA increases when a secondary endoleakdevelops in a previously isolated AAA following successful endoluminal repair.

Bernhard24 (pers. com., 1998) in reviewing an extensive series of endovasculartechnologies (EVT) (Endovascular Technologies, Menlo Park, CA, USA) patientsreported that type II endoleaks were more likely to seal spontaneously then type I. It hasalso been suggested that type II endoleaks may be less likely to rupture. This may be adangerous supposition, however, since the Albany group25 have reported rupture of an AAA due to collateral channels in patients treated by ligation and bypass. Untreatedendoleak (type I), resulting in AAA rupture, has now been reported on a number ofoccasions.25–28


Management of the endoleak

Endoleak may be managed by:

1. observation; 2. a further endovascular procedure comprising either a supplementary endoluminal

repair or embolization;

Figure 10.6 Kaplan-Meier curves for survival following a concurrent study of endoluminal vs open repair of abdominal aortic aneurysms. (From May et al., 1988,5 with permission.)


Figure 10.7 Kaplan-Meier curve for graft failure following endoluminal repair. (From May et al., 1988;5 withpermission.)

3. surgical band ligature of the aneurysm neck; and 4. conversion to open repair of the aneurysm where supplement ntary endoluminal repair

is not possible or has failed.

Results

The authors in a concurrent comparison of endoluminal versus open repair of AAA hasdemonstrated that the endoluminal method is safe.5

Despite having 44% high-risk patients, the endoluminal group had the same perioperative mortality (5.6%) as the open group. Kaplan-Meier curves for survival following endoluminal and open repair of 303 patients treated concurrently showed nosignificant difference when analysed by log rank test (Figure 10.6). Demonstration of this acceptable survival probability of 83% at 5 years in the endoluminal group is important,considering the cost of endoluminal prostheses.

Graft failure rate was significantly higher in the endoluminal group compared with theopen group. The success probability at 3 years was 70% (Figure 10.7). The higher failure rate, however, was compensated for by a decrease in blood loss at operation, and need for


intensive care and length of hospital stay. In a more recent report29 a concurrent comparison of endoluminal repair using second

generation prostheses versus open repair demonstrated superior survival in theendoluminal group.

References

1. Parodi JC. Endovascular repair of transfemoral intraluminal graft for abdominal aortic aneurysms and other arterial lesions. J Vasc Surg 1995; 21:549–57.

2. White GH, Yu W, May J, Chaufour X, Stephen MS. Endoleak as a complication of endoluminal grafting of abdominal aortic aneurysms: classification, incidence, diagnosis, and management. J Endovasc Surg 1997; 4:152–68.

3. May J, White GH, Endovascular leak—a complication unique to endovascular grafting. In: A Whittemore D Bandyk, J Cronenwett, N Hertcer, R White (ed.) Advances in vascular surgery. St Louis, MO: Mosby Inc, 1998; 6:65–78.

4. White GH, May J, McGahan T et al. Historic control comparison of outcome for matched groups of patients undergoing endolyminal versus open repair of abdominal aortic aneurysms. J Vasc Surg 1996; 2: 201–12.

5. May J, White GH, Yu W et al Concurrent comparison of endoluminal versus open repair in the treatment of abdominal aortic aneurysms: analysis of 303 patients by life table method. J Vasc Surg 1998; 27:213–22.

6. Kee WW. Surgery. Its principles and practice. Philadelphia, PA: WB Saunders, 1921; 216–49.

7. Barker WF. Clio Chirurgica. The Arteries, Part 1, Austin, T: Silvergirl Inc., 1988. 8. Power, DA, Sir. The palliative treatment of aneurysms by ‘wiring’ with Colt’s

apparatus. Br J Surg 1921; 9:27. 9. Blakemore AH, King BG. Electrothermic coagulation of aortic aneurysms. JAMA

1983; 111:1821–4. 10. May J, White GH, Yu W et al Conversion from endoluminal to open repair of

abdominal aortic aneurysms: a hazardous procedure. Eur J Vasc Endovasc Surg 1997; 14:4–11.

11. May J, White GH, Yu W et al. Endovascular grafting for abdominal aortic aneurysms: changing incidence and indications for conversion to open operation. Cardiovasc Surg 1998; 6(2): 194–7.

12. May J, Woodburn K, White GH. Basic data underlying clinical decision making: endovascular treatment of infrarenal abdominal aortic aneurysms. Ann Vasc Surg 1998; 12:391–5.

13. May J, White GH, Yu, W et al Importance of graft configuration in outcome of endoluminal aortic aneurysm repair: a 5-years analysis by the life table method. Eur J Vasc Endovasc Surg 1968; 15:406–11.

14. May J, White GH, Yu W et al Endoluminal grafting of abdominal aortic aneurysms: causes of failure and their prevention. J ndovasc Surg 1994; 1:44–52.

15. Rutherford R (ed.) Endovascular Treatment of aortic aneurysms. In: Vascular surgery. 5th edition. London: W.B. Saunders.

16. Whittemore A, Bandyk D, Cronenwett J, Hertcer N; White R (eds.) Advances in vascular surgery. St Louis, MA: Mosby Inc. (in press).

17. White GH, May J, Waugh RC, Yu W. Type I and Type II endoleak: a more useful


classification for reporting results of endoluminal repair of AAA [Letter]. J Endovasc Surg 1998; 5(2): 189–91.

18. Moore WS, Rutherford RB for the EVT Investigators. Transfemoral endovascular repair of abdominal aortic aneurysm: results of the North American EVT phase 1 trial. J Vasc Surg 1996; 23:543–53.

19. Marin ML, Veith FJ, Cynamon J et al. Initial experience with transluminally placed endovascular grafts for the treatment of complex vascular lesions. Ann Surg 1995; 222:449–69.

20. Blum U, Voshage G, Lammer J et al Endoluminal stent-grafts for infrarenal abdominal aortic aneurysms. N Engl J Med 1997; 336: 13–20.

21. May J, White GH, Yu W, Waugh R, Stephens MS, Harris JP. Repair of abdominal aoritc aneurysms by the endoluminal method: outcome in the first 100 patients. Med J Aust 1996; 165:549–51.

22. May J, White GH, Yu W, Waugh R, Stephen M, Harris J. A prospective study of anatomico-pathological changes in abdominal aortic aneurysms following endoluminal repair: Is the aneurysmal process reversed? Eur J Vasc Endovasc Surg1996; 12:11–17.

23. Matsumara JS, Pearce WH, McCarthy WJ, Yao JST for the EVT Investigators. Reduction in aortic aneurysm size: early results after endovascular graft placement. J Vasc Surg 1997; 25:113–23.

24. Malina M, Invacev K, Chuter TAM et al. Changing aneurysmal morphology after endovascular grafting: relation to leakage or persistent perfusion. J Endovasc Surg 1997; 4:23–30.

25. Lloyd WE, Darling RC, Chang BB, Shar DM, Paty PJK, Leather RP. The fate of the excluded abdominal aortic aneurysm sac: long term follow up of 852 patients. Poster presentation, SVS/ISCVS meeting, New Orleans, 1995.

26. Lumsden AB, Allen RC, Chaikof EL et al. Delayed rupture of aortic aneurysms following endovascular stent grafting. Am J Surg 1995; 170:174–8.

27. Parodi JC, Barone A, Piraino R, Schonholz C. Endovascular treatment of abdominal aortic aneurysms: lessons learned. J Endovasc Surg 1997; 4:102–10.

28. White GH, Yu W, May J et al Three-year experience with the White-Yu endovascular GAD graft for transluminal repair of aortic and iliac aneurysms. J Endovasc Surg 1997; 4:124–36.

29. May J, White GH, Waugh R, Ly CN, Stephen MS, Harris JP. Improved survival after endoluminal repair with second generation protheses compared with open repair in the treatment of abdominal aortic aneurysms: A 5-year concurrent comparison using life table method. J Vasc Surg 2001; 33: S21–6.


Insertion of an aorto-uni-iliac graft for the treatment of aortic aneurysms

11 P.R.F. BELL AND M.M. THOMPSON

Introduction

Ideally aortic aneurysms should be dealt with by the insertion of a bifurcated graft if at allpossible, supplying both internal iliac arteries as well as the limbs.1 This approach has, over many years, been found to be satisfactory when open repair is used and there is noreason to do any differently if endovascular techniques are employed instead. However,when it is impossible to insert a bifurcated device, then an aorto-uni-iliac graft offers an opportunity to avoid an open procedure, which is particularly important in older or unfitpatients, where the mortality for open repair may be higher. The restrictions imposed onthe use of bifurcated grafts usually relate to the distal anatomy of the aorta, as theproximal requirements both for the uni-iliac and the bifurcated systems is similar, namely a segment of reasonably normal aorta between the renal arteries and the commencementof the sac. This segment should between 1 and 1.5 cm long and up to about 2.8 cm indiameter. Distally, most of the bifurcated systems require a segment of iliac artery that isnot aneurysmal and where the maximum diameter is about 16mm. Another limitingfactor is aortic or iliac tortuosity (Figure 11.1). Whether these conditions can be metdepends upon the threshold for treatment of abdominal aortic aneurysms (AAA). Thegreater the diameter of the aneurysm when treatment is begun, the more unlikely it is thata bifurcated graft can be inserted because many of the adverse features mentioned abovewill then be present. For example, if 5.5 cm is the starting point for intervention, as is thecase in our centre, then relatively few (in our experience, about 30%) of bifurcated grafts,can be inserted into these patients. If aneurysms less than 5 cm are treated, then manymore grafts of the bifurcated variety can be placed.2 The insertion of uni-iliac devices is therefore usually into patients who have iliac arteries larger than 16–18mm and which might even be aneurysmal. However, the continued evolution of bifurcated systems doesmean that more patients will be treated with these devices in years to come.

Figure 11.1 A 1–1.5 cm neck is required by the aneurysm sac proximally, and distally the iliac artery should be no more than 16mm for bifurcated grafts. Excess of tortuosity is also a problem.


Uni-iliac grafts plus cross-over

Even for this type of graft, two approaches are possible: one is to use an aorto-uni-iliac system with the lower end of the graft attached to a common iliac artery on one side,which is 16–18mm in diameter, thereby preserving the internal iliac artery on that side(Figure 11.2). This is particularly useful if the other common iliac artery is aneurysmal or narrow,

Figure 11.2 An aorto-uni-iliac graft with the lower end fixed in the common iliac artery. The opposite iliac artery can be blocked at (a) of (b) using a covered stent.

Insertion of an aorto-uni-iliac graft for the treatment of aortic aneurysms 233

Figure 11.3 The aorto-uni-iliac graft in this case is taken down to the groin via a dacron conduit and sewn to the cross-over graft. The ipsilateral internal iliac is occluded with a coil and the contralateral common iliac with a covered stent.

in which case the internal on that side can be occluded by embolization and the commonfemoral ligated in the groin preventing retrograde flow.3 The second approach is useful if the iliac artery is wider than this diameter on one or both sides. In this case, the graft canbe taken right down to the groin and sutured directly to a cross-over graft, allowing blood


to flow back up into the opposite internal iliac artery with occlusion of the common iliacon that side by a covered stent (Figure 11.3). This technique is very useful, as precise measurements of the length of the graft are not needed. Almost 80% of cases can be dealtwith using this method. Between 50 and 60% of cases can be dealt with using thetechnique where the lower end of the graft is placed in the common iliac artery on oneside.

Insertion of an aorto-uni-iliac graft with a lower attachment to a cross-over graft in the groin

Patient selection

Patient selection for this procedure usually occurs where the aneurysm is greater than 5.5cm in diameter. Assessment is done initially using computed axial tomography (CAT)scanning (Figure 11.4), and a marker catheter and angiography if the anatomy appears suitable (Figure 11..5). For the system that we use, a proximal aortic neck of about 1.5 cm is necessary, although it is possible to attach the stent above the renal arteries using anuncovered portion for this purpose. The diameter of the proximal neck must be no morethan 28 mm in order to allow the insertion of a 30mm Palmaz stent, to allow for laterdilatation of the neck. The extent of the dilatation of the iliac arteries or the tortuosity ofthe upper neck is of no real importance with this method. Upper-end tortuosity can be compensated for by abdominal pressure on the aneurysm to

Figure 11.4 A computed tomography scan is used to assess the length of the neck and the diameter of the aorta above the sac.


Figure 11.5 In suitable cases, a marker catheter is inserted and an angiogram performed to measure the length required and also to estimate the tortuosity of the iliac.

straighten it while the wire is passed, and distal tortuosity can be straightened out asdescribed later (Figure 11.6). Usually, patients under 65 are not treated in this waybecause of the lack of long-term data after endovascular repair, but there are no otherexclusions.

The graft is produced on site from 8 mm polytetrafluoroethene (PTFE) [Impra] under sterile conditions. A 15 mm balloon (Cook Inc., Bloomington, IN, USA) is first insertedinto the graft, which is distended slowly throughout its length to 15 mm using an air-filled 20 ml syringe (Figure 11.7). An achalasia balloon (Boston Scientific Inc., Watertown, MA, USA) is then inserted into one end of the the dilated graft, which isexpanded with air. This is done slowly without touching the graft, which can otherwisedisintegrate. The achalasia balloon allows the PTFE to be stretched to more than 30 mm(Figure 11.8). A suture on a straight hand-held needle is then placed through the narrow end of the graft and the needle allowed to drop down the inside of a 21F peel-away sheath (Cook) (Figure 11.9). Once the needle has traversed the sheath, it is possible to pull the narrow end of the graft through it until it emerges. A 30 mm Palmaz stent is thenpartly expanded using the dilator from within the sheath. The stent is then placed insidethe expanded part of the PTFE, which is sutured to it with two 5/0 prolene sutures, one oneach side for the


Figure 11.6 Tortuosity of an iliac artery can be dealt with using an extraperitoneal iliac incision to mobilize the artery and then pull it downwards.

circumference of the stent, leaving the upper ring of the Palmaz stent uncovered. Smallpieces of PTFE are used to reinforce these sutures (Figure 11.10). A 30 mm balloon (Cook) is then passed inside the PTFE to lie at the upper end inside the Palmaz stentwhich is then crimped tightly over it (Figure 11.11). The expanded PTFE is folded around the stent and pulled back into the sheath leaving the tip of the balloon protrudingfrom the sheath (Figure 11.12). The device is then packed in a sterile intestinal bag for later use.


Insertion of the graft

The patient is prepared in the usual way and can be given either spinal anaesthesia orgeneral anaesthesia and placed on the operating table in the prone position. It is, ofcourse, important to ensure that the table top is one that will allow X-rays to be taken. It is also essential to have appropriate X-ray equipment in the theatre; the minimum would be a C-arm, ideally with a 12′′ picture. All staff must wear appropriate radiation protection around the neck and body during the procedure.

The patient is prepared with the usual sterile techniques, exposing the groin and the entire abdomen in case urgent conversion is required.

Selecting the surgical approach

Pre-operative examination with a CT scan or angiogram will have allowed a decision tobe made about which side to access and also where the incision is to be made. Obliqueangiograms are essential in order to inform this decision.

Figure 11.7 A 15 mm balloon is inserted into the polytetrafluoroethene, which is stretched throughout its length.


Figure 11.8 An achalasia balloon is inserted into one end of the partially stretched polytetrafluoroethene and expanded to more than 30 mm.


Figure 11.9 A suture is passed through the narrow end of the polytetrafluoroethene graft and the needle dropped through a 21F Cook sheath.

Generally speaking, if both vessels are relatively straight, either side can be chosen andgroin incisions will suffice. If, however, the vessels are tortuous, it is best to use the leasttortuous side, and an incision above the inguinal ligament to expose the retroperitonealexternal iliac artery may be necessary. This will also be required if it is necessary toligate the common iliac artery on the opposite side to prevent retrograde flow,particularly if placement of a gianturco stent covered with PTFE is not possible becausethe iliac artery is too large. When the route has been chosen, the initial procedure is toexpose both femoral arteries in the groin using a vertical incision.


Figure 11.10 The Palmaz stent is stitched to the expanded graft using 5/0 nylon sutures buttressed with a piece of polytetrafluoroethene.

Figure 11.11 The Palmaz stent is crimped over the 30 mm balloon and the expanded polytetrafluoroethene wrapped around it.


Figure 11.12 The stent and graft are then pulled back into the 21F sheath, leaving the balloon projecting from the end of it.


Operative procedure

Both femoral arteries are exposed through a vertical incision and the profundafemoris andthe superficial and common femoral arteries are controlled. If a groin approach is thoughtto be appropriate then it will be necessary to expose the common femoral artery on theside through which the device is to be inserted, sufficiently high to attach a piece of10mm dacron [Vascutek] to it as an aid to entry, in order to prevent damage to the accessartery. When both vessels have been dissected, a piece of 10 mm coated dacron is soakedin rifampacin for infection control and sutured endto-side to the front of both common femoral arteries after being tunnelled under the skin; 5/0 prolene is used to do this (Figure 11.13). Prior to starting the procedure, the patient should be heparinized with 5000 units of heparin and given prophylactic antibiotics. When this has been done, the rest of theother half of the 10 mm dacron is sutured end-to-side, with the common femoral arteryabove the cross-over graft on the side chosen to insert the prosthesis (Figure 11.13). A ligature is then placed between the end-to-side graft and the cross-over graft to prevent reflux later (Figure 11.14). This need not be tied at this stage. The end-to-side graft is attached using a vertical arteriotomy and 4 or 5/0 prolene. The anastomosis should belarge enough to allow the passage of a 25F sheath.

Figure 11.13 A 10 mm rifampacin-soaked knitted dacron is sutured to each femoral artery with a cross-over graft. A conduit for access is sutured to the common femoral artery above it.

Iliac approach

If the vessels are too tortuous or if it is thought that the common iliac artery will need tobe ligated, a muscle-cutting incision is made above the inguinal ligament and the retroperitoneal space entered. The external iliac artery is controlled and the internal iliacartery ligated to prevent reflux later. A piece of 10 mm dacron is then sutured endto-side with the external iliac artery just below the bifurcation and tunnelled to the groin (Figure 11.15).


Figure 11.14 The ligature is tied between the conduit and the cross-over graft to prevent reflux of blood into the sac.

Figure 11.15 In cases where a tortuous iliac artery is present, the conduit is sewn to the external iliac artery and tunnelled into the groin.

Occlusion of the ipsilateral internal iliac artery

If a groin incision is used, the ipsilateral internal iliac artery is first occluded by passing awire into the right internal iliac artery through the ipsi- or contralateral femoral artery and embolizing this with one or two 8 mm coils (Figure 11.16). This can be done the day before in the angio suite to save time, as it is often difficult to enter the vessel because ofthe angle of calcification. If the iliac approach is being used, the internal iliac artery canbe simply ligated.


Insertion of the device

Access is via the end-to-side conduit. This is done by inserting a standard needle into theconduit and passing a wire up into the neck of the aneurysm and beyond. If the standardwire cannot be inserted, a Terumo guidewire is used after the insertion of a sheath or VanAndel catheter. Once the wire has reached the neck of the sac a Van Andel catheter ispassed over the wire to lie above the sac. The guide-wire is removed and replaced with a Lundqvist wire to straighten out the various tortuous parts of the aortoiliac system. Whenthis is in place, the Van Andel catheter is removed. A needle is then placed in the crossover graft on the opposite side and a wire followed by a pigtail catheter is placed in theneck of the sac for later

Figure 11.16 An embolus is passed into the ipsilateral internal iliac artery to occlude it. A coil is used for this purpose.


Figure 11.17 With the cross-over graft in place, a Lundqvist wire is inserted in the aorta or the aneurysm via the conduit and a pigtail catheter is passed up the contralateral side via the cross-over graft.

angiography (Figure 11.17). A 25F peel-away sheath (Cook) is then passed over thelundqvist wire via the conduit and an incision made in the conduit little by little to allowentry of the dilator and the 25F sheath (Figure 11.18). This size sheath fits the 10 mm conduit in an almost bloodtight fashion. The sheath is then advanced slowly inside theiliac artery over the lundqvist wire, screening all the while to monitor its progress. Do notpush too hard and gradually advance the sheath over the lundqvist wire until it rests in theaorta above the aneurysm near the renal arteries (Figure 11.19). When this has been done,


an angiogram

Figure 11.18 The 25F sheath and dilater is then passed into the aneurysm sac via the conduit.


Figure 11.19 An angiogram is performed to show the. relationship of the renal arteries to the conduit.

Figure 11.20 The position of the renal arteries is marked by a piece of thread fixed to the screen of the viewing box. The C-arm is then fixed.

using the contralaterally placed pigtail catheter is performed to locate the renal arteries(Figure 11.20). These can then be marked in a variety of ways. Our preference is to fix the C-arm and to place a piece of thread on the viewing box to mark the position of the vessels (Figure 11.21). Another method is to use roadmapping, which we think isinferior. When this has been done the dilator is removed from the sheath along with thelundqvist wire and the sheath clamped to prevent blood loss (Figure 11.22). The wire is


Figure 11.21 The central dilater has been removed and the empty sheath damped to prevent blood loss.


Figure 11.22 The device contained inside the 21F sheath is now pushed up inside the 25 sheath.


then backloaded into the previously constructed device, which is then passed forward into the already clamped sheath; again, a 21F sheath produces a relatively good seal in the25F sheath (Figure 11.23). As the device is advanced up the sheath, the lundqvist wire ispushed before it and placed back into the aorta above the sac. The pigtail catheter is nowpulled back into the sac itself. Once the device reaches the level for deployment, which isjudged by the string marking the renal arteries, the 25F sheath is peeled away until wellinto the sac (Figure 11.24). This requires an assistant to maintain the position of the device with upward pressure. The 21F sheath is then peeled away in the same fashionuntil the stent in the balloon is expanded, again maintaining the position of the device.The balloon is then inflated to 2 atm using an inflater, with no contrast in the balloon(Figure 11.25), moving the stent slightly up or down to maximize its position as shortening occurs. Precise deployment of the stent can be achieved in this fashion. Theballoon is left inflated for 1 min and then let down. It is then filled with dilute contrastand reexpanded in a slightly different radial direction. The mean blood pressure ismaintained at a mean of 70mmHg during this phase and both peel-away sheaths removed completely. The PTFE at the lower end is then clamped and the conduit cut back toexpose the PTFE (Figure 11.25). This is then sutured to the cross-over graft, which is appropriately clamped after removing a disc of dacron from that graft. Once this is done,the balloon is deflated and removed under X-ray vision prior to completion of theanastomosis, which is then released; blood should now flow down both limbs of thecross-over graft. We have found it useful to monitor flow down one of the limbs using a transcranial doppler probe placed over the femoral artery, which gives a good idea ofvolume flow into the lower extremities, the adequacy of the graft, and the absence of anykinking.

Occlusion of contralateral common iliac artery

In cases where the common iliac artery is aneurysmal it has to be tied off through a smalliliac incision. However, if it is of the correct size to accommodate a gianturco stent ofabout 20 mm it can be dealt with retrogradely. The Gianturco stent is covered with apiece of the PTFE cut from the original graft, so that it is closed completely (Figure 11.26). A wire is then passed into the common iliac artery via the cross-over graft, followed by a Van Andel catheter, and replaced with a lundqvist wire (Figure 11.27). A 21F sheath and dilater is then passed over the lundqvist wire and positioned in thecommon iliac artery (Figure 11.28). The dilater is then bevelled flat and used to push the covered gianturco stent up the 21F sheath to be deployed in the common iliac artery(Figure 11.29). The wire and sheath are then removed and the defect in the graftoversewn. Finally, a needle is inserted into the cross’ over graft opposite the entry of the PTFE, and a wire passed


Figure 11.23 The 25 sheath is now peeled away to expose the 21F sheath inside the aorta.


Figure 11.24 The balloon is inflated to allow precise deployment of the stent. The condiut is cut away to expose the PTFE.


Figure 11.25 A piece of the expanded PTFE is sewn over the gianturco stent from a covered graft—stent combination.

up into the PTFE and the aorta above the device. A pigtail catheter is inserted and anangiogram performed using a pump to show flow down the device and also across the legand up into the internal iliac artery. Two runs are usually required to show this (Figure 11.30). This will show if there is a leak and if satisfactory flow into the other leg is occurring (Figure 11.31).

Problems

If the correct patient is chosen for this technique the problems are relatively few. Themain difficulty is that sometimes the stent slips off the balloon and cannot be positionedproperly. This can be rectified by partly inflating the balloon and pushing the stent intoplace and then fully inflating after withdrawing the wire. Apart from this, no other majorproblems have been experienced using this approach. If the neck is not long enough toaccommodate the device as described here, an alternative is to stitch the PTFE lowerdown the stent and cover the renal vessels with the open part. We have done this on onlytwo occasions but have seen no changes in renal function. We have now done of theseprocedures; two stents needed open conversion because of inexperience when we firststarted using these grafts. The first was because we were inserting the stent into a bell-shaped aortic neck, which is a contraindication, and in the second


Figure 11.26 A wire is passed into the contralateral iliac artery via the cross-over graft.


Figure 11.27 A 21F sheath is passed over the wire and a dilator with the end blunted used to push out the Gianturco stent into the common iliac artery.


Figure 11.28 The deployment is complete, in the common iliac artery with the internal open for retrograde perfusion.


Figure 11.29 An X-ray showing the common iliac artery occluded.

Figure 11.30 Completion angiogram, showing no leakage from the upper end.


Figure 11.31 An angiogram showing good flow across the cross-over iliac into the internal iliac artery, with no leakage of the contralateral common iliac.

thrombus was present in the neck. There has been one late leak, which was due to thestent slipping when it was first inserted. In one other case, the graft has occluded acutelyat 6 weeks, needing a graft between the axillary artery and the cross-over to solve the problem. The only other prob-lem is buttock claudication, which affects about 15% ofthese patients but is not usually a serious difficulty in terms of quality of life.4

References

1. May J, White GH, Yu W et al. Endoluminal repair of abdominal aortic aneurysms, strength and weaknesses of various prostheses observed in a 4–5 year experience. J Endovasc Surg 1997; 4:147–51.

2. Schumaker H, Eckestein HH, Kallinowski F et al. Morphometry and classification in abdominal aortic aneurysms: patient selection for endovascular and open surgery. J Endovasc Surg 1997; 4:39–44.

3. Yusuf S W, Whitaker SC, Chuter TAM et al. Early results of endovascular aortic aneurysm repair with aorto uni iliac graft and femorofemoral crossover. J Vasc Surg 1997; 25:165–72.

4. Thompson MM, Boyle JR, Fishwick G, Bell PRF. Aorto-uni-iliac endovascular aneurysm repair utilizing PTFE and balloon expandable stents. The Leicester experience. In: RM Greenhalgh (ed.) Indications in vascular and endovascular surgery. London: W.B. Saunders, 1998, 229–39.


Endovascular repair of abdominal aortic aneurysm: the aorto-biiliac approach

12 WESLEY S.MOORE

Introduction

Endovascular repair of abdominal aortic aneurysm is now in an advanced stage of clinicalinvestigation worldwide. From a historical perspective, the groundwork for placingvascular prostheses within the arterial lumen, as a minimally invasive approach, beganwith Charles Dotter in 1969, who demonstrated that coils could be successfully placedwithin the arteries of experimental animals with maintenance of patency.1 However, the concept of repairing an abdominal aortic aneurysm through the remote deployment of anendograft can be attributed to two investigators: Juan Parodi of Buenos Aires, Argentina,and Harrison Lazarus of Salt Lake City, Utah. These investigators, unknown to oneanother, began to develop experimental prototypes for tube graft deployment in the late1970s. Parodi was the first to place a clinical endograft and reported this experience in1991.2 His prosthesis utilized commercially available components including a light-weight fabric graft to which a Palmaz stent was sewn to the proximal end and balloonexpanded for fixation below the renal arteries. Initially, the distal portion of the graft wasallowed to selfexpand and did not have any means of fixation. Subsequently, a distalPalmaz stent was added to improve the distal seal of the endograft. Lazarus, working withindustrial collaboration, in a company later to be called Endovascular Technologies(EVT), developed a catheter-based graft delivery system that was fabricated specificallyfor the purposes of endovascular repair of abdominal aortic aneurysm.3, 4 The first successful clinical implant took place at the University of California, Los Angeles(UCLA) Medical Center on 10 February, 1993, as a part of a phase 1, trial for clinicalinvestigation approved by the Food and Drug Administration (FDA).5–9

Chuter et al. having studied the anatomic patterns of aortic aneurysm by computed tomography (CT) scanning, concluded that most aneurysms extended to the aorticbifurcation, and therefore a bifurcated prosthesis would have greater utility in managing alarger percentage of patients with aortic aneurysm.10, 11 He was the first to successfully develop a method for deploying a unit body aortic prosthesis.

Currently, endovascular repair of abdominal aortic aneurysm is being carried out usingaortic tube grafts, aortic bifurcation grafts of varying design, and aorto-uni-iliac with crossover femoral-femoral prostheses. This chapter will focus on the aorto-biiliac approach for endovascular aneurysm repair.

Types of aorto-biiliac grafts

The prostheses that are in current clinical investigation can generally be divided into twotypes: the unit body bifurcation graft and the modular bifurcation graft.

The unit body bifurcation graft

While the original unit body bifurcation graft was developed by Chuter and was subjectto initial clinical trial, that graft is currently not commercially available.11 The bifurcation graft developed by EVT has undergone the largest implantation experience and will bediscussed in detail. The EVT bifurcation graft is a light-weight woven prosthesis with self-expanding attachment systems located at the proximal end of the body and at the distal ends of each graft limb (Figure 12.1). Hooks are incorporated into the attachment systems, and further seating of the attachment systems are carried out with successiveballoon inflation (Figure 12.2). The bifurcation graft is compressed and pack-

Figure 12.1 The Endovascular Technologies bifurcation graft is a woven polyester prosthesis. The limbs are crimped in order to provide protection from kinking with angulation. Note the proximal and distal metallic attachment systems.

aged in a catheter delivery system, and covered with a retractable jacket (Figure 12.3). A pull-wire is attached to the distal capsule of the contralateral graft limb and emergesthrough the leading edge of the catheter delivery system (Figure 12.4). Passage of the pull-wire up the ipsilateral iliac artery into the aorta and subsequent capture of the pull-wire by a snare introduced from the contralateral femoral artery into the aorta permits thedrawing of the pull-wire into the contralateral femoral artery and the sub


Figure 12.2 This is the end-on appearance of the proximal attachment system, showing the hooks in profile.

Figure 12.3 This is the distal end of the graft delivery system. The bifurcated graft is compressed into a capsule and covered with a jacket. An inflatable balloon represents the distal end of the device that functions in an over-the-wire configuration.

sequent direction of the contralateral graft limb into the contralateral iliac artery positiononce the jacket is retracted and the limbs of the bifurcation graft allowed to separate.

Endovascular repair of abdominal aortic aneurysm: the aorto-biiliac approach 263

The modular bifurcation graft

There are several commercially fabricated modular prostheses that are currently inclinical trial. These include the Vanguard, the AneuRx (Medtronic), the Talent (WorldMedical), the Corvita, and the White-Yu endograft. The basic principle of the modular system involves the ability to add components of the endograft once the basic graft bodyhas been placed in the aortic position. Thus, the contralateral limb, as well as limb andbody extensions, may be added in order to build a bifurcation prosthesis in situ. The advantage of this approach is the opportunity to customize the final graft configuration tothe needs of an individual patient.

Figure 12.4 This is a close-up view of the distal end of the capsule. Note the pull-wire emerging from the leading edge of the distal capsule.

Patient selection

At the present time, there are certain limitations in the use of endovascular grafting foraneurysm repair. Clearly, all patients with abdominal aortic aneurysm are not candidatesfor this approach. As certain technical improvements or modifications take place, nodoubt a larger percentage of patients with abdominal aortic aneurysm will be consideredfor endovascular repair, as an alternative to conventional open repair.

In general, in order for a patient to be considered for endovascular repair, there must be a sufficient length of relatively normal aorta between the lowest renal artery and thebeginning of the aortic aneurysmal dilatation. This proximal neck should be an optimumlength of at least 15mm. The EVT bifurcation graft maximum proximal diameter is 26mm. Thus, patients with neck diameters that exceed 26 mm would be excluded. Othermanufacturers are able to accommodate patients with necks between 26 and 28 mm, andno doubt this limitation will be overcome by enlarged graft diameters available fromother manufacturers. Secondary exclusions involving the proximal neck includeexcessive calcification, irregularity, or the presence of mural thrombus. Elongation of theaneurysm resulting in profound angulation between the aneurysm sac and the proximalneck in excess of 45 degrees is also a relative contraindication.

Aneurysmal dilatation of the common iliac arteries is a contraindication toimplantation using the unit body bifurcation graft construction. This may be


accommodated in some of the modular graft design systems. In addition, if one is willingto sacrifice one hypogastric artery, that vessel can be occluded by coil embolization and amodular limb extended into the external iliac artery in order to extend the indications topatients with iliac artery aneurysm. The presence of occlusive lesions in the common orexternal iliac arteries is also a relative contraindication if one assumes that the lesionswould prohibit the passage of the graft delivery system. Finally, patients who have smalliliac arteries that prevent the passage of a sheath or delivery system also preclude the useof endovascular graft repair for treatment of their aneurysm. Relative contraindicationsinclude iliac artery tortuosity or angulation.

A recent review of our own experience in evaluating patients for endovascular repairreveals that only 25% of the patients we were asked to evaluate were candidates for eithera tube or an EVT bifurcation graft.12

Technique of implantation

There are several overlapping features common to the implantation of the currentendovascular prostheses. For the purposes of this chapter, I describe implantation of threedifferent grafts. These include the EVT unit body bifurcation graft, the MedtronicAneuRx modular graft, and the World Medical Talent modular graft.

All the current graft designs require the open exposure of both femoral arteries. Whileit is conceivable to do this under local or regional anaesthesia in a radiology suite, frommy perspective it is far safer to perform this procedure in an operating room undergeneral anaesthesia. The possible need for conversion to an open repair, sometimes underemergent conditions, does exist. Thus, having a patient in the operating room, undergeneral anaesthesia, with the abdomen prepared for prompt laparotomy is a distinct safetyfeature. In addition, since we are implanting a prosthetic device in the vascular system,risk of infection is a possibility. In my opinion, an operating room environment offersconsiderable advantage over a radiology suite from the standpoint of aseptic technique.These limitations are being addressed in some institutions by developing endovascularsuites adjacent to or as a part of an operating room suite. This approach has the advantageof combined optimum imaging equipment in an operating room environment.

Implantation of the EVT Guidant bifurcation graft system

Following review of the angiogram, one femoral artery is designated as the ipsilateralside, and the opposite the contralateral side. Designation of the ipsilateral femoral arterymeans that the large sheath and graft catheter delivery system will be placed on that side.Considerations for ipsilateral designation include the presence or absence of tortuosity ofthe iliac system, iliac artery angulation, and the smooth pathway for passage of the guide-wire and graft catheter delivery system in order to achieve optimal geometric relationshipwith the proximal neck of the aneurysm. When either side would be acceptable forpassage, it is usually easier for a right-handed operator to select the right femoral artery.

The common femoral arteries are surgically exposed from the inguinal ligament to the femoral bifurcation. The ipsilateral side is circumferentially mobilized. The contralateral


side is mobilized sufficiently for placement of a smaller sheath. If the external iliac arteries are tortuous they can be straightened by the retroperitoneal mobilization of thevessel, beneath the inguinal ligament, thus permitting the vessel to be pulled down andproviding a straighter course for passage of the sheath. Once the vessels are exposed, theipsilateral femoral artery is then punctured with an angiogram needle, through which an0.035′′ flexible-tip guidewire is passed under fluoroscopic control and manipulated intothe suprarenal aorta. The needle is removed and replaced with a 7 F angiogram sheath. Apigtail angiogram catheter with 1.0cm radio-opaque marks is then loaded over the guide-wire, advanced into the aorta, and positioned just above the renal arteries. An aortogram,using a pressure injector, is then performed with roadmap imaging (Figure 12.5). The location of the renal arteries and aortic bifurca

Figure 12.5 This is an aortogram of a patient with an abdominal aortic aneurysm. Note the radio-opaque marks on the catheter. These are set at 1.0cm intervals and provide the opportunity for precise intraluminal measurement.


tion is then marked. It is generally our practice to place the patient on a cassette withhorizontal radio-opaque cursors that can be manipulated and used to delineate theposition of the renal arteries and the aortic bifurcation.

At this point, the contralateral femoral artery is punctured with an angiogram needlethrough which an 0.035′′ guide-wire with a flexible tip is advanced into the aorta. The needle is removed and replaced with a 12F sheath. An Amplatz sheath is then loaded overthe guide-wire and advanced under fluoroscopic control to be positioned in the neck of the aneurysm. The guide-wire is then removed and an Amplatz snare is then passed up the implant sheath to allow the snare to open in the superior portion of the aneurysm orthe aneurysm neck (Figure 12.6). The patient is then systemically anticoagulated with5000 units of heparin. A 0.035 Amplatz super-stiff guide-wire is then passed up the angiogram catheter and advanced into the thoracic aorta. The angiogram catheter isremoved. The femoral artery is then clamped distally and the 7F angiogram sheath isremoved. The proximal femoral artery is clamped over the guide-wire using a soft-jawed clamp. The sheath puncture site is used as a focal point for enlarging the arteriotomylaterally and medially into a modified oblique transverse arteriotomy. An EVT sheath23F in diameter is loaded over the guide-wire and manipulated into the arteriotomy. Theproximal clamp is removed, and the sheath is inserted into the femoral artery. The sheathis advanced up the iliac system toward the aorta under fluoroscopic control (Figure 12.7). Once the sheath is fully inserted, an obturator within the sheath is then advanced in orderto fully expand the sheath for catheter passage. The diameter of the bifurcated graft hasbeen previously selected based upon prior CT scanning and angiogram measurement. Thelength of the graft is determined using the intraluminal marker angiogram catheter. Thegraft catheter delivery system appropriate for size is then prepared. A pull-wire comes off the leading edge of the graft catheter delivery system. This pull-wire is connected to the contralateral limb of the graft within the graft capsule. The graft catheter delivery systemis then loaded over the Amplatz superstiff guide-wire and brought into proximity with the sheath. The pull-wire is then passed through the double-valve system of the sheath up into the aorta. Under fluoroscopic control, the pull-wire is passed through the open loop of the Amplatz snare. Once it has been passed through the loop of the snare, the snare isclosed by advancing the sheath over the snare, thus trapping the pull-wire. By advancing the pull-wire through the ipsilateral sheath and retracting the captured pull-wire with the Amplatz snare down the proximal iliac system, the pull-wire is gently drawn into the contralateral iliac system and out of the contralateral sheath (Figure 12.8). We have now achieved bilateral control of the bifurcation graft.


Figure 12.6 This cartoon illustrates the Amplatz catheter and snare system. The snare wire is in the open position.

The graft catheter delivery system is now advanced over the guide-wire through the double-valve system of the sheath and passed up the iliac system into the aorta. At this


point, it is crucial to determine whether or not the pull-wire circles the superstiff guide-wire. It is possible to determine, fluoroscopically, whether the pull-wire is properly separated from the guide-wire. If the pull-wire has encircled the guide-wire, it is necessary to rotate the entire graft delivery system until this encirclement is corrected andthe pull-wire is separated from the guide-wire (Figure 12.9). Once that is accomplished, the graft catheter delivery system is advanced into the suprarenal aorta. The jacket of thegraft catheter delivery system is then retracted. This allows the body of the graft and bothgraft limbs to separate. The entire system is then drawn distally so that the proximalattachment system is positioned immediately below the lowest renal artery and each graftlimb is positioned in their respective iliac arteries (Figure 12.10). The proximal attachment release is then pulled, which allows the self-expanding stent to deploy. The balloon catheter lock is then opened, and the balloon is pulled back into position oppositethe proximal attachment system. An endoflator, which has been connected to the ballooncatheter, is then compressed to allow the intrinsic balloon to dilate and seat the pins of theproximal attachment system into the aortic wall. The balloon inflation pressure is 2.0 atm(Figure 12.11). Three separate inflations for 1 minute each are carried out, in order to seat the attachment system fully.

At this point, a torque catheter is loaded over the pullwire, which emerges from thecontralateral sheath and passed under fluoroscopic control. The torque catheter thenengages the distal attachment system of the contralateral limb. Radio-opaque markers are present along the graft limb, and these are checked under fluoroscopy to make sure thatthey are properly aligned. If there is rotation, these can be straightened using the torquecatheter (Figure 12.12). As soon as the graft is appropriately aligned, the contralateralattachment capsule is retracted, which allows the attachment system to self-expand and to engage the wall of the iliac artery. A fine nitinol guide-wire is carefully left in place and advanced up the iliac limb. A high-pressure balloon catheter of appropriate diameter tothe graft limb is passed over the guide-wire and advanced into the distal attachmentsystem.


Figure 12.7 (a) An undeployed Endovascular Technologies arterial access sheath. The sheath contains a double- valve system for haemosta-sis. An obturator is in position. Once the sheath is inserted, the obturator is advanced forward to fully dilate the sheath over the guide-wire. (b) The Endovascular Technologies sheath in position on the right femoral artery with the obturator being extracted. The Amplatz snare catheter is in position for receiving the pull-wire.

The balloon is inflated in order to seat the distal attachment system. This balloon is thenadvanced up the graft limb and expanded so that the graft limb is fully expanded. If thereis any extrinsic compression on the graft limb from atherosclerotic plaquing, particularlyat the aortic bifurcation, angioplasty through the graft limb can be accomplished.

The final part of the deployment is the release of the ipsilateral distal attachment system. The cover of the distal attachment system is then retracted, and the distalattachment system release is activated on the operating handle. The whole cathetersystem, including the balloon catheter, is now retracted through the lumen of the graft sothat the aortic balloon catheter is positioned opposite the ipsilateral distal attachmentsystem. The balloon catheter is inflated to seat the device, and then the balloon is deflatedand the spent catheter delivery system removed. This leaves the principal guide-wire through the ipsilateral graft limb. A high-pressure balloon catheter is then advanced overthe guide-wire up the ipsilateral side, and a series of simultaneous inflations of high-pressure balloon catheters on both the ipsilateral and contralateral sides are carried outthroughout the length of both graft limbs in a ‘kissing balloon’ manner (Figure 12.13). Once we are certain that both graft limbs are fully expanded, the balloons are removed.An angiogram catheter is then passed up the ipsilateral side, and a completion angiogramis obtained to make certain that flow is present through both graft limbs and to determinewhether or not there is any evidence of perigraft leak into the aneurysm sac (Figure 12.14). Following this, the guide-wires and sheaths are removed and the femoral arteries are repaired. Subcutaneous tissues and skin are closed in the usual manner. Steriledressings are applied, and the patient is allowed to recover from anaesthesia.

Most patients will then go to a standard hospital room for overnight observation. Ifthere are no untoward events during the next 12h, the patient can be discharged from thehospital the following morning. The patient will return for a postoperative visit within thenext few days, at which time imaging studies, including duplex ultrasound, plain films ofthe abdomen, and contrast-enhanced CT scanning of the abdomen and pelvis are carriedout to establish a baseline and to determine whether or not an endoleak is present.


Figure 12.8 (a) The pull-wire of the graft catheter delivery system has been passed up the Endovascular Technologies sheath and through the loop of the Amplatz snare. (b) The pull-wire has been captured with the Amplatz snare and drawn into the contralateral iliac artery.


Figure 12.9 When advancing the device behind the pull-wire, it is possible to encircle the guide-wire (see insert). It is important that this is recognized and the device rotated such that the guide-wire and pull-wire are separated.


Figure 12.10 Once the jacket has been retracted, the bifurcated graft sys-tem is opened and the limbs are allowed to separate. The device is then retracted so that the proximal attachment system is immediately below the renal arteries and the ipsilateral and contralateral graft limbs are in the common iliac arteries respectively.


Figure 12.11 The proximal attachment system is deployed, and the balloon catheter is inflated so as to seat the hooks into the aorta.

Deployment of the Medtronic AneuRx Endograft

[The text and illustrations of this section are provided courtesy of Dr Thomas J. Fogarty,Professor of Surgery, Stanford University School of Medicine Stanford, CA, USA).]

Both femoral arteries are exposed via small oblique incisions. The patient issystemically heparinized and introducer sheaths are inserted high in each common


Figure 12.12 A torque catheter has been attached to the contralateral distal capsule. By observing the radio-opaque markers on the limb (see insert), it is possible to rotate the torque catheter in order to accurately align the radio-opaque markers and to prevent graft limb twist.

femoral artery. An 0.035′′ guide-wire and angiographic catheter are passed through thesheath and placed just above the renal arteries. An aortogram is obtained to documentanatomy and landing zones for the bifurcation graft. An intravascular ultrasound (IVUS)catheter may now replace the angiogram catheter to obtain precise intraluminalmeasurements. After making IVUS recordings, the multiside-hole angiogram catheter is reinserted in the contralateral femoral sheath. The smaller sheath is removed from themain access site (ipsilateral femoral artery), an arteriotomy is performed, and a 21 F


sheath is inserted. Using continuous fluoroscopy, the AneuRx primary bifurcatedendograft delivery catheter is inserted and initially positioned above the renal arteries.The device is positioned properly by orienting a nosecone, a distal notch, and radio-opaque markers, toward the contralateral limb. The graft cover is then retracted 2–3 cm, while observing deployment under fluoroscopy.

Figure 12.13 The fluoroscopic image, demonstrating simultaneous inflation of high-pressure balloons in the iliac limbs located at the anatomic aortic bifurcation in a ‘kissing balloon’ configuration.

Small adjustments can be made to obtain proper alignment, while the endograft is slowlypulled down to just below the renal arteries. The angiographic catheter is then removed.The graft cover is carefully pulled down, allowing the endograft to expand in fulldeployment. For safe deployment, the cover should be pulled down to just below thedistal radio-opaque marker. The nosecone and runners are then retracted into the delivery catheter under fluoroscopy.

After removing the main balloon catheter, the contralateral limb is accessed via aguide-wire. IVUS evaluation is performed and the ultrasound catheter is replaced with asuperstiff wire and positioned in the descending thoracic aorta. The small 8 F sheath isremoved and replaced with a 16 F sheath under fluoroscopy. A delivery catheter isinserted into the sheath and up into the gate area. Radio-opaque markers on the contralateral graft limb are used to obtain proper alignment in the gate area. The 16 Fsheath is pulled back to the end of the graft cover, and the iliac limb deployed in a similarmanner to the main graft, assuring position by noting removal of the cover to just belowthe distal radioopaque markers. Once again, nosecone and runners are retracted into thedelivery catheter, and all are removed. Angiograms are performed from the renal arteriesto the hypogastric arteries in order to check endograft seals at both proximal and iliacapposition sites. Extension cuffs may be placed on the graft limbs if necessary, or otheradjunctive procedures performed at this time, followed by removal of sheaths and wires(Figure 12.15). The femoral incision sites are closed in the usual manner. Finally, distallower extremity perfusion is checked before leaving the operating room.


Figure 12.14 (a) A preparatory intraoperative aortogram prior to aneurysm repair. (b) A completion angiogram on the same patient, following deploy’ ment of a bifurcated graft.

Figure 12.15 (a) The components of the AneuRx graft system. (b) The assembled components of the AneuRx graft system.


Talent bifurcated graft insertion

The text and illustrations of this section are provided courtesy of Dr Syde A. Taheri.Following bilateral femoral artery dissection, the larger femoral artery is selected forinsertion of the bifurcated graft. Five thousand units of heparin are administeredintravenously. The femoral artery is controlled proximally and distally, and anarteriotomy is performed. An aortogram using image amplification is performed so thatthe renal arteries are visualized and marked externally. The Talent bifurcated graft ispassed over a stiff guide-wire that has been inserted into the aorta. Using imageamplification, the Talent’s two proximal stents are deployed above the renal arteries initially and then the device is pulled down to the lower renal artery landmark. Byinflating the integrated balloon, the proximal aortic graft is secured to the aortic wall.Maintaining inflation of the balloon releases the remaining stents of the graft. Bysequentially inflating and deflating the integrated balloon, the stent graft carefully modelsthe Talent device to the vasculature. To ensure that the integrity of the iliac artery is notdisrupted, gentle pressure should be applied to the distal stent balloon inflation. Guide-wire cannulation of the short limb is then performed from the contralateral femoral arteryor the brachial artery. The contralateral limb is then passed over the stiff guidewire forproper docking position and deployment of the first two stents above the docking area.After pulling the contralateral limb into proper position and centring the integratedballoon, inflation of the balloon to fixate the proximal contralateral limb of the mainTalent stent graft is accomplished. While maintaining the balloon inflation, the sheath iswithdrawn to expose the self-expanding stents and complete the stent graft deployment. Inflation and deflation of the integrated balloon accomplishes graft modelling. Finally, anaortogram is obtained to document complete exclusion of the abdominal aortic aneurysm(Figure 12.16).

Figure 12.16 (a) The Talent graft components. (b) The assembled Talent graft.


Results

The EVT Guidant bifurcated graft has completed phase II trials and is currently in phaseIII. The same is true of the Medtronic AneuRx bifurcated graft system. Investigators forboth devices reported the results of the phase II trials in June 1998 at the InternationalSociety for Cardiovascular Surgery (North American Chapter) meeting in San Diego,California.13–15 Both phaseII reports compared their results with a concurrent non-randomized control group. EVT Guidant entered 88 patients using an endovascularbifurcated graft system and compared them with 105 patients undergoing standardaneurysm repair, who served as controls. The 88 patients undergoing an endovascularbifurcated graft system were the results of attempting placement of a bifurcated graft in96 patients. This provided a 92% immediate success rate. The 30-day mortality rate in the endovascular group was 2.0% and included one patient who required conversion tostandard aneurysm repair. The mortality rate in the standard aneurysm repair controlgroup was 3.8%. Other postoperative complications were compared. The incidence ofperioperative fatal myocardial infarction, congestive heart failure/arrhythmia, colonischaemia, arterial embolism, and wound infection were not statistically differentbetween the experimental and control groups. There was a statistically significantreduction in blood loss and blood replacement in the endovascular graft group whencompared with the open repair group. There was a statistically significant difference inpulmonary complications, including pneumonia and atelectasis, favouring endovascularversus open repair. Finally, there was an increased incidence of temporary renaldysfunction in the endovascular group compared with the control group. There was noinstance of aneurysm rupture in the endovascular group during the period of observation.

The Medtronic AneuRx investigators reported their experience with 150 patients entered in phase II, compared with 60 patients who served as a control group. The 30-day mortality rate was 2.0% in the phase II experimental group, and none in the controlgroup. Blood replacement averaged 3.8 units in the open surgical group compared to 1.2units in the phase II experimental group. Hospital stay averaged 8.4 days in the controlgroup, compared to 3.1 days in the experimental group. Endograft deployment wassuccessful in 98% of their patients, with only 2.0% requiring surgical conversion. At 30days, primary aneurysm exclusion rate without endoleak was 91%, and graft patency was100%. The authors concluded that endoprosthetic stent graft repair of abdominal aorticaneurysm compared favourably with open surgical repair with reduced morbidity, bloodloss, shorter intensive care unit and hospital stay, earlier ambulation, and a return toactivity.

The other bifurcated graft systems are currently in phase II trials and will no doubt report their results in the near future.

References

1. Dotter CT. transluminally-placed coil spring endarterial tube grafts: long term patency in canine popliteal artery. Invest Radiol 1969; 4:329–32.



3. Lazarus HM. Intraluminal graft device, system and method. US Patent No. 4 787 899, 1988.

4. Lazarus HM. Endovascular grafting for the treatment of abdominal aortic aneurysms. Surg Clin North Am 1992; 72:959–68.

5. Moore WS. Endovascular grafting technique: a feasibility study. In: JST Yao, WH Pearce (eds) Aneurysms: new findings and treatments. Norwalk, CT: Appleton and Lange, 1993:333–40.

6. Moore WS, Vescera CL. Repair of abdominal aortic aneurysm by transfemoral endovascular graft placement. Ann Surg 1994; 220: 331–41.

7. Moore WS. Transfemoral endovascular repair of abdominal aortic aneurysm using the endovascular graft system device. In: RM Greenhalgh ed. Vascular and endovascular surgical techniques: an atlas. 3rd edition. Philadelphia, PA: W.B. Saunders, 1994: 78–91.

8. Moore WS. The role of endovascular grafting technique in the treatment of infrarenal abdominal aortic aneurysm. Cardiovasc Surg 1995; 3:109–14.

9. Colburn MD, Moore WS. Endovascular repair of abdominal aortic aneurysms using the EGS tube and bifurcated graft systems. World J Surg 1996; 20:664–72.

10. Chuter TAN, Green RN, Ouriel K, Fiori WM, DeWeese JA. Transfemoral endovascular aortic graft placement. J Vasc Surg 1993; 18: 185–97.

11. Chuter TA, Wendt G, Hopkinson BR et al. Transfemoral insertion of a bifurcated endovascular graft for aortic aneurysm repair: the first 22 patients. Cardiovasc Surg 1995; 3:121–8.

12. Sarkar R, Moore WS, Quiñones-Baldrich WJ, Gomes AS. Endovascular repair of abdominal aortic aneurysm using the EVT device: limited increased utilization with availability of a bifurcated graft. J Endovasc Surg 1999; 6(2): 131–5.

13. Goldstone J, Brewster DC, Chaikoff ER, Katzen BT, Moore WS, Pierce WH for the EVT Investigators. Endoluminal repair versus standard open repair of abdominal aortic aneurysm: early results of a prospective clinical comparison trial. Presentation Iscus Meeting, 1998.

14. Moore WS, Brewster DC, Bernhard VM et al. Aorto-uni-iliac endograft for complex aortoiliar aneurysm compared with tube/bifurcation endografts: results of the EVT/Guidant Trial. J Vasc Surg 2001; 33: 511–12.

15. Zarins CK, White RA, Shwarten DE et al. Medtronic AneuRx stent graft system versus open surgical repair of AAA: Multi-center clinical trial. J Vasc Surg 1999; 29:292–308.


Aneurysm exclusion using hand-assisted laparoscopy

13 R.KOLVENBACH AND L.DA SILVA

Introduction

Minimally invasive techniques have revolutionized general surgery over the past decade.Laparoscopic surgery is increasingly used as an alternative to conventional open surgerybecause of its advantages compared to open procedures, such as less trauma and pain,reduced hospitalization, and a quicker recovery. However, more advanced surgicalprocedures such as aortoiliac reconstructions are only reluctantly accepted. The lack oftactile feedback, which is essential in abdominal surgery to perform a safe dissection,prevents many surgeons from performing advanced laparoscopic procedures.

There are a number of operative techniques that can be used to perform video-endoscopic aorto-iliac reconstructions. Most of these operations can only be offered to a small group of highly selected patients. Therefore laparoscopic aorto-iliac surgery is only performed in a few surgical centres due to the complex and time-consuming nature of these procedures.1–3 Patients with severely calcified vessels present a particular challenge to laparoscopic surgery because most vascular clamps do not permit safe occlusion of theinfrarenal aorta.4 The tactile senses of the surgeon cannot be used in laparoscopicsurgery, yet they are required to assess the degree of calcification, and to determine theoptimal site to place the clamp. We tried to overcome these disadvantages by using anovel laparoscopic technique, which permits the surgeon to use his non-dominant hand in the operative field while maintaining the pneumoperitoneum. Hand-assisted laparoscopy was used in patients with an infrarenal abdominal aortic aneurysm (AAA).

Transperitoneal hand-assisted laparoscopic surgery in patients with an abdominal aortic aneurysm (AAA)

Laparoscopic aneurysm surgery can be performed in two different ways. The aneurysmcan be excluded by using a linear surgical stapler to ligate the aorta and the iliac arteries.A bifurcated graft is anastomosed with the infrarenal aorta and the external iliac arteriesafter exclusion of the aorta. Alternatively, hand-assisted laparoscopy can be used toperform a mini-incision aneurysm resection. The latter technique requires a largerincision, however it permits the surgeon to use a tube graft after resection of the AAA.The original Creech technique is performed in these cases using a mini-laparotomy only.

Exclusion technique

In all cases after induction of general anaesthesia and establishment of controlledventilation, orogastric decompression of the stomach is performed. Haemodynamicmonitoring is performed using an arterial line and a central venous catheter.

The patient is placed in a supine position on the operating table, with the operating surgeon standing on the right side of the patient (Figure 3.1). All operations are carried out with one assistant. A 1 cm incision is performed in the upper abdomen and the 30°-angled laparoscopic video camera is inserted. A second 10 mm port is placed in the leftlower abdomen. Both ports are required for the laparoscopic camera. Laparoscopy isperformed to determine the optimal site for the mini-laparotomy. Using a 6 cm incision, an airtight seal is attached to the abdominal wall, which enables the surgeon to use hishand while maintaining the pneumoperi-

Figure 13.1 All operations are performed by the operating surgeon, his or her first assistant and a scrub nurse.

toneum to perform laparoscopy (HandPort®, Smith & Nephew Surgical, Andover, MA,USA). The protector retractor device has an open-ended cylinder with a flexible ring at each end. One ring is inserted through the incision into the peritoneal cavity and the other


remains outside the incision. The retractor holds the incision open. The surgeon can passhis or her non-dominant hand through the 6 cm mini-laparotomy into the abdominal cavity (Figure 13.2). A third 10mm trocar is placed in the lower abdomen, as far aspossible from the other ports (Figure 13.3). This port is required for laparoscopicinstruments including suction. Laparoscopic dissection is started at the level of the aorticbifurcation. Both common iliac arteries are dissected free, including the right and leftureters. The inferior mesenteric artery is dissected free and ligated. Dissection iscontinued proximally up to the renal arteries. The neck of the aneurysm is dissected freecircumferentially. The aorta is exposed by dissection using laparoscopic instruments andthe surgeon’s hand. The procedure is facilitated by placing the patient in a 60°Trendelenburg position and by tilting the table to the right. Hand-assisted laparoscopy permits digital exploration of the aorta to determine the optimal site for placing the clampand for performing the proximal anastomosis. We try to clip all lumbar arteries that areaccessible.

Figure 13.2 Drawing of the surgeon’s hand in the operative field using a transperitoneal laparoscopic access to dissect the aorta free.

Aneurysm exclusion using hand-assisted laparoscopy 285

The common iliac arteries are dissected free circumferentially after identifying the ureter. Both common iliac arteries are ligated using a linear stapler (TA 30, US Surgical,Norwalk, Connecticut, USA). The external iliac arteries are exposed using two small,oblique incisions above the inguinal ligament. Tunnelling is performed from both groins under digital control and under direct vision of the laparoscopic video camera. The camera is inserted through the trocar in the upperabdomen. This step is usually followed by the loss of the pneumoperitoneum andtherefore accomplished at the end of the laparoscopic part of the operation.

When dissection of the aorta is completed the protector retractor device is removed andtwo 2.5cm blades of a conventional retractor (Omnitract, Minneapolis, Minnesota, USA)are inserted. The aorta is clamped using regular vascular clamps. The sac of the aneurysmis evacuated and the aorta is transsected after staple occlusion to achieve completeexclusion of the aneurysm.

The patient is kept in the Trendelenburg position, and the proximal anastomosis is sutured using conventional instruments. We always perform an end-to-end anastomosis in inlay technique using a running 3–0 Prolene suture. The distal anastomosis is alwaysperformed by two teams simultaneously.

After completing the proximal anastomosis, laparoscopy is performed to inspect theabdominal cavity and the left hemicolon. Special care is taken to close theretroperitoneum over the graft laparoscopically with a running suture. In patients withconcomitant iliac artery occlusive disease an aortofemoral bypass procedure isperformed.

Mini-incision hand-assisted transperitoneal aneurysm resection

Dissection of the aneurysm and the neck of the aneurysm are identical to that describedfor the exclusion technique. Instead of ligating the sac of the AAA and the common iliacarteries a mini-laparotomy is performed, through an incision similar in size to the lengthof the AAA. A conventional crossclamp is inserted through the upper trocar site. The sacof the aneurysm is opened and the lumbar arteries are ligated. If possible, a tube graft isinserted. In most cases, an 8–10 cm incision is sufficient to perform AAA resection.


Figure 13.3 Schematic drawing showing triangulation of the. laparoscopic instruments and the HandPort device to achieve an optimal degree of freedom of all devices.

Materials and methods

A consecutive series of 18 patients who were admitted for AAA surgery within a periodof 6 months were evaluated for laparoscopic surgery and exclusion bypass (Table 13.1). The age varied from 49 to 81 years. Obesity was no contraindication for the laparoscopicprocedure. Exclusion criteria were juxtarenal aneurysms or iliac artery aneurysms.Patients in the American Society of Anesthesiology (ASA) classification IV wereoperated conventionally or using endovascular techniques. During the study period, fivepatients were excluded from the laparoscopic operation. Two of these were operatedconventionally and in three patients the AAA was excluded using a stent graft. The mean


body mass index (BMI) was 25.1 (range 23–28). The operations took 100–230 min (mean: 153 min), with a clamping time varying from 22 to 40min. The estimated bloodloss varied from 250 to 900ml. The length of the incision, where the HandPort devicewas inserted, was measured, and varied from 5.8 to 8.2 cm.

Most patients were initially returned postoperatively in the intensive care unit, wherethey were discharged after a mean period of 0.77 days (range 0–3). All patients left hospital after a mean postoperative interval of 5.7 days (range 4–10 days). The mean size of the aneurysm was 6.1cm (range 4.9–8.1 cm). After a mean follow-up of 13 months the excluded aneurysm had shrunk to a mean size of 2.5 cm (range 1.6–4.1 cm).

In two cases conversion to a conventional operation with an incision of more than 12 cm was required. In both cases subdiaphragmatic crossclamping was performed. In threepatients there were minor local complications: a lymphatic fistula in two cases and ahaematoma in the groin in one patient.

Major complications were observed in two cases. One patient developed an acutepancreatitis and was treated

conservatively. Postoperative graft thrombosis occurred in one case and was treated bythrombectomy and a femoropopliteal bypass.

Discussion

Therapeutic laparoscopy has substantially improved the postoperative course of patientssuffering from hepatobil iary, gastric, or colonic disease. In vascular surgery a minimalinvasive approach was primarily preferred by radiologists to treat patients with iliacocclusive disease.5 The primary advantage of these minimal invasive endoscopic procedures is the reduced incidence of respiratory complications and diminished pain.Patients with AAA treated with conventional surgery are at a high risk for postoperativecomplications, and a minimally invasive procedure may favourably affect theirpostoperative course.6 Laparoscopic vascular surgery for AAA exclusion is feasible, safe and effective.7 In a prospective study we showed that surgical trauma was reduced, as measured by the concentration of interleukin 6 and the acute-phase proteins in patients treated using a laparoscopy-assisted approach versus those treated by conventional

Table 13.1

Variable Mean Std dev. Minimum Maximum

Age 64.60 9.42 49.00 81.00

Op.time 164.94 mm 25.52 min 124.00 min 210.00 min

Clamp time 43.05 min 10.00 min 28.00 min 61.00 min

Incision size 6.73 cm 0.80 cm 5.70 cm 8.20 cm

Blood loss 785.55 ml 321.92 ml 105.00ml 1900.00 ml


surgery.8 Transperitoneal access can be difficult in obese patients or in those with ahostile abdomen. Meanwhile, we routinely use an extraperitoneal laparoscopic approachin these cases (Figure 13.4). Expo-sure of the retroperitoneal structures can be facilitatedif the surgeon can use his hand in the operative field for blunt

Figure 13.4 Retroperitoneal laparoscopic access. The hand in the operative field is used to mobilize the peritoneal sac medially.


Figure 13.5 The HandPort device in a patient with a transperitoneal access.

dissection (Figure 13.5). The HandPort used in the cases described here is an example ofa new surgical device that can help to make laparoscopic aorto-iliac reconstructions and other complex procedures easier (Figure 13.5).9, 10

The combination of a pneumoperitoneum and a gasless laparoscopic technique seems to offer several benefits for the patient. While the pneumoperitoneum can easily be usedfor exposure of the iliac arteries and the aorta, it is difficult to maintain once the tunnelsto the outflow vessels have been established. It becomes nearly impossible to sustainonce the graft has been inserted into the abdominal cavity. The mini-laparotomy permits the surgeon to use a wider array of instruments. He can use conventional clamps andmore efficient suction devices or needle holders without fear of compromising theoperative cavity (Figure 13.6).

Patients with AAA are increasingly treated using endovascular techniques, however,


there continues to be a certain number of patients with arterial occlusive disease orjuxtarenal aneurysms who require conventional surgical therapy. With furtherimprovement of laparoscopic techniques and instruments a minimal invasive alternativecan be offered to this group of patients. Meanwhile, we have operated on patients withhand-assisted laparoscopy where suprarenal crossclamping was required using aminilaparotomy only. Aortic crossclamp times and the total operative time of a video-assisted procedure are significantly shorter than a total laparoscopic approach, which

Figure 13.6 Schematic drawing of the mini-laparotomy required for a retroperitoneal laparoscopic exposure of the aorta.


can be offered to a highly selected group of patients only. Due to the long crossclamptimes there is prolonged distal ischaemia with an increased risk of a reperfusion injury.Further studies have to assess whether the mini-laparotomy required for a laparoscopy-assisted procedure makes any difference compared to a total laparoscopic operation.

It is conceivable that by using a combined approach, consisting of endovascular techniques as well as a laparoscopic access, a larger number of patients can be treated ina minimally invasive way.11 Further clinical controlled studies must prove whether or notaneurysm patients can benefit from these videoendoscopic procedures.12

Mini-laparotomy aortic surgery

In a recent paper, minimal incision repair was reported as an alternative less invasivetechnique compared to open or laparoscopic surgery.13 In our own experience a small laparotomy of about 10–12 cm is required for this technique in contrast to the 7 cm mini-incision used in laparoscopy assisted techniques. This does not necessarily affect thepostoperative course of aneurysm patients, but laparo scopically we can inspect the wholeabdomen which increases the safety of the procedure especially in obese patients withadhesions. It can be very challenging to perform an aortic reconstruction with abifurcated graft when only very limited conventional dissection can be performed.Laparoscopic exposure gives us the safety and optimal exposure we need to preventinjuring the ureter or other intraabdominal organs particularly when tunnelling to thegroin.

Operative technique

The night before surgery an oral bowel preparation is given. A small periumbilicalincision is made and for aneurysms the incision is extended cephalad.

The exact position of the aneurysm is located by palpation. Directly above the aneurysm a 10–12 cm incision is performed just like in conventional surgery. The bowelis placed in the right upper abdomen and a table-mounted retractor is inserted. Either large laparotomy sponges or a special vacuum bag (Space OR, Advanced SurgicalConcepts, Dublin, Ireland) is inserted to retract the bowel. With good muscle relaxation,the abdominal wall and its incision can be moved cephalad and or caudad for sequentialdissection and exposure of the infrarenal aorta and the bifurcation. The low-profile Cosgrove arterial clamps (Baxter, Irvine, CA) are used for this procedure (Figure 13.7). They are preferred because they avoid any vertical cutter in the operating field. Suturingis done with long needle holders avoiding the need for hand placement in the operativefield. The rest of the procedure is carried out just like in open surgery. According toTurnipseed operating times are not significantly longer compared to conventionalsurgery, but postoperative recovery is much faster.14


Figure 13.7 Illustration showing the circular ring of the table mounted Bookwalter retractor we have used in mini-laparotomy aortic surgery.13

Discussion

A major disadvantage of this technique is the fact that the abdomen cannot be inspected.In our laparoscopic experience more than 70% of our patients have varying degrees ofadhesions in the abdomen. Therefore blind retraction can cause bowel damage thatcannot be noticed during the primary procedure. In a feasibility study involving 22 caseswe had more complications in the mini-laparotomy group compared to the laparoscopy assisted procedures. In both groups there was a rather large number of obese patients.

One of the criteria of a minimal invasive procedure is that the sequelae of a standardlaparotomy are significantly reduced. Particularly in aneurysm patients this means thatthe incidence of incisional hernias and of intraabdominal adhesions should be lowercompared to conventional surgery. According to our own data from 17 patients with amini-laparotomy and a laparoscopy assisted procedure who were readmitted with an incisional hernia this procedure cannot be a minimal invasive alternative to laparoscopy.It seems that the predisposition of aneurysm patients to incisional hernias in combinationwith extensive retraction of the abdominal wall might explain the increased incidence ofabdominal wall hernias. Since all 17 patients were treated laparoscopically with a PTFEmesh we had a unique opportunity to inspect the abdomen several months after mini-incision aortic surgery. In 15 out of 17 cases there was a substantial amount of adhesionsbetween the midline mini-laparotomy and small bowel or omentum although some of the


incsions were only 5 cm in length. It is a proven fact in surgery that midline incisions areworse than any other abdominal access. This is true for hernias as well as forpostoperative restrictions in pulmonary function. Therefore we should use thelaparoscopic technique to perform retroperitoneal dissection in a way that a mini-laparotomy can be placed in a ‘strategically’ better position.

Laparoscopy assisted procedures are intermediate techniques towards a total laparoscopic approach. Several studies managed to show until today that the metabolicresponse, e.g. of mini-incision cholecystectomy is significantly more severe compared tolaparoscopic cholecystectomy. Optimal vision combined with a more ‘physiologic’ incision can probably reduce the intraoperative and late complications of aortic surgery.

References

1. Dion Y-M, Karkhouda N, Rouleau C. Laparoscopy-assisted aortobifemoral bypass. Surg Laparoscop Endoscop 1993; 3:425–9.

2. Berens E, Herde J. Laparoscopic vascular surgery: four case reports. J Vasc Surg 1995; 22:73–7.

3. Jones BD, Thompson RW, Soper N. Development and comparison of transperitoneal and retroperitoneal approaches to laparoscopic-assisted aortofemoral bypass in a porcine model. J Vasc Surg 1996; 23: 466–71.

4. Johnson JR, Mc Loughlin GA, Wake PN. Comparison of extraperitoneal and transperitoneal methods of aorto-iliac reconstruction. J Cardiovasc Surg 1986; 27:561–4.

5. Palmaz JC, Laborde JC, Rivera FJ. Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovasc Intervent Radiol 1992; 15:291–7.

6. Ahn SS, Clem M, Braithwaite MA. Laparoscopic aortofemoral bypass. Ann Surg 1995; 5:677–83.

7. Dion YM, Gracia CR. A new technique for laparoscopic aortobifemoral grafting in occlusive aortoiliac disease. J Vasc Surg 1997; 26:685–92.

8. Kolvenbach R. The role of video assisted vascular surgery. Eur J Vasc Endovasc Surg 1998; 15(5): 377–9.

9. O’Reilly MJ, Saye WB, Mullins SG, Pinto SE, Falkner PT. Technique of hand-assisted laparoscopic surgery. J Laparoendosc Surg 1996; 6: 239–44.

10. Memon MA, Fitzgibbons RJ. Hand-assisted laparoscopic surgery: a useful technique for complex laparoscopic abdominal procedures. J Laparoendosc Adv Surg Tech A. 1998; 8:143–50.

11. Chen MHM, Murphy EA, Halpern V, Cohen JR. Laparoscopic-asissted abdominal aortic aneurysm repair. Surg Endosc 1995; 9: 905–7.

12. Kolvenbach R, Deling O, Schwierz E, Landers B. Reducing the operative trauma in aortoiliac reconstructions—a prospective study to evaluate the role of video-assisted vascular surgery. Eur J Vasc Endovasc Surg 1998; 15, 483–8.

13 Turnipseed WD. A less invasive minilaparotomy technique for repair of aortic aneurysm and occlusive disease. J Vasc Surg 2001; 33: 431–4.

14 Cerveira J, Halpern V, Faust G, Cohen JR. Minimal incision abdominal aortic aneurysm repair. J Vasc Surg 1999; 30:977–84.


Thoracic aneurysmal disease

14 STEPHEN T.KEE AND MICHAEL D.DAKE

Introduction

The incidence of thoracic aortic aneurysms ranges between 1 and 4% in various autopsystudies.1 True aneurysms of the thoracic aorta were once dominated by the syphiliticvariety, but improved diagnosis and treatment of that condition have now made theseextremely rare. The most common aetiology is now atherosclerosis, usually of thedescending thoracic aorta. This leads to progressive damage of the medial layer of theaorta, with degenerative weakness of the vessel wall and subsequent aortic dilatation andaneurysm formation.2 This medial degenerative disease can also be secondary to myxoiddegeneration, Marfan’s syndrome, etc. Other aeti-ologies include aortic dissection, aortitis (Takayasu’s, syphilitic), mycotic, and traumatic aneurysms.3 These aneurysms are potentially life-threatening and studies of the natural history of untreated lesions estimatea 50% 5-year, and 70% 10-year mortality rate.1 Only half of these deaths can beattributed to actual aneurysmal rupture—a catastrophic event—the remaining deaths being secondary to coexisting medical disease, principally hypertension and diffusecardiovascular pathology.3, 4

Conventional treatment for a thoracic aortic aneurysm is surgical repair. Variousdefinitions of aneurysmal dilation of the aorta exist, and the optimal time for surgicalintervention is controversial; however, size greater than 6 cm diameter (especially whenincreasing on serial imaging studies), aortic regurgitation, or acute chest or back pain, areconsidered indications for intervention. Traditional surgical techniques involve resectionand replacement of the aneurysm with prosthetic graft material. When the aneurysm isconfined to the descending thoracic aorta, surgery can be performed without the need forextracorporeal circulation.5, 6 The surgical mortality, even in the most experiencedinstitutions and in low-risk patients, approaches 15%.5, 7 Morbidity is also high, with paraplegia reported in 5–12%.5–7 The mortality rate approaches 50% in patients withpoor cardiac reserve or emergency cases.3, 7

Transluminally placed endovascular stent-grafts offer an alternative method oftreatment that is potentially less invasive, expensive, and hazardous than conventionalrepair. Dotter introduced the concept of treating experimentally induced aneurysms withendovascular stent-grafts in 1969, and since then a number of animal studies haveconfirmed the potential of this technique.8–14 The first human cases of endovascularstent-graft placement for abdominal aortic aneurysms were reported by Parodi and colleagues in 1991.15 They deployed a stent above the aneurysm with a limb of polyestergraft material attached. The initial results were favourable with aneurysm thrombosis;

however, the pressure transmission from the lower unstented portion of the graft materialinto the thrombosed aneurysm led to continued expansion and rupture. Since this earlystudy, investigators have concentrated on excluding the entire aneurysm from the arterialcirculation either using a stent above and below the aneurysm, or placing covered stentsthroughout the aneurysmal portion of the vessel.

Over the past 7 years we have placed endovascular devices in 149 patients withdescending thoracic aneurysms. Initial results with a first-generation device were obtained in 129 patients, commencing in July 1992; more recently a second-generation device was implanted in 20 patients. This chapter reviews the principles used in thedevelopment of an endovascular device for deployment in the thoracic aorta.

Anatomic considerations

The most important feature to be considered when evaluating an aortic aneurysm forendovascular stent-graft placement is the presence of an adequate proximal and distalneck. It is important to allow at least 15 mm of neck distal to the left subclavian artery, orproximal to the celiac artery to provide for secure anchoring without inadvertentlycovering the ostium of that vessel. In order to assess the suitability of the anatomy ofeach individual, all patients undergo an extensive work-up, including aortography, and spiral computed tomography (CT) with three dimensional reconstructions. Theinformation from these studies is used to calculate the length of the aneurysm and thediameters of the proximal and distal normal aorta. In cases where the left subclavianartery is less than 15 mm from the aneurysm sac, a more favourable neck may be createdby transposing this vessel onto the left common carotid artery. The origin of thesubclavian vessel can then be covered with the proximal portion of the stent-graft without leading to arm ischaemia (see Figure 14.5).

The overall length of the stent-graft is kept to a minimum to limit the number of intercostal arteries that are excluded from flow, and to hopefully reduce the incidence ofparaplegia.

The other important anatomic consideration is the size of the proposed conduit vessel for introduction of the stentgraft. Currently available stent-grafts require introducer sheaths of up to 24 F outside diameter. To facilitate advancement of such a sheaththrough the iliac vessels and the aorta, the pelvic vessels must be ≥9 mm in diameter. Where this is not the case, a retroperitoneal approach to the iliac vessels or lowerabdominal aorta can be performed. After surgically exposing the infrarenal aorta througha retroperitoneal incision, a purse-string suture is placed around the introduction site andthe aorta is subsequently punctured using the standard Seldinger technique.

Technical considerations

Stents

The stent is the metallic framework to which the graft material is secured. Stents are


currently manufactured from stainless steel, nitinol, or tantalum. Two basic types ofstents are available: balloon expandable, such as the Palmaz stent (J+J Inc., Warren, NJ,USA) and self-expanding stents, such as the Wallstent (Boston Scientific Inc.,Watertown, MA, USA) and the modified Gianturco Z-stent (Cook Inc., Bloomington, IN, USA). Balloon-expandable stents are mounted on an angioplasty catheter, which is expanded when in position, whereas self-expanding stents return to a preformed shapeand size when released from a restraining sheath.

The large diameter of the human thoracic aorta precludes the use of balloon-expandable stents. The largest available angioplasty balloons on the market in the USAmeasure 25 mm, and the mean diameter of the stents necessary to treat thoracic aorticaneurysms is 36 mm. A further problem with balloon-expandable devices is the forces exerted by flowing blood, which could cause migration of the device downstream whilebeing deployed. Selfexpanding devices can be designed to fit the sizes required anddeploy sufficiently rapidly so as to offer little resistance to the blood flow.

In the early development work undertaken in Stanford Medical Center, the modified Gianturco Z-stent was the best available prosthesis. This consists of 0.020′′ surgicalgrade stainless steel wire formed into Z-shaped elements. Individual stent bodies are 2.5cm inlength, and are available in diameters ranging from 24 to 45 mm. The individual stentbodies can be sewn together, using 2:0 polypropylene sutures, to achieve the overalldesired length (Figure 14.1). The Z-stent endoskeleton is used to support the entire lengthof the graft material necessary to bridge the aneurysm. This design helps prevent kinkingor collapse of the prosthesis within the aneurysm. No hooks or anchoring wires wereused.

Trials are currently underway in the US investigating lower profile adaptations of the original stent-grafts. These newer stent-grafts utilize nitinol as the basic metallic framework to support the graft material. These stents are also

Figure 14.1 Stent-graft and deployment system. The stent-graft has tem-porary ties at one end to assist in introducing the device into the loading cartridge.

Thoracic aneurysmal disease 297

self-expanding and are released from deployment sheaths using various methods of deployment.

Grafts

The graft material used in the devices manufactured in Stanford is polyethyleneterephthate (Cooley Veri-Soft, Meadox Medicals Inc., Oakland, NJ, USA). This material is resistant to radial stretch, relatively non-porous and thin. A single piece of graft material is cut to the appropriate length and secured to the stent endoskeleton withmultiple interrupted sutures of 6:0 polypropylene at both ends (Figure 14.1). When complete, the entire device is gas-sterilized with ethylene oxide.

In the more modern devices mentioned earlier, the graft material most commonly utilized is polytetrafluoroethylene (Gore Inc., Flagstaff, AZ, USA). This material issomewhat easier to work with than polyethylene terephthate and is also thinner.

Delivery system

The delivery system consists of four components:

1. a 24 F Teflon sheath (Desilet-Hoffman, Cook Inc., Bloomington, IN) with an external haemostatic valve apparatus;

2. a tapered dilator that allows the sheath to be advanced over an 0.035′′ guide-wire; 3. a 24 F loading cartridge in which the stent-graft is placed to facilitate introduction; and 4. a 24 F solid Teflon mandrill that is used as a pusher to advance the stent-graft through

the delivery system (Figure 14.1).

Patient preparation

All patients are evaluated by the cardiothoracic surgeons and interventionalists and fullinformed consent is obtained for both conventional surgery and stent-graft procedures. All stent-graft procedures are performed in the operating suite, or in an operating room-compatible angiography suite, with the patient intubated and under general anaesthesia.The operating suite is prepared as for aortic surgery, with the patient placed on the tablein a shallow right decubitus position. The patient’s thorax is prepared with antiseptic and draped as for a left thoracotomy. For an approach via the common femoral artery, afemoral cut-down is performed. When the arteries are of insufficient size, a lower leftabdominal approach is preferred.

High-quality fluoroscopic equipment is essential to ensure accurate placement of the device and a portable Carm with digital subtraction capabilities is moved into positionand centred over the thorax.

Procedure

Based on the preprocedural imaging, a cut-down is performed on the relevant femoralartery, and an 18-gauge needle inserted and soft-tipped wire advanced into the thoracic


aorta. Aortography is performed using a pigtail catheter. The proximal and distalaneurysmal necks are identified and their location either marked on the skin with radio-opaque markers or correlated with stationary bony structures. An exchange length (260cm) 0.035′′ extra-stiff guide-wire is placed through the pigtail catheter, the catheterremoved, and a transverse arteriotomy performed. The patient is then fully anticoagulatedwith intravenous heparin (300IU/kg). The 24 F sheath and dilator assembly are advancedover the guide-wire under fluoroscopic guidance. When the sheath is located proximal tothe upper neck of the aneurysm, the dilator and guide-wire are withdrawn. The stent-graft is then introduced into the sheath from its loading cartridge using the Teflon pusher. Thedevice is advanced through the sheath until it approaches the tip.

The arterial blood pressure is lowered to a mean of 60–70 mmHg, using a nitroprusside infusion to prevent downstream migration of the device during deployment due to theforce of blood flow in the aorta. Immediately following deployment, the nitroprusside isdiscontinued, allowing the blood pressure to normalize.

Figure 14.2 A 28-year-old man, 2 days’ status post motorcycle versus tree injury with multiple orthopaedic problems, including long leg fractures bilaterally. There was also a question of irreversible CNS damage; however, the patient was able to move all extremities. (a) Aortogram demonstrates pseudoaneurysm of the proximal descending thoracic aorta following traumatic injury. (b) Aortogram performed following stent-graft placement across the pseudoaneurysm. No evidence of perigraft leak or other associated abnormality.


Figure 14.3 A 48-year-old woman with fusiform aneurysm of the mid descending thoracic aorta. (a) A thoracic aortogram demonstrates suitable anatomy with sufficient proximal and distal necks for stent-graft placement. (b) Following stent-graft deployment, repeat aortogram demonstrates the device in good position without perigraft leak or other associated abnormalities.

A postdeployment aortogram is then performed (Figures 14.2–14.4). A faint persistent leak of contrast into the aneurysm is not uncommon and is due to the porosity of the graftmaterial. This will usually cease when the patient’s clotting status returns to normal. Should a major contrast leakage be identified, it may be necessary to place an additionalstent-graft either at the superior or inferior aspect of the aneurysm. If no leak is identified, the patient’s anti-coagulation is reversed with protamine sulphate, the delivery sheath isremoved, and the arteriotomy repaired surgically. For stent placement through theretroperitoneal aorta, the procedure has a more extensive surgical component; however,the technique is similar.


Figure 14.4 A 32-year-old female 5 days post gunshot wound to the upper abdomen, with persistent back pain following duodenal laceration repair. (a) A lateral lower thoracic aortogram identifies a pseudoaneurysm extending from the posterior wall of the aorta, just superior to the level of origin of the celiac artery. (b) Repeat aortogram following stent-graft placement, showing accurate positioning of the device above the celiac artery origin. The pseudoaneurysm was successfully treated.

Postprocedural monitoring

The patients usually spend the initial 24 h postprocedure in the intensive care unit, 1–2 days in a regular ward, and are then discharged on oral aspirin. A spiral CT is performedprior to discharge to evaluate any persistent filling of the aneurysm. Should a leak beidentified at this stage, angiographic evaluation is performed and the leak treated eitherwith a further device or by using embolization coils to close the channel. Patients haverepeat spiral CT examinations 6 months after placement, and yearly thereafter.

Results/complications

The primary success of the procedure in terms of aneurysm thrombosis was 73±5%. The


secondary success was 11%, yielding an ultimately successful outcome in 84±4%. The operative mortality rate was 9±3% on an intent-to-treat analysis and included all deaths that occurred within 30 days of the procedure. In terms of late survival, there were 14 latedeaths, two associated with aneurysm rupture, and six sudden unexplained deaths. Theother six deaths were unrelated to the aneurysm or the stent-graft procedure. The overall survival at 2 years was 80±5%.

Four cases of paraplegia (3.1%) complicated the stentgraft procedure. Three of the four cases occurred in patients in whom a stent-graft was used to repair a descending thoracicaortic aneurysm combined with surgical resection of an abdominal aortic aneurysm underthe same general anaesthesia. The other patient had operative repair of an abdominal aortic aneurysm 3 months prior to thoracic stent-graft placement. Four patients (3.1%)had a stroke associated with stent-graft deployment; in two patients it was related to intracerebral haemorrhage and heparin anticoagulation administered to preventthrombotic complications caused by the large delivery sheath.

Modern devices

A number of trials are currently underway in the USA to evaluate user-friendly low-profile devices. Stanford Medical Center is a participant in a phase 1 Food and DrugAdministration (FDA) trial using the Excluder thoracic stentgrant (Gore Inc., Flagstaff,AZ, USA). Stent-grafts have so far been placed in 20 patients at Stanford. The device stillrequires a 22 or 24 F introduction sheath, but is much easier to deploy accurately (Figure 14.5). Preliminary results appear extremely favourable, and rapid transition to phase 2 isexpected.

Discussion

The transluminal placement of endovascular stent-grafts has been shown to be of benefit in the treatment of a variety of lesions, including abdominal aortic aneurysms.15–19 While a less common entity than abdominal aortic aneurysms, thoracic aortic aneurysms are amajor health hazard, and are associated with a poor prognosis if left untreated.4Unfortunately, the standard surgical repair is associated with considerable morbidity andmortality. For this reason, a less invasive alternative such as an endoluminal prosthesis isideally suited to the treatment of this condition.3, 5–7

In contrast to abdominal aortic aneurysm repair the descending thoracic aorta is a relatively simple structure. As the device does not have to accommodate the bifurcation,it can be manufactured as a straight tube and can be inserted using one access site. Theoverall completion diameter of the deployed device is large, requiring a substantialintroduction sheath. This will continue to ensure that the procedure requires a teamapproach to access, deployment, and vessel repair. Currently, the largest introducersheath size that can be repaired using a minor surgical technique is 11 F. The proximityof the left subclavian artery to the superior aspect of the aneurysm is the most commonanatomical problem encountered during the work-up of these patients. A considerable


number will require a surgical transposition of the subclavian to carotid artery prior tostenting.

Modern advances in the speed and reconstruction techniques of CT scanners havemade this examination the procedure of choice in the work-up and measurement of the required prosthesis for these patients.20 The diameter of the iliac arteries, however, isusually 6–9 mm. At these small diameters, the CT unit may underestimate the size of these vessels, leading to access problems. For this reason, we usually perform anaortogram and pelvic arteriogram prior to scheduling the patient, to ensure that thecorrect access site is chosen.

During the continued follow-up of these patients the thrombosed aneurysm will usually begin to shrink, due to the absence of transmitted pressure from the blood flow. The lackof any reduction in aneurysm sac size after 6 months to 1 year follow-up should raise concerns for continued pressure transmission, and prompt detailed review of the imagingstudies.21

Complications are not uncommon with the use of these devices. Problems related tothe procedure are, however, relatively rare, and definitely decrease with experience. Thedevelopment of paraplegia in four of our patients is worrying; however, in all of thesepatients the abdominal aorta was either simultaneously repaired, or had been fixedpreviously. The interruption of a significant number of intraabdominal lumbar arteries, aswell as thoracic intercostals, appears to significantly increase the risk of this devastatingcomplication. For this reason it is our current policy to delay repair of one or otherproblem for a period of time following the initial repair to allow for increased collateraldevelopment. A significant number of postprocedural complications were identified,several of which were due to the relatively high-risk nature of the patients enrolled in thestudy. With continued and more widespread use of these procedures in a younger andhealthier population, these problems should decrease.

The current investigations will make this a procedure that can be performed by physicians with substantially less training in endovascular techniques than that requiredto utilize the equipment used in our first 121 patients. This factor will contribute to theconsiderable debate regarding which specialty should lead the way in the application ofthese endovascular technologies. In our institution, a combined approach by the vascularsurgeon and interventional radiologist has proved feasible and has been associated withconsiderable success. This may not be possible in all


Figure 14.5 A 58-year-old male 15 years after a motor vehicle accident. Recent routine chest radiograph identified a large thoracic aortic aneurysm (a) Contrast-enhanced computed tomography scan shows a 7cm proximal descending thoracic aortic aneurysm. (b) Thoracic aortogram reveals a short proximal neck above the aneurysm. The left subclavian artery can be seen to arise within 1 cm from the superior aspect of the aneurysm. (c) Gore excluder thoracic aortic stent-graft device, a self-expanding nitinol stent with the interior surface lined by polytetrafluoroethylene. (d) Following deployment of the stent-graft, a large, specially manufactured balloon is inflated to secure the proximal and distal aspects of the stent-graft. (e) Computed tomography scan identifies complete thrombosis of the excluded aneurysm sac. (f) Repeat aortogram following stent-grafting shows flow through the device without perigraft leak. The left subclavian artery has been transplanted onto the left common carotid artery to extend the length of the superior neck.


institutions; however, we feel that the team approach is clearly advisable. While astraightforward procedure may not require considerable catheter skills, a complex, andpossibly complicated one will need these. The operator will need skills to preventcontinued aneurysm filling, such as coil embolization of persistent leaks, balloonangioplasty of the devices, and addition of further stents or stent-grafts.

The morbidity and mortality encountered in our early series compares favourably with even the best reported surgical results. These numbers will certainly continue to improvewith continued experience and the development of lower profile devices. Although theultimate safety, durability and efficacy of this procedure awaits long-term followup, our initial experience would suggest that endovascular stent-grafts offer a feasible alternative to the extensive surgical procedures currently employed in the treatment of descendingthoracic aortic aneurysms.

Reference

1. Joyce J, Fairbairn JI, Kincaid O, Juergens J. Aneurysms of the thoracic aorta: a clinical study with special reference to prognosis. Circulation 1964; 29:176–81.

2. Lindsay J, DeBakey M, Beall A. Diagnosis and treatment of diseases of the aorta. In: R Schlant, R Alexander (eds.) The heart. 8th edition. New York: McGraw-Hill, 1994; 2163–80.

3. Pressler V, McNamara J. Thoracic aortic aneurysm: natural history and treatment. J Thorac Cardiovasc Surg 1980; 79:489–98.

4. Bickerstaff L, Pairolero P, Hollier L et al. Thoracic aortic aneurysms: a population-based study. Surgery 1982; 92:1103–8.

5. DeBakey M, McCollum C, Graham J. Surgical treatment of aneurysms of the descending thoracic aorta: long term results in five hundred patients. J Cardiovasc Surg 1978; 19:571–6.

6. Crawford E, Rubio P. Reappraisal of adjuncts to avoid ischemia in the treatment of aneurysms of the descending thoracic aorta. J Thorac Cardiovasc Surg 1973; 66:693–704.

7. Moreno-Cabral C, Miller D, Mitchell R et al. Degenerative and atherosclerotic aneurysms of the thoracic aorta: determinants of early and late surgical outcome. J Thorac Cardiovasc Surg 1984; 88: 1020–32.

8. Dotter C. Transluminally placed coilspring endarterial tube grafts: long-term patency in canine popliteal artery. Invest Radiol 1969; 4: 329–32.

9. Laborde J, Parodi J, Clem M et al. Intraluminal bypass of abdominal aortic aneurysm: feasibility study. Radiology 1992; 184:185–90.

10. Chuter T, Green R, Ouriel K, Fiore W, DeWeese J. Transfemoral endovascular aortic graft placement. J Vasc Surg 1993; 18:185–97.

11. Mirich D, Wright K, Wallace S et al. Percutaneously placed endovascular grafts for aortic aneurysms: feasability study. Radiology 1989; 170(3): 1033–37.

12. Lawrence DJ, Chansangavej C, Wright K, Gianturco C, Wallace S. Percutaneous endovascular graft: experimental evaluation. Radiology 1987; 163:357–60.

13. Balko A, Piasecki G, Shah D, Carney W, Hopkins R, Jackson B. Transfemoral placement of intraluminal polyurethane prosthesis for abdominal aortic aneurysm. J Surg Res 1986; 40:305–9.

14. Yoshioka T, Wright K, Wallace S, Lawrence DJ, Gianturco C. Selfexpanding


endovascular graft: an experimental study in dogs. AJR 1988; 151:673–6. 15. Parodi J, Palmaz J, Barone H. Transfemoral intraluminal graft implantation for

abdominal aortic aneurysms. Ann Vasc Surg 1991; 5: 491–9. 16. Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP. Transluminal

placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 1994; 331(26): 1729–34.

17. May J, White G, Waugh R, Yu W, Harris J. Transluminal placement of a prosthetic graft-stent device for treatment of subclavian artery aneurysms. J Vasc Surg 1993; 18:1056–9.

18. Marin M, Veith F, Panetta T et al. Percutaneous transfemoral insertion of a stented graft to repair a traumatic femoral arteriovenous fistula. J Vasc Surg 1993; 18:299–302.

19. Craff A, Dake M. Percutaneous femoropopliteal graft placement. Radiology 1993; 187:643–8.

20. Quint LE, Francis IR, Williams DM et al. Evaluation of thoracic aortic disease with the use of helical CT and multiplanar reconstructions: comparison with surgical findings. Radiology 1996; 201(1): 37–41.

21. May J, White G, Yu W, Waugh R, Stephen M, Harris J. A prospective study of anatomico-pathological changes in abdominal aortic aneurysms following endoluminal repair: is the aneurysmal process reversed? Eur J Endovasc Surg 1996; 12:11–17.


Laparoscopic aorto-femoral bypass

15 S.S. AHN AND K.M. RO

Introduction

Advocates of endovascular surgery have heralded its advantages over conventional openrevision; specifically minimal tissue trauma and scarring, decreased risk of contaminationand quicker recovery. Although in their infancy, laparoscopic techniques applied to intra-abdominal vascular repair are gaining increased acceptance due to their noted value inreducing postoperative pain, morbidity, and hospital stay, as well as enhancing earlierrehabilitation. Their feasibility has been previous documented in several studies reportedby Ahn,1, 2 Berens,3 Dion,4 and Barbera,5 who, utilizing slightly different techniques, have successfully performed laparoscopic vascular procedures. Using carbon dioxideinsufflation, Ahn and colleagues reported studies in both a porcine model and a patient,showing that a completely laparoscopic aorto-ileofemoral bypass grafting is not onlytechnically feasible, but also safe.1, 2 Conventional abdominal procedures for the treatment of aortic and iliac artery occlusive disease include aortofemoral bypass,extraanatomic bypass, endarterectomy and/or angioplasty, with a 5-year patency rate of approximately 90% and 1–8% mortality rate.6, 7 However, laparoscopic intra-abdominal repair has the potential to deliver comparable results when compared to open revision,with the benefits associated with minimally invasive techniques. The transperitonealapproach to laparoscopic aorto-ileofemoral bypass surgery is outlined below.

Instruments

1. Two video monitors. 2. Veress needle. 3. 30° angled endoscope. 4. Central epigastric subxiphoid port. 5. Versaports. 6. Endo-Babcock clamp. 7. Reticulating fanned endoretractor. 8. Suction/irrigator. 9. Electrocauterized endo-Metzenbaum scissors. 10. Reticulating endodissectors. 11. Rumel tourniquets. 12. Endoclips.

13. Endodissector. 14. Curved endomicro-Metzenbaum scissors. 15. 4–0 Surgipro stay sutures. 16. 16×8 mm Hemashield bifurcated Dacron graft. 17. Curved CV-23 tapered needle. 18. Endoneedle driver. 19. Endoknot pusher.

Preparation

Anaesthesia/position

The patient should undergo a mechanical bowel preparation on an outpatient basis the dayprior to surgery. The patient should be placed in the supine position and induced undergeneral endotracheal anaesthesia. An arterial line and central venous catheter should beinserted. With the ankle padded and secured tightly to the table, place the patient in asteep Trendelenberg position with a 20-degree right lateral tilt (Figure 15.1a). Prepare theabdomen and groin in the usual sterile fashion.

Ports

Seven incisions are required to position the laparoscopic ports and trocars (Figure 15.1b).Four Versaports (4–12 mm, US Surgical Corp. [USSC], Norwalk, CT, USA), one in eachquadrant, should be introduced via stab incision. Two additional Versaports are required:one positioned in the right lower abdomen for bowel retraction using an Endobabcockclamp and/or reticulating fanned endoretractor, and the other in the suprapubic region foran endoscope/suction/ irrigation. The two stay sutures should be placed laterally on eitherside.


Figure 15.1 (a) Patient in steep Trendelenberg position with a 20-degree right lateral tilt. (b) Transperitoneal placement of seven laparoscopic ports/ trocars via stab incisions. Also, note lateral placement of two stay sutures.

Laparoscopic aorto-femoral bypass 309

Procedure

1. Induce a carbon dioxide pneumoperitoneum with a Veress needle (USSC) and maintain it at 9–16mmHg.

2. Insert the 30° angled endoscope (Karl Storz Inc., Culver City, CA, USA) connected to two television monitors through the central epigastric subxiphoid port (11mm, Ethicon Endosurgery, Cincinnati, OH, USA) (Figure 15.1b).

3. Insert one Versaport into each quadrant. 4. Insert two additional Versaports: one in the right lateral abdomen to allow for bowel

retraction using an endoBabcock clamp or a reticulating fanned endoretractor and another in the suprapubic region for an endoscope or suction/irrigation.

5. Circumferentially dissect an 8 cm section of the infrarenal aorta using electrocauterized endo-Metzenbaum scissors (MicroSurge Inc., Needham, MA, USA) and reticulating endodissectors (USSC). Control the dissection proximally and distally with Rumel tourniquets consisting of red Robinson catheter tubing and umbilical tape (Figure 15.2a). If the aorta is calcified, an intraluminal balloon or laparoscopic vascular clamp is used.

Figure 15.2 (a) The circumferentially dissected region of the infrarenal aorta is occluded proximally and distally by Rumel tourniquets, consisting of Robinson catheter tubing and umbilical tape. The lumbar arteries are doubly clipped. (b) A 16×8mm Hemashield bifurcated Dacron graft cut at an angle to match the arteriotomy.


6. The femoral vessels should be exposed and controlled bilaterally; vascular control should be obtained using conventional open techniques.

7. Doubly clip two pairs of lumbar arteries with an Endoclip (Ethicon Endosurgery). The inferior mesenteric artery can be controlled with a loosely applied endoclip, which is removed at a later stage.

8. Administer 5000 units of intravenous heparin and tighten the Rumel tourniquets, and inflate the intra-aortic balloons, or apply vascular clamps for aortic occlusion.

9. Make a 3 cm aortotomy using a no. 11 blade secured to an endodissector (USSC) and curved endomicro-Metzenbaum scissors (Microsurge Inc., Needham, MA, USA).

10. Place two Surgipro stay sutures in the aorta and pass them externally through a needle-stab incision.

11. Cut a 16×8mm Hemashield bifurcated Dacron graft (Meadox Medical Inc., Oakland, NJ, USA) at an angle to match the arteriotomy. Place a horizontal U-stitch at the graft heel using a double-armed Surgipro suture on a curved CV-23 tapered needle (USSC) (Figure 15.2b).

12. Introduce the graft and suture into the abdomen through a 12 mm lower quadrant port.

13. Using an endoneedle driver, suture the graft to the aorta end-to-side in a continuous running fashion. Secure the knots extracorporeally using an endoknot pusher (USSC) (Figure 15.3a).

14. Pass long aortic clamps retroperitoneally from the exposed groins to the aorta to pull the left and right limbs of the graft through their respective tunnels into the femoral region (Figure 15.3b).

15. Release the distal and proximal aortic Rumel tourniquets. Check the aortic graft anastomosis for haemostasis.

16. Flush the graft with heparinized saline solution and clamp the two distal limbs. 17. Anastomose the respective graft limbs to the corresponding common femoral artery

with a running 5–0 Prolene suture using conventional open techniques. 18. Confirm palpable femoral pulses and a haemostatic aortic anastomosis. Pedal artery

signals can be detected by Doppler. 19. Remove all instruments and close port sites with a 3–0 polyglycolic acid for fascia

and staples for skin.


Figure 15.3 (a) The bifurcated Dacron graft is sutured to the aorta end-to-side in a continuous running fashion. (b) Dacron graft sutured to the aorta with the left and right limbs of the graft pulled in to the femoral region through their respective tunnels.

Postoperative care

Appropriate pain control medications should be administered postoperatively. On postoperative day 1, the bladder catheter should be removed and the patient started on a clear diet. Ambulation is initiated and the diet advanced as tolerated. Hospital stay should average 2–3 days. Follow-up examination should be conducted using standard vascular protocol.

Discussion

Technical difficulties have limited the progression and widespread dissemination of intra-abdominal laparoscopic surgery. Albeit feasible, laparoscopic transperitoneal aorto-ileofemoral bypass still requires additional experience and specialized instruments to be effective in reducing operating time and duration of general anaesthesia. In our


experience, using a totally laparoscopic transperitoneal approach with induction of apneumoperitoneum, the primary difficulty we encountered was in retracting the boweland obtaining total aortic occlusion with Rumel tourniquets; however, the relatively largenumber of incisions and laparoscopic ports utilized for this procedure are well tolerated,as indicated by the reduced postoperative analgesia required. Moreover, the totalcombined length of the port incisions is still less than the abdominal incision associatedwith conventional aortobifemoral bypass.

Berens and Herde reported their experience with four laparoscopically performedaorto-iliac procedures performed using a gasless transperitoneal approach, only one ofwhich was an aortobifemoral bypass. While no complications were reported, the authorsfound the vascular anastomosis to be challenging and time-consuming. In 1997, Dion and others reported their results compiled from 6 years of in vitro and animal experiments utilizing a completely laparoscopic retroperitoneal approach without carbon dioxideinsufflation. Their technique, which evolved from a retroperitoneal approach usingcarbon dioxide insufflation, involved separating the intraperitoneal organs from the con-tents of the retroperitoneal cavity using a ‘peritoneal apron’. The authors believe that this technique offers several advantages, including a larger retroperitoneal cavity and easierretraction of the abdominal contents. In a recent study published in 1998, Dion and othersreported a series of 10 patients using this technique and successfully decreased theoperative time from 510 to 245 min. However, three out of 10 patients were converted toopen procedures and three patients had postoperative complications.

Recently, Barbera and colleagues reported a series of 24 laparoscopically performedvascular procedures for aorto-iliac occlusive disease, 11 of which were aortobifemoral bypass procedures. Similar to Ahn et al., Barbera and colleagues performed theirprocedures with pneumoperitoneum. This offered the advantage of proper visualizationof the operative field and the enlarged abdominal cavity enhanced the manoeuvrability ofthe suturing device. However, they too had difficulty in retracting the bowel andobtaining total aortic occlusion with Rumel tourniquets. They reported a mean blood lossof 563 ml, with two patients requiring red blood cell transfusion and one patientexperienced respiratory failure postoperatively due to the lengthy surgery time. Using agasless technique, Kolvenbach and associates,8 examined the influence of aortic access relative to the extent of the surgical trauma. By comparing the pre- and postoperative cytokine levels in the laparoscopic versus open aortoiliac reconstruction, they were ableto obtain a physiological determinant of the extent of surgical trauma and found adampened immunological response, with a significant reduction in cytokine release in thelaparoscopic group.

Although the use of laparoscopic procedures for the treatment of aortic aneurysmsrequires additional confirmation, Edoga and associates9 successfully performed laparoscopic surgery for the treatment of infrarenal abdominal aneurysms in 20 out of 22patients. Postoperatively, of the 20 patients, nine complication and two deaths post-operatively were reported. They found the patients’ postoperative course to require shorter intensive care unit and hospital stay and fewer postoperative analgesics whencompared to patients undergoing open transabdominal aortic resection at the sameinstitution.

Surgeons should first refine their laparoscopic vascular anastomosis skills using an


animal model. Contraindications may include a heavily calcified aorta, morbid obesity,and previous aortic surgery, as all these factors can increase the possibility ofcomplications and conversion to open surgery. Potential problems also include difficultyin retracting the bowel and obtaining total aortic occlusion with Rumel tourniquets;however, the availability of large laparoscopic fan retractors, as well as otherlaparoscopic vascular occluders, may help to minimize this problem and facilitatelaparoscopic exposure of the aorta. In a diseased human aorta, total occlusion may bedifficult and require intermittent suctioning of the operative field while performing theaortic graft anastomosis; high blood loss is possible. In spite of these factors, thedecreased hospital stay and accelerated ambulation are remarkable when compared to thetypical postoperative course following a conventional aortobifemoral bypass grafting.

References

1. Ahn SS, Hiyama DT, Rudkin GH, Fuchs GJ, Ro KM, Concepcion B. Laparoscopic aortobifemoral bypass. J Vasc Surg 1997; 26:128–32.

2. Ahn SS, Clem MF, Braithwaite BD, Concepcion B, Petrik PV, Moore WS. Laparoscopic aortofemoral bypass: initial experience in an animal model. Ann Surg 1995; 222:677–83.

3. Berens ES, Herde JR. Laparoscopic vascular surgery: four case reports. J Vasc Surg 1995; 22:73–9.

4. Dion YM, Gracia CR. A new technique for laparoscopic aortobifemoral grafting in occlusive aortoiliac disease. J Vasc Surg 1997; 26: 685–92.

5. Barbera L, Mumme A, Metin S, Zumtobel V, Kemen M. Operative results and outcome of twenty four totally laparoscopic vascular pro-cedures for aortoiliac occlusive disease. J Vasc Surg 1998; 28:136–42.

6. Ameli FM, Stein M, Provan JL, Aro L, Prosser R. Predictors of surgical outcome in patients undergoing aortobifemoral bypass reconstruction. J Cardiovasc Surg 1990; 31:333–9.

7. Ameli FM. Aortobifemoral bypass: an enduring operation. Can J Surg 1992; 35:237–41.

8. Kolvenbach R, Deling O, Schwierz E, Landers B. Reducing the operative trauma in aortoiliac reconstructions-a prospective study to evaluate the role of video-assisted vascular surgery. Eur J Vasc Endovasc Surg 1998; 15:483–8.

9. Edoga JK, Asgarian K, Singh D et al. Laparoscopic surgery for abdominal aortic aneurysms: technical elements of the procedure and a preliminary report of the first 22 patients. Surg Endosc 1998; 12(8): 1064–72.


Minimal access in situ vein bypass grafting

16 C.H.A. WITTENS

Introduction

The first successful femoropopliteal in situ saphenous vein bypass was reported by Hallin 1962.1 Due to this success, more surgeons became interested in this bypass procedure, which was theoretically superior, especially when compared to the use of a reversed veinbypass. There are theoretical advantages physiologically, minimizing endothelial injuryby leaving the vasa vasorum intact; mechanically, as a result of the gradual vessel taperand minimal anastomotic discrepancy favourable flow characteristics, reducinghaemodynamic injury; and technically, the in situ saphenous vein allowing for greater utilization of small saphenous veins that were previously deemed inadequate. Possibledisadvantages related to the technique provide challenges with regards to valve ablationand ligation of venous sidebranches. Although some surgeons still believe the in situbypass procedure to be more demanding, improved instrumentation, appropriate trainingand attention to detail, have led to a more acceptable procedure in patients requiring aninfrageniculate or crural bypass.

Over the past two decades, a substantial number of papers have been published relatingto the use of the in situ bypass2–8 and its comparison with other techniques,6 often with the reversed vein bypass.9–11 Taking these papers into consideration, it may be concluded that the theoretical advantages did not translate into a marked improvement onperformance, but if carried out properly, in situ vein grafting clearly has advantages inpatients requiring a distal crural or pedal bypass. One potential advantage of the in situbypass is that it can accommodate a minimally invasive procedure.

This chapter will not address all the possible indications or alternatives for in situbypasses, but it will summarize the technical points of minimally invasive surgery. Themain objectives in performing such a procedure are a reduction of wound-related problems, a shorter hospital stay, improved cosmesis and equally good patency rates. Thetwo main components of the minimally invasive in situ procedure are disabling the saphenous vein valves and occlusion of the venous side-branches.

Vein valve lysis

When the in situ bypass was first introduced, valves had to be excised directly.1 Later, Hall invented the Hall valve cutter, which disrupted the commissures of the valve cusps,leaving behind the incompetent cusps.12 Clinical experience did not show any

disadvantage of the incompetent cusps remnant inside the vessel. Cartier and Leather alsoinvented valvulotomes which work well.13, 14 The vein is dilated under pressure, from proximal to distal to close the valves, which allows the valvulotome to divide the valves(Figure 16.1). Complete valve lysis can be confirmed by antegrade and retrogradehydrostatic pressure measurement15 or by using angioscopy.16

Hollis et al. 17 subsequently recommended completion of the proximal anastomosis before the valves are cut. This modification eliminated the need for hydrostatic dilatationof the vein by means of an heparinized solution; the vein is dilated physiologically by thenative arterial pressure (Figure 16.2). There are no published data comparing the different valve cutters. The Hall, Leather or Cartier valve cutters can all be used, as proposed byHollis, as long as the vein is completely exposed.

Another problem with these valve cutters is sizing. They have to be introduced throughthe narrow distal end of the vein, but as this vein is tapered more proximally there is adiameter mismatch. This was the reason why blind valvulotomy with valve cutters wasunpopular. In order to avoid the need of visual control and to preserve Hollis’ method, a variable valve cutter was designed (Figure 16.3). This

Figure 16.1 The action of the valve cutter within the vein. Proximal pressure distension of the vein is important, both to allow the cutter to float within the lumen and to avoid traumatizing the walls of the vein, while engaging the closed valve cusps cleanly.

valve cutter automatically adjusted its size to the vein diameter from 2.5 up to 10 mm.This facilitates an atraumatic introduction at the distal end of the vein and also enablesblind proximal valve lysis, due to proper diameter adjustment (Figure 16.4). Van Dijk published a series of approximately 50 patients, using this valve cutter successfully in acompletely closed bypass procedure, confirming the safety of the procedure.18

Minimal access in situ vein bypass grafting 317

Figure 16.2 Valve cutter in situ after the proximal end-to-side anastomosis is completed. The arterial pressure adequately deploys the cusps for for easy lysis.

Figure 16.3 This variable nitinol valve cutter adjusts its size automatically to the size of the vein, varying from 10 to 2.5mm, allowing blind lysis of the valve cusps from groin to ankle (VaVaCut™, Cook®).


Figure 16.4 A schematic drawing of the variable valve cutter, as used during the operations.

A good valve cutter has to be safe. A valve cutter must avoid damage to the vein wall, which can occur by catching a side-branch, and it should also avoid extensivelydamaging the endothelium.19

After a successful disruption of all cusps, the surgeon has to perform angiography,duplex or Doppler to identify possible stenoses related to persistent competent valvecusps. These should be treated when detected.

Tributary occlusion

Over the past three decades, several attempts have been made to perform in situ bypass grafting using the saphenous vein with minimal dissection. It was known that completeexposure of the vein (Figure 16.5) led to an increased number of postoperative wound


complications. Reifsnijder20 published a retrospective study with an incidence of 44%and Schwartz21 showed an incidence of 33%. Wound complications are more frequently seen in prospective studies. In a randomized trial between open and closed in situ bypass procedures, van Dijk noted an incidence of 72%.18

Tributaries can be occluded either by ligation of the vessel or through occlusion from within, the latter being an endoluminar approach. Table 16.1 shows the options available for minimally invasive tributary occlusion for in situ vein bypass.

The diameter of the long saphenous vein could be properly quantified using duplex. A preoperative diameter of more than 2.5 mm is associated with a higher success rate.22

The knowledge of venous duplications or triplications in advance also helps. Preoperative identification of side-branches has been performed using a great variety

of methods. Preoperative

Figure 16.5 Completely prepared vein, causing a significant number of wound problems.

Table 16.1 Options available for minimally invasive tributary occlusion for in situvein bypass Extraluminal occlusion of tributaries

Selective Angiography

Doppler

Duplex

Angioscopy

All Endoscopic

Endoluminal occlusion of tributaries

Angioscopically assisted Occlusion gel gel

Detachable balloons

Coils


angioscopy has been studied most frequently16, 23 but other possibilities such as Doppler,24, 25 electromagnetic flow measurement,26 duplex27 and angiography28 have also been used.

If any of these techniques are to be used intraoperatively, the proximal anastomosis has to be performed prior to sidebranch occlusion. This precludes the use of angioscopy, asthe proximal anastomosis cannot be completed first. A special irrigation system has to beapplied as an aid to angioscopically controlled side-branch ligation. The angioscope with irrigation systems may be inserted proximally or distally. Proximal insertion requiresvalve lysis before angioscopy. A disadvantage of endoscopy with the distal approach isthat side-branches can be missed because of the anatomical orientation of the side-branch orifices. With proximal insertion of the angioscope, the side-branches may be visualized more directly after valve cutting. After detection, the light of the angioscopetransluminates the skin, where consequently, a small stab incision is made (Figure 16.6). After the side-branch has been dissected, it is ligated or clipped. In general, proximal to distal angioscopy is advocated, due to the orifice orientation of all the sidebranches.

Doppler24, 25 or electromagnetic measurements can be used to detect fistulas. Themethod is based on cessation of the flow signal in the graft by obstructing it proximal to afistula, while the flow signal persists if the graft is obstructed just distal to the fistula.This is known as the ‘null point method’ (Figure 16.7). Side-branches with competent valves are missed. Duplex27 or angiography28 can be applied after completion of the distal anastomoses. Duplex is able

Figure 16.6This diagram shows the angioscope and valvulotome in situ. The stab incisions are made after translumination of the skin at a tributary site.

Fluorscopically assisted Occlusion gel

Detachable balloons

Coils


to detect the side-branches easily, but if flow is impaired as a result of a competent side-branch valve, it may easily be missed. Using a set of small needles at 5–10cm intervals inserted in the overlying skin as radiographic markers, angiography also will only imagethe side-branches without valves and does not visualize side-branches with competent valves.28

New endoscopic techniques have been developed in order to harvest the longsaphenous vein for coronary bypass surgery. Special tools have been developed toperform this endoscopic method.29 Special equipment allows for circular dissection of the vein, which ensures that all side-branches are dissected (Figure 16.8). Because of the experience that most and vascular surgeons have with video assisted endoscopic surgeryand the fact that most of the equipment is quite common, this technique might becomeuseful in in situ vein bypass grafting. Because extensive subcutaneous dissection isnecessary, haematomas or seroma formations can occur. No data on woundcomplications are available and therefore randomized trials still have to be performed.

Endoluminal occlusion of tributaries

Endovascular occlusion of the side-branches can be achieved with different materialsunder angioscopic or fluoroscopic guidance.

Pigott published the use of an occlusion gel (Figure 16.9). This technique allowed the occlusion of vein side-branches in dogs. Due to the potential risk of lung embolisms, nofurther studies have been pursued.30 The use of detachable balloons has been reported; however, this is very expensive.

Most experience has been gathered with the use of coils. essentially consisting of apiece of guide-wire with

Figure 16.7 The ‘null point method’ to detect fistulas


Figure 16.8 Special equipment for endoscopic long saphenous vein harvesting (Vasoview Uniport™ Systems).

Figure 16.9 Angioscopically controlled occlusion of tributary using Ethibloc® occlusion gel.


Figure 16.10 A 3 F coil-delivery catheter with a coil in position.

dacron threads (Figure 16.10), are used to occlude sidebranches in in situ vein bypasses. These can be introduced in patients without the need for further laboratory in vitro or in vivo studies, as there is already extensive experience using coils in the vascular system.Several methods have been developed to introduce coils into side-branches, but for effective delivery the side branches must be visualized. Rosenthal developed a techniqueusing the angioscope as an aid to perform a valvulotomy under direct vision, and he usedthe angioscope as a side-branch detector.31–33 After its detection, a nitinol steerable catheter was introduced into the side-branch and a coil delivered. Multicentre studies showed good results with this technique, with reduction of wound-healing problems and a short hospital stay. Stierli and colleagues modified a Mills valvulotome, which made itpossible to deliver coils through this new device (Figure 16.11).34 Here also, the angioscope was used to identify side-branches. The disadvantages of these systems arethe high costs of the angioscopes and the fact that no


Figure 16.11 A modified Mills valvulotome for angioscopically guided occlusion of tributaries using coils.

information is gathered about the exact anatomy of the side-branch, as only the orifice is visualized. The latter may cause problems, such as positioning a coil that is too long for aside-branch, which will protrude into the main long saphenous vein lumen (Figure 16.12). If this is not corrected promptly, it will probably cause an occlusion of the graft.32

Another problem might be the fact that some sidebranches have secondary branchesimmediately after their orifice, where one coil is insufficient to neutralize all the branches(Figure 16.13). A third problem might be caused by inserting an undersized coil into a side-branch, resulting in the coil being flushed into the deep venous system. Finally, no information is gathered about the side-branch being a cutaneous or perforating vein.

All these possible problems can be addressed by using fluoroscopy. Wittens hasdeveloped a fluoroscopy assisted coil

Figure 16.12 (a) A coil protruding into the long saphenous vein after a misplacement; (b) a properly placed coil in a side-branch.


Figure 16.13 (a) A coil positioned beyond a secondary branch, leaving a persistent AV-fistula; (b) properly occluded side-branch with a coil in each secondary branch; (c) a coil positioned between the long saphenous vein and the secondary branching (cave: protruding in long saphenous vein).

Figure 16.14 Co-axial embolization catheter system for coil delivery (Cook®).

delivery system using a 7 F co-axial catheter system (Figure 16.14).35 The 7 F catheter is introduced through a long side-branch of the proximal long saphenous vein after completion of the bypass. Valves are cut using a specially designed variable valve cutter(Figure 16.3 and 16.4). This 7 F catheter is guided down to the distal anastomoses and,under fluoroscopic guidance, the catheter is pulled back until a side-branch is visualized. A guide-wire is then brought into the side-branch, along which a 3 F catheter isintroduced (Figure 16.15). Under fluoroscopy, side-branch anatomy is defined, whether itis a cutaneous branch or a perforating vein, and whether secondary branching is involvedor not. Coils of appropriate length and diameter can be delivered, causing completeocclusion of the side-branch. Advantages of this system are that it is less expensive, and fluoroscopy establishes precise positioning of the coils and provides online informationabout the anatomy of the side-branch. Fluoroscopy is also used to assess the distalanastomoses and its outflow. One disadvantage that should be mentioned is that a side-


branch can be missed during fluoroscopy if it has a competent valve positioned directly atits orifice, but this does not appear to be a major problem. Van Dijk published aprospective randomized trial between the open and closed in situ vein method, showing a significant reduction in wound complications.20 Another important issue of the study was that the catheter manipulation in the vein might impair the patency rate. The patency rateof the closed technique was shown to be better, but without a statistical significance. Acost-benefit analysis was carried out and this showed the closed method to be more cost-effective than the complete open method.36 Cikrit also performed a series

Figure 16.15 A schematic drawing of the deposition of an embolization coil in a side-branch via the co-axial catheter.


Figure 16.16 Angiogram of an in situ bypass with coil embolized side-branches: (a) preoperatively; (b) 1 month postoperatively.

using fluoroscopy and angioscopy and concluded that angioscopy did not add anyadvantage compared to using fluoroscopy alone.37

Arteriovenous fistulae

By not dissecting the long saphenous vein completely and trying to occlude side-branches selectively, extra- or endovascularly, a number of side-branches can be missed. These persistent side-branches will remain as an arteriovenous fistula after the procedure. This problem of persistent arteriovenous fistulae is addressed by Leather and Van Dijk.2, 38 It can be concluded from these data that if duplex-detected arteriovenous (AV) fistula39 do not cause any skin circulation problems or impair haemodynamic performance of thebypass, they can be left and not tied off. One-third of the AV fistulae will occlude within several months, onethird will not cause any problem, whereas the remaining one-third will influence the clinical performance of the bypass, especially if a stenosis is present inthe bypass.40 Only 6% of the patients that had received a closed in situ bypass required AV fistula occlusion.39, 41 Two methods were used to occlude these AV fistulae. One is apercutaneous technique, through which the side-branches are occluded using coil embolization.42 The second is a surgical technique using a stab incision with directligation under local anaesthesia after localization with duplex ultrasound. Coil occlusionof side-branches does not occur immediately, but takes up to 3 days. Angiography at theend of the procedure and after 1 week illustrates this finding (Figure 16.16).


Conclusion

After analysis of all the data, the standard for in situ saphenous vein bypass surgery should be an endovascular method, showing a much lower morbidity, a shorter hospitalstay, better cosmesis and lower costs. Fluoroscopic control has advantages related to coil placement and anatomical information. There is a learning curve associated with thesemethods, and ultimately the choice will be influenced by the availability of resources.

References

1. Hall KV. The great saphenous vein used in situ as an arterial shunt after extirpation of the vein valves. Surgery 1962; 51:492–5.

2. Leather RP, Shah DM, Chang BB, Kaufman JL. Resurrection of the in situ saphenous vein bypass 1000 cases later. Ann Surg 1988; 208: 435–42.

3. Bandyk DF, Kaebnick HW, Stewart GW, Towne JB. Durability of the in situ saphenous vein arterial bypass: a comparison of primary and secondary patency. J Vasc Surg 1987; 5:256–68.

4. Shah DM, Leather RP, Darling III RC, Chang BB, Paty PSK, Lloyd WE. Long term results of using the in situ saphenous vein bypass. Advan Surg 1997; 30:123–40.

5. Anderson CB, Stevens SL, Allen BT, Sicard GA. In situ saphenous vein for lower extremity revascularization. Surgery 1992; 112: 6–12.

6. Shah DM, Darling III RC, Chang BB, Kaufman JL, Fitzgerald KM, Leather RP. Is long vein bypass from groin to ankle a durable procedure? An analysis of a ten-year experience. J Vasc Surg 1992; 15: 402–8.

7. Connolly JE. In situ saphenous vein bypass: 1962 to 1987. Am J Surg 1987; 154:2–10. 8. Shah DM, Darling III RC, Chang BB, Fitzgerald KM, Paty PSK, Leather RP. Long-

term results of in situ saphenous vein bypasses. Analysis of 2058 cases. Ann Surg 1995; 222:438–48.

9. Moody AP, Edwards PR, Harris PL. In situ versus reversed femoropopliteal vein grafts: long term follow-up of a prospective, randomised trial. Br J Surg 1992; 79:750–2.

10. Wengerter KR, Veith FJ, Gupta SK et al. Prospective randomised multicenter comparison of in situ and reversed vein infrapopliteal bypasses. J Vasc Surg 1991; 13:189–99.

11. Veith FJ, Wengerter KR, Gupta SK. In situ or reversed vein bypass for lower limb revascularization? Acta Chir Scand 1990; 455: 43.

12. Skageth G, Hall KV. In situ bypass experience with a new vein stripper. Surgery 1972; 6:1–6.

13. Becquemin JP, Haiduc F, Labastie J, Melliere D. Femoropopliteal in situ saphenous vein bypass: technical aspects and factors determining patency. Ann Vasc Surg 1987; 1:432–40.

14. Leather RP, Shah DM, Corson JD et al Instrumental evolution of the valve incision method of in situ saphenous vein bypass. J Vasc Surg 1984; 1 113–23.

15. Christopoulos D, Galloway JMD, Grigg MJ. A perioperative technique for detection of retained valve cusps in the in situ vein graft. Surgery 1989; 105:553–5.


16. Maini BS, Andrews L, Salimi T, Hendershott TH, O’Mara P. A modified, angioscopically assisted technique for in situ saphenous vein bypass: impact on patency, complications, and length of stay. J Vasc Surg 1993; 17:1041–9.

17. Hollis HW, Gottesman L, Wright CB, Podore PC. A modified technique for use of the intraluminal valve cutter in in situ saphenous vein grafts. J Vasc Surg 1987; 6:124–6.

18. Van Dijk LC, Van Urk H, Du Bois NA et al. A new ‘closed’ in situ vein bypass technique in a reduced wound complication rate. Eur J Vasc Endovasc Surg 1995; 10:162–7.

19. Sayers RD, Watt PAC, Muller S, Bell PRF, Thurston H. Endothelial cell injury secondary to surgical preparation of reversed and in situ saphenous vein bypass grafts. Eur J Vasc Surg 1992; 6:354–61.

20. Van Dijk LC, Van Urk H, Du Bois NAJJ et al. A new ‘closed’ in situ vein bypass technique results in a reduced wound complication rate. Eur J Vasc Endovasc Surg1995; 10:162–7.

21. Schwartz ME, Harrington EB, Schanzer H. Wound complications after in situ bypass. J Vasc Surg 1988; 7:802–7.

22. Leopold PW, Shandall A, Kupinkski AM et al. Role of B-mode venous mapping in infrainguinal in situ vein-arterial bypasses. Br J Surg 1989; 76:305–7.

23. Grundfest WS, Litvack F, Glick D et al. Intraoperative decisions based on angioscopy in peripheral vascular surgery. Circulation 1988; 78(suppl. 1): I-13–17.

24. Corson JD, Shmma AR, Meng RL. In situ saphenous vein bypass . In: JJ Bergan, JST Yao (eds) Arterial surgery, new diagnostic and operative techniques. Orlando, FL: Grune & Stratton, 1988, 507–22.

25. Leather RP, Karmody AK, Shah DM, Corson JD. The in situ saphenous vein arterial bypass. In: JJ Bergan, JST Yao (eds) Reoperative arterial surgery. Orlando, FL: Grune & Stratton, 1986, 299–310.

26. Heather BP, Green IL, McCollum CN, Greenhalgh RM. Intraoperative detection of arterio-venous fistulae after in-situ vein bypass. In: RM Greenhalgh (ed.) Diagnostic techniques and assessment procedures in vascular surgery. Orlando, FL: Grune & Stratton, 1985, 297–302.

27. Bandyk DF, Johnson BL, Gupta AK, Esses GE. Nature and management of duplex abnormalities encountered during infrainguinal vein bypass grafting. J Vasc Surg 1996; 24:430–8.

28. Nadler LH, Tiefenbrun J. Roentgenographic marking using surgical staples after in situ saphenous venous bypass. Surg Gynecol Obstetr 1990; 170:361–2.

29. Johnson PR, Tan SL, Chin AK. Endoscopic femoral-popliteal/distal bypass grafting: a preliminary report. J Am Coll Surg 1998; 186: 331–6.

30. Pigott JP, Donovan DL, Fink JA, Sharp WV. Angioscope-assisted occlusion of venous tributaries with prolamine in in situ femoropopliteal bypass: preliminary results of canine experiments. J Vasc Surg 1989; 9:704–9.

31. Rosenthal D, Dickson C, Rodriguez FJ et al. Infrainguinal endovascular in situ saphenous vein bypass: ongoing results. J Vasc Surg 1994; 20:389–95.

32. Rosenthal D, Herring MB, O’Donovan TG, Cikrit DF, Comerota AJ, Corson JD. Endovascular infrainguinal in situ saphenous vein bypass: a multicenter preliminary report. J Vasc Surg 1992; 16:453–8.

33. Rosenthal D. Endoscopic in situ bypass. Surg Clin N Am 1995; 75: 703–13. 34. Stierli P, Aeberhard P. In situ femorodistal bypass: novel technique for angioscope-

assisted intraluminal side-branch occlusion and valvulotomy. A preliminary report. Br


J Surg 1991; 78:1376–8. 35. Wittens CHA, Van Dijk LC, Du Bois NAJJ, Van Urk H. A new ‘closed’ in situ vein

bypass technique. Eur J Vasc Surg 1994; 8: 166–70. 36. Van Dijk LC, Seerden R, Van Urk H, Wittens CHA. Comparison of cost affecting

parameters and costs of the ‘closed’ and ‘open’ in situ bypass technique. Eur J Vasc Endovasc Surg 1997; 13:460–3.

37. Cikrit DF, Dalsing MC, Lalka SG et al. Early results of endovascular-assisted in situ saphenous vein bypass grafting. J Vasc Surg 1994; 19:778–87.

38. Van Dijk LC, Van Urk H, Laméris JS, Wittens CHA. Residual arteriovenous fistulae after ‘closed’ in situ bypass grafting: an overrated problem. Eur J Vasc Endovasc Surg 1997; 13:439–42.

39. Londrey GL, Hodgson KJ, Spadone DP, Ramsey DE, Barkmeier LD, Sumner DS. Initial experience with color-flow duplex scanning of infrainguinal bypass grafts. J Vasc Surg 1990; 12:284–90.

40. Nielsen TG, Djurhuus C, Pedersen EM, Laustsen J, Hasenkam JM, Schroeder TV. Arteriovenous fistulas aggravate the haemodynamic effect of vein bypass stenoses: an in vitro study. J Vasc Surg 1996; 24:1043–9.

41. Chang BB, Leopold PW, Kupinski AM, Kaufman JL, Leather RP, Shah DM. In situ bypass hemodynamics. J Cardiovasc Surg 1989; 30: 843–7.

42. Sniderman KW, Kalman PG, Shewchun J, Goldberg REA. Lowerextremity in situ saphenous vein grafts: angiographic interventions. Radiology 1989; 170:1023–7.


Intravascular ultrasound

17 EDWARD B.DIETHRICH

Introduction

Intravascular ultrasound (IVUS) has demonstrated success in both diagnostic andinterventional settings.1–7 The new American Heart Association classification of coronary atherosclerosis pathology can be evaluated using IVUS, and studies of atheromaregression and progression may also be performed.8 Serial IVUS studies have been used to examine the natural history of the restenosis process and to identify both adaptive andpathological remodelling.9 IVUS also allows quantitative measurement for calculation ofplaque volume.10

Diagnostic uses of IVUS in the coronary vessels also include visualization ofcompensatory coronary artery enlargement and assessment of intermediate lesions, andleft main stem disease and arteriosclerosis that is not visible with angiography.11 Optimal device selection may be aided by IVUS and significant increases in postproceduralluminal diameters attained.12, 13 Determination of pre-interventional plaque burden and postinterventional lumen dimensions with IVUS may be predictive of angiographic in-stent restenosis.14 In addition, the effects of angioplasty on vessel wall morphology may be studied using IVUS. IVUS imaging has also contributed substantially to theunderstanding of aortic dissection and pulmonary hypertension.11

IVUS has proved useful in the peripheral arteries as well. During renal artery stent placement, IVUS yields information that allows additional ballooning and lumenenlargement as compared to angiography.15 Comparison of IVUS and single-plane arteriography in the iliac arteries indicates that sensitivity and specificity are higher withIVUS than with arteriography in predicting haemodynamically significant stenoses, asdefined by duplex scanning.16 IVUS has also been used to determine the results ofdirectional atherectomy used in the treatment of femoropopliteal artery stenosis.

In endovascular stent-graft procedures, IVUS has proved to be a valuable adjunct formanagement of peripheral aneurysms, particularly when the initial procedure isunsatisfactory, or when intraprocedural angiographic studies are inconclusive.17 IVUS has also been used for intraoperative assessment of semiclosed thromboendarterectomy;material left behind after the procedure may be identified using IVUS and thenremoved.18

Although interest in IVUS is slowly increasing, disparity between the cost ofequipment and potential Medicare reimbursement creates financial disincentive to applythe technology. While IVUS technology has a number of routine uses in cardiology andendovascular surgery, at present it is used sparingly. It is certainly unfortunate that the

use of a valuable technique like IVUS has been limited by cost and technicaldevelopment problems because it remains a powerful tool with numerous applications indiagnosis and intervention. Hopefully, the introduction of new billing codes for IVUSprocedures will encourage its use. In this chapter, the role of IVUS in endovascularprocedures is examined, and the results of clinical study are reviewed.

The creation of IVUS images

Advancements in ultrasound technology have resulted in the ability to convert two-dimensional IVUS images into three-dimensional images (Figure 17.l).19 Serial images are stacked by the computer during a single ‘pull-through’ and reassembled into a three-dimensional reconstruction that allows the whole length of the artery to be displayed atone time. Images may be examined from any angle, slice, or rotation-an advance we have found particularly helpful in peripheral interventions.20

Three-dimensional IVUS images may be presented either as ‘longitudinal’ or ‘volume’ views (Figure 17.2). The former are immediately available in the operating room,

Figure 17.1 Example of three-dimensional images using a pull-through technique: (a) incompletely deployed iliac stent; (b) incompletely deployed Wallstent. This is a highly useful technique to assess arterial pathology and the results of endoluminal therapy.

enabling the physician to make rapid clinical decisions following a pull-through. Longitudinal views are similar in appearance to an angiogram and define vessel wallmorphology; rotation of these images also provides a lateral perspective. The creation ofvolume images takes several minutes but provides a three-dimensional cylindrical view of the vessel that can be turned over or revolved. Computer software allows hemisectionof the cylinder along its length for inspection of the luminal aspect of the artery.

The use of IVUS in angioplasty and stenting

Angioplasty and stenting have changed traditional vascular surgical proceduressubstantially, and successful use of these new endovascular techniques relies on adequateimaging capability. IVUS provides useful perspectives during angioplasty and stenting

Intravascular ultrasound 333

and can be used as an adjunct to more traditional imaging techniques.

Coronary arteries

In coronary interventions, IVUS allows optimal device selection and may guide stentexpansion such that significant increases in postprocedural luminal diameters areattained.12, 13 Volumetric IVUS analysis has been used to demonstrate that late lumen volume loss following directional coronary atherectomy is a result of a decrease in thevolume of the external elastic membrane.21 Increasing luminal diameter is thought tolimit restenosis over the long term,22 and determination of postinterventional lumen dimensions using IVUS may allow prediction of angiographic in-stent restenosis.14 Using IVUS to guide additional ballooning has the potential to optimize the stent lumen cross-sectional area and limit restenosis.23

IVUS technology has been somewhat limited by the size of the imaging catheter. The development of a 30 MHz ultrasonic imaging device with the same dimension as an0.01822 guide-wire is an advance that allows greater

Figure 17.2 Intravascular ultrasound images may be presented either in (a) longitudinal; or (b) volume views.

manoeuvrability and compatibility with balloon catheters without degradation of imagequality.24

Peripheral arteries

Although the manufacturers of IVUS equipment for use in the coronary system have beenrelatively responsive to the imaging needs of cardiologists,25 the development of ultrasound probes for use in the peripheral circulation has not been as rapid or successful.At present, the coronary configurations for the 0.014′′ and 0.018′′ wires are not appropriate for use in the peripheral arteries, where 0.035′′ wires are used routinely. Likewise, while a monorail system may be satisfactory in the coronaries or in someperipheral applications, an over-the-wire coaxial system is much more desirable for traversing tortuous arteries or passage across long distances, such as those encountered inthoracic and abdominal aortic investigations. Unfortunately, the corporate world does notyet appreciate these nuances, and the ideal IVUS catheter has not yet been developed forperipheral use.


Carotid artery

Carotid angioplasty and stenting are controversial alternatives to carotidendarterectomy.26 Indeed, there is heated debate about the appropriateness of carotid angioplasty and stenting, and it has become clear that some carotid lesions areconsiderably more amenable to endovascular treatment than others. IVUS has animportant role in distinguishing lesion morphology and in detecting inadequate stentdeployment27 that is not visible on the completion angiogram.

In the common carotid artery, disease is frequently pre-sent at the origin. Accurate location of the origin is difficult with angiography alone because the aortic arch oftencovers and masks it. The IVUS image demonstrates the origin precisely, and its site maythen be noted on fluoroscopy. IVUS may also be useful in detecting stenotic diseaseuntreated by the initial application of a stent.

In some lesions, the decision to deploy a carotid stent without preliminary angioplasty may be aided by information provided by IVUS imaging. In these cases, the IVUScatheter is carefully negotiated through the diseased artery to allow measurement of theminimum lumen diameter and an evaluation of the plaque morphology (Figure 17.3). Although this technique may provide useful images, colour flow Doppler ultrasound mayyield a similar assessment with less risk of embolization.28

Figure 17.3 Three-dimaasional reconstniction of an intravascular ultra-sound study in the carotid artery. An ulcer was identified that was probably responsible for the patient’s transient ischaemic attacks.

When IVUS is used for imaging following stent placement, a 3.5F, 30 MHz IVUScatheter is advanced into the cephalic internal carotid artery on a 0.018′′ guide-wire. The artery is usually free of disease at this level, and luminal diameters are measured. Thecatheter is pulled through the stent so that deployment may be assessed and the minimumstent diameter measured. The deployed stent should be uniformly expanded along itslength, and there should be no space between the stent and the artery wall. The IVUSoperator should confirm that the stent covers the lesion and that no proximal or distaldisease is left untreated. A careful examination for any intimal dissection should also bemade. In general, a minimum stent diameter of greater than 4 mm is desired in theinternal carotid artery.


Stenotic plaque is often heavily calcified in the carotid (Figure 17.4).27 Calcifications and fibrotic tissue resist complete stent expansion, and this is often seen on IVUS as mid-stent ‘waisting’ which usually responds to redilation with a larger balloon. In some cases, external fibrosis prevents complete, uniform expansion. IVUS may also demonstrateincomplete apposition of the stent to the artery wall. The internal carotid artery is oftenwider at its

Figure 17.4 Three-dimensional images identifying calcified plaque proximal to a carotid stent.

origin than it is distally, and even a stent that is uniformly expanded in the majority of thecarotid may not appose to the wider origin. IVUS images may detect such deficiencies instent expansion and indicate the need for additional ballooning.28

Subclavian and innominate arteries

Despite initial concerns over the potential for thromboembolic complications andrestenosis, angioplasty of subclavian artery stenosis has been in frequent use for a numberyears. More recently, stenting has been used successfully in this region to improveluminal diameter and restore flow in occluded arteries.

IVUS provides useful preliminary assessments of the subclavian and innominate arteries prior to stenting. Disease is most commonly found at the origins and is well-suited to treatment with angioplasty and stenting. In this setting, a 3.5F, 30 MHz IVUScatheter is guided from a brachial artery approach. The pull-through is used to measure the artery diameter and the length of disease, as well as to locate the vessel’s origin. The morphology of these lesions is usually soft, and stent expansion is generally satisfactoryafter the initial deployment. When disease is present in the second part of the subclavianartery, angioplasty and stenting may compromise a patent vertebral artery. The use ofIVUS here can define the proximity of disease to the vertebral artery origin.

Iliac artery

In the iliac arteries, IVUS is useful in determining the success of balloon angioplasty andmay indicate the need for stenting if intimal flap dissection or plaque recoil occur. Boththe Palmaz stent (Cordis, Warren, NJ, USA), and the Schneider Wallstent (Schneider,


Minneapolis, MN, USA) have US Food and Drug Administration (FDA) approval for theiliac arterial location. When applied in the larger-sized vessels with diameters of >6 mm, the results of stenting in these locations is excellent.29–32 Occasionally, IVUS demonstrates a clinically suspected lesion that is not demonstrable with angiography.Indeed, comparison of IVUS and single-plane arteriography in the iliac arteries indicates that sensitivity and specificity are higher with IVUS than with arteriography in predictinghaemodynamically significant stenoses, as defined by duplex scanning.18 IVUS is a valuable technique for assessing adequacy of arterial stent deployment and may improvethe long-term clinical outcome of balloon angio plasty and stenting in aorto-iliac lesions.33

Renal artery

In patients with severe renal failure, who cannot tolerate X-ray contrast dye, IVUS may be a valuable imaging alternative. We have used IVUS as a sole imaging tool to guidestent deployment in the renal artery. IVUS images have allowed us to make decisionsabout balloon and stent size and to confirm accurate placement in the renal artery. Ascompared to angiography, IVUS frequently yields information that allows additionalballooning and lumen enlargement during renal artery stent placement.15

The use of IVUS in atherectomy

Mechanical removal of plaque with atherectomy devices has been used alone and inconjunction with other revascularization strategies. The use of IVUS in atherectomyprocedures may provide important information about the effects of the procedure on thearterial wall and on residual plaque volume. IVUS also allows measurement of theluminal diameter and demonstrates residual plaque more accurately than angiography. Inaddition, the use of IVUS allows visualization of intimal flap dissection and may guideselection of the appropriate burr.7

As a result of information obtained via IVUS, directional atherectomy has been shownto stretch the arterial wall and to remove normal tissue.34, 35 The use of IVUS before and during directional atherectomy procedures may guide the clinician’s use of the cutting blade and allow optimal debulking. Indeed, IVUS may be quite useful in evaluating thevessel and preventing injury and perforation. In rotational atherectomy procedures, whereangiography has documented adequate results, evaluation with IVUS has revealedresidual plaque in cross-sectional areas of the vessel and allowed additional interventionin selected cases. Results of the GUIDE study (Guidance by Ultrasound Imaging forDecision Endpoints) indicate that IVUS frequently influences the decision to removemore tissue and treat additional vessel segments.36

The use of IVUS in endoluminal grafting

IVUS has proven to be a useful adjunct in endovascular stent-graft procedures for


management of peripheral aneurysms, particularly when the initial procedure isunsatisfactory, or when intraprocedural angiographic studies are inconclusive.17

Intraluminal resurfacing is an idea that dates back 30 years,37 but Parodi and colleagues38

were the first to introduce a Dacron tube graft-Palmaz stent device for aneurysm exclusion in clinical applications. Since the first clinical experience with endoluminalgrafts (ELGs), ELG devices and deployment techniques have been studied throughout theworld, with some encouraging results. Combining IVUS with information obtained fromangiography, magnetic resonance imaging (MRI), and computed tomography (CT)allows optimal sizing of devices and may help the operator choose optimal fixation sitesthat help prevent endoleaks and maintain luminal patency acutely and in the long term.39

Three-dimensional reconstruction is useful in assessing proper deployment of ELGs in the peripheral circulation (Figure 17.5).

Treatment of aortic aneurysms

Exclusion of abdominal aortic aneurysms using non-surgical, endoluminal technology has attracted worldwide attention. Initially, the procedure was designed for use in patientswith cardiac pathologies, pulmonary insufficiency, a hostile abdomen, or other conditionsthat heighten the risk of classical surgical intervention.36 The use of endoluminal techniques for exclusion of abdominal aortic aneurysms has now been proposed for usein patients without comorbid conditions and even in those with small, asymptomaticaneurysms.40 IVUS has also demonstrated value in identifying aortic injuries that are undetected by arteriography, and it allows assessment of precise measurements forendograft fabrication and deployment.41

In the aorta, a 6F, 12.5 MHz catheter is most suitable for the large vessel diameter. IVUS assists in accurate placement of devices so that encroachment of the subclavian,celiac, renal, or iliac arteries may be avoided. It is also vital that the diameters of the iliacarteries are measured at the narrowest point to ensure that the delivery system canadvance safely through the iliac artery. On more than one

Figure 17.5 Three-dimensional intravascular ultrasound of an endoluminal graft used to exclude a popliteal aneurysm.

occasion, we have elected not to proceed to endoluminal grafting because of iliac diseaseelucidated by IVUS.

In the imaging of abdominal aortic aneurysms, we have found IVUS particularly


helpful in the preoperative assessment (Figure 17.6). Under local anaesthetic and fluoroscopic control, the IVUS catheter is advanced from the groin to a level just abovethe renal arteries. A steady and continuous pull-through allows three-dimensional IVUS reconstruction. The proximal and distal necks of the aneurysm are measured, and theendoluminal length requiring grafting is calculated. The amount of calcification andmural clot are noted. An assessment of the shape of the proximal and distal necks oftengives an indication of how well an ELG will exclude the aneurysm. The proximal neck isusually circular, and the distal neck is often oval and calcified.

Treatment of lesions in the limbs

Although angioplasty and stenting of occlusive disease in the femoral and poplitealarteries may be quite successful acutely, long-term patency in these lesions is seldom areality. ELG placement in the femoral and popliteal arteries has been tried as analternative, but the results have been somewhat disappointing. Nevertheless, theseprocedures may be viable options for patients who are not candidates for surgicalintervention, and ELG treatment may become a standard for the treatment of poplitealaneurysms in those patients who have no other treatment options.

IVUS and arteriography have been compared as control procedures after femoropopliteal angioplasty. IVUS allowed identification of calcification, dissection orplaque rupture, and determination of residual stenosis less than 70%; these factors werepredictive of patency following angioplasty.42 Angiography was less sensitive than IVUS for detecting lesion eccentricity, calcification, and vascular damage in thefemoropopliteal artery.43

Figure 17.6 Preoperative assessment of an abdominal aortic aneurysm prior to exclusion with an endoluminal graft.

In endoluminal grafting of the femoropopliteal arteries, IVUS provides preoperative assessment of the artery and allows determination of the balloon size required to expandthe ELG. A long pull-through is usually necessary, and the IVUS operator must set the acquisition frame rate for three-dimensional reconstruction accordingly. Following ELG deployment, IVUS detects any minor abnormalities in the graft’s expansion. This expansion is normally caused by external atherosclerotic plaque; however, it is rarelynecessary to treat this condition.


Observations from clinical experience at the Arizona Heart Institute and Heart Hospital

Our experience at the Arizona Heart Institute and Heart Hospital indicates that IVUS isvery useful in preoperative assessment and measurement of the vessels. IVUS was alsoquite valuable in determining accurate placement of the ELG. Indeed, the use of IVUShas frequently revealed inaccurate stent deployment in patients in whom satisfactory stentdeployment was demonstrated on angiography (Figure 17.7 and 17.8). The most accurate predictor of restenosis after balloon angioplasty and stenting in the coronary arteries isthe minimum lumen diameter immediately after the procedure,22 and increasing luminal diameter may reduce the risk of acute arterial occlusion and long-term restenosis. Our observations indicate that minimum stent diameters may be increased by an average ofapproximately 20% in patients who undergo additional IVUS-guided ballooning.

In the carotid arteries, additional ballooning may improve in-stent diameter considerably. However, when IVUS does allow detection of incomplete deployment, thedecision whether to balloon again or place another stent must be weighed up carefully.The risks associated with overinstrumentation of the vessel include intimal dissection,spasm, thrombosis, or embolism.

We are hopeful that improvements in the design of IVUS catheters may allowdevelopment of devices that are easier to manoeuvre and less likely to disturb plaque inthe arterial wall. Coaxial configurations allow safer movement through diseased ortortuous vessels, and the Wise Wire (Boston Scientific, Watertown, MA, USA) containsan IVUS transducer that is introduced through the central channel of an angioplastyballoon catheter to guide realtime IVUS imaging during the intervention. The‘forwardlooking’ IVUS catheter is another innovation that allows accurate cannulation through total arterial occlusions and negotiation of tight stenoses.44 While the early forwardlooking IVUS catheters were mechanically complex and quite bulky, smaller 5Fand 8F catheters have been developed.45 The new Endodonics catheter has a 0.025′′coaxial configuration and does not require any complicated preparation before use. Ourrecent studies with the device have been encouraging.


Figure 17.7 (a) Initial three-dimensional intravascular ultrasound following endoluminal graft deployment to exclude an abdominal aortic aneurysm. The study shows poor apposition of the stent to the arterial wall. (b) Follow-up study after additional ballooning.


Figure 17.8 (a)Example of a two-dimensional intravascular ultrasound in which the stent in the abdominal aorta was incompletely deployed. (b) The angiogram did not detect this condition, but it was easily corrected by inflation with a larger diameter balloon.


Summary

The field of endovascular surgery is constantly changing as new techniques and devicesare adopted. The introduction of stent technology has been a very important breakthroughin the treatment of coronary and peripheral lesions, and the use of modern innovations inimaging techniques such as angioscopy and IVUS have helped to provide theinterventionist with indispensable information about lesion morphology and appropriatestent placement. The profusion of new endovascular devices available for percutaneousintervention is staggering, and successful use of new equipment relies heavily onadequate imaging capability using sophisticated techniques such as IVUS.

IVUS is an important adjunct to angiography and angioscopy, providing luminal dimensions (pre- and post procedure) and precise determination of arterial architecture and lesion pathology. In many cases, IVUS examination plays a significant role both indetermining the need for device placement and in assessing adequate deployment.Detection of incomplete stent deployment with IVUS may improve patient outcomes byallowing the clinician to increase luminal diameter. We have found IVUS indispensablein our endoluminal graft programme and hope that it will become a standard tool in avariety of endovascular procedures.

References

1. Gussenhoven EJ, van der Lugt A, Pasterkamp G et al. Intravascular ultrasound predictors of outcome after peripheral balloon angioplasty. Eur J Vasc Endovasc Surg 1995; 10:279–88.

2. Cavaye DM, Diethrich EB, Santiago OJ et al. Intravascular ultrasound imaging: an essential component of angioplasty assessment and vascular stent deployment. Int Angiol 1993; 12:212–20.

3. Katzen BT, Benenati JF, Becker GJ et al. Role of intravascular ultrasound in peripheral atherectomy and stent deployment [Abstract] Circulation 1991; 84:2152.

4. White RA, Scoccianti M, Back M et al Innovations in vascular imaging; arteriography, three-dimensional CT scans, and two- and threedimensional intravascular ultrasound evaluation of an abdominal aortic aneurysm. Ann Vasc Surg 1994; 8:285–9.

5. The SHK, Gussenhoven EJ, Zhong Y et al. Effect of balloon angioplasty on femoral artery evaluated with intravascular ultrasound imaging. Circulation 1992; 86:483–93.

6. Kopchock GE, White RA, Guthrie C et al. Intraluminal vascular ultrasound: preliminary report of dimensional and morphological accuracy. Ann Vasc Surg 1990; 4:291–6.

7. Scoccianti M, Verbin CS, Kopchock GE et al. Intravascular ultrasound guidance for peripheral vascular interventions. J Endovasc Surg 1994; 1:71–80.

8. Gotsman MS, Mosseri M, Rozenman Y, Admon D, Lotan C, Nassar H. Atherosclerosis studies by intracoronary ultrasound. Adv Exp Med Biol 1997; 430:197–212.

9. Mintz GS, Kent KM, Pichard AD, Popma JJ, Satler LF, Leon MB. Intravascular ultrasound insights into mechanisms of stenosis formation and restenosis. Cardiol Clin 1997; 15:17–29.


10. Bom N, Li W, van der Steen AF, Lancee CT, Cespedes EI, Slager CJ, de Korte CL. New developments in intravascular ultrasound imaging. Eur J Ultrasound 1998; 7:9–14.

11. Gorge G, Ge J, Baumgart D, von Birgelen C, Erbel R. In vivo tomographic assessment of the heart and blood vessels with intravascular ultrasound. Basic Res Cardiol 1998; 93:219–40.

12. Gorge G, Ge J, Erbel R. Role of intravascular ultrasound in the evaluation of mechanisms of coronary interventions and restenosis. Am J Cardiol 1998; 81(12A): 91G–95G.

13. Stone GW, Hodgson JM, St Goar FG et al. Improved procedural results of coronary angioplasty with intravascular ultrasound-guided balloon sizing: the CLOUT Pilot Trial. Circulation 1997; 95:2044–52.

14. Hoffmann R, Mintz GS, Mehran R et al. Intravascular ultrasound predictors of angiographic restenosis in lesions treated with Palmaz-Schatz stents. J Am Coll Cardiol 1998; 31:43–9.

15. Leertouwer TC, Gussenhoven EJ, van Overhagen H, Man in’t Veld AJ, van Jaarsveld BC. Stent placement for treatment of renal artery stenosis guided by intravascular ultrasound. J Vasc Interven Radiol 1998; 9:945–52.

16. Vogt KC, Rasmussen JG, Skovgaard LT, Just S, Schroeder TV. Quantification of iliac artery stenoses: a methodological comparative study between intravascular ultrasound, arteriography, and duplex scanning. Ultrasound Med Biol 1998; 24:963–70.

17. van Sambeek MR, Gussenhoven EJ, van Overhagen H et al. Intravascular ultrasound in endovascular stent-grafts for peripheral aneursyms: a clinical study. J Endovasc Surg 1998; 5(2): 106–12.

18. Vogt KC, Sillesen H, Schroeder TV. The use of intravascular ultrasound for intraoperative assessment during semiclosed thromboendarterectomy. Ultrasound Med Biol 1998; 24:21–5.

19. Rosenfield K, Losordo DW, Ramaswamy K et al. Three-dimensional reconstruction of human coronary and peripheral arteries from images recorded during two-dimensional intravascular ultrasound examination. Circulation 1991; 84:1938–56.

20. Reid DB, Douglas M, Diethrich EB. The clinical value of threedimensional intravascular ultrasound imaging. J Endovas Surg 1995; 2:356–64.

21. de Vrey EA, Mintz GS, von Birgelen C et al. Serial volumetric (three dimensional) intravascular ultrasound analysis of restenosis after directional coronary atherectomy. J Am Coll Cardiol 1998; 32: 1874–80.

22. Fischman DL, Leon MB, Bain DS et al. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med 1994; 331:496–501.

23. Kasaoka S, Tobis JM, Akiyama T et al. Angiographic and intravascular ultrasound predictors of in-stent restenosis. J Am Coll Cardiol 1998; 32:1630–35.

24. Hiro T, Hall P, Maiello L et al. Clinical feasibility of 0.018-inch intravascular ultrasound imaging device. Am J Heart 1998; 136: 1017–20.

25. Colombo A, Hall P, Nakamura S et al. Intracoronary stenting wihout anticoagulation accomplished with intravascular ultrasound guidance. Circulation 1995; 91:1676–88.

26. Diethrich EB, Ndiaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 1996; 3:42–62.

27. Reid DB, Diethrich EB, Marx P et al. Intravascular ultrasound assessment in carotid interventions. J Endovasc Surg 1996; 3:203–10.


28. Diethrich EB, Marx P, Wrasper R. Percutaneous techniques for endoluminal carotid interventions. J Endovasc Surg 1996; 3:182–202.

29. Nöldge G, Richter GM, Rören T et al. A randomized trial of iliac stenting versus PTA in iliac artery stenoses and occlusions: updated 6-year results. [Abstract]. J Endovasc Surg 1996; 3:99–100.

30. Murphy KD, Encarnacion CE, Le VA, Palmaz JC. Iliac artery stent placement with the Palmaz stent: follow-up study. J Vasc Intervent Radiol 1995; 6(3): 321–9.

31. Murphy TP, Webb MS, Lambiase RE et al. Percutaneous revascularization of complex iliac artery stenoses and occlusions with use of Wallstents: three-year experience. Vasc Intervent Radiol 1996; 7(1): 21–7.

32. Vorwerk D, Guenther RW, Schürmann K et al. Primary stent placement for chronic iliac artery occlusions: follow-up results in 103 patients. Radiology 1995; 194:745–9.

33. Arko F, Mettauer M, McCollough R et al. Use of intravascular ultrasound improves long-term clinical outcome in the endovascular management of atherosclerotic aortoiliac occlusive disease. J Vasc Surg 1998; 27:614–23.

34. Schnitt SJ, Safian RD, Kuntz RE, Schmidt DA, Baim DS. Histologic findings in specimens obtained by percutaneous directional coronary atherectomy. Hum Pathol 1992; 23:415–20.

35. Serruys PW, Umans VA, Strauss BH, van Suylen RJ, van den Brand M, Suryapranata H. Quantitative angiography after directional coronary atherectomy. Br Heart J 1991; 66:122–9.

36. The GUIDE Trial Investigators. Impact of intravascular ultrasound on device selection and end-point assessment of interventions: phase I of the GUIDE trial [abstract]. J Am Coll Cardiol 1993; 21:134A.

37. Dotter CT. Transluminally placed coil-spring endarterial tube grafts: long-term patency in canine popliteal artery. Invest Radiol 1969; 4: 329–32.


39. White RA, Donayre C, Kopchok G, Walot I, Wilson E, deVirgilio C. Intravascular ultrasound: the ultimate tool for abdominal aortic aneurysm assessment and endovascular graft delivery. J Endovasc Surg 1997; 4:45–55.

40. May J, White G, Yu W, Waugh R, Stephen MS, Harris J. Concurrent comparison of endoluminal repair versus no treatment for small abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 1997; 13: 472–6.

41. White R, Donayre C, Walot I, Kopchok GE, Wilson E, Klein S. Endograft repair of an aortic pseudoaneurysm following gunshot wound injury: impact of imaging on diagnosis and planning intervention. J Endovasc Surg 1997; 4:344–5.

42. Vogt KC, Just S, Rasmussen JG, Schroeder TV. Prediction of outcome after femoropopliteal balloon angioplasy by intravascular ultrasound. Eur J Vasc Endovasc Surg 1997; 13:563–8.

43. van Lankeren W, Gussenhoven EJ, Pieterman H, van Sambeek MR, van der Lugt A. Comparison of angiography and intravascular ultrasound before and after balloon angioplasty of the femoropopliteal artery. Cardiovasc Intervent Radiol 1998; 21:367–74.

44. Back MR, Kopchock GE, White RA et al. Forward looking intravascular ultrasonography: in-vitro imaging of normal and atherosclerotic human arteries. Am Surg 1994; 60:738–43.

45. Liang DH, Hu BS. A forward-viewing intravascular ultrasound catheter suitable for intracoronary use. Biomed Instrum Technol 1997; 31:45–53.


Subfascial endoscopic perforator vein surgery

18 A.D.K. HILL, D.BOUCHIER-HAYES AND A.L. LEAHY

Introduction

Leg ulcers caused by chronic venous insufficiency are a widespread, though oftenunderestimated problem. Approximately 0.5% of the populations of the USA and the UKhave chronic venous insufficiency,1 with an estimated loss of 2 million work days per year in the USA.2 At the turn of this century John Homans elegantly described thepathophysiological interactions of the deep, superficial and communicating venoussystems.3 Linton devised an operation to interrupt the incompetent perforating veins.4Although healing of venous ulcers after ligation of the perforating veins has beenreported, the original procedure as described by Linton is seldom performed today. Themain reasons for this technique being abandoned were frequent wound complications anda need for prolonged hospitalization because of the long skin incision necessary to ligatethe perforators. Other researchers have developed alternate procedures that use shorterskin incisions and avoid incisions in the area of stasis dermatitis and underlyinglipodermatosclerosis.5–7 Edwards8 recommended that a shearing instrument be passedblindly in the subfascial plane to interrupt the perforating veins.

Hauer9 introduced the endoscopic technique for division of perforating veins in 1985.His work was soon followed by other investigators in Europe,10–13 who used different types of endoscope to perform the surgery with direct vision through a single incisionmade in the proximal calf. The use of laparoscopic instruments was described byO’Donnell,14 who infused saline solution beneath the fascia to facilitate the visualization and dissection of the subfascial plane. In Australia, Conrad15 began using carbon dioxide insufflation in 1993 and published a report on his first seven patients in 1994- Using videoscopes, subfascial endoscopic perforator surgery (SEPS) has been shown to betechnically feasible, with minimal perioperative morbidity and shorter hospital stay.

Patient evaluation and selection

Patients should undergo non-invasive evaluation via colour duplex ultrasound imaging ofthe leg to document the presence of a patent deep system and to confirm incompetence ofthe perforating veins of the lower leg. The sites of the incompetent veins are marked onthe skin for reference at the time of surgery. If indicated, the superficial incompetentsystem is also marked on the skin for surgical stripping and ligation. Given the accuracyof duplex imaging, venography is not used. Venography is more invasive and less

informative in identifying incompetent perforators. Subfascial vein interruption is offered to patients with preulcerative

lipodermatosclerosis (pain, pigmentation), refractory ulcerative, and active ulcerativevenous disease states that do not respond to compression therapy.

Surgical instrumentation (Figure 18.1)

The majority of the instruments used in this procedure are currently used for laparoscopiccholecystectomy. Instrumentation includes an insufflator to introduce carbon dioxide tomaintain the working space, a rigid 5 mm or 10 mm endoscope, a three-chip video camera with xenon light source, and a monitor. The rigid endoscope is introduced into theworking space via a 10mm cannula, but a 5 mm cannula is used for all other equipment.

Several additional instruments are particularly important for the successful and expedient performance of the operation. One is the balloon dissector. Although dissectionof the subfascial plane can be accomplished manually via endoscopic instruments, theballoon dissector significantly

Figure 18.1 Instrumentation overview for endoscopic subfascial perforator interruption.

Subfascial endoscopic perforator vein surgery 347

expedites the dissection process and helps create a large unencumbered operativeworking space. A second useful instrument is a 5 mm roticulating grasper. Thecombination of tip articulation and rotation offers a high degree of manoeuvrability. The5 mm clip applier needs only a 5mm port. Its small size also affords greatermanoeuvrability and visibility when working in the tunnel-like confines of the endoscopic working space. The applier delivers an 8mm long (medium/large) clip in aconvenient multifire configuration.

Table 18.1 shows the suggested operating theatre set-up.

Surgical technique (Figure 18.2)

After the induction of general or epidural anaesthesia, the affected leg and the groin areprepared and draped in a sterile fashion. The operating table is placed in a 10-degree Tredelenburg position. The pneumatic tourniquet is placed on the proximal third of theleg and the leg is exsanguinated with an Esmarch bandage. The tourniquet is then inflated

Table 18.1 Suggested operating theatre set-up

● Vascular balloon dissector

● (2) 60cm3 syringes

● 300 cm3 saline solution

● Allis clamps

● Standard laparoscopic cart positioned at feet, including camera, light source, and CO2 insufflator

● 10 mm 0 degree and/or 30 degree laparoscope

● 5 mm trocar

● 5 mm endoscopic clip applier with medium/large clips

● 5 mm tight angle dissector

● 5 mm endoscopic scissors, graspers and dissectors

● Suction/irrigation


Figure 18.2 Leg position for subfascial endoscopic perforator surgery (SEPS). The lower leg is elevated parallel to the table using a padded strand at the ankle and a stack of towels behind the knee. A 10mm trocar is used for the endoscope, and a 5 mm port is placed 5 cm lateral and distal to accommodate the working instruments.

to 300 mmHg and is continuously monitored during surgery with a pressure gauge. Thetime of insufflation is also monitored.

Two 15 mm longitudinal incisions are made about 5 cm apart in the medial aspect of the calf 8–10 cm distal to the level of the tibial tuberosity. The first incision is placed 3cm below the medial edge of the tibia. This incision is carried through the subcutaneoustissue under direct vision. Any varicose vein identified in this area is excised; ifencountered the saphenous nerve is carefully preserved. With the assistance of smallretractors the subcutaneous fascia is exposed and incised.

Dissection may then be facilitated by the use of a balloon dissector. Although thistechnique is not used by all surgeons, it is described here. If used, the balloon dissector isthen introduced into the fascial incision and directed towards the medial malleolus(Figure 18.3). After removal of the peel-away balloon cover sheet, the dissection balloonis inflated with saline to a volume of 200–300cm3 (Figure 18.4). The balloon is constructed in such a way that the radial expansion occurs initially, followed by distalpropagation towards the malleolus. As the balloon everts distally, dissection by theballoon occurs along planes of least resistance; thus, the perforating veins are notdisrupted in the process. Once the dissection is accomplished, the balloon is deflated andremoved. CO2 at a pressure of 15 mmHg is then insufflated to create the working space.A straight length 10mm camera is inserted to visually confirm the operative field (Figure 18.5). Should the port be misplaced, emphysema in the subcutaneous tissue would beapparent, and the camera would visualize the subcutaneous fatty tissue.

After the camera is positioned properly, the second 10mm laparoscopic port is placedunder direct vision


Figure 18.3 Insertion of balloon dissector.

Figure 18.4 Inflation of balloon dissector with saline.

through the second skin incision. This port is inserted over a trocar introducer, which canbe visualized by the camera when it enters the subfascial space. The loose connectivetissue that bridges the space between the muscle and the fascia can be bluntly dissectedunder videoscopic control with forceps or a grasper. Perforating veins are easilyvisualized as larger structures bridging the gap between the muscle and the fascia.Because the leg was exsanguinated, the veins have a whitish appearance. Some perforatorveins are accompanied by fine nerves or small arteries, which are preserved unless theyprevent full exploration of the subfascial space. In these cases they are also divided orincluded in the clip. It is the author’s belief that the only veins that should actually bedivided are those identified pre-operatively on duplex scanning to be incompetent perforators. After the veins are isolated, a 10mm stapling device is used to clip the veinsin two areas, between which the vessel is divided with endoscopic scissors (Figure 18.6). Alternatively, bipolar diathermy can be used. Unipolar diathermy cannot be used as itcauses muscle contraction. Dissection proceeds medially down to the edge of the tibia,laterally to the posterior midline, and distally to the level of the ankle. The mostsignificant perforating veins are the Cockett perforators, which


Figure 18.5 Insertion of endoscope.

Figure 18.6 Division of perforating vein.

connect the posterior arch vein with the posterior tibial veins. Exploring the area close tothe tibia and, if necessary, incising the paratibial fascia, reveals whether the paratibialperforators, which were previously emphasized by Bergan can also be divided.Eventually, the entire area between the medial malleolus and the laparoscopic portinsertion site can be visualized, and all perforating veins can be interrupted. In theauthor’s view, directing the dissection using the marks of the perforators on the skin is important. This minimizes unnecessary dissection.

After the procedure is complete, the instruments and ports are removed and thetourniquet is released. In patients with incompetent greater or lesser saphenous veins,stripping is performed. The incision used for the first port can be used to introduce thestripper into the greater saphenous vein. Stab avulsion of the varicose tributaries is thenperformed in the usual fashion. At the completion of the procedure, the skin incisions thatwere used to insert the laparoscopic ports are closed with 2–0 sutures for the subcutaneous tissue and 4–0 sutures for the skin. The leg is wrapped with an elasticbandage. After surgery the legs are elevated to 30 degrees; ambulation to the bathroom ispermitted after 3 h. After overnight observation, patients are usually discharged within 24h of surgery. They are instructed to use elastic bandages for a period of 10 days to 2weeks and to use firm compression (30–40 mmHg) graduated elastic stockings afterwards. Patients with active open ulcers also are instructed in the proper care of theround.


Discussion

Chronic venous insufficiency afflicts 3–4% of our population, and 10% of these patients ultimately have venous ulceration.16 Incompetence of the perforating veins plays animportant role in venous hypertension, and in the development of stasis changes of theskin and subcutaneous tissue of the leg. Although physical examination can suggest thelocation of incompetent perforating veins in many patients, using the double tourniquettests or identifying fascial defects in the Linton line, imaging of incompetent perforatorsis required to confirm the diagnosis and to map their location. Duplex scanning is themost useful for this purpose.

Interruption of incompetent perforators has been demonstrated to be effective in healing ulcers and decreasing symptoms. Wilkinson and Maclaren6 reported excellent or good long-term results in 80% of patients treated with subfascial or subcutaneous ligationof perforating veins. With a modified Linton procedure, Cikrit et al.7 observed a complete healing in 81% of legs during a 4-year observation period; however, they also reported an 18% perioperative complication rate and a 22% ulcer rate. Woundcomplications of incisions performed in areas where the skin is significantly diseased arefrequent. The advantage of endoscopic techniques is not only that incisions can beperformed in an area remote from the diseased skin, but also that all perforating veinsfrom the insertion site of the port down to the level of the ankle can be interrupted.Duplex mapping greatly facilitates this.

The advantage of the single-port technique used by Hauer,9 is that it does not require an expensive set-up of laparoscopic equipment and video monitoring. The disadvantageis that a single port used both for visual control and instrumentation is quite restricted.The visual field of the surgeon in the subfascial plane is significantly smaller than intechniques in which insufflation is not used. Laparoscopic instruments and videoequipment are available in most hospitals and we feel that subfascial ligation ofincompetent veins using endoscopic equipment is justified.

In one large series, Jugenheimer and Junginger11 reported on subfascial division of perforators performed in 103 limbs with a single-port endoscope. Changes in most of thelimbs were limited to swelling or dermatitis. Of 17 legs that had ulcers, healing wasobserved in 16 of them. In a series of 10 patients reported by Couto and Baptista,10 two patients required direct ligation of perforators through separate small incisions after theveins were identified through a rigid scope.

Treatment of incompetent perforating veins using minimally invasive techniques provides a significant advance in the management of these difficult patients. Division ofincompetent perforating veins using the Linton and Cockett subfascial ligation techniques has been reserved for patients with intractable diseases, because both these openprocedures carry considerable morbidity. By approaching the veins subfascially fromremotely placed ports, morbidity from both complications is more or less eliminated.

Refinements in port placement and technique have reduced the operative time of thisprocedure. It has also been reported that balloon dissection may also reduce operativetime by quickly creating a large operative working space which, when expanded withgas, facilitates rapid identification and exposure of the perforating veins. How’ ever, this


adds to the cost of the procedure.

Conclusion

Endoscopic subfascial division of the perforating veins appears to be a useful and safeprocedure. It should be studied in a multicentre, prospective, randomized trial to assess itsbenefit compared with best medical management for patients with severe forms oflipodermatosclerosis or healed or active venous stasis ulcers.

References

1. Boyd AM, Jepson RP, Ratcliffe RH, Rose SS. The logical management of chronic venous ulcers of the leg. Angiology 1952; 3:207–15.

2. Browse NL, Burnand KG. The postphlebitic syndrome: a new look. In: JJ Bergan, JST Yao (eds). Venous problems. Chicago: Year Book Medical Publishers, 1978, 395–406.

3. Homans J. The etiology and treatment of varicose ulcer of the leg. Surg Gynecol Obstet 1917; 24:300–11.

4. Linton R. The communicating veins of the lower leg and the operative technique for their ligation. Ann Surg 1938; 107: 582–93.

5. De Palma RG. Surgical therapy for venous stasis. Surgery 1974; 76: 910–7. 6. Wilkinson GE, Maclaren IF. Long term review of procedures for venous perforator

insufficiency. Surg Gynecol Obstet 1986; 163: 117–20. 7. Cikrit DF, Nichols WK, Silver D. Surgical management of refractory venous stasis

ulceration. J Vasc Surg 1988; 7:473–8. 8. Edwards JM. Shearing operation for incompetent perforating vein. Br J Surg 1976;

63:885–6. 9. Hauer G. The endoscopic subfascial division of the perforating veins - preliminary

report [in German]. VASA 1985; 14:59–61. 10. Couto JS, Baptista AL. Endoscopic ligation of perforator leg veins. Lancet 1991;

337:1480. 11. Jugenheimer M, Junginger T. Endoscopic fascial sectioning of incompetent

perforating veins in treatment of primary varicosis. World J Surg 1992; 16:971–5. 12. Wittens CHA, Pierik RGJ, van Urk H. The surgical treatment of incompetent

perforating veins. Eur J Vasc Endovasc Surg 1995; 9: 19–23. 13. Pierik EGJM, Wittens CHA, van Urk H. Subfascial endoscopic ligation in the

treatment of incompetent perforating veins. Eur J Vasc Endovasc Surg 1995; 9:38–41. 14. O’Donnell TF. Surgical treatment of incompetent communicating veins. In: JJ

Bergan, RL Kistner (eds) Atlas of venous surgery. Philadelphia, PA: WB Saunders, 1992:111–24.

15. Conrad P. Endoscopic exploration of the subfascial space of the lower leg with perforator vein interruption using laparoscopic equipment: a preliminary report. Phlebology 1994; 9:154–7.

16. Shami SK, Shields DA, Scurr JH, Smith PDC. Leg ulceration in venous disease. Postgrad Med J 1992; 68:779–85.


Endoscopic venous valve surgery

19 J.M. SCRIVEN AND N.J.M. LONDON

Introduction

With the advent of non-invasive duplex scanning it has become apparent that deepvenous reflux as the sole cause of chronic venous insufficiency (CVI) and ulceration isless common than originally thought.1 However, significant deep venous incompetence remains an important factor in approximately one-third of ulcerated limbs. Subfascial endoscopic perforating vein surgery (SEPS) has been proposed as a method of removingdeep to superficial venous communications in the calf, which are thought by some to beimportant in the development of CVI and venous ulceration.2 Also, superficial venous surgery has a useful role to play in limbs with normal deep veins.3 However, neither SEPS nor superficial venous surgery have been demon-strated to influence extensive deep venous reflux, especially if this is post-thrombotic in nature.

With the appropriate application of superficial venous surgery or multilayercompression bandaging, many ulcerated limbs can be successfully healed. However, anumber of limbs remain unhealed despite what can be considered to be ‘best current practice’. The ulcerated limbs of many of these patients exhibit extensive deep venousreflux, often involving the full length of the deep venous system, and have either normalsuperficial veins, or, more commonly, these patients have already undergone extensivesuperficial and perforating vein surgery in previous attempts to heal their ulcers. Thismay have resulted in an ulcerated limb possessing marked venous hypertension with deepvenous reflux as the cause. With this in mind, it is necessary to address ways ofcorrecting deep venous incompetence as a therapeutic manoeuvre for those patients withrecalcitrant venous ulceration caused by ‘full length’ deep venous reflux. A number of open operative procedures are described to repair or replace incompetent venous valvesand more recently, following advances in endovascular technology, reports are appearingin the literature describing endovascular procedures that have restored venouscompetence. This chapter outlines the open procedures available, reviews the reportsdescribing endovascular surgery of venous valves, and describes the clinical applicationof an endovenous valve transplant in our unit (Department of Vascular Surgery, LeicesterRoyal Infirmary).

Open deep venous valve surgery

In 1968, Kistner described a technique of venous valve repair in human limbs4 with

successful correction of deep venous reflux. Prior to this, only a small number of caninemodels of venous valve surgery had been reported.5

Failure of the deep venous valves may occur as a primary phenomenon, in which valvular incompetence results from dilatation of the valve annulus associated withotherwise normal valve cusps, or secondary to venous thrombosis, in which the valvecusps are destroyed or scarred such that apposition is no longer possible. Primary valvefailure can be corrected by plication valvuloplasty6–9 a procedure in which valve leaflets are tightened by ‘reefing’ the valve leaflet commissures; this can be aided by angioscopicvisualization of the valve leaflets.10 An alternative is external band valvuloplasty, in which a prosthetic cuff is placed around the valve annulus, reducing the circumferenceand hence aiding valve apposition.11,12

Post-thrombotic valve failure, where no repairable venous valves are present, requires the introduction of a competent valve by way of venous transposition;13, 14 autogenous valve transplantation15 or prosthetic valve surgery.16

All these open procedures are hampered by variable clinical outcomes. Johnson andcolleagues (1981)17 described an 18-month follow-up of 10 patients (twelve post-thrombotic limbs) that had undergone transposition of a competent segment of vein (longsaphenous or profunda vein) into the femoral vein at the groin. They found that although11 of the 12 limbs demonstrated normalization of venous filling times immediately aftersurgery, nine of these limbs had deteriorated to the presurgery level at the 12 or 18months follow-up visit. The authors concluded from this that femoral venous valve reconstruction was inadequate without associated superficial venous surgery, which wasomitted in their 10 patients.

Similar haemodynamic changes were described in a series of canine experimental venous transplantations complicated by thrombosis and subsequent recanalization, thusresulting in long-term patency but incompetence of the transplanted segments.18 A thorough review of venous valve surgery (transposition and valvuloplasty), over aminimum 4-year follow-up period, described similar poor clinical outcomes in limbsundergoing valve transposition/transplantation because of post-thrombotic damage19

(only 43% of limbs in this study demonstrated a good result). This same paper reportsgood clinical outcomes for limbs undergoing valvuloplasty for primary deep venousreflux in 73% of limbs operated on, the implication being that deep venous valve surgeryin post-thrombotic limbs is less successful than that performed in limbs with primaryvalve failure.

The reasons for transplanted valve failure are likely to be multifactorial, relating to the operative procedure, valve segment used and the general thrombogenicity of therecipient. Previous episodes of deep vein thrombosis can result in scarred veins andperivenous tissues making the surgery lengthy and complicated by local swelling, both ofwhich contribute to further deep vein thrombosis.20 The segment of vein undergoing transplantation receives a certain degree of handling and manipulation, resulting inevolving endothelial damage (20 min to 28 days following surgery), culminating in cellloss and exposure of the basement membrane.21 Whether these changes are mechanical or ischaemic remains unclear, but either way the result is increased thrombogenicity of thetransplanted segment. Since vein transplantation is used in post-thrombotic limbs, there is already a predisposition towards further deep vein/graft thrombosis, possibly because of


an underlying thrombophilia in combination with some element of mechanical venousoutflow obstruction from previous episodes of thrombosis.

Despite these shortcomings, encouraging results have been reported in axillary veintransplants to the popliteal vein in post-thrombotic limbs22 with eight out of 10 patients reporting maintenance of ulcer healing 2 years following surgery.

Endovascular venous transplantation

The development of endovascular technology detailed in the preceding chapters haspermitted the manipulation of various devices within the vascular tree distant from thesite of vascular access. Open surgery and thus dissection at the site of valve failure wherethe post-thrombotic perivascular tissues are scarred and fibrotic could be minimized ifsuch technology were applied to venous reflux disease. To date, three reports haveappeared in the literature describing the placement of intraluminal autogenous vein/stentdevices, initially in animal models using goats23 and dogs,24 and also in post-thrombotic human limbs.25 These reports outline the feasibility of the technique using both balloon and self-expanding metallic stent devices and have suggested that the intraluminallocation of the valve/stent device may prevent the late valve dilatation and incompetencereported in open valve transplantation. In addition, this approach avoids extensivedissection and theoretically may thus reduce the risks of thrombosis of the transplantedsegment of vein.

Dalsing and colleagues24 constructed a dog model (five animals) using a length ofexternal jugular vein containing a competent valve. This length of vein was placed withina self-expanding Z-stent such that the vein protruded beyond the ends of the stent. Theseoverhanging ends of vein were wrapped over the stent struts and sutured, such that nopart of the stent was exposed to the lumen after deployment. The complete device wasdeployed within the external iliac vein of the same dog. Venographic patency wasdetermined at 3–7 days and histological examination of the stent and vein device performed between 1 and 4 weeks after deployment. Sadly only two devicesdemonstrated early patency, and by 4 weeks only one valve remained patent. Ofenlochand colleagues23 also used selfexpanding stents (‘Wallstent’), containing a segment of competent external jugular vein in a goat model of endovenous valve repair, with successin five of six animals at 6 weeks. In this device, the stent protruded beyond the end of thetransplanted vein segment and the entire device was loaded into a sheath and deployed inthe contralateral external jugular vein of the same goat. After 1 week (five subjects), alltransplanted segments were patent and competent using the manual strip test; however,angioscopy demonstrated thrombus attached to the exposed stent struts at the downstreamend of the device. This would suggest that all of the stent metalwork should be coveredand kept out of contact with the venous blood, although in these cases the exposed lengths of stent were fully covered by endothelium. At 6 weeks, all devices remainedpatent, but only five were found to be competent. The one incompetent valve was scarredand trabeculated, suggesting that the patency was due to recanalization of an earlierthrombosis.

In 1996, Richer de Forge25 presented some early work on the first human studies of

Endoscopic venous valve surgery 357

endovenous valve repair to the International Society for Endovascular Surgery. To date,only an abstract of this work is available for study. Two balloon expandable stents wereattached to each end of a segment of axillary vein containing a competent valve. Thisdevice was passed into the superficial femoral vein (SFV) via the exposedsaphenofemoral junction (SFJ) rendering the SFV competent. Unfortunately, no dataregarding patient selection or follow-up patency are given.

The design of an endovenous device for the correction of popliteal vein reflux

Encouraged by the above reports23–25 the bio-prosthetic valve/stent device describedbelow was developed and employed for the correction of deep venous reflux. Theunderlying principle was the endovascular placement and anchorage of a competentvenous valve in the proximal popliteal/distal SFV to reconstitute a functional‘gatekeeper’ mechanism. It was proposed that placing the transplant segment inside thenative vein might prevent dilatation of the valve in the long term and that deploy

Figure 19.1 The valve stent device inside the recipient segment of vein. Note that the ends of the donor vein are wrapped over the stent, excluding all metalwork for the circulation once deployed. The orientation of the valve is distal (left), proximal (right).

ment by the endovascular route would remove the need for extensive soft-tissue dissection and thus be less thrombogenic.

Preliminary work using fresh cadaveric saphenous (donor segment) and SFV (recipient) demonstrated the feasibility of constructing such a device. Two balloonexpandable metal stents were sutured over the top of the donor vein segment, with theends of the vein overhanging the stent allowing complete coverage of the metal struts(Figure 19.1). The entire device (seven examples) was mounted over an angioplastyballoon catheter and advanced into the recipient segment of vein (SFV) where the stentswere deployed, anchoring the valved vein segment. Pressure studies confirmed thepatency and competency of the device after deployment and the ability of thetransplanted valve/stent device to withstand supraphysiological hydrostatic pressuresacross the valve (Figure 19.2). Encouraged by these findings and reports of animal andearly human work, the next section describes the first use of this device in a humansubject.


Figure 19.2 Histogram demonstrating the burst pressure for the seven devices constructed. Note that two devices exceed a burst pressure of 300mmHg and all devices exceed the important pressure of 100 mmHg encountered in the ambulant lower limb.

The axillary vein was chosen as the donor vein because minimal disability would ensue from removal of a segment of this vein.26, 27 In addition, the diameter of the axillary vein approximates to that of the popliteal vein into which it would be transplanted. This isimportant to prevent the introduction of any stenosis (and possible obstructive effects)into an otherwise patent but refluxing lower limb venous system. The use of balloonexpandable stents was felt to be appropriate, because they are available in suitabledimensions and previous experience using such stents within our institution ensuredaccurate and reliable deployment.

The clinical application of an endovenous stent device for the correction of popliteal vein reflux

At the time this work began at the Leicester Royal Infirmary, no account of endovenousvalve transplantation had been reported. It was felt that the first patient to receive anendovenous valve transplant would undergo such a procedure as a final therapeuticoption to achieve ulcer healing. The degree of ulceration in the patient chosen was ofsuch a degree that the only alternative was amputation. Although this posed a ‘challenge’ for our first case, we felt it unethical to attempt such novel surgery in a patient withanything less than ‘end-stage venous disease’.

Patient

A 57-year-old female with intermittent venous ulceration of her right leg for ten years


and a continuous ulcer for two years at presentation was selected. Twenty-six years previously she had undergone right-sided high ligation, stripping of the long saphenous vein to the calf and avulsion of calf varicosities for varicose veins. Three years followingthis she sustained a right leg deep vein thrombosis treated with warfarin for 6 weeks. Shewas a non-smoker and was not diabetic. The ankle brachial pressure index in the ulcerated leg was 1.0 and initial venous investigation by colour duplex scanning andfunctional venography demonstrated deep venous reflux without obstruction involvingthe common femoral vein down to the calf veins at the ankle. In addition, there wasrecurrent long saphenous reflux from an SFJ to the calf, with reflux in six-calf perforating veins. These abnormalities were treated by recurrent SFJ disconnection and calf-perforating vein surgery via a ‘mini’ Cocketts’ incision. At the time of functionalvenography, three perforating veins were successfully embolized with metal coils,rendering them thrombosed and thus non-refluxing. Thereafter, despite a period of hospital inpatient bed rest, the ulcer deteriorated from an initial area of 105 cm2 to 256 cm2. Further laboratory investigations demonstrated the following blood results:haemoglobin 11.6 g/dl, glucose 4.9 mM, albumin 40 g/l, urea 4.8 mmol/l and creatinine92 µmol/l, thus excluding any major systemic abnormality. A full thrombophilia screen,including examination of antithrombin III, protein S and protein C, was normal.

Pre-operative imaging and assessment

Prior to endovenous stenting, further duplex and venographic studies clarified the venousanatomy, demonstrating numerous axillary and subclavian vein valves within suitablelengths of vein (Figure 19.3). The right axillary vein proximal and distal to a suitablevalve had diameters of 8.0mm and 7.5 mm, respectively. Dimensions of the rightpopliteal vein were examined with the limb dependent at rest and on performing aValsalva manoeuvre to assess any degree of dilatation with raised venous pressure (Table 19.1). Lower limb venography demonstrated no further superficial venous reflux, deepvenous reflux along the full length of the common femoral vein (CFV) into the distalcrural veins and no obvious venous valves precluding any attempt at valve repair (Figure 19.4). Duplex examination of the left leg demonstrated no suitable venous valves to usefor the transplant.

Table 19.1 The diameter (mm) of the right popliteal vein in the dependent limb at rest and performing a Valsalva manoeuvre, as assessed by colour duplex scanning

Segment of popliteal vein examined

Diameter dependent at rest (mm)

Diameter dependent with Valsalva (mm)

Above knee 10.4 11.3

Level of knee joint line 6.2 6.2

Below knee 8.2 8.6


Figure 19.3 An upper limb venogram demonstrating a bifid proximal brachial and single axillary vein with valve sinuses full of contrast medium.

The above findings dictated the use of 9 mm balloon expandable stents to be deployedusing 5 mm balloons to stabilize each stent in position separately, followed by fulldeployment with 10mm balloons.

The operative procedure and result

Full informed consent and local ethical committee approval were obtained. Under generalanaesthesia the patient was positioned supine with the right arm abducted to 90 degrees atthe shoulder on a supporting arm board. Skin preparation and drapes exposed the rightleg (ulcerated distal part enclosed in drapes) and right arm and shoulder. A longitudinalincision was made in the right axilla, exposing the axillary and proximal brachial veins.The external diameter of the exposed axillary vein was measured at 10mm. A suitablevalve was identified using the ‘strip test’ to demonstrate unidirectional flow, and this valve was excised with 3 cm of axillary vein on each side of the valve ring (Figure 19.5). The divided ends were ligated and the


Figure 19.4 A lower leg venogram demonstrating valveless refluxing superficial femoral vein, popliteal and crural veins.


Figure 19.5 An operative photograph of the segment of axillary vein used for the transplant. Unequal marking sutures identify proximal/distal orientation of the valve. Tributaries are ligated with silk.

wound closed over a single vacuum ‘Redivac’ drain. Synchronous exposure and control of the common femoral vein below the entry of the profunda vein and construction of thevein stent device followed. The endovenous device was constructed on the shaft of a5mm diameter balloon (Figures 19.6 and 19.7). After the intravenous administration of5000 units of heparin, a transverse venotomy was created in the CFV and a guide-wire passed through the popliteal vein to the below-knee venous confluence, under X-ray screening, The endovenous device, premounted and crimped by the ‘distal’ stent onto the balloon catheter was passed over the guide-wire and ‘screened’ to a suitable site. This ensured that the device would not be deformed on knee flexion. Initial stabilization of thedistal stent, was obtained using the 5mm balloon on which the device had beenconstructed. The wire was then withdrawn a short distance under screening and relocatedunder the proximal stent, which was similarly stabilized. This part of the procedure wasperformed maintaining some degree of tension in the device to prevent any folding orrotation of the device during deployment, as this would probably render the valvemechanism ineffective. This balloon was replaced by a 10 mm diameter balloon and thestents fully deployed (Figure 19.8). A completion venogram performed before removal of the catheter and guide-wire demonstrated the patency and competence of the device. Thevenotomy and wound were closed over a ‘Redivac’ drain. A colour duplex scan on completion of the procedure with the legs dependent demonstrated a patent and fullycompetent venous valve. The patient was fully anticoagulated


Figure 19.6 An operative photograph demonstrating the passage of the guide-wire across the valve.

Figure 19.7 An operative photograph demonstrating the method of sutur-ing the vein segment onto the two stents. Note the partially inflated angioplasty balloon and the eversion of the vein ends over the stents struts excluding these from the circulation once deployed.

with intravenous heparin, initially at 1000 units per h and subsequently warfarinized to aninternational normalized ratio (INR) of 2 to 3. At 7 days postoperatively, a colour duplexscan confirmed the patency and competence of the device. Duplex scanning on day 13after surgery found that the device had occluded and from then on a conservative


Figure 19.8 A screening X-ray demonstrating the final position of the device in the popliteal vein. The shoulders of the angioplasty balloon are identified by the radio-opaque markers on either side of the distal stent.

course of compression therapy was followed, with a good response for the following 4months. Thereafter, the ulcer enlarged and a below-knee amputation had to be performed.

Discussion

This first experience with such a bioprosthetic device and endovenous approach todeployment of such a device has demonstrated the feasibility of this technique. Theprocedure successfully deployed a competent autogenous venous valve into the poplitealvein, abolishing deep venous reflux. The device only remained patient for two weeks, butduring this time the patient described significant subjective symptomatic relief, with lesspain.

This early experience with endovenous stent devices is encouraging; however, the reasons for device occlusion remain unclear. The patient was systemically anticoagulatedand duplex examination demonstrated marked ‘hyperaemic flow’ in the deep veins, most probably because of the large inflamed ulcer. With these factors in mind, mechanicalocclusion followed by thrombosis or native venous endothelial damage are the mostlikely events to have precipitated thrombotic occlusion. Others have reported valvepatency in goats at 6 weeks after transplantation.23

This patient was chosen to be the first subject because of the degree of ulceration, such


that an amputation may have been the only alternative form of symptom control availableto us. It is possible that had a patient with a nonthrombotic history (despite a negativethrombophilia screen) been used, then the end result may have been an intact and healedleg. It is possible that the choice of a patient with ‘end-stage venous disease’ introduced a degree of bias away from ultimate success and healing, as it is possible that such adamaged limb would not have healed with any form of treatment.

Conclusion

This chapter has suggested a novel technique for restoring popliteal vein competency.This work remains in its infancy but is supported by two animal studies demonstratingfeasibility. The only other experience in humans we are aware of has not appeared in thepeer-reviewed literature and our work represents only a single case report. This work encourages further such procedures within the confines of a research programme andalthough the results are encouraging, the technique cannot yet be recommended forroutine use in clinical practice. A significant number of questions remain to be answered.In particular, the reasons for thrombosis and the response of the venous endothelium toauto transplantation need to be understood.

References

1. Scriven JM, Hartshorne T, Thrush AJ, Bell PRF, Naylor AR, London NJM. A single visit venous ulcer assessment clinic: the first year. Br J Surg 1997; 84:334–6.

2. Gloviczki P, Cambria RA, Rhee RY, Canton LG, McKusick MA. Surgical technique and preliminary results of endoscopic subfascial division of perforating veins. J Vasc Surg 1996; 23: 517–23.

3. Scriven JM, Hartshorne T, Thrush AJ, Bell PRF, Naylor AR, London NJM. The role of saphenous vein surgery in the treatment of venous ulceration. Br J Surg 1998; 85:781–4.

4. Kistner RL. Surgical repair of a venous valve. Straub Clin Proc 1968; 34:41–3. 5. Wilson NM, Rutt DL, Browse NL. Repair and replacement of deep vein valves in the

treatment of venous insufficiency. Br J Surg 1991; 78:388–94. 6. Kistner RL. Surgical repair of the incompetent femoral vein valve. Arch Surg 1975;

110:1336–42. 7. Kistner RL. Primary venous valve incompetence of the leg. Am J Surg 1980; 140:218–

24. 8 Raju S. Venous insufficiency of the lower limb and stasis ulceration. Changing

concepts and management. Ann Surg 1983; 197: 688–97. 9. Jones JW, Elliot F, Kerstein MD. Triangular venous valvuloplasty: a new procedure

for correction of venous incompetence. Arch Surg 1982; 117:1250–1. 10. Welch HJ, McLaughlin RL, O’Donnell TF, Jr. Femoral vein valvuloplasty:

intraoperative angioscopic evaluation and hemodynamic improvement. J Vasc Surg 1992; 16:694–700.

11. Hallberg D. A method for repairing incompetent valves in deep veins. Acta Chir Scand 1972; 138:143–5.


12. Guarnera G, Furgiuele S, Camilli S. The role of external banding valvuloplasty with the Venocuff in the treatment of primary deep venous insufficiency. Phlebology 1994; 9:150–3.

13. Kistner RL, Sparkuhl MD. Surgery in acute and chronic venous disease. Surgery 1979; 85:31–40.

14. Ferris EB, Kistner RL. Femoral vein reconstruction in the management of chronic venous insufficiency. Arch Surg 1982; 117: 1571–9.

15. Taheri SA, Lazar L, Elias SM. Vein valve transplant. Surgery 1982; 91:28–33. 16. Taheri SA, Schultz RO. Experimental prosthetic vein valve longterm results.

Angiology 1995; 46:299–303. 17. Johnson ND, Queral LA, Flinn WR, Yao JST, Bergan JJ. Late objective assessment

of venous valve surgery. Arch Surg 1981; 116: 1461–6. 18. De Weese JA, Niguidula F. The replacement of short segments of veins with

functional autogenous venous grafts. Surg Gynecol Obstet 1960; 110:303–8. 19. Masuda EM, Kistner RL. Long-term results of venous valve reconstruction: a four- to

twenty-one-year follow-up. J Vasc Surg 1994; 19: 391–403. 20. Kistner RL, Eklof B, Masuda EM. Deep venous valve reconstruction. Cardiovasc

Surg 1995; 3:129–40. 21. Raju S, Perry JT. The response of venous valvular endothelium to autotransplantation

and in vitro preservation. Surgery 1983; 94:770–5. 22. O’Donnell TF, Mackey WC, Shepard AD, Callow AD. Clinical, haemodynamic, and

anatomic follow-up of direct venous reconstruction. Arch Surg 1987; 122:474–82. 23. Ofenloch JC, Chen C, Hughes JD, Lumsden AB. Endoscopic venous valve

transplantation with a valve-stent device. Ann Vasc Surg 1997; 11:62–7. 24. Dalsing MC, Sawchuk AP, Lalka SG, Cikrit DF. An early experience with

endovascular venous valve transplantation. J Vasc Surg 1996; 24:903–5. 25. Richer de Forges M, Lermusiaux P, Artru B. Minimal invasive endovenous

transplantation of valved venous segment for postthrombotic femoro popliteal reflux [abstract]. Int Soc Endovasc Surg 1996.

26. Raju S. Axillary Vein Transfer for postphlebitic syndrome. In: JJ Bergan, RL Kistner (eds). Atlas of venous surgery. Philadelphia, PA: WB Saunders, 1992, 147–152.

27. Raju S, Neglen P, Doolittle J, Meydrech EF. Axillary vein transfer in trabeculated postthrombotic veins. J Vasc Surg 1999; 29: 1050–64.


Minimally invasive varicose vein surgery: transilluminated powered phlebectomy

20 GREGORY A.SPITZ

Introduction

Outpatient varicose vein surgery seeks to remove the sources of venous hypertension andthe superficial venous abnormalities produced by such abnormal forces. Removal ofvaricosities, now called ambulatory phlebectomy, has been widely used in the treatmentof varicose veins for many years. One of the earliest descriptions of the procedure was byCelsus (56 BC-30 AD). He described how ‘blunt hooks are passed under the vein to hookit. [The veins are] pulled out with the hook and avulsed.’ Before Celsus, a Roman counsel endured the first recorded varicose vein procedure in 86 BC. He ‘endured most excessive torments in the cutting, never either flinching or complaining; but when the surgeon wentto the other leg, he declined to have it done, saying “I see the cure is not worth the pain"'1

Nothing has changed substantially with hook phlebectomy since ancient times.Anaesthesia and antisepsis have been added. However, the key to success of present-day varicose vein operations is that the operation becomes min’ imally invasive, gives good cosmetic results, provides relief of vein pain and leg fatigue, and can be done in anoutpatient setting. Although there has been a trend towards minimal incisions, shorteroperative and anaesthetic times, and outpatient surgery, the operations are still fraughtwith multiple incisions required to remove friable and easily fragmented vein segments.The operations are essentially blind, with no confirmation of total removal of varicoseclusters. In some hands the procedures have proved to be tedious, and impossible toperform in limbs with chronic venous insufficiency and even early lipodermatosclerosis.The operations are particularly difficult in limbs subjected to liposuction or thoseexperiencing previous superficial thrombophlebitis.

Preoperative evaluation

General medical history and physical examination should be obtained in all cases, withspecific attention given to venous insufficiency symptoms, previous treatment, andprevious complications of chronic venous insufficiency. Duplex examination should bedone and a treatment plan formulated for each limb. This plan should take intoconsideration the incompetence or absence of incompetence of the greater saphenousvein and location of varicose vein clusters in relation to named perforating veins.

Each patient undergoes an ultrasound duplex examination using reflux diagnostic

techniques. Records are made of reflux at the saphenofemoral junction above the kneeand below the knee, saphenopopliteal junction, the lesser saphenous vein, andgastrocnemius veins. The deep venous system is studied through the common femoralvein and superficial femoral vein, popliteal vein, and posterior tibial vein. Perforatingveins are searched for in limbs with chronic venous insufficiency. The patient’s varicose vein pattern is marked immediately before surgery using an indelible marker with a nylontip. The marking of the veins should simply be an outline of the affected areas thatrequire resection. If the marks cover the veins themselves it may obscure visualizationduring transillumination.

Technique

Operation is performed under general, spinal or epidural anaesthesia. We prefer a light‘fast track’ anaesthesia using a laryngeal mask airway (LMA) utilizing propofol and a short-acting narcotic. Tumescent anaesthesia is obtained by infusions of 1000 ml of 0.9%normal saline with 40 ml of 2% lidocaine and 1 ml of 1:1000 epinephrine added.Tumescent anaesthesia is obtained using an infusion pump with a minimal pressure of600–700 mmHg and is directed utilizing the tumescent cannula illuminator (TCI) to visualize the varicose vein clusters. Transillumination is also obtained with the TCI froma 300 watt xenon light source, specifically designed for this purpose (see Figures20.1 and 20.2). The bevel is aimed upwards to transilluminate the subcutaneous tissue andhighlight the venous clusters. The vein resector is a powered morcellator with suctionapplied to it. Blades within the resector are engineered with a tube within a tube design,purpose-built for varicose veins. Irrigation between the inner are outer sheaths keep the device from clogging with resected tissue. The device is actually a rotating, tubular innercannula encased in a stationary outer sheath dissector. The working tip opening is placedon the side of the sheath and it is through this opening that the vein is sucked in,morcellated, and removed. Using suction through the handpiece, the vein is ultimatelydirected into a suction container and standard wall suction supplies the aspirationmechanism. Blade speeds are set at 1000rpm for forward and/or reverse and may be set tooscillate at 1000 rpm.

Oscillation is used to break up larger and tougher varicose vein clusters. Forward andreverse are used to clean up and smooth out smaller bits of tissue. The working bladelength is 13 cm. The vein extractor is inserted through 2–3 mm incisions and the rotation of the blade is controlled by the surgeon with buttons on the handpiece.

The operation is performed supine, with the affected leg elevated 30 degrees (see Figure 20.3). The saphenofemoral junction is exposed through a 12 mm groin incision and the greater saphenous vein ligated and divided flush with the femoral vein. Thesaphenous vein is removed to the knee using inversion techniques. The TCI is used at thistime to hydrodissect the saphenous vein prior to inversion and in

Minimally invasive varicose vein surgery: transilluminated powered phlebectomy 369

Figure 20.1 TCI resector.

Figure 20.2 TriVex resector.

effect decreases bleeding and postoperative pain. The groin incision is closed and the firststage of staged operative tumescent technique (SOTT) is performed. Incisions are madeadequate to insert the TCI. Transillumination guides placement of the tumescentanaesthesia along the pathways of the previously marked varicose vein clusters (seeFigure 20.4). In the first stage of SOTT it is important to instill the solution to the point where the vein is reduced in size as much as possible, while still being able to visualizeits course. Tumescent anaesthesia introduction performs the hydrodissection, which aidsremoval of the veins. It also increases the radius of visualization by the transilluminationlight.

The blade extractor is introduced through 2–3 mm incisions, and manipulated toremove all visible varicose vein clusters, as visualized by transillumination. The use ofthe device requires pulsing the device on and off removing the veins 1–2 cm at a time on the first pass. A minimal number of incisions are made to allow the full 13 cm length of


Figure 20.3 Elevation of the affected leg by 30°. Makings show incisions used for the entire leg.

Figure 20.4 Transillumination guides placement of transcent anaesthesia along pathways of the previously marked various vein cluster. (a) Internal; (b) external

the resector to be utilized. The strategy for incision placement should take into accountcosmetic results as well as the need to use the incisions effectively for tumescence,transillumination and resection. Holding the skin taut makes the vein easier to removeand prevents the skin from getting caught in the working tip. As experience grows, theuser lets the dissector do the resection while holding the handpiece with a relatively lightgrip. The veins marked on the posterior aspect of the thigh and leg are reached bestutilizing the 30-degree leg elevation technique. Inward and outward rotation of the flexed knee allows visualization of posterior varicosities.

After the vein extractor has been utilized to its fullest extent, the second stage of SOTTis performed through the available incisions. The tumescent anaesthesia is utilized underfull pressure, achieving a peau d’orange effect. The objective of this second-stage


tumescent anaesthesia is to minimize haematoma formation, bleeding, and to ensurepostoperative comfort.

Incisions are closed without suture by Steri-Strips and an occlusive pressure dressing applied from toes to the proximal third of the thigh (see Figure 20.5). When appropriate, the patient is discharged from the postanaesthesia unit and encouraged to ambulate. Thepatient should be advised

Figure 20.5 (a) Preoperative, (b) two days postoperatve, and (c) six weeks postoperative.

that temporary bruising and numbness in the areas of dissection are expected. Dressingsare changed at 48 h and the patient should wear a 20–30mmHg graded compression stocking until the bruising is resolved, usually in 2–3 weeks. Postoperative therapeutic ultrasound seems to speed up the recovery on most patients.

Complications

Postoperatively, patients are cautioned about numbness and tingling for various lengthsof time, commensurate with the number of veins removed and the amount of tumescentanaesthesia used. In our experience, with 350 patients using transilluminated poweredphlebectomy (TIPP), we experienced paresthesias in 14 patients (4%). Most of these werein the early experience, while using higher resection speeds and poorer visualization withearlier forms of transillumination. Now with higher pressure for the TCI and pulsedtechnique to remove the veins we have less than 1% paresthesias. Cellulitis has occurredin 12 patients (3.4%), when defined as redness in a diameter greater than 2 cm. Thesewere all treated with oral antibiotics and resolved. Haematoma requiring needle drainageoccurred in one patient and may have been related to poor compliance with postoperativecompression. Persistent veins are a relatively rare occasion and have occurred in sixpatients (1.7%) in our earlier experience (requiring one session of sclerotherapy toobliterate the vein). With a stronger light source we have not seen any missed veins. If avein was persistent it often thrombosed spontaneously if close to an area of resection.


Conclusions

Transilluminated powered phlebectomy (TIPP) with SOTT is an exciting new procedurefor varicose vein removal as an outpatient procedure. The procedure should save time, iseasy to perform, gives direct visualization and a distinct end-point of the removal of veins. It is less tedious to perform and gives good cosmetic results, with significant painrelief. The procedure is complete with verification of removal at the time of surgery.There is now an option for veins previously treated with sclerotherapy or surgery that arepersistent or recurrent. It can be used with lipodermatosclerosis, previousthrombophlebitis, chronic venous insufficiency and previous liposuction. With the use ofpowered instruments for this otherwise tedious task, more patients can be treatedeffectively in a shorter time period. Since in our experience the procedure is easy to learn,surgeons may well be willing to use it in preference to other techniques.

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(10): 947–54. 19. Smith SR, Goldman MP. Tumescent anesthesia in ambulatory phlebectomy.

Dermatol Surg 1998; 24:453–6. 20. Tong Y, Royle J. Recurrent varicose veins after short saphenous vein surgery: a

duplex ultrasound study. Cardiovasc Surg 1996; 4(3): 364–7. 21. Weiss RA, Goldman MP. Transillumination mapping prior to ambulatory

phlebectomy. Dermatol Surg 1998; 24:447–50.


Dialysis grafts

21 MATTHEW A.MAURO AND LANCE L.ARNDER

Introduction

In the USA alone, there are over 214000 patients undergoing some form of dialysis,providing the renal replacement therapy necessary for life.1 The cost of maintaining this haemodialysis access in the USA was between 750 and 900 million dollars in 1995 andhas easily exceeded $1 billion in 1996. Despite the fact that it has been acknowledgedthat the native fistula (e.g. Brescia-Cimino radiocephalic fistula) is the haemodialysis access of choice, only 15–20% of patients in the USA have this type of access. The overwhelming majority have artificial (polytetrafluoroethylene [PTFE]) conduits orcatheters.2, 3 These remarkable percentages are in direct contrast with the European and Japanese experience, where nearly 90% of dialysis patients have the preferable nativefistulae. One of the major urgent goals in the USA is to increase the percentage ofpatients receiving native fistulae to the 40% level.1

As a result of the high proportion of synthetic access grafts, haemodialysis accessfailure is a major cause for morbidity for this group of patients.4 In the USA, haemodialysis access failure is the most frequent cause of hospital admission andaccounts for the largest number of hospital days among end-stage renal disease (ESRD) patients.3–6 It has also been established that an aggressive programme of monitoringdialysis graft (DG) patency will extend graft life and minimize graft thrombosis.7, 8 Thus, in addition to increasing the placement of native arterio-venous (AV) fistulae, another major goal of a dialysis programme is to detect (and subsequently treat) accessdysfunction prior to access thrombosis.

The ensuing discussion will focus on:

1. monitoring dialysis grafts for stenoses; 2. percutaneous treatment of the dysfunctional dialysis graft; 3. percutaneous treatment of the thrombosed dialysis graft; and 4. percutaneous treatment of complications and miscellaneous conditions.

For the purposes of this chapter, percutaneous management of dysfunctional orthrombosed dialysis grafts is defined as the use of catheter-based endovascular techniques to restore or maintain adequate blood flow within the DG to supporthaemodialysis. A dysfunctional dialysis graft is defined as a DG that has ahaemodynamically significant stenosis or one that cannot be successfully punctured toperform dialysis. A thrombosed dialysis graft is defined as a synthetic conduit thatcontains occlusive thrombus with no significant blood flow. This thrombus may extend

into the inflow arteries or outflow veins.

Monitoring dialysis grafts for stenoses

The most frequent cause of a dysfunctional or thrombosed DG is progressive venousoutflow stenosis secondary to intimal hyperplasia, typically at the venous anastomosis.7, 9–16 Until this problem is controlled, any salvage effort to provide long-term results will be disappointing. As the severity of this outflow stenosis increases, the intra-access pressures increase and DG blood flow decreases. This eventually leads to DG thrombosis,the leading cause of access loss. When access flows are repeatedly measured, decreasingflow rates are predictive of access stenosis. Dialysis grafts with flow rates below 600ml/min have a significantly higher rate of thrombosis than grafts with flows greater than600ml/min.17–19 Interventions with either percutaneous transluminal angioplasty (PTA)or surgical revision to correct the stenosis reduce the rate of DG thrombosis and graftloss. In one report, the baseline DG thrombosis rate was 0.58 thrombosis per patient perhaemodialysis year. After the introduction of a screening programme to detect andcorrect the stenosis with PTA, the thrombosis rate dramatically fell to 0.19 thrombosisper patient per haemodialysis year. 7 In another study, a screening programme led to a thrombosis rate of 0.15 thrombosis per patient dialysis year, equal to that in patientswithout stenoses.8 In addition, patients who had stenoses based on a screeningexamination but who declined subsequent therapy had thrombosis rates of 1.4 per patientdialysis year—a significant increase.

A detailed description of the various screening procedures and their protocols arebeyond the scope of this discussion. However, these details can be found in the NationalKidney Foundation Dialysis Outcomes Quality Initiative1 and a review by Sullivan and Besarab.20 Monitoring techniques (not mutually exclusive) that can be used to detect DG stenoses include intra-access flow, static venous pressures, dynamic venous pressures, measurement of recirculation using urea concentrations, measurement of recirculationusing dilution techniques, unexplained decreases in the measured amount ofhaemodialysis delivered, physical examination findings, including persistent armswelling, clotting of the graft, prolonged bleeding following needle withdrawal, or alteredcharacteristics of the pulse or thrill within the graft, elevated negative arterial prepumppressures that prevent acceptable blood flows, and ultrasound (Doppler, colour).1

Sequential repetitive measurement of DG flow is the preferred method of monitoring. Doppler flow, ultrasound dilution and magnetic resonance can perform access-flow evaluation. Doppler flow and magnetic resonance are difficult to perform during dialysissessions. However, flow measurements using ultrasound velocity in blood dilution isaccurate and reliable and can be done on-line during dialysis. It is anticipated that, as technology evolves and expands into the clinical area, ultrasound dilution flowmeasurements performed on-line will become the standard technique.1

Measuring venous pressures is easy and inexpensive and has acceptable sensitivity andspecificity.8, 11 It is critically important to standardize protocols, including blood tubing, needle size and haemodialysis machine. Static dialysis pressures are even more stronglypredictive of outflow stenoses but do require specialized devices.7, 21 It may be possible


to adapt existing haemodialysis machines for static pressure measurements, making thistechnique very attractive.22

Regular physical examination may supplement and enhance a screening programme.11, 23, 24 Findings suggestive of an outflow stenosis include a swollen arm, prolonged bleeding following needle removal and changes in the pulse/thrill of the DG. A palpablethrill at the arterial, mid-graft and venous limbs indicates flows greater than 450ml/min.24

Conversion of a thrill to a pulse indicates lower flows. When any test suggests thepresence of a stenosis, venography or fistulography is indicated to confirm the lesion anddirect therapy.1

Treatment of the dysfunctional dialysis graft

The primary indication for intervention of a dysfunctional dialysis graft is for thetreatment of a haemodynamically significant stenosis. A haemodynamically significantstenosis is defined as a greater than 50% reduction of the normal vessel diameter,accompanied by a haemodynamic, functional or clinical abnormality, including abnormalrecirculation values, elevated venous pressures obtained during dialysis (dynamic orstatic), decreased graft blood flow, swollen extremity, prolonged bleeding, reducedthrill/pulse, or elevated negative arterial prepump pressures.1 The treatment of haemodynamically significant stenoses reduces the rate of DG thrombosis and prolongsthe life of the graft.7, 8, 12, 25, 26 The long-term patency of the DG is improved when stenoses are treated prior to thrombus formation, compared to treatment after graftocclusion. In a retrospective study, 50% of thrombosed DGs treated with thrombolysisand PTA were patent 4 weeks later. When PTA was performed prior to DG thrombosis,50% of the grafts were patent 24–28 weeks later.27 There is no evidence to support the treatment of stenoses that are not associated with a haemodynamic, functional or clinicalabnormality.

Of DG thromboses, 85–90% are associated with venous outflow stenotic lesions due tointimal hyperplasia, typically at the venous anastomosis. Other sites of stenoses includearterial anastomosis, outflow vein distal to the venous anastomosis, central vein stenosis,intragraft stenosis, inflow artery proximal to the arterial anastomosis, and extrinsiccompression (graft kinking, pseudoaneurysm).1, 14

Balloon angioplasty

PTA is the primary endovascular technique for the treatment of stenotic lesions (Figure 21.1). Access is typically obtained via the graft and the lesion is treated with pro-

Dialysis grafts 377

Figure 21.1 Angioplasty of venous anastomosis stenosis. (a) Predilatation; (b) postdilatation.

longed inflations (up to 10min). Because the standard diameter of the PTFE graft is 6mm, most interventionalists use 6–8 mm high-pressure balloons for the PTA. Intraprocedural heparin is also commonly used. The clinical success and patency ratesfrom PTA are illustrated in Table 21.1. These figures reflect results reported in the literature using modern techniques and life-table analysis 14,28,29 Clinical success is defined as the presence of a continuous palpable thrill extending from the arterialanastomosis following therapy. Primary patency is defined as the uninterrupted patencyfollowing intervention until the next re-intervention or graft thrombosis. Secondarypatency is the time between initial intervention and surgical declotting, revision or graftloss. In general, the treated lesions are solitary and less than 6cm in length. Stenoseslonger in length or previously treated will have poorer patency rates. If PTA is requiredmore than twice within 3 months, a surgical revision should be considered if such anoption is available, and the patient is a surgical candidate. When only synthetic DGs areconsidered, a goal of 40% 6-month primary patency should be achievable.1 PTA is a safe procedure. Complications relating to the PTA range from 3 to 4.8%.30, 31 The more common com

Table 21.1 Treatment of a dysfunctional dialysis graft

Rates (%)

Clinical success 85–98

Patency

6-month primary 38–63


12-month secondary 81–82


plications include angioplasty site rupture, acute access thrombosis, and delayedpseudoaneurysm formation. Less frequent complications include puncture site bleeding,bacteraemia, balloon fragment retrieval, and contrast media reaction. 32

Atherectomy

The primary mechanism of balloon angioplasty in the treatment of the intimalhyperplastic lesion is probably vesselwall stretch with or without a mural tear.33, 34 The Simpson directional atherectomy catheter (Mallinckrodt Inc., St Louis, MO, USA) allowsshaving and removal of the obstructive hyperplastic material. Gray and colleaguesreported the results of 32 lesions in 24 patients with PTFE grafts. Eighty-one per cent were initial treatment success’ es with 88% of the venous lesions requiring supplemental balloon angioplasty.33 The recurrence rates were similar to those for PTA alone.Directional atherectomy is primarily used for balloon-resistant lesions, and intrastent stenoses (Figure 21.2). A minority of lesions resist balloon expansion, despite the use of high-pressure balloons. In these cases, shaving the lesion with a directional atherectomycatheter will remove some of the hyperplastic material and allow subsequent full-balloon expansion.34 Directional atherectomy can be used for recurrent intrastent stenoses when repeat PTA fails to provide an adequate channel.35 This approach may be preferable tothe placement of a stent within a stent or to abandoning the access.

Although not an atherectomy device, balloon-resistant venous lesions can also be treated with a ‘cutting’ balloon.36 Cutting balloons were initially developed for coronary angioplasty to control neointimal hyperplasia and reduce the rate of restenosis. Theballoons have four longitudinally oriented blades on the balloon surface, which incise the intimal hyperplastic lesion within the vein allowing full subsequent conventional balloondilatation. Cutting balloons are now available with 5–6 mm diameters.

Dialysis grafts 379

Figure 21.2 Atherectomy of balloon-resistant venous stenosis. (a) High-grade stenosis; (b) balloon inflation with resistant stenosis; (c) directional atherec-tomy catheter adjacent to balloon catheter; (d) repeat balloon inflation with full expansion; (e) improved vein calibre.


Metallic stents

The full role of stents is not well defined and continually evolving. Presently, the primaryindications for metallic stent placement include:

1. a peripheral outflow lesion that has failed angioplasty and where surgical access is difficult or contraindicated or there are limited remaining sites;

2. central venous lesion that has either failed angioplasty or recurred within a 3-month period following successful PTA (Figure 21.3); and

3. rupture of an outflow vein following angioplasty (Figure 21.4). In a randomized prospective study, Hoffer and colleagues compared PTA with PTA and Wallstent in the treatment of stenoses at the vein-graft junction or within a peripheral outflow vein that had recurred within 6 months of a prior PTA.37 They found no difference in primary and secondary patency rates for the two groups, concluding that stent placement for recurrent stenoses added no advantage for those lesions adequately dilated with balloon angioplasty. In a retro-spective study, which included central as well as peripheral venous lesions, Turmel-Rodriques and colleagues found that the use of stents doubled the interval between re-interventions for early (< 6 months) recurrent stenoses.38 In a study limited to the placement of Wallstents across the venous anastomosis for PTA failure, rapid restenosis and vessel perforation, Patel and Colleagues found that stenting can salvage access function (Figure 21.4).39 Their findings supported the use of stents for those indications and furthermore reported a 50% 1-year secondary patency rate.

Central venous stenoses and occlusions can be treated with endovascular stents whenangioplasty fails in order to salvage the haemodialysis access (Figure 21.3).11, 15, 40–44

Central venous bypass, the surgical alternative, has been reported in small series but hasnot gained widespread acceptance. The most common cause of stent failure is neo-intimal hyperplasia within and adjacent to the stent (Figure 21.5). With aggressive follow-up and retreatment (angioplasty, atherectomy), Gray and colleagues were able to achieve assistedprimary patency rates of 76% at 6 months and 33% at 12 months.44 Spontaneous migrations have not been reported with the Wallstent or Gianturco stent. In general, therehas been enough accumulated clinical experience to indicate that stent deployment is safeand will provide a high initial access salvage rate in cases where PTA fails.

Dialysis grafts 381

Figure 21.3 Central venous recanalization. (a) Occluded (L) innomi-nate vein; (b) poor result following angioplasty; (c) successful recanalization following stenting.


Figure 21.4 Venous perforation. (a) Venous perforation following balloon angioplasty; (b) successful treatment following stenting.

Figure 21.5 Intimal hyperplasia. (a) Recurrent stenosis within metallic stent; (b) successful balloon dilatation.

Treatment of the thrombosed dialysis graft

Patients with thrombosed DGs should be evaluated as soon as possible in order to avoidthe placement of temporary dialysis catheters.1 The only absolute contraindication to percutaneous treatment is infection of the access site. Relative contraindications includesevere contrast allergy, lifethreatening conditions that require immediate dialysis,contraindications to fibrinolytic therapy, right-to-left shunts and severe pulmonary disease.

The standard percutaneous declot procedure can be divided into five components.

• Step 1: Access the DG directed towards the venous anastomosis; the anastomosis is traversed with a guide-wire and catheter and a venogram of the venous outflow is performed. This first component is important in order to determine whether you should proceed with the graft declot procedure or immediately refer the patient for surgical

Dialysis grafts 383

revision or a new access. If the venous anastomosis cannot be traversed with a guide-wire and catheter, the underlying venous stenosis will not be able to be corrected by endovascular techniques. Similarly, if the outflow venous system is diffusely and severely diseased with long-segment stenoses and/or occlusions, endovascular techniques will probably not yield a satisfactory result. In these circumstances, the declot procedure is terminated and the patient is referred for surgical revision or the placement of an entirely new access.

• Step 2: A second access is created in the DG near the venous anastomosis, directed toward the arterial limb. The graft is then declotted using either pharmacological or mechanical techniques.

• Step 3: The endovascular treatment of underlying stenoses is accomplished with the same techniques (PTA, atherectomy and stents) used in the treatment of the dysfunctional DG.

• Step 4: The arterial plug that forms next to the arterial anastomosis is mobilized and removed—usually with a Fogarty balloon catheter.

• Step 5: removal of the catheters/sheaths (Figure 21.6).45

The removal of thrombus within the DG can be accomplished by two basic endovasculartechniques pharmacological thrombolysis and mechanical declotting. Pharmacologicalthombolysis of DG was first performed in the mid-1980s using streptokinase. Urokinasebecame the preferred agent and was initially used as a drip infusion. Infusion timesranged from 2 to 20 h and nearly 50% of patients experienced bleeding difficulties.46–49

Pulse-Spray pharmacomechanical thrombolysis was developed to reduce treatment times,urokinase doses and bleeding complications.50–52 The pulse-spraytechnique relies on boththe mechanical disruption of the clot from the spray as well as the pharmacological lyticeffect of the direct plasminogen activator, urokinase. This pulse-spray technique has beenfur-ther modified to include early fragmentation of the clot with a balloon catheter, theaddition of concentrated heparin to the concentrated urokinase solution for intrathrombicinjection, and the use of a Fogarty balloon catheter to mechanically remove the lysis-resistant plug at the arterial anastomosis, as well as any residual clots within the DG. Byusing this modified pulse-spray technique, the mean throm bolytic infusion time wasreduced to 23 min and the initial success rate increased to 96%.50 The 30- and 90-dayprimary patency rates with the modified pulse-spray technique are reported to be 70 and50%, respectively.29, 53–55

Cynamon and colleagues have recently described a simplified lytic method for thetreatment of thrombosed DGs, termed the ‘lyse and wait’ technique.56 Before the patientis brought to the angiographic lab, a 22 or 20 G angiocath is placed in the DG near thearterial anastomosis (straight grafts) or apex (looped grafts) pointing towards the venousanastomosis. Confirmation of intragraft position includes visualizing blood or clot in thecatheter or the easy insertion of a 0.018′′ guide-wire. A mixture of 250000 units ofurokinase in 5 ml with 5000 units of heparin in 1 ml is then slowly infused into the graft(over 1–2 min), while manually compressing both the arterial and venous ends of the DG.After 45 min, the patient is brought to the angiographic laboratory. A second puncture inthe DG is made near the venous anastomosis, heading towards the arterial limb. Thearterial plug is mobilized, along with any residual clot, with the use of a Fogarty balloon.The venous stenosis is then treated with PTA. Clinical success (graft declotting with thrill


and a successful dialysis) was achieved in 96% of patients. There were no reported casesof arterial emboli secondary to the urokinase infusion.45

Figure 21.6 Dialysis graft declot procedure. (a) Access with catheterizatian of venous anastomotic stenosis; (b) access with catheterization towards arterial inanastamosis and placement of thrombolytic catheter or mechanical thrombectomy device; (c) dilatation of venous anastamosis; (d) removal of arterial plug and any residual thrombus with Fogarty balloon.

A variety of mechanical devices have been developed to address the deficiencies ofexisting methods (pharmacologic thrombolysis) to remove thrombus from a clottedDG.57 The goals of these devices include a faster, safer and less expensive method of clot removal. To date, results from mechanical clot removal utilizing any of these devices hasbeen equivalent to those from standard pharmacological techniques. A brief review ofseveral of the devices is included. A more detailed review of percutaneous mechanicalthrombectomy can be found in a three-part series by Sharafuddin and Hicks.58–60

Mechanical devices canbegrouped into those that expand to make vessel wall contact and

Dialysis grafts 385

those that produce clot fragmentation by a variety of processes such as fluid penetration,suction and recirculation. The first group physically detaches clot from the wall, oftenwith subsequent maceration.57 Examples of this group of devices include the Fogarty-type thrombectomy balloon catheter (Baxter Healthcare, Santa Anna, CA, USA) (Figure 21.7a), the Arrow-Trerotola percutaneous thrombectomy device (Arrow International Inc., Reading, PA, USA) (Figure 21.7b), and the Cragg/Castaneda thrombolytic brush(Micro Therapeutics Inc., San Clemente, CA, USA) (Figure 21.7c). The Fogarty balloon catheter can treat chronic thrombus and the ‘arterial plug’, but there is limited thrombus fragmentation. Its primary current use is as an adjunctive technique to remove the arterialplug and residual clot. However, the thrombectomy balloon catheter can be used as thesole method of clot removal.58 The Arrow and Cragg devices are both easy to use and effective in removing thrombus from DGs.57, 59 A potential limitation is vascular injuryand distal arterial embolization.60–62

Figure 21.7 Thrombectomy devices. (a) Fogarty balloon treating arterial plug and residual thrombus; (b) Arrow-Trerotola basket; (c) Cragg/ Castaneda brush—the actual brush is radiolucent, but is located distal to opaque mark where thrombus is seen.

The second group of devices tend to produce smaller particles, which can then be easily suctioned or allowed to embolize.59 These devices include the multiside-hole


pulse-spray catheter, the Amplatz thrombectomy device (Microvena Corporation, White Bear Lake, MN, USA), the AngioJet rheolytic thrombectomy system (Possis Medical, Minneapolis, MN, USA), the Trac-Wright catheter (Dow Corning Wright/Theratek International, Auburn, MI), the Hydrolyser mechanical thrombectomy device (JJIS-Cordis Endovascular, Warren, NJ, USA), and the Gelbfish EndoVac (NeovascularTechnologies, New York, NY).60–62

A more simplified endovascular mechanical technique that directly removes thrombusis catheter thromboaspiration.63 This technique involves two accesses within the DG andthe use of 7 or 8 F non-tapered angled guiding catheters. The thrombus is manually aspirated via these non-tapered catheters, as their tips are rotated so that contact is madewith the wall of the graft. Turmel-Rodrigues reported on his experience with thistechnique in 43 PTFE grafts. The mean procedure time was 119min and the 1-, 6-, and 12-month primary patency rates were 85%, 33% and 24%, respectively.63

It should be realized that the successful treatment of a thrombosed DG is more difficult to achieve than the stenosis associated with a dysfunctional DG.1 The report’ ed patency rates for pharmacological thrombolysis and mechanical thrombectomy are similar and areshown in Table 21.2.29, 50, 52–55, 64–69 A 40% primary patency rate at 90 days is anacceptable goal and should be achievable with current techniques.1

Major and minor complications occur in up to 10% of patients. Complications are lowerwhen treating dysfunc-tional DGs. Complications include symptomatic arterial embolization (1–9%), remote haematoma (2–3%), vascular rupture (2–4%), symptomatic pulmonary embolism (<1%), and puncture site complications (<1%).51,70,71

Percutaneous treatment of complications and other conditions

The majority of arterial emboli resulting from DG declotting procedures areasymptomatic.72 Arterial emboli may occur from vigorous flushing within the closed DGsystem, the passing of catheters through the arterial anastomosis, or the actual macerationand removal of the arterial plug. Imaging of the forearm arterial circulation should be apart of the completion angiographic study. Treatment of arterial emboli includesendovascular and open surgical techniques. Endovascular techniques include bothmechanical and thrombolytic procedures. In turn, mechanical endovascular techniquesinclude:

Table 21.2 Treatment of a thrombosed dialysis graft Rates(%)

Clinical success 75–94

Patency



6-month secondary 62–80

Dialysis grafts 387

1. backbleeding technique—placement of a Fogarty balloon catheter into the artery proximal to the anastomosis allowing backbleeding to flush the emboli back into the graft;73

2. thromboaspiration—direct aspiration and removal of the emboli with a non-tapered guiding catheter; and

3. mobilization with an over-the-wire balloon catheter.72

If these mechanical techniques fail, catheter-directed thrombolysis can be performed.Because the arterial plug is relatively resistant to lysis, an infusion will be required.

When venous rupture occurs secondary to the PTA, it is critically important tocomplete the declotting procedure and re-establish brisk antegrade flow. This is now best accomplished with the placement of a Wallstent across the perforation. Although theWallstent has interstices, the brisk antegrade blood flow prevents leakage and allows theperforation to heal.74, 75

A well-known problem associated with multiple DG punctures is the development of pseudoaneurysms. These pseudoaneurysms can be treated with embolization techniques(direct puncture with coil/balloon occlusion), which tends to be tedious and expensive.76

More recently, pseudoaneurysms have also been treated with the endoluminaldeployment of a covered stent.77 A tattoo can be placed on the skin overlying the coveredstent to be sure that this area is not punctured with a needle. Occasionally, due to thelarge amount of flow through the graft, the ipsilateral arm becomes ischaemic—a steal phenomenon, or the extremity becomes markedly swollen due to a proximal venousocclusion. When indicated, the DG can be intentionally occluded with endovascularembolization techniques. Due to the high flow, an overnight inflation of an occlusionballoon (with or without coils) is often necessary. The occlusion is simply documentedwith colour-flow ultrasound and the occlusion balloon is removed.

Summary

Until the problem of neointimal hyperplasia is effectively controlled, long-term results of either surgical or endovascular techniques will be disappointing in the maintenance ofsynthetic dialysis grafts. A shift in practice to the placement of more native fistulas willhelp this patient population significantly. There are no clear-cut differences between surgical thrombectomy with revision and percutaneous methods. Comparative studieshave shown conflicting results.25, 49, 78–81 Even in those studies reporting superior results with surgical revision, percutaneous revision is often initially performed. The initialpreference to percutaneous therapy is due to the following:

1. Percutaneous techniques are minimally invasive with low risk. 2. They are often available on the same or next day, thereby avoiding temporary

catheters. 3. They preserve existing venous anatomy. 4. They can be repeated. These benefits have made percutaneous techniques the initial

therapy in many centres, reserving surgery for early recurrences and fail-ures. The National Kidney Foundation recommends surgical revision for stenoses requiring PTA


more than twice within a 3 month period if this option is available.1

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47. Schilling J, Eiser A, Slifkin R et al. The role of thrombolysis in hemodialysis access occlusion. Am J Kidney Dis 1987; 10:92–7.

48. Brunner M, Matalon T, Patel S et al. Ultrarapid urokinase in hemodialysis access occlusion. JVIR 1991; 2:503–6.

49. Summers S, Drazan K, Gomes A. Urokinase therapy for thrombosed hemodialysis access grafts. Surg Gynecol Obstet 1993; 176:534–8.

50. Valji K, Bookstein J, Roberts A et al. Pulse-spray pharmacomechanical thrombolysis of thrombosed hemodialysis access grafts: long-term experience and comparison of original and current techniques. Am J Roentgenol 1995; 164:1495–500.

51. Roberts A, Valji K, Bookstein J et al. Pulse-spray pharmacomechanical thrombolysis for treatment of thrombosed dialysis access grafts. Am J Surg 1993;166:221–6.

52. Valji K, Bookstein J, Roberts A et al. Pharmacomechanical thrombolysis and angioplasty in the management of clotted hemodialysis grafts: early and late clinical results. Radiology 1991; 178:243–7.

53. Beathard G. Mechanical versus pharmacomechanical thrombolysis for the treatment of thrombosed dialysis access grafts. Kidney Int 1994; 45(5): 1401–6.

54. Cohen M, Kumpe D, Durham J et al. Improved treatment of thrombosed hemodialysis access sites with thrombolysis and angioplasty. Kidney Int 1994; 46:1375–80.

55. Berger M, Aruny J, Skibo L. Recurrent thrombosis of polytetrafluoroethylene dialysis fistulas after recent surgical thrombectomy: salvage by means of thrombolysis and angioplasty. JVIR 1994; 5:725–30.

56. Cynamon J, Lakritz P, Wahl S et al. Hemodialysis graft declotting: description of the ‘Lyse and Wait’ technique. JVIR 1997; 8:825–9.

57. Crain M. Percutaneous mechanical thrombolysis and thrombectomy. Tech Vasc Intervent Radiol 1998; 1:235–43.

58. Soulen M, Zaetta J, Amygdalos M et al. Mechanical declotting of thrombosed dialysis grafts: experience in 86 cases. JVIR 1997; 8: 563–7.

59. Trerotola S, Vesely T, Lund G et al. Treatment of thrombosed hemodialysis access grafts: arrow-trerotola percutaneous thrombolytic device versus pulse-spray thrombolysis. Radiology 1998; 206:403–14.

60. Sharafuddin M, Hicks M. Current status of percutaneous mechanical thrombectomy, Part II. Devices and mechanisms of action. JVIR 1998; 9:15–31.

61. Sharafuddin M, Hicks M. Current status of percutaneous mechanical thrombectomy, Part III. Present and future applications. JVIR 1998; 9:209–24.

62. Sharafuddin MJA, Hicks M. Current status of percutaneous mechanical thrombectomy. Part III. Present and future applications. JVIR 1998; 9:209–24.

63. Turmel-Rodrigues L, Sapoval M, Pengloan J et al. Manual thromboaspiration and dilation of thrombosed dialysis access: mid-term results of a simple concept. JVIR 1997; 8:813–24.

Dialysis grafts 391

64. Davis G, Dowd C, Bookstein J et al. Thrombosed dialysis grafts: efficacy of intrathrombic deposition of concentrated urokinase, clot maceration, and angioplasty. Am J Roentgenol 1989; 149: 177–81.

65. Sands J, Patel S, Plaviak D et al. Pharmacomechanical thrombolysis with urokinase for treatment of thrombosed hemodialysis access grafts. ASAIO J 1994; 40: m886–8.

66. Swan T, Smyth S, Ruffenach S. Pulmonary embolism following hemodialysis access thrombolysis/thrombectomy. JVIR 1995; 6: 683–6.

67. Trerotola S, Lund G, Scheel P. Thrombosed dialysis access grafts: percutaneous mechanical declotting without urokinase. Radiology 1995; 191:721–6.

68. Vorwerk D, Sohn M, Schurmann K et al. Hydrodynamic thrombectomy of hemodialysis fistulas: first clinical results. JVIR 1994; 5: 813–21.

69. Beathard G, Welch B, Maidment H. Mechanical thrombolysis for the treatment of thrombosed hemodialysis access grafts. Radiology 1996; 200:711–16.

70. Uflacker R, Rajagapolan P, Viljic I et al. Treatment of thrombosed dialysis access grafts with the Amplatz device. JVIR 1996; 7: 185.

71. Sharafuddin M, Kadir S, Joshi S, Parr D. Percutaneous balloon-assisted aspiration thrombectomy of clotted hemodialysis access grafts. JVIR 1996; 7:177–83.

72. Trerotola S, Johnson M, Shah H et al. Incidence and management of arterial emboli from hemodialysis graft surgical thrombectomy. JVIR 1997; 8:557–62.

73. Trerotola S, Johnson M, Shah H, Namyslowski J. Backbleeding technique for treatment of arterial emboli resulting from dialysis graft thrombolysis. JVIR 1998; 9:141–3.

74. Raynaud A, Angel C, Sapoval M et al. Treatment of hemodialysis access rupture during PTA with wallstent implantation. JVIR 1998; 9:437–42.

75. Rundback J, Leonardo R, Poplausky M, Rozenblit G. Venous rupture complicating hemodialysis access angioplasty: percutaneous treat-ment and outcomes in seven patients. AJR 1998; 171:1081–4.

76. Selby J, Pruett T, Westervelt JR F et al. Treatment of hemodialysis fistula pseudoaneurysms with detachable balloons: technique and preliminary results. JVIR 1992; 3:505–10.

77. Hausegger K, Tiessenhausen K, Klimpfinger M et al. Aneurysms of hemodialysis access grafts: treatment with covered stents: a report of three cases. Cardiovasc Intervent Radiol 1998; 21:334–7.

78. Beathard G. Thrombolysis versus surgery for the treatment of thrombosed dialysis access grafts. J Am Soc Nephrol 1995; 6:1619–24.

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80. Schwartz C, McBrayer C, Sloan J et al. Thrombosed dialysis grafts: comparison of treatment with transluminal angioplasty and surgical revision. Radiology 1995; 194:337–41.

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Inferior vena cava filters

22 ANNE C.ROBERTS AND THOMAS B.KINNEY

Introduction

Interruption of the inferior vena cava (IVC) for the treatment of pulmonary embolism(PE) was first proposed by Trousseau in 1868 and first performed by Bottini in 1893.Since that time, partial or complete caval interruption has been viewed as an alternativetherapy when anticoagulation is contraindicated or has failed. Ligation of the IVC or ofthe femoral veins is now almost never performed. The second generation of therapy,surgical plication using external clips, such as the Adams-DeWeese clip, has also been largely abandoned, used only occasionally if the patient is undergoing retroperitoneal orabdominal surgery for other reasons (Figure 22.1). The third generation of therapy, the IVC filters, has become the therapeutic approach of choice and has undergone markedchanges over the past 15 years.

The early transvenous devices, the Hunter balloon1,2 and Mobin-Uddin umbrella (Figure 22.2),3 are no longer used because of unacceptable rates of caval occlusion, andin the case of the Mobin-Uddin filter, migration.4–7 Thegoldstandard for transvenous caval interruption is the Greenfield filter (also referred to as the Kimray-Greenfield or KG filter). The Greenfield filter was originally described in 1973 and there is anextensive published literature of its efficacy and complications.8–14 It was originally described as being placed via a surgical cutdown of the internal jugular or femoral vein.In the mid-1980s, the percutaneous placement of the filter was described, and now percutaneous placement of filters has become the approach of choice in most centres.15–18 The fourth generation of therapy is represented by the development of newerpercutaneous filter devices, and there are a variety of filters from which to choose.

The eight Food and Drug Administration (FDA)approved filters presently on the US market include the 24 F Greenfield filter (Meditech/Boston Scientific Corporation,Natick; MA, USA), the percutaneous over-the-wire

Figure 22.1 (a) Transverse; and (b) sagittal reformation CT images of an inferior vena cava clip obtained in a patient during routine evaluation for another suspected abdominal condition.

stainless steel Greenfield filter (Meditech), the titanium Greenfield filter (Meditech), the Bird’s Nest and Gunther Tulip filters (Cook Inc., Bloomington, IN, USA), the VenaTechLGM filter now with a low-profile configuration (B. Braun Inc, Bethlehem, PA), theSimon nitinol filter (Nitinol Technologies, Woburn, MA, USA), and the TrapEase filter(Cordis, Miami, FL, USA). A fifth genera tion of caval interruption therapy, temporaryfilters, is now being developed.19–21 Also in the developmental stages are filters in which there is the option to leave the filter in place indefinitely or the ability to remove the filterpercutaneously at various times remote from the IVC filter insertion procedure. Outsidethe USA the Gunther Tulip filter is now used in such a manner.

Interruption of the IVC continues to be an important adjunct in the treatment of thromboembolic disease, despite recent improvements in anticoagulation regimes. Asubstantial number of patients develop deep venous thrombosis (DVT). It has beenestimated that there are 5 million cases of DVT in the USA22 and as many as 650 000 cases of symptomatic PE.23–25

Approximately 80–90% of PEs originate from DVTs in the lower extremities or pelvis.IVC filters have been specifically designed to trap such potential emboli within the IVC,thus preventing PE. Although most of these patients with thromboembolic disease can betreated with anticoagulation, there are some patients who are not candidates foranticoagulation and who require cava interruption for protection from fatal PE. Industrysources estimate that approximately 40000 IVC filters are inserted in the USA each year.The mortality rate of untreated PE has been estimated to be 30%.24 Treatment of patients who have proximal DVT with unfractionated heparin followed by oral anticoagulationfor 3 months prevents PE in 95% of patients. A wide diversity of aetiological risk factorshave been identified for thromboembolic disease (Table 22.1).


Figure 22.2 Example of imaging characteristics of the Mobin- Uddin inferior vena cava (IVC) umbrella. The patient was being evaluated for possible recurrent deep venous thrombosis with lower extremity ultrasound studies. Review of the patient history indicated a remote history of prior IVC filter insertion, as shown on the plain film of the abdomen (a). The filter projects over the third lumbar vertebral body and the conical tip of the filter points inferiorly in comparison to current generation conical IVC filters. A CT scan of the abdomen demonstrated an occluded IVC (b-d, selected axial images ordered in a cranial-caudal direction).

Inferior vena cava filters 395

Indications for IVC filter placement

IVC filters have been primarily placed for certain welldefined indications (Table 22.2):

Table 22.1 Risk factors for deep venous thrombosis and pulmonary embolism (adapted from Stephen and Feied, 1995)97 Acute myocardial infarction Intravenous drug abuse

AIDS Malignant disease

Antithrombin III deficiency Multiple injuries

Burns Obesity

Chemotherapy Oral contraceptives

Congestive heart failure Polycythaemia

Disorders of plasminogen activators Postoperative period

Postpartum period

Drug-induced lupus anticoagulant Pregnancy

Previous history of DVT

Dysfibrinogenaemia Protein C deficiency

Dysplasminogenaemia Protein S deficiency

Fractures Systemic lupus

Heparin-induced thrombocytopenia Thrombocytosis

Ulcerative colitis

Immobilization Venography

Indwelling venous catheters Venous pacemakers

DVT: deep venous thrombosis.

Table 22.2 Indications for inferior vena cava filter placement

Well-accepted indications

• Contraindication to anticoagulation

• Complication of anticoagulation

• Failure of anticoagulation

• Chronic pulmonary thromboembolism

Expanded indications

• Free-floating thrombus


The most common and well-accepted indication is a patient with known thromboembolic disease (i.e. PE and/or DVT) and a contraindication to anticoagulation. Commoncontraindications include presence of neurological conditions, such as intracranialtumour, neurological trauma, or haemorrhagic stroke. Treating such a patient withanticoagulation might result in intracranial haemorrhage. Recent gastrointestinalbleeding, recent major surgery or trauma, or a bleeding diathesis are also reasons to avoidanticoagulation. Patients with cancer may also have a higher risk of complications whentreated with anticoagulation.26, 27

Known thromboembolic disease in a patient who has developed a complication ofanticoagulation is another reason for IVC filter placement. Bleeding is the most frequentcomplication. However, heparin-induced thrombocytopenia is becoming a morefrequently recognized complication of heparin therapy. The risk of major bleedingrequiring transfusion with heparin therapy is 1.5–20%. The risk of heparin-induced thrombocytopenia is 5–15%. Anticoagulant therapy carries a mortality rate of 5–12%. These risks increase with the longer duration of treatment and increasing age of thepatient. Coumadin therapy has its own complications including coumadin-associated necrosis. The use of low-molecular weight heparin may decrease some of these complications; however, if complications develop, an IVC filter will be required.

A small number of patients with known thromboembolic disease will have a failure ofanticoagulation therapy. In a relative minority of these cases, there is objectivedocumentation with imaging of recurrent PE or progressive DVT occurring despite therapeutic levels of anticoagulation. Unfortunately, in the majority of these cases thehistory is not so clear. A common situation is a patient with a documented DVT, nosymptoms of PE and no objective evaluation for PE. The patient is placed on heparin, andlater develops some respiratory symptoms. At this point a concern for PE arises. Aventilation/perfusion ratio (V/Q) scan is performed and is positive for a PE. The patienthas been on adequate anticoagulation and is thus considered a failure of medical therapy.Unfortunately, since there was no previous evaluation for PE, it is possible that thepatient originally had a PE that was not clinically evident. The clot gradually moveddistally and became occlusive with the development of a small infarct that causedsymptoms. At this point, the patient is evaluated for PE and now the patient iscategorized as a failure of anticoagulation. Is the patient a failure? Since there is noprevious study documenting the presence or lack of PE, the conservative approach isapplied, which assumes that any finding is new and thus the patient must be treated as afailure of anticoagulation.

The most controversial reason to place an IVC filter is for prophylaxis. What is meant by prophylaxis varies. Some patients have thromboembolic disease and can be treated

• DVT and underlying severe cardiac or pulmonary disease

• Severe trauma

• Surgical procedures in patients with a history of venous thromboembolism

• Venous thrombolysis

DVT: deep venous thrombosis.


with anticoagulation, but filter placement is required to further protect the patient fromPE. Such patients include patients with chronic PE who have limited cardiopulmonaryreserve to tolerate additional embolic insults. Such patients may undergo pulmonarythrombendarterectomy and IVC filter placement is used as an adjunct to anticoagulation.Patients with very large acute PE may also be felt to require a filter to supplementanticoagulation and/or thrombolytic therapy. These patients are not truly in the categoryof prophylaxis. They do have thromboembolic disease and the filter is being used asadjunctive treatment with anticoagulation to help prevent another PE. Patients withsevere chronic obstructive pulmonary disease (COPD) and DVT may also benefit fromfilter placement because of their poor prognosis if they suffer a PE.28

True prophylactic filter placement in a patient who is at high risk for thromboembolic disease is controversial. Such patients do not yet have thromboembolic disease but areconsidered to be at high risk for both DVT and bleeding from prophylacticanticoagulation (e.g. patients with stroke, paraplegia, pelvic fractures or postoperativepatients from neurosurgical, or orthopaedic procedures).29–33 Part of the controversy revolves around the fact that these patients can often be treated with lower extremityintermittent pneumatic compression devices, with low-dose heparin, or with serial ultrasound surveillance studies instead of IVC filter placement.

Trauma patients with head injury, spinal cord injury, multiple long bone and pelvic fractures are at particularly high risk for PE and there is a trend to treat these patientsprophylactically.34–49 The patterns of injury that place patients in a high-risk category are being further refined.44

Patients with a relative contraindication to heparin and iliofemoral DVT, particularly a free-floating thrombus, may require filter placement.50–53 This is based on data indicating the iliofemoral region as the source of 75% of lethal emboli. In some patients with a largeburden of clot, the use of filters as a therapeutic adjunct to heparin therapy has beenadvocated. Finally, another relative indication for IVC filter insertion is in the patientwho is considered to be poorly compliant with anticoagulation treatment.

Contraindications to IVC filter placement

There are no absolute contraindications to IVC filter placement. Lack of access sitescould prohibit placement of a filter, but with the newer filter designs, some filters can beplaced from any of the larger veins (femoral and jugular) or even the smaller veins suchas an antecubital vein. If there is clot present between the venous access and the filterdeployment site, another access site should be chosen. Patients with a severecoagulopathy that cannot be corrected have a relative contraindication to filter placement,although using an antecubital venous access may be feasible. Placing a filter in a patientwith septic thromboembolism is controversial, but in animal studies, the Greenfield filterwas found to be well tolerated as long as antibiotics were given to treat the infection.14

Insertion of IVC filters in paediatric patients should be strictly scrutinized, as the long-term efficacy and durability of such devices in these cases are not well known.


Characteristics of the various IVC filters (Table 22.3)

Stainless steel 24F Greenfield IVC filter (Meditech/ Boston Scientific Corporation, Natick, MA, USA)

The ‘gold standard’ of filters, this is a stainless steel filter, with a conical structure madeup of six 0.015′′ wires extending from

a central hub (Figure 22.3). Hooks at the inferior ends of the wire legs engage the caval wall, and prevent filter migration. The legs are spaced 2 mm apart at the apex andapproximately 6mm at the base. The length of the filter is 46mm and the maximaldiameter of the base is 30 mm. It can be placed in a cava measuring 28 mm or less. Thefilter design permits filling of 70% of the depth of the cone by blood clot with a reductionin the filter’s effective cross-sectional area of only 50%.54 A central hole in the filter apex allows the filter to be placed over a wire. The carrier of the filter is 24F and it is placedvia a 28F (outer diameter) sheath.

Table 22.3 Characteristics of various Food and Drug Administration-inferior vena cava Filter Size of delivery

system (OD) Maximum caval diameter (mm)

Artifactsa Magnetic resonance

Original 24F SS Greenfield

28F 28 + ++

Modified hook titanium Greenfield

14.3F 28 −

Percutaneous OTW-SS Greenfield

15F 28 ++

Bird’s nest filter 14F 40 ++++

Gunther Tulip filter 8.5F 30 +

VenaTech LGM filter’ 13.6F 28 +

VenaTech low profile ; 9F 30 +

TrapEase filter . 6F 30 +

Simon nitinol filter : 9F 28(24 mm)b +

OD= outside diameter. aArbitrary classification of magnetic resonance artifacts caused by inferior vena cava filters with increasing degree of artitacts with a number of +a. bManufacturer recommends a. cava diameter of 24 mm or less if the patient is to undergo surgery within 14 days offilter insertion.


Concerns have been raised with all three Greenfield filter designs regarding possibledecreased filtration when it is deployed more than 15 degrees off the long axis of thevessel.55–59 The clinical importance of this tilting remains unclear.

Modified hook titanium Greenfield IVC filter (Meditech/Boston Scientific Corporation)

This version of the Greenfield filter was specifically designed for percutaneousplacement (Figure 22.4). The filter is made of a titanium alloy and has a similar design tothe original Greenfield filter. The elastic properties of titanium

Figure 22.3 (a) Frontal and (b) axial views of the 24F stainless steel Greenfield IVC filter.

allow the filter to be compressed into a much smaller 12F carrier. The filter and carrierare placed via a 14.3F (outer diameter) sheath. The base of the filter is broader,measuring 38 mm, but the manufacturer continues to recommend that the filter be placedin a cava measuring 28 mm or less. The apex of the filter has no hole, which means thatthe filter can not be placed over a guide-wire. This can cause some difficulty with placement, particularly from a left femoral approach, because the carrier device can causethe sheath to kink at the region of the pelvic brim, where there may be a relatively acuteangulation of the iliac vein. The first version of this filter was withdrawn from the marketbecause of caudal migration and caval wall penetration. The hook design was modified tominimize perforation of the cava as well as to stabilize the filter within the IVC. Thetitanium alloy used to construct the filter is compatible for magnetic resonance imaging(MRI).


Percutaneous over-the-wire stainless steel Greenfield IVC filter (Meditech/Boston Scientific Corporation)

This is the most recent modification of the Greenfield filter (Figure 22.5). The design is similar to the other Greenfield filters, with a conical shape and six wire legs. The filter ismade of stainless steel. The filter is packaged in a 12F carrier and is delivered through asheath that is 15F (outer diameter). The delivery system is similar to the titanium filter,but the stainless steel filter has a hole at the apex, allowing it to be placed over a wire. Asuper-stiff guide-wire (0.035") comes as part of the kit, and facilitates passage of thefilter through tortuous venous anatomy, and over the pelvic brim. There has also been aredesign of the filter capsule used for femoral approaches. The capsule covering the filteris now plastic rather than metal, and this adds flexibility to the delivery system. Thedelivery sheath has a haemostatic rotating valve, which minimizes blood loss when thesheath dilator is being removed and the delivery device is being placed. The height of thefilter is 49mm and it has a base diameter of 32mm. Although the base diameter is large,the manufacturer recommends that placement be limited to an IVC of 28 mm or less. Thehooks on the end of four legs point upwards and two hooks on opposite sites of the filterpoint downwards. This is to help stabilize the filter and prevent tilting.

Bird’s nest IVC filter (Cook, Inc., Bloomington, IN, USA)

The Gianturco-Roehm Bird’s nest filter (BNF) is the most unique of the filter designs(Figure 22.6). All the other filters are essentially modifications of the Greenfield conical design, but the BNF is completely different. The filter con-

Figure 22.4 (a) Frontal; and (b) axial views of the modified hood titanium Greenfield inferior vena cava filter.


Figure 22.5 (a) Frontal; and (b) axial views of the percutaneous over-the-wire stainless steel Greenfield inferior vena cava filter.

sists of four 304 stainless steel wires attached to two vshaped struts, which are 0.46 mmin diameter. The wires are 25 cm long and 0.018 mm wide. The wires are arranged in acrisscrossing fashion and are fixed to the struts. The struts have small barbs on their ends,providing fixation to the cava wall. The struts are pushed into the wall of the cava (a stopon the end of the strut prevents complete IVC perforation) and the four stainless steelwires are extruded into the cava in a random fashion, resembling a bird’s nest. The carrier for the filter is 11F and the sheath through which it is placed has a 14F outer diameter.

A unique aspect of the BNF is that, it is not limited to the 28 mm IVC diameter. It canbe placed in a cava up to 40 mm in diameter. The filter is the longest of all the IVCfilters, measuring approximately 70 mm in length (requiring a relatively long length ofinfra-renal IVC to deploy), but the actual length varies because of the random positioning of the small wires when the filter is released. The small wires may prolapse above theupper filter struts, increasing the length of the filter. This randomness in positioning doesnot seem to decrease the effectiveness of the filter,58 however, it may increase the IVC occlusion rate.60 Rotating the delivery sheath two or three 360-degree twists during deployment of the fine wires may decrease the occurrence of wire prolapse.61 The original design of the filter allowed migration of the filter. It was redesigned in 1986 tostrengthen the struts, preventing migration.


The filter comes as a jugular or femoral set. The only difference between the two sets is the length of the sheath, with the jugular sheath having a longer sheath (75 cm versus40 cm). The filter and deployment is identical, so many institutions keep only the jugularfilter in stock, using it for either jugular or femoral approach. The filter is pushed throughthe sheath without a guide-wire for support. In contrast to the titanium Greenfield filter orthe VenaTech filter (see below), the flexibility of the filter makes it less likely to kink asit is placed through tortuous anatomy.

Gunther Tulip filter (Cook, Inc., Bloomington, IN, USA)

The Gunther Tulip filter is similar in appearance to the Greenfield filter, it has a conicaldesign with four main struts. Each strut has an elongated wire loop that extends alongthreequarters of the length of the strut. Each strut has a hook, which anchors the filter tothe wall of the inferior vena cava. The filter is made of an alloy. The filter comes loadedin an introducer and is placed through a 8.5 French Introducer sheath. Filters arepackaged a femoral system which is 45 cm long, or a jugular system which is 80 cm long.The filter can be placed in a cava up to 30 mm. The length of the filter is 45 mm. Thefilter is MRI compatible with minimal MRI artifact. The filter is prepackaged in anintroducing device that is placed through a sheath. When the filter is in the appropriatelocation, the covering over the filter is pulled back releasing the filter into the inferiorvena cava. The Gunther Tulip filter also has a hook at the top of the filter. Outside theUSA the filter is marketed as a removable filter. The filter is accessed from a jugularapproach and the hook is engaged and the filter can be drawn up into a sheath andremoved. This feature is not yet available in the USA but is in testing and approval by theFDA is anticipated.


Figure 22.6 (a) Frontal; and (b) axial views of the Bird’s Nest inferior vena cava filter.


Figure 22.7 (a) Frontal; and (b) axial views of the Gunther Tulip inferior vena cava filter.


VenaTech/LGM IVC filter (B.Braun, Bethlehem, PA, USA; L.G. Medical, France)

This filter is similar in appearance to the Greenfield filter. It has a conical design but withthe addition of metallic struts or side-rails attached to the filter legs (Figure 22.8). Along the length of the struts there are small hooks that engage the caval wall and provide fixation of the filter to the IVC. The new low profile Vena Tech filter has thinner side-rails with fewer stabilizing hooks (Figure 22.8c). The side-rail design optimizes filter centring within the cava and helps prevent filter tilting with deployment. The original filter material is Elgiloy, a non-ferromagnetic alloy also used for pacemaker wires, which is MRI compatible. The lowprofile filter is made withPhynox ™ a non-ferromagnetic alloy which is MRI compatible. The original filter is placed via a 13.6 F (outer diameter) sheath. The low profile filter design is placed via a9F sheath. Both styles of filters are preloaded in a carrier device that allows the filter tobe loaded into the sheath in either a jugular or femoral orientation (only one filter needsto be kept in inventory). For the original filter, the cava size should not be larger than28mm in diameter, but the width of the low profile filter is 30mm in width. The origionalfilter measures 38mm in length, and the, low profile filter measures 43mm. The firstversion of the original filter allowed incomplete opening of the filter, which decreased thefilter’s clot-trapping ability.62–65 The redesign of the filter in 1991 alleviated the problemof incomplete opening and decreased the caudal migration that was seen with theorigional filter. The filters are pushed through the sheath without any guidewire support;this can lead to problems of kinking of the sheath if there is marked angulation of thesheath. If kinking occurs, the filter should not be used, as there is a chance of pushing thefilter through the wall of the vein. The sheath should be removed and another type offilter or another access should be used.


Figure 22.8 (a) Frontal; (b) axial views of the VenaTech inferior vena cava filter and (c) frontal of low profile VenaTech.


Figure 22.9 (a)Frontal; and (b) axial views of the Simon nitinol infe-rior vena cava filter.


Simon nitinol IVC filter (Nitinol Medical Technologies, Woburn, MA, USA)

This filter is made of nitinol, a nickel and titanium alloy, which has a unique thermalmemory (Figure 22.9). This alloy enables the filter to exist as straightened wires at cooltemperatures and to reform into a predetermined filter shape at body temperatures. Thefilter construction consists of six legs in a conical design, topped by a dome ofoverlapping loops. This design gives the filter two levels of filtration. It cannot be placedin a cava greater than 28 mm and the manufacturer suggests not placing it in a cavagreater than 24 mm if the patient is to undergo surgery with general anaesthetic in thefollowing 2 weeks. The filter is contained in a 7F carrier that is placed via a 9F sheath.The sheath is infused with saline while the filter is being pushed through the sheath. Noguide-wire is used, but the flexibility of the filter makes kinking unlikely. The flexibilityof the filter and the small diameter of the sheath also allow this filter to be placed easilyfrom almost any access site, including the left jugular approach, and even an antecubitalvein. While in the sheath, the filter measures more than 8 cm in length. During filterdeployment, there is significant foreshortening of the filter to approximately 4.5 cm inlength. The foreshortening may make accurate deployment of this filter more difficultthan with the other filters. Moreover, the filter may take several hours to achieve its finalconfiguration in certain cases. The filter is MRI compatible, with minimal MRI artifacts.

TrapEase Filter (Cordis Endovascular, Miami, FL, USA)

The TrapEase filter is also made of nitinol. It is unique design composed of two basketscomposed of struts forming six diamond shapes (Figure 22.10). The baskets are connected by six straight struts. These struts contain a proximal and distal hook designedfor fixation of the filter to the caval wall. The filter is symmetrical and because of thissymmetry can be place from either a jugular or femoral approach. The filter is packagedin a plastic storage tube which is used to load the filter into a sheath. A pushing device isused to advance the filter through the sheath to the appropriate level in the inferior venacava, then the sheath is pulled back, exposing and releasing the filter. There are twosheath lengths. A 55 cm length which can be used for a right jugular or femoral approach,and a 90 cm length which can be used to place the filter from a jugular vein, femoral veinor antecubital vein. The flexibility of the filter due to the nitinol material allows for the placement of the filter through the tortuosity of the arm veins, or from the left jugularvein. The sheath is 6 F, the smallest of any of the filter sheaths. The filter is indicated forIVC diameters to 30 mm. The filter will expand to the diameter of the cava, and this willvary the length of the filter between 65 mm (the maximum length of the unexpandedfilter is 65 mm) and 50 mm. The filter is MRI compatible.


Figure 22.10 (a) Frontal; and (b) axial views of the TrapEase inferior vena cava filter.


Approach to IVC filter placement

The patient should be assessed to determine whether there is an appropriate indication forfilter placement. If such an indication is present, then an assessment of the patient’s clinical status, including BUN/creatinine and coagulation parameters, should beperformed. Patients with markedly elevated prothrombin time or platelet counts of lessthan 50 000 should have these deficiencies corrected. A discussion should be held withthe patient or family regarding the risks, benefits, and alternatives to the procedure, andconsent should be obtained.

Technique of IVC filter placement

The technique of filter placement is similar for all the filters, although there are minorvariations with individual filters.

The transfemoral approach is usually the approach of choice and is well tolerated by the patient. This approach is also convenient and comfortable for the operator. The rightfemoral vein is the most commonly used. This allows a relatively straight approach to theIVC and is the easiest to negotiate. The second choice for a site is debatable. Manyoperators prefer the left femoral vein to the right jugular. The left femoral route does havesome disadvantages, the primary of being greater resistance to filter passage due to theangle of the common iliac vein with the IVC. However, except for this disadvantage,which can usually be overcome with some minor technical manoeuvres, the left femoralapproach has the same level of comfort for the patient and the physician. The rightjugular approach is favoured by some as the primary and/or secondary site of choice.There are some disadvantages to the jugular approach. It tends to be more awkward, withless room for manoeuvring equipment, and the sterility of the procedure is more difficultto maintain. The pressure on the patient’s neck required when placing the filter may cause discomfort. Finally, using the neck approach requires negotiation past the clavicle,through the heart and eustachian valves, past the hepatic veins and past the renal andgonadal veins. When one sees filter misplacements, it gives an appreciation of thepossible pitfalls awaiting the unwary operator (Figure 22.11)!

When the access site is evaluated, it should be assessed for possible pre-existing infection, which would preclude using that entrance site. Information should also beobtained regarding possible thrombosis of the site. If ultrasound or


Figure 22.11 Examples of misplaced inferior vena cava filters. (a and b) The first case demonstrates two 24F Greenfield filters, one of which appears to be placed in the right renal vein and one in the right iliac vein. Note that a filter placed in the right gonadal vein may appear similarity as the more cephalad closer to the right hemidiaphragm. (c) The second case demonstrates a 24F Greenfield inferior vena cava filter, which was deployed within the superior vena cava.

computerized tomography (CT) examinations that include the proposed access site havepreviously been performed, these studies should be evaluated. If previous abdominal CTscans are available, these should also be evaluated. Important information that may bediscerned includes the size of the IVC, the presence of thrombus, the presence of cavalanomalies such as a left-sided cava, duplication of the IVC, or the presence of renal veinanomalies (Figure 22.12).


Evaluation of the IVC

Use of a one-wall needle with continuous suction is preferred for the puncture of either the femoral or jugular vein. The one-wall needle will help to ensure that an arterial structure is not transgressed inadvertently during venopuncture, thus avoiding thecomplication of arteriovenous fistula. Prior to using an 18-gauge needle to puncture the jugular vein, a 22-gauge needle can be used to find the vein and the larger needle placed in a parallel course (lessening the possibility of puncturing the carotid artery).Alternatively, a micropuncture set can be used to gain access. Use of ultrasound imagingguidance for the jugular puncture will lessen the possible complications of arterialpuncture or pneumothorax.

After achieving access, a hand injection of contrast can be done to check for clot in theiliac veins. A 5F pigtail catheter is then placed in the inferior vena cava and an IVC gram is performed to evaluate the diameter and patency of the cava, to assess the cava forpossible anomalies, evaluate the cava for clot and to determine the level of the renalveins. These studies may determine the access to the cava by demonstrating clot in thefemoral/iliac veins or proximal IVC, and may influence the choice of a filter. The IVCgram is performed using a catheter that can deliver contrast at a rate of 20 cm3/s for a total of 30–40 cm3. It is important to give an adequate amount of contrast in order tomaximize the chances of demonstrating venous anomalies. Some operators performselective renal venography to maximize the evaluation for significant venous anomalies,but this is not a standard practice.66 In situations where standard iodinated contrast material cannot be used to image the venous system, utilization of carbon dioxide orgadolinium is generally adequate.

The position of the renal veins is identified either by demonstrating reflux into the veins or inflow of unopacified blood into the IVC from the renal veins. Placement of thefilter below the lowest renal vein is standard. This minimizes the risk of renal veinthrombosis if the filter captures a large clot or if the filter causes IVC thrombosis.

Venous anomalies include duplication of the IVC, a leftsided IVC, multiple renal veinsand a circumaortic renal vein (Figure 22.12). The incidence of a left-sided IVC is 0.2–3%, and duplicated IVC are present in 3%.67 A duplicated IVC is most easily identifiedfrom a left-sided approach; however, since a right-sided approach is most commonly used, the operator must be alert to findings that suggest a caval anomaly.


Figure 22.12 Illustrative cases where review of other imaging studies provided useful information to help plan the inferior vena cava (IVC) filter insertion procedure (a and b). The first case demonstrates caval size in a 44-year-old female who suffered massive trauma and required bedside IVC filter insertion because of unstable patient haemodynamics. The IVC diameters were measured at 19.6mm and 23.3mm in the antero-posterior and lateral dimensions, respectively. The right common femoral vein is patent with a normal Doppler waveform pattern during performance of an augmentation manoeuvre. The filter was inserted with the aid of portable fluoroscopy. (c) The second case demonstrates a large thrombus extending into the IVC from the left lower extremity on a coronal CT reformation. The cause of the thrombosis was felt to be due to May-Thurner syndrome. This information indicated that the IVC filter insertion procedure should be performed via a jugular route. (d) The final case demonstrates sequential axial CT images in a patient with a left-sided IVC. In this case, Filter insertion would require a left common femoral vein access. (e—h) Shown over page.


Figure 22.12 Continued. (e-h) The final case demonstrates sequential axial CT images in a patient with a left-sided IVC. In this case, Filter insertion would require a left common femoral vein access.

Such findings include a small diameter IVC, lack of reflux or lack of inflow from the leftiliac vein, and increased inflow from the left renal vein, suggesting termination of theleft-sided IVC into the left renal vein. If such findings are identified, then further work-up to confirm the presence of a left-sided cava is essential. If duplication of the IVC is confirmed, then a second filter should be placed in the duplicated cava to prevent embolithrough the duplicated system. If multiple renal veins or a circumaortic renal vein isfound, then the filter must be placed either below the lower vein, or less commonly, inthe suprarenal IVC. A filter placed between the renal veins has the theoretical potential ofallowing clot to pass from the lower renal vein into the upper renal vein, thus bypassingthe filter.

Accurate measurement of the IVC diameter is important since all of the filters exceptthe Bird’s nest filter are limited to a caval diameter of 28–30 mm or less. If the cava is larger than 28–30 mm on the anteroposterior projection, a lateral cavagram should beobtained, since a 28–30 mm wide but flat IVC will have a diameter much less than 28–30 mm when it is made circular by placing a filter.68 Use of a radio-opaque measuring device or a marking catheter will facilitate proper measurement. Not only the diameter,but also the length of cava available for filter placement must be considered whenchoosing the type of filter. The length of the cava between the iliac confluence and thelowest renal vein may be too short to accommodate some filters particularly withduplication of the renal veins, or when using the Bird’s nest filter. If the cava diameter is greater than 28–30 mm and a Bird’s nest filter is not available, filters can then be placed in both common iliac veins.


Figure 22.13 Important venous anomalies, which potentially effect placement of inferior vena cava (IVC) filters. (a) The first case demonstrates a duplicated IVC in a patient who suffered massive trauma and required prophylactic IVC filter insertion. In this case, two Greenfield IVC filters were inserted. The size of the cava is determined by comparison with the radio-opaque ruler placed under the patient. (b) The second case demonstrates a left-sided IVC. (c) The final case demonstrates a circumaortic left renal vein (the lower renal vein). In this particular case, the IVC filter was inserted below the lower left renal vein.


If thrombus is identified on injection into the femoral vein, or on the IVC gram, an alternative approach to filter placement is usually required. Again, the length of IVCabove the thrombus may be an important factor in selecting the filter to be placed. Ifthrombus is present in the suprarenal IVC, then filter placement may not be possible.

IVC filter deployment

Following the evaluation of the IVC and associated venous structures, the diagnostic IVCcatheter is exchanged for a dilator(s). The placement site is dilated to an appropriate size for the filter. For the original stainless steel 24F Green-field filter, an 8 mm angioplasty balloon catheter is used to dilate the subcutaneous tissues and venous entrance site. As the dilatation is beingdone, and the filter introducer is inserted, it is crucial that the guide-wire is not withdrawn and re-advanced. This avoids the possibility that the wire inadvertently becomespositioned in a tributary of the IVC, such as an ascending lumbar vein (femoral approach)or renal or gonadal vein (jugular approach).

The filter is then placed into the IVC below the level of the renal veins. The position of the renal veins is determined from the cavagram. An internal or external reference for thelevel of the renal veins needs to be established. A common internal reference is avertebral body level. External references might be a radio-opaque scale placed under/on the patient’s back prior to the procedure, or a clamp placed anteriorly over the patient following the cavagram (Figure 22.13a). Efforts should be made not to move the table in relationship to the image intensifier following the cavagram, since significant parallaxmay develop which could result in filter misplacement. If the table is moved, then carefulreview of the reference landmarks is necessary prior to placement of the filter.

In special circumstances, a suprarenal filter may be required. Such circumstances include thrombus in the cava extending to or above the renal veins, renal vein thrombosis,thrombosis of an enlarged ovarian or gonadal vein, or recurrent pulmonary embolismfollowing thrombosis of a previously placed IVC filter, or IVC ligation (Figures 22.14).69

The presence of tumour thrombus from IVC extension from a renal cell carcinoma isanother less common indication.70 A less well-defined reason for suprarenal IVC filter placement would be in a pregnant woman or a woman who is anticipating futurepregnancies.50, 71 The rational for suprarenal placement is to avoid compression of the filter by the gravid uterus and to protect against any possible ovarian veinthromboembolism.

Following filter deployment, a digital cavagram may be performed to demonstrate the appropriate deployment of the filter and the degree of caval coverage. If a cavagram isnot done, a radiograph documenting the filter position needs to be obtained.

The filter placement device is removed and gentle compression is applied to the vein to obtain haemostasis. Once haemostasis is obtained, a Band-Aid or steri-strips can be applied to the skin. The patient is cautioned to keep the leg straight for 4–6 h (longer if the patient is anticoagulated). If the jugular approach has been used, the patient is usuallyplaced in a semi-upright position. The patient should be closely monitored for 4 h, withfrequent checks of the puncture site.


The timing of IVC filter insertion procedure

The timing of IVC filter insertion of patients with thrombo-embolism must be determined by the indications for the IVC filter. Patients with absolute contraindications toanticoagulation should have a filter placed when the diagnosis of DVT or PE is made,regardless of the time of day. Similarly, patients who have documented new or recurrentPE while adequately anticoagulated should also have a filter inserted at the time ofdiagnosis. In certain cases, a delay of several hours may be reasonable in patients whodevelop a complication of anticoagulation, or in whom DVT has progressed despiteadequate anticoagulation without evidence of PE.

Specific situations

Although most of the filters can be deployed easily and correctly in most patients, thereare a few special circumstances that may be handled more easily with a specific filter.

If the length of the IVC between the renal veins and the iliac confluence is short, perhaps because of a low-lying renal vein, or duplicated renal veins, the Bird’s nest filter may be too long. The Bird’s nest filter may also be too long if a suprarenal filter is required; the thin wires may prolapse into the right atrium or even the right ventricle.

If the IVC is larger than 28–30 mm (defined as a megacava, incidence 1–3%), then a Bird’s nest filter would be the best choice. If a Bird’s nest filter is not available in the setting of an enlarged cava, then bilateral common iliac filters will be required.

If a left-sided femoral or jugular vein approach is required, a flexible filter deliverysystem such as the Simon nitinol filter or the Bird’s nest filter would be preferable. TheVenaTech Gunther or Greenfield titanium filters, which are not placed over a wire guide,maybe poor choices when the venous anatomy is tortuous. The Simon nitinol andTrapEase filters have the additional advantage of being able to be placed from anantecubital approach.72 This is


Figure 22.14 Illustrative situations requiring that a suprarenal inferior vena cava (IVC) filter be inserted. (a and b) The first case demonstrates a large, free-floating thrombus within the IVC, extending up from the left lower extremity in a 30-year-old patient with ulcerative colitis. The thrombus extended up to the level of the renal veins, so a filter was inserted in a suprarenal IVC location via the right internal jugular approach. (c–d) The second case demonstrates a 42-year-old patient with an IVC sarcoma diagnosed by percutaneous biopsy. The tumor was located just below the renal veins. The patient was felt to be at risk for embolization and developed a bleeding complication while on anticoagulation. There was insufficient room in the cava to place the filter below the renal veins, so that it was placed in a suprarenal location. The final case concerns a 30-year-old female with pelvic malignancy who developed right-sided ovarian vein thrombosis, well demonstrated on the contrast-enhanced CT images. This case required a suprarenal IVC filter as well. (e–j) Shown over page.


(e–j) The second case demonstrates a 42-year-old patient with an IVC sarcoma diagnosed by percutaneous biopsy. The tumor was located just below the renal veins. The patient was felt to be at risk for embolization and developed a bleeding complication while on anticoagulation. There was insufficient room in the cava to place the filter below the renal veins, so that it was placed in a suprarenal location. The final case concerns a 30-year-old female with pelvic malignancy who developed right-sided ovarian vein thrombosis, well demonstrated on the contrast-enhanced CT images. This case required a suprarenal IVC filter as well.


advantageous if other access sites are not available, or if the patient has a bleeding diathesis. The peripheral venous access allows easier observation and control of bleedingat the access site.

Complications of IVC filters

Complications can be divided into several categories, which include those associated withplacement of the filter and the longer-term problems associated with IVC filtration (Table 22.4). The longer-term complications will be discussed in the following performancesection.

Procedural complications involve the puncture site, including haematoma, infection, arterial-venous fistula, and access site thrombosis. If a jugular approach is used, puncture of the carotid or vertebral arteries can occur, as well as vocal cord paralysis, arrhythmia,and pneumothorax. Delivery problems include air embolism, misplacement of the filter,and perforation of venous structures.

IVC filter performance

There have been few studies with long-term focused followup of IVC filters. Objectiveevaluation of IVC filters

Table 22.4 Complications of inferiro vena cava filter placement

• Recurrent pulmonary embolism,

• Access site thrombosis

• Inferior vena cava thrombosis

• Filter migration

• Inferior vena cava perforation

• Filter breakage

• Guide-wire entrapment

• Operator errors


should ideally include a multiplicity of criteria (Table 22.5). Reported problems are largely anecdotal. Series of various filters differ in how filter evaluation is performed, butthis depends largely on clinical symptoms, rather than objective data.

Recurrent clinically symptomatic pulmonary embolism following filter placementappears to be uncommon, with pulmonary embolism being reported in approximately 2–5%.60, 73 However, since pulmonary emboli are commonly asymptomatic, it is unclear whether filter patients may be having asymptomatic emboli. Also, since pulmonaryembolism can be a difficult diagnosis, it is possible that due to a lack of objective datarecurrent pulmonary embolism is higher than reported.

Thrombotic complications following filter placement also seems to be uncommon. Thrombosis can involve the insertion site, and the inferior vena cava. Insertion sitethrombosis has been reported with all filter types and occurs in both the femoral andjugular veins (Figure 22.15). The initial concern for insertion site thrombosis developed with the percutaneous placement of the 24F Greenfield filter. With changes in technique,there was a decrease in the thrombosis rate with placement of the large delivery system.The incidence

Table 22.5 Inferior vena cava filter performance criteria

• Percutaneous insertion

• Ease of deployment

• Effective filtration

• Maintenance of caval patency

• Biological compatibility

• Mechanical stability

• Cost

• Magnetic resonance imaging compatibility

• Retrievability


Figure 22.15 An example of access site thrombosis. The patient had a catheter inserted into the right common femoral vein several days before the inferior vena cava (IVC) filter insertion; this catheter had been removed prior to the cavagram. On the cavagram, performed from the jugular approach, a filling defect is identified within the right common femoral vein. Access site thrombosis from IVC filter insertion procedures appears similarly.

of insertion site thrombosis has been reported with rates from 2 to 35%.57, 63, 74–76 This wide range represents the difference between evaluation of asymptomatic accessthrombosis (higher end of the scale) and symptomatic femoral vein thrombosis (lowerend of the scale). Unfortunately, no study has been performed with objective evaluationof the insertion site in all patients undergoing filter placement.

A similar lack of objective evaluation plagues the statistics regarding IVC occlusion.The mechanism of IVC occlusion may be variable (Figure 22.16). Possible causes can be trapping of a large embolus that causes occlusion of the filter, thrombus forming de novowithin the filter, or the development of intimal hyperplasia caused by the presence of thefilter. The caval occlusion rate is probably between 4 and 15%, with no demonstrabledifference between the various filters.60, 63, 76 These figures represent symptomatic caval occlusion rates. The asymptomatic caval occlusion rate is considerably higher, up to22%.9, 73, 76, 77 However, no study has been performed that objectively evaluates caval occlusion on a consistent basis. Both femoral vein and IVC thrombosis can lead tophlegmasia cerulea dolens, which can be severe and represent a threat to life and limb.

Migration has been reported with all of the filters (Figure 22.17). The most common migration is caudal migration, particularly with the original stainless steel Greenfieldfilter. Fortunately, major migration into another area of the


Figure 22.16 An example of a thrombotic complication following infe-rior vena cava (IVC) filter insertion. The patient developed a deep venous thrombosis after a cerebral vascular accident (subarachnoid haemorrhage from a ruptured aneurysm). A Simon nitinol IVC filter was inserted. Approximately 8 weeks after IVC filter insertion, the patient developed lower extremity swelling, which upon work-up was determined to be due to the thrombosed IVC.

body (i.e. heart or lungs) is rare. A specific migration problem reported recently is theaccidental capturing of the filter by wires, which are being used to place central lines.78–82 The VenaTech and the over-the-wire Greenfield 12F stainless steel filters appear to be prone to this complication.83 The use of a J-guide-wire seems to be particularly prone toentanglement in the filters.83

Although the filters would seem to be most prone to this complication in the earlyperiod after placement, some of the displaced filters had been placed more than a monthpreviously. Because the operators may not realize why they are having difficultyremoving the wire after it is entangled, there is the tendency to pull harder on the wire,which leads to fracturing of the filter and relocation of the filter. These filters have beenreported as being displaced into the right atrium and brachiocephalic veins.

Perforation of the wall of the cava has been reported with most filters, particularly the Greenfield designs and the Bird’s nest filter (Figure 22.17).73 Fortunately, perforation is usually clinically insignificant and the patients are asymptomatic. Occasionallyperforation will lead to retroperitoneal haemorrhage, particularly in patients who areanticoagulated.84 Perforations into the small bowel, aorta, and lumbar sympathetic ganglion, have all been reported.85, 86 Quadraplegic patients who undergo the ‘quad cough’ procedure to improve their respiratory status are particularly subject to filter migration and perforation of the cava wall.87, 88


Figure 22.17 Examples of inferior vena cava (IVC) filter migration and perforation. (a) The patient sustained a cervical spine injury and had a prophylactic titanium Greenfield IVC filter inserted. A repeat cavogram—anteroposterior projection (b) and lateral projection (c)—was performed because of change in position of the IVC filter detected on plain film of the abdomen approximately 90 days after insertion. The anteroposterior projection demonstrates that the filter has migrated inferiorly such that it is a full vertebral body below the renal veins. On the lateral cavagram, a filter strut is positioned anterior to the IVC, consistent with caval perforation. (d) A CT scan demonstrates that the strut is located within the second portion of the duodenum. The patient had the perforated strut removed surgically. Note that the patient had been treated with a form of respiratory therapy consisting of the ‘quadriplegic cough’, a form of assisted coughing, to help clear pulmonary secretions. The forces exerted upon the filter during this type of abdominal compression probably cause the filter strut perforation.


Filter breakage has been reported with all the filters. Breakage of the legs of the Greenfield filters, the struts of the Bird’s nest filter, the struts of the VenaTech and nitinolfilter have all been described. In most cases the filter will not change in appearance orposition, but in some cases the broken filter pieces may embolize through the vascularsystem or migrate through the wall of the cava.

Despite almost 30 years of experience with various IVC filters, there is a surprisinglack of prospective studies concerning the effectiveness of filters in preventing PEs. Mostseries of IVC filters have demonstrated reduced rates of PEs with filters when comparedto historical controls.

In 1998, the first prospective clinical trial of IVC filters in preventing PE in patients with proximal DVT was reported.89 The study was a two-by-two factorial design in which a total of 400 patients with proximal DVT at risk for PE were enrolled to receivean IVC filter (200 patients) or no filter (200 patients), and to receive lowmolecularweight heparin (195 patients) or unfractionated heparin (205 patients). The rates of recurrent thromboembolism, death, and major bleeding were analysed at day 12 and at 2 years after filter insertion. The study demonstrated astatistically significant reduction in PE rates at 12 days with IVC filters (1.1% with afilter versus 4.8% without a filter, p=0.03). However, the 2 year follow-up demonstrated an excessive rethrombosis rate in the filtered population (20.8% with filters versus 12.6%without a filter, p=0.02). At 2 years follow-up, the recurrent PE rates were not statistically significantly different (3.4% with a filter versus 6.3% without a filter,p=0.16). No mortality benefit occurred with IVC filtration.

While providing useful performance data, the study has been criticized for severalreasons. First, only approximately one-half of the original planned patient enrollment wasmet when the study was stopped. It is possible that with a larger patient population, thetrend in differences with PE rates at 2 years may have become significant. Second, intheir discussion, the authors state that ‘at two years the initial benefits of filters were counterbalanced by a significant increase in recurrent DVT, which may be related tothrombosis at the filter site’. The result must be interpreted with caution due to the difficulties in detecting recurrent thromboembolism in such cases. It is entirely possiblethat the higher recurrent thrombosis rate was a result of the filters performing theirfunction. A number of different IVC filters were inserted in the trial. Finally, the studyhas been criticized for using filters in addition to anticoagulation, which is often notpossible. Despite these criticisms, it is hoped that the study will provide impetus foradditional prospective IVC filter studies, which will help to better define the operationalcharacteristics of these devices in different patient populations.

Future directions

The next innovation in IVC filters will probably be the temporary filters (Figure 22.18). Temporary filters are placed into the inferior vena cava with some type of mechanism,attached to the filter, that remains outside the venous system and that allows the filter tobe removed after some limited period of time.90–92 The filter needs to be removed before it becomes incorporated into the caval wall. Presently, there are no devices available that


have been tested and approved by the FDA for temporary caval interruption. Sometemporary filters have been used in Europe, and have started clinical trials in the USA.

Unfortunately, there have been several deaths associated with the use of one of thetemporary filters, the Tempofilter (B. Braun-Celsa, Chasseneuil, France)93 Temporary filters would be ideal for patients who only need short-term protection, such as trauma patients, patients in the peri-operative period (particularly orthopaedic surgery), patients with large iliocaval thrombus, pregnant patients, and patients with temporary restrictedmobility. Use of this filter will require an improved understanding of the patients who areat risk for DVT and pulmonary embolism.19

Retrievable filters are another experimental approach to IVC filtration.20, 94–96 These filters are detached into the IVC and are later removed using some type of snare device.The filters usually have some type of hook that allows them to be captured, drawn into asheath and removed from the body. The Gunther Tulip filter is used as a retrievable filteroutside the USA, and is in an FDA trial in the USA. Approval for retrieval indication isexpected. The time period over which the filters can be removed is limited to a fewweeks, after which this become endothelialized and retrieval is unreliable.

Figure 22.18 An example of a temporary inferior vena cava (IVC) filter called the Tempofilter. The filter is essentially a VenaTech filter supported in place by a tether, which is placed subcutaneously in the neck. The filter can be left in place for a period of 6 weeks, when removal. is attempted. The filter strut lack hooks, which facilitates its removal

Conclusions

IVC filter placement has become a common and acceptable procedure for protectingpatients at risk of PE who cannot be anticoagulated or who have failed anticoagulation.With the relative safety and ease of percutaneous placement of IVC filters there has been an expansion of the indications for filter placement. The most common and accepted of


the expanded indications is for specific categories of severely injured trauma patients.Patients with head trauma, spinal cord injury, multiple long-bone and pelvic fractures are considered to be at very high risk for PE and are often patients who can not beanticoagulated. These patients, as well as many patients with traditional indications, onlyneed IVC filters for a limited time. Some of these patients would be candidates for atemporary/retrievable filter, once such a filter is available.

A primary difficulty in choosing a device is the paucity of well-designed studies with good clinical and objective followup data. The published literature does not demonstratethat any one filter is clearly superior. In the absence of such data, the operator shouldchoose a device based on an understanding of the filter characteristics, the operator’s comfort with the deployment characteristics of the device, and the constraints of anindividual patient’s anatomy. Ideally, largescale studies of filters would be performed to evaluate the relative safety and effectiveness of all the filters currently available.

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34. Khansarinia S, Dennis JW, Veldenz HC, Butcher JL, Hartland L. Prophylactic Greenfield filter placement in selected high-risk trauma patients. J Vasc Surg 1995; 22


(3): 231–6. 35. Rogers FB, Shackford SR, Ricci MA, Wilson JT, Parsons S. Routine prophylactic

vena cava filter insertion in severely injured trauma patients decrease the incidence of pulmonary embolism. J Am Coll Surg 1995; 180(6): 641–7.

36. Winchell RJ, Hoyt DB, Walsh JC, Simons RK, Eastman AB. Risk factors associated with pulmonary embolism despite routine prophylaxis: implications for improved protection. J Trauma 1994; 37(4): 600–6.

37. Brasel KJ, Borgstrom DC, Weigelt JA. Cost-effective prevention of pulmonary embolus in high-risk trauma patients. J Trauma 1997; 42(3): 456–60; discussion 60–2.

38. Britt LD, Zolfaghari D, Kennedy E, Pagel KJ, Minghini A. Incidence and prophylaxis of deep vein thrombosis in a high risk trauma population. Am J Surg 1996; 172(1): 13–14.

39. Gosin JS, Graham AM, Ciocca RG, Hammond JS. Efficacy of prophylactic vena cava filters in high-risk trauma patients. Ann Vasc Surg 1997; 11(1): 100–5.

40. Headrick JR, Jr, Barker DE, Pate LM, Horne K, Russell WL, Burns RP. The role of ultrasonography and inferior vena cava filter placement in high-risk trauma patients. Am Surg 1997; 63(1): 1–8.

41. Montgomery KD, Geerts WH, Potter HG, Helfet DL. Thromboembolic complications in patients with pelvic trauma. Clin Orthop 1996; 329:68–87.

42. Nagy KK, Duarte B. Post-traumatic inferior vena caval thrombosis: case report. J Trauma 1990; 30(2): 218–21.

43. Nunn CR, Neuzil D, Naslund T et al. Cost-effective method for bedside insertion of vena caval filters in trauma patients [see comments]. J Trauma 1997; 43(5): 752–8.

44. Quirke TE, Ritota PC, Swan KG. Inferior vena caval filter use in U.S. trauma centers: a practitioner survey. J Trauma 1997; 43(2): 333–7.

45. Rogers FB, Shackford SR, Ricci MA, Huber BM, Atkins T. Prophylactic vena cava filter insertion in selected high-risk orthopaedic trauma patients. J Orthop Trauma 1997; 11(4): 267–72.

46. Rogers FB, Strindberg G, Shackford SR et al. Five-year follow-up of prophylactic vena cava filters in high-risk trauma patients. Arch Surg 1998; 133(4): 406–11; discussion 12.

47. Rosenthal D, McKinsey JF, Levy AM, Lamis PA, Clark MD. Use of the Greenfield filter in patients with major trauma. Cardiovasc Surg 1994; 2(1): 52–5.

48. Spain DA, Richardson JD, Polk HC, Jr, Bergamini TM, Wilson MA, Miller FB. Venous thromboembolism in the high-risk trauma patient: do risks justify aggressive screening and prophylaxis? J Trauma 1997; 42(3): 463–7; discussion 7–9.

49. Zolfaghari D, Johnson B, Weireter LJ, Britt LD. Expanded use of inferior vena cava filters in the trauma population. Surg Ann 1995; 27: 99–105.

50. Teodorescu V, Schanzer H. Management of thrombophlebitis in the prepartum period. A case report. J Cardiovasc Surg 1992; 33(4): 448–50.

51. Dorfman GS. Percutaneous inferior vena caval filters. Radiology 1990; 174(3 Pt 2): 987–92.

52. Simon M, Palestrant AM. Transvenous devices for management of pulmonary embolism. Cardiovasc Intervent Radiol 1980; 3:308–18.

53. Norris SC, Greenfield LJ, Herrmann JB. Free-floating iliofemoral thrombus: a risk of pulmonary embolism. Arch Surg 1985; 120: 806–8.

54. Greenfield LJ, McCurdy JR, Brown PP, Elkins RC. A new intracaval filter permitting continued flow and resolution of emboli. Surgery 1973; 73:599.

55. Kinney TB, Rose SC, Weingarten KE, Valji K, Oglevie SB, Roberts AC. IVC filter


tilt and asymmetry: comparison of the over-the-wire stainless-steel and titanium Greenfield IVC filters. JVIR 1997; 8(6): 1029–37.

56. Sweeney TJ, Van Aman ME. Deployment problems with the titanium Greenfield filter [see comments]. JVIR 1993; 4(5): 691–4.

57. Greenfield LJ, Cho KJ, Proctor M et al. Results of a multicenter study of the modified hook-titanium Greenfield filter. J Vasc Surg 1991; 14(3): 253–7.

58. Katsamouris AA, Waltman AC, Delichatsios MA, Athanasoulis CA. Inferior vena cava filters: in vitro comparison of clot trapping and flow dynamics. Radiology 1988; 166(2): 361–6.

59. Thompson BH, Cragg AH, Smith TP, Barenieweskih, Barnhart WH, De Jong SC. Thrombus trapping efficiency of the Greenfield filter in vivo. Radiology 1989; 172:979–81.

60. Mohan CR, Hoballah JJ, Sharp WJ, Kresowik TF, Lu CT, Corson JD. Comparative efficacy and complications of vena caval filters. J Vasc Surg 1995; 21(2): 235–45; discussion 45–6.

61. Roehm JO, Jr, Thomas JW. The twist technique: a method to minimize wire prolapse during Bird’s Nest filter placement. J Vasc Interven Radiol 1995; 6(3): 455–9.

62. Cull DL, Wheeler JR, Gregory RT, Synder SO, Jr, Gayle RG, Parent FN. The Vena Tech filter: evaluation of a new inferior vena cava interruption device. J Cardiovasc Surg 1991; 32(5): 691–6.

63. Murphy TP, Dorfman GS, Yedlicka JW et al. LGM vena cava filter: objective evaluation of early results. JVIR 1991; 2(1): 107–15.

64. Ricco JB, Dubreuil F, Reynaud P et al. The LGM Vena-Tech caval filter: results of a multicenter study. Ann Vasc Surg 1995; 9 Suppl: S89–100.

65. Reed RA, Teitelbaum GP, Taylor FC et al. Incomplete opening of LGM (Vena Tech) filters inserted via the transjugular approach. JVIR 1991; 2:441–5.

66. Hicks ME, Malden ES, Vesely TM, Picus D, Darcy MD. Prospective anatomic study of the inferior vena cava and renal veins: comparison of selective renal venography with cavography and relevance in filter placement. JVIR 1995; 6(5): 721–9.

67. Sardi A, Minken SL. The placement of intracaval filters in an anomalous (left-sided) vena cava. J Vasc Surg 1987; 6(1): 84–6.

68. Prince MR, Novelline RA, Athanasoulis CA, Simon M. The diameter of the inferior vena cava and its implications for the use of vena caval filters. Radiology 1983; 149(3): 687–9.

69. Orsini RA, Jarrell BE. Suprarenal placement of vena caval filters: indications, techniques, and results. J Vasc Surg 1984; 1(1): 124–35.

70. Brenner DW, Brenner CJ, Scott J, Wehberg K, Granger JP, Schellhammer PF. Suprarenal Greenfield filter placement to prevent pul-monary embolus in patients with vena caval tumor thrombi. J Urol 1992; 147(1): 19–23.

71. Matchett WJ, Jones MP, McFarland DR, Ferris EJ. Suprarenal vena caval filter placement: follow-up of four filter types in 22 patients. JVIR 1998; 9(4): 588–93.

72. Kim D, Schlam BW, Porter DH, Simon M. Insertion of the Simon Nitinol caval filter: value of the antecubital vein approach. AJR 1991; 157:521–2.

73. Ferris EJ, McCowan TC, Carver DK, McFarland DR. Percutaneous inferior vena caval filters: follow-up of seven designs in 320 patients [see comments]. Radiology 1993; 188(3): 851–6.

74. Hicks ME, Middleton WD, Picus D, Darcy MD, Kleinhoffer MA. Prevalence of local venous thrombosis after transfemoral placment of a Bird’s Nest vena caval filter. JVIR 1990; 1:63–8.


75. Molgaard CP, Yucel EK, Geller SC, Knox TA, Waltman AC. Accesssite thrombosis after placement of inferior vena cava filters with 12–14-F delivery sheaths [see comments]. Radiology 1992; 185(1): 257–61.

76. Millward SF, Marsh JI, Peterson RA et al. LGM (VenaTech) vena cava filter: clinical experience in 64 patients [see comments]. JVIR 1991; 2(4): 429–33.

77. Roehm JOF, Johnsrude IS, Barth MH, Gianturco C. The bird’s nest inferior vena cava filter: progress report. Radiology 1988; 168: 745–9.

78. Johnson D, Harshfield D. Radiological case of the month. Inadvertant guidewire entrapment by IVC filter during subclavian line place-ment. J Arkan Med Soc 1993; 89(10): 517–8.

79. Loesberg A, Taylor FC, Awh MH. Dislodgement of inferior vena caval filters during “blind” insertion of central venous catheters. AJR 1993; 161:637–8.

80. Amesbury S, Vargish T, Hall J. An unusual complication of central venous catheterization. Chest 1994; 105:905–7.

81. Marelich GP, Tharratt RS. Greenfield inferior vena cava filter dislodged during central venous catheter placement. Chest 1994; 106(3): 957–9.

82. Urbaneja A, Fontaine AB, Bruckner M, Spigos DG. Evulsion on a Vena Tech filter during insertion of a central venous catheter. JVIR 1994; 5:783–5.

83. Kaufman JA, Thomas JW, Geller SC, Rivitz SM, Waltman AC. Guide-wire entrapment by inferior vena caval filters: in vitro evalu-ation. Radiology 1996; 198(1): 71–6.

84. Howerton RM, Watkins M, Feldman L. Late arterial hemorrhage secondary to a Greenfield filter requiring operative intervention. Surgery 1991; 109:265–8.

85. Appleberg M, Crozier JA. Duodenal penetration by a Greenfield caval filter. Aus N Z J Surg 1991; 61(12): 957–60.

86. al Zahrani HA. Bird’s nest inferior vena caval filter migration into the duodenum: a rare cause of upper gastrointestinal bleeding. J Endovasc Surg 1995; 2(4): 372–5.

87. Balshi DD, Contelmo NDL, Monzoian JO. Complications of caval interruption by Greenfield filter for deep venous thrombosis in quadriplegics. J Vasc Surg 1989; 9:558–62.

88. Kinney TB, Rose SC, Valji K, Oglevie SB, Roberts AC. Does cervical spinal cord injury induce a higher incidence of complications after prophylactic Greenfield inferior vena cava filter usage? JVIR 1996; 7:907–15.

89. Decousus H, Leizorovicz A, Parent F et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. N Engl J Med 1998; 338:409–15.

90. Thery C, Asseman P, Amrouni N et al. Use of a new removable vena cava filter in order to prevent pulmonary embolism in patients submitted to thrombolysis. Eur Heart J 1990; 11:334–41.

91. Nakagawa N, Cragg AH, Smith TP, Castaneda F, Barnhart WH, DeJong SC. A retrievable nitinol vena cava filter: experimental and initial clinical results. J Vasc Intervent Radiol 1994; 5(3): 507–12.

92. Vorwerk D, Schmitz-Rode T, Schurmann K, Tacke J, Guenther RW. Use of a temporary caval filter to assist percutaneous iliocaval thrombectomy: experimental results. JVIR 1995; 6:737–40.

93. Rossi P, Arata FM, Bonaiuti P, Pedicini V. Fatal outcome in atrial migration of the Tempofilter. Cardiovasc Intervent Radiol 1999; 22(3): 227–31.

94. Neuerburg J, Gunther RW, Rassmussen E et al. New retrievable percutaneous vena cava filter: experimental in vitro and in vivo evaluation. CVIR 1993; 16:224–9.


95. Millward SF, Bormanis J, Burbridge BE, Markman SJ, Peterson RA. Preliminary clinical experience with the Gunther temporary inferior vena cava filter. J Vasc Intervent Radiol 1994; 5(6): 863–8.

96. Epstein DH, Darcy MD, Hunter DW et al. Experience with the Amplatz retrievable vena cava filter. Radiology 1989; 172(1): 105–10.

97. Stephen JM, Feied CF. Venous thrombosis. Postgrad Med 1995; 97(1): 36–46.


blank.

Training in endovascular surgery

23 P.R.F BELL

Introduction

With the increasing trend for vascular procedures to be dealt with by endovasculartechniques, the necessity of surgeons to become proficient in endovascular surgerybecomes more obvious. The question is not whether this is necessary, but how to achieveit. Most vascular societies throughout the world are now trying to evolve programmes fortraining and recognition.1

We start from a situation where interventional radiologists have been the providers ofendovascular treatment. This is partly historical, based on their involvement withangiography and the need for imaging of high quality to allow accurate placement ofvarious devices. The increasing use of duplex technology means that diagnosticangiography is being performed less and less frequently, taking away the training groundfor radiologists and others, who used to learn to pass catheters and wires whileperforming routine angiography. Therefore, the question of who does the endovascularprocedures is of less relevance than how those individuals are to be trained. In 19932 a paper was published by the American Vascular Surgical Society setting out what they feltwere the credentialling and training requirements for vascular surgeons. The currentpublication1 sets out what is required at present in the way of training in order thatvascular surgeons can be competent in the basic skills needed to perform all presentlyaccepted diagnostic and therapeutic endovascular procedures safety and effectively,though this is not meant to be limiting for the future. As there are no set criteria forEurope, those published in the USA are worth mentioning. Although these regulations areset out for surgeons, in future the barriers or divisions between interventionalists, whetherradiologists or cardiologists, and surgeons will become increasingly blurred and a set ofcriteria needs to be developed for everyone who intends to practice endovascular surgery.Most interventional societies differ in their requirements for training because no oneactually knows how many of any procedure is enough. However, it would seem frompublished work that approximately 100 catheterizations or angiograms and approximately50 interventions are a starting point.

Training should certainly start by those involved being aware of the wide variety of equipment available. This should be followed by training to pass wires and catheters inmany of the excellent models now available, first with the naked eye and then in anenclosed box system. After this has been accomplished, and after the trainer feels they arecapable, then the skills can be translated to the operating theatre under supervision, firstusing exposed vessels for entry and C-arm in theatre and the percutaneous puncture in the

Xray suite. The basic need is for individuals aspiring to become qualified in endovasculartechniques to learn to pass wires and catheters percutaneously, so that they can be locatedat any point in the vascular tree. The techniques needed for this are readily learnt bysurgeons who already have significant tactile skills. Once the trainee has learned the artof wire passing and placing catheters he can progress to the next stage, which would be toinsert stents or stent/graft combinations after learning to inflate balloons. As mentionedearlier, time spent learning about the equipment available is vital, and a good deal of timeshould be spent doing this. The language is completely new to surgical trainees and needsto be appreciated by those entering this field. The trainee need not learn about all thewires and catheters available, but there is a basic set with which he/she should befamiliar.

Before the practitioner can work on his own, he needs to be able to get out of problemsthat he may create and should be versed in the techniques of aspiration of thrombus andthe insertion of coils to prevent bleeding from ruptured vessels. Because he is a surgeon,ultimately operative treatment to rescue a patient from an endovascular procedure thatgoes wrong is possible.

Fundamental skills necessary

These include gaining access to the vascular system, positioning catheters in variouslocations, dilatation of stenoses and assessment using angiography, and can be learnedfirst of all on models, which should be available in any training department. The traineewill require instruction on how to use the models and how to direct wires towards variousvessels. It is important that the trainee progresses from being able to see what he is doingto a model where the wire cannot be seen by the naked eye. The range of day-to-day equipment such as J-wires, straight wires, Terumo wires and various catheters such as a pigtail for angiography, cobra catheter, renal catheter, a sidewinder or a road runner,should all be necessary starting points on this model. Using this variety of catheter itshould be possible to instruct the trainee on how to gain access to most of the vessels inthe model. Once the trainee is proficient at this, it is then necessary to encourage the sameactivity in animal models, which is not possible in the UK but is in the USA, Ireland andparts of Europe. Animal models are a very useful way of learning to pass wires in vivoand should be used if available. If not, an alternative is to learn to pass wires in theatre,using exposed arteries, in the groin for example, and carrying out angiography pre- and postoperatively. This will allow adequate training to be gained.

Finally, the trainee can be taught how to pass wires subcutaneously using local anaesthesia in patients.

Interventions

Once the trainee is proficient at passing wires and entering vessels, the relatively simpletechnique of balloon angioplasty should be learnt, again first on the model and then inanimals or patients, after appropriate training. During this phase of training the trainee


will need to become aware of the sizes of balloons and stents used in various arteries andalso of the way in which angiography is performed and the concentrations of contrastused to minimize renal damage.

As mentioned earlier, the requirement should probably be that the surgeon or trainershould have been involved in 100 catheterizations and 50 interventions such asangioplasty or stent deployment. Of the catheterizations, 75% should be arterial and 25%can be venous; the same would be true of the interventions.

These will be the basic requirements for training both trainers and trainees. Thereafter, there would need to be special training for more complex interventions, such as insertingcoils and stent graft combinations. Each training session might be device specific and atleast require exposure to a lecturer or in vitro sessions with guidance from a proctor for the first two or three cases. This will always be necessary as the indications forendovascular procedures increase.

Exactly how much training is required remains uncertain. One of the real questions is how the trainee obtains the training outlined in this brief chapter. At present, becausemany of the existing vascular surgeons have not achieved the minimum requirements setout here, it would be a much more practical and reasonable way forward if some form ofjoint accreditation could be obtained between the College of Radiologists and thevascular surgeons. For example, this might entail a trainee in vascular surgery spending 6months in a radiology department, with teaching from the interventionalists. This couldresult in a recognition of that training from the radiologists. At the same time, it should bepossible for radiologists wishing to do endovascular work to spend 6 months on asurgical rotation, where they could be trained in some of the basic requirements of patientcare, outpatient consultation and exposing arteries such as the femoral, radial, etc. andsuturing of arteriotomies. Again, this could result in some form of recognition from thesurgical colleges, giving dual accreditation. In future it is likely that this will be necessarybecause diagnostic arteriography is becoming less and less common with the use ofduplex scanning to diagnose and treat obstructive disease of the arteries and also of theveins. This means that the number of diagnostic angiographic and diagnosticinterventions will decrease year by year, and it will become more common and perhapsnecessary to learn wire-passing skills in the operating theatre during other interventionssuch as aneurysm repair or procedures to deal with limb ischaemia. This, in itself, maybring the various practitioners together. Therefore, the future is in collaboration withvascular surgeons and radiologists, both of whom will be involved in therapeuticinterventions.

References

1. White RA, Hodgson KJ, Ahn SS, Hobson RW, Veith FJ. Endovascular interventions, training and credentialing for vascular surgeons. J Vansc Surg 1999; 29(1): 117–86.

2. White RA, Fogarty TJ, Baker WH, Ahn SS, String ST. Endovascular surgery credentialling and training for vascular surgeons. J Vansc Surg 1993; 17:1095–102.

Training in endovascular surgery 437

The risks of endovascular techniques and the patient’s rights

24 ROGER N.BAIRD

Introduction

As doctors we enjoy a considerable measure of autonomy in treating our patients.However, the legal framework of our society imposes a duty on us to exercise reasonablecare and skill. ‘Tort’ is the term used in the public sector for the breach of that duty whereby an injured patient acquires the right to sue for damages. The courts recognizethat negligent mistakes, isolated lapses of good practice, can happen to competentpractitioners of good professional standing. In recent years, there has been a markedincrease in claims for medical negligence,1 by patients who come from a more consumerist and litigation-prone population. The rapid progress in medical technology, including the development of endovascular techniques, has brought enormous benefits.At the same time, new problems have emerged, as described earlier in this book.Nowadays, the expectations of patients are much greater than before and we doctors aresometimes overoptimistic.

No longer is it for us alone to decide the standards by which medicine is practised. It isinsufficient justification for us to rely on the worthy motive of good intentions whencomplications arise. The patient has the right to choose whether or not to accept the riskof serious damage. In this chapter, these principles will be applied to issues of consent,reasonable care and skill in clinical practice, and the introduction of new procedures.

Consent

The traditional view of the courts in the UK has been that the extent of informationdisclosed to a patient about the risks of a procedure is solely a matter for responsiblemed-ical opinion. This approach was given credence by the House of Lords in 1985 in a case called Sidaway,2 in which a body of experienced and skilled neurosurgeons regarded it as acceptable not to warn Mrs Sidaway of a slight, but well-recognized, risk of paralysis, which she did in fact suffer following operation on her cervical disc.

In his dissenting opinion, Lord Scarman argued unsuccessfully that the doctor’s duty fell to be determined by the patient’s rights. His proposition that Mrs Sidaway had theright to choose whether to accept a slight, but well recognized, risk of paralysis did notprevail at the time. However, this decision now has to be viewed in the context of theBolitho case (vide infra). Supreme Courts in other jurisdictions, notably Canada and

Australia, have ruled that the doctor’s duty is to pass on ‘that information which a reasonable patient would wish to know, and not merely that which doctors might thinkappropriate’. In the vascular context, all would agree that the risk of paralysis has to be disclosed prior to procedures for thoracic aneurysms.

Which risks should be disclosed?

The risks to be disclosed depend on the proposed intervention. For example, in patients inwhom a carotid endarterectomy is advised, the chance of stroke with and without theintervention needs to be understood by the patient and, just as importantly, by theirfamily. Also the general hazards of interventions in patients with atherosclerosis, such asperioperative myocardial infarction, need to be explained. Similar considerations apply tothe new procedures of carotid angioplasty and stenting. Furthermore, the magnitude ofthe risks quoted should be specifically from the personal experience of the surgeon or radiologist and not a general figure quoted from literature. This principle was laid downby the General Medical Council in their recent judgements on adverse outcomes inpaediatric cardiac surgery.

In practice, a doctrine of proportionality prevails regarding the rigour with which issues of consent are pursued. For example, a patient with a leaking aortic aneurysm willdie unless operation is undertaken, and a brief explanation and consent will normallysuffice.

On the other hand, a full discussion is required prior to an intervention for a lessthreatening condition such as thoracoscopic sympathectomy for hyperhidrosis, includingthe fact that the procedure is more effective in causing dryness of the palms than of theaxillae, the risk of Horner’s syndrome, and the frequent postoperative development ofcompensatory hyperhidrosis of the trunk.

In femoral angiography for leg ischaemia, where the risk of amputation is slight (of the order of 0.1%) and not usually disclosed beforehand, the accountability of theinterventionalist for an adverse outcome will depend on whether independent experts feelthat his or her clinical judgement and technical skill were of a reasonable standard, asoutlined in the next section.

Reasonable care and skill

The patient has the right to expect that the doctor will exercise reasonable care and skill.For example, transection of the common femoral vein during disconnection of the longsaphenous vein in the groin cannot be condoned. Neither can division or ligation of thecommon peroneal nerve during disconnection of the short saphenous vein in the poplitealfossa. That is not to say that all adverse events following an intervention are the practitioner’s fault—far from it. We surgeons and radiologists cannot guarantee success.However, it is only natural that our actions are called into question when complicationsoccur. After all, we would expect no less if we were the patient!

Sometimes, things unexpectedly go wrong. For example, balloon angioplasty of the

The risks of endovascular techniques and the patient’s rights 439

superficial femoral artery may be complicated by thrombosis distal to the site of thedilation. Some or all of thrombolysis, mechanical removal of thrombus by catheteraspiration, open embolectomy and surgical bypass may be required. The result will fallwithin the range shown in Table 24.1.

If the symptoms are unchanged or worse, then the patient has the right to a rational explanation. This is best given without delay by the senior radiologist and/or surgeon,who then writes personally in the case notes. It is bet

ter to satisfy the patient at the time than to explain the matter later. In the event that acomplaint or claim is later lodged, the contemporary entries in the hospital records andthe angiograms will be minutely scrutinized by independent experts and lawyers.

It is disappointing that the only confirmations of an angioplasty are often the postdilation film in the X-ray department and entries in the nursing record following thepatient’s return to the ward.

It is good practice to verify the continued patency of the dilated arterial segment directly by non-invasive imaging with duplex ultrasound and indirectly by documentingimproved distal arterial perfusion by the warmth of the foot by palpating distal arterialpulses and by measuring the Doppler systolic ankle pressure before the patient leaves thehospital.

Liability and causation

The following example may serve to illustrate the terms ‘liability’ and ‘causation’.

A 50-year-old insulin-dependent diabetic company director, who smoked 20 cigarettes a day, consulted a vascular surgeon with right calf claudication at 200 yards. A Duplex. ultrasound scan revealed a localized stenosis of the distal superficial femoral artery, a diseased and patent popliteal artery (SFA), and a single patent calf run-off artery,

The stenosis of the superficial femoral artery was dilated by a radiologist with a satisfactory postdilation film. That night, according to the nursing notes, the patient complained of pain in his right foot and oral analgesia was required. The following day, the house officer’s brief discharge note recorded the procedure, but not the outcome. Within a few days, the patient was readmitted with ischaemic rest pain of his foot. Arterial reconstruction was not technically

Table 24.1 Results of thrombolysis following ballroom dilation

Dilation Distal thrombus Patient’s symptoms

Successful Cleared Improved

Unsuccessful Cleared Unchanged

Unsuccessful Not cleared Worse


feasible and the leg had to be amputated. The patient, who was overweight, and was unable to return to work, consulted a lawyer and a claim for damages of £500 000 was lodged.

Independent radiologists and surgeons were reluctant to support the decision of the clinicians to dilate an SFA stenosis for mild claudication in the presence of poor run-off. They felt that the dilated arterial segment and distal run-off prob-ably thrombosed during the evening following the procedure and that the amputation might have been prevented if the ischaemic foot had been examined by the following morning and thrombolysis instituted before the patient left hospital. They criticized the poor quality of record keeping.

A barrister advised that the case could not be successfully defended. Liability was admitted and an out-of-court settlement of £350 000 was negotiated.

In this case, the lawyers advised that a judge would find against the surgeon andradiologist on liability if the case came to court.

On the other hand, if the limb had been critically ischaemic, and an angioplasty hadfailed to prevent the amputation, a defence on causation could have been run. In thatinstance, the court might find that the patient’s vasculature was in such a parlous state thatan amputation was inevitable, even with the best of care.

The legal test

The test by which the doctor fulfils his duty of care to the patient is to act ‘in accordancewith the practice accepted as proper by a responsible body of medical men skilled in thatparticular art’. This legal principle was established in the UK more than 40 years ago inthe Bolam case.3 Put simply, all that a doctor needs to do to answer a claim of breach ofduty is to show that he or she had done what fellow doctors would have done.

This principle stood unchanged for 40 years until the Bolitho case,4 in which the Houseof Lords held that a court can disregard an expert’s opinion if the judge feels that it isincapable of withstanding logical analysis.

New techniques

In my professional lifetime, there have been revolutionary advances in endovasculartechniques, including Thomas Fogarty’s embolectomy catheter in the 1960s and AndreasGruntzig’s angioplasty catheter a decade later. In the twenty-first century, Juan Parodi’sgroundbreaking work on stent grafting for aortic aneurysms has borne fruit andcommercially available endoprostheses have become available. We rely on pioneers tomake advances into previously uncharted territory. Once the initial steps have been taken,each new technique has to withstand rigorous scientific review before becoming widelyadopted. As stent graft manufacturing techniques evolve, the endoprostheses become evereasier to implant and can be used for an extended range of aneurysm types. Even so, weshould be cautious in recommending this new technique, especially in younger patients,

The risks of endovascular techniques and the patient’s rights 441

until there are results to show that problems of endoleaks and graft limb occlusion havebeen solved. In addition, as the requirement for randomized clinical trials increases,sufficient time has to be set aside for the unhurried provision of patient information bythe specialist, who is often assisted in this duty by a specialist nurse.

References

1. Baird RN. The vascular patient as a litigant. Ann R Coll Surg Engl 1996; 78:278–82. 2. Sidaway v Board of Governors of the Bethlem Royal Hospital and the Maudsley

Hospital [1985]. AC 871. 3. Bolam v Friern Hospital Management Committee [1957] 1 WLR 582. 4. Bolitho v City and Hackney Health Authority [1998] AC 232.


Index

Abbokinase 164 Abdominal

aortic investigations 347 approach 311 cavity 296, 302, 326 condition 409 musculature 217 pain 80 pressure 244 surgery 294, 408 wall 295, 304–6

Abdominal access 305 Abdominal aorta 122, 144, 309, 315, 354 Abdominal aortic aneurysms 78, 90, 227–8, 232–7, 240, 294, 296–302, 308, 315, 351

exclusion 299 resection 298 rupture 236 surgery 299

Above-knee amputation 42 Access site 79, 286, 315, 397, 414, 423–7, 438 Access site thrombosis 438 Accurate cannulation 353 Accurate placement 109, 117, 311, 350–2, 452 Accurate positioning 92–3, 154, 314 Achalasia balloon 245, 247 Acoustic cavitation 197 Aortic arch, acute 143, 148 Aortic dissection, acute 53, 72 Arterial thromboses, acute 72 Acylated human plasminogen 164 American Heart Association

categories 4, 9, 345 guidelines 2, 5, 11

American Society of Anesthesiology 299 Amplatz

catheter 277 guide-wire 140 sheath 276 snare catheter 279 snare 277–81

superstiff guide-wire 276 thrombectomy device 181, 186, 399

Amputations, major 10, 389 Aneurysm sac 99, 227–8, 231–2, 240, 254, 274, 281, 309, 315–6 Angiography 7, 14, 25, 43, 79, 84, 89, 98–102, 105–7, 110, 116–8, 121, 129, 139–45, 154––168, 178, 231, 234, 244, 255, 311, 332–4, 342, 345, 348–56, 452–3, 456 AngioJet 182, 186–93, 401 Angioplasty balloon catheter 105, 352, 371, 434 Angioscope 334–6 Angioscopy 140, 330, 333, 341, 356, 371 Animal models 370, 453 Anisoylated plasminogen streptokinase activator 164 Ankle brachial pressure index 2, 65, 106, 112, 373, 457 Antecubital vein 414, 423

access 414 Anticoagulation failure 411–3 Aortic

aneurysms 5, 77, 78, 90, 227–37, 240, 244, 247, 252, 257, 261, 264, 269, 271, 274–7, 281, 285, 288, 291, 294, 308–9, 315, 318, 326, 351, 458 arch 116–7, 121, 136–40, 144–8, 157, 348 balloon catheter 279 bifurcation 15–6, 41, 84, 122, 231, 271, 276, 279, 287, 296 bifurcation grafts 271 dissection 53, 72, 308, 345 graft anastomosis 323, 326 injuries 351 lumen 122 occlusion 324–6 position 273 prosthesis 271 reconstruction 304 regurgitation 308 surgery 304–5, 311, 326 tube grafts 271 wall 279, 289

Aortobifemoral bypass 326 Aorto-bi-iliac approach 271, 274, 277, 281, 286, 288, 292 Aortofemoral bypass 298, 320 Aortography 117, 230–1, 276, 285–8, 312–6 Aorto-iliac

procedures 326 region 180

Aorto-iliac sac 229 Aorto-uni-iliac graft 240–4, 247, 252, 257, 261, 264, 269 Arm

ischaemia 309 pain 210

Arrhythmia 290, 438

Index 444

Arrow-Trerotola percutaneous thrombectomy device 398 Arterial

anastomosis 390–1, 398, 402 pressure 139, 207, 312, 330 wall 105, 140, 177, 193, 349, 353

Arteries of experimental animals 271 Arteriograms 136 Arteriography 345, 350–1, 454 Arteriolar resistance vessels 216 Arteriosclerosis/medial degeneration 80 Arteriovenous fistulae 90, 341, 389, 429 Artery

aneurysm 78–80, 96–7, 274 diameter 34, 349 diseased 348 forceps 208 wall 105, 348

Ascending lumbar vein 434 Atherectomy 1, 181–5, 345–7, 350, 393–4, 398

device 185, 393 Atheroma regression 345 Atheromatous stenoses 136 Atherosclerosis 79, 99, 136, 140, 143, 147, 150, 154, 159, 163, 308, 345, 456 Atherosclerotic cardiovascular disease 7 Atherosclerotic plaquing 281 Atherosclerotic stenoses 1, 116

Bacteraemia 393 Balloon

angioplasty 90, 136, 150, 318, 349, 352, 390–1, 395–7, 453, 456 catheters 43, 54, 105, 281, 347 dilatation 24, 57, 120, 154, 179, 394–7 dissection 218, 366 dissector 217, 223, 361–3 expandable devices 16, 19, 309 expansion 91, 393 fragment retrieval 393 inflation pressure 279 length 32, 34, 54 mounted Palmaz 120 predilatation 122 size 43, 108, 352 surface 394 technique, atherosclerotic disease 14 technique 14–6, 30, 43 technology 12

Below-knee amputation 379

Index 445

venous confluence 377 Bifurcated graft 230, 240, 272, 277, 282, 287–91, 294, 304 Bifurcation graft 271–4, 277, 285 Bifurcation prosthesis 272 Bird’s nest filter 410, 414–8, 430, 434, 440 Bladder catheter 325 Blood loss 65, 71, 227, 238, 257, 291, 299, 326, 416 Blood pressure 65, 71, 139, 186, 231, 259, 312 Bolus, intravenous 164, 176 Brachial artery 51, 116–7, 231, 289, 349 Brachial plexus 208–10 Brachiocephalic veins 441 Bradycardia 139 Brain embolism 139, 144, 157 Brescia-Cimino radiocephalic fistula 389 Bypass

procedure 296, 329–30 surgery 8, 12, 66, 71–3, 320, 335, 342 therapy 12

Calcified

aorta 327 lesions 139 vessel 45, 52, 64, 73, 294

Calf claudication 17, 44, 457 cramping 13, 37 veins 374 vessel run-off 6

Capacitance vessels 216 Carbon dioxide

insufflation 320, 326, 360 pneumoperitoneum 322

Cardiac mural thrombi 163 pathologies 351 status 136, 160 thrombus 163

Cardiovascular surgery 232, 290 Carotid

angioplasty 136, 140, 159, 348, 456 artery 116, 136, 140–3, 148, 153–, 159, 309, 315–7, 348, 429, 455 atheromatous lesion 150 atherosclerosis 136, 140, 143, 147, 150, 154, 159 bifurcation 136, 140, 145, 159 bypass grafting 160 endarterectomy 348, 456 endoluminal treatment 136

Index 446

lesions 348 puncture 145 stenoses 136, 155 vessels 157

Catheter exchanges 109, 173, 178 intervention 121 lumen 179 manipulation 65, 108, 109, 340 passage 276 size 179 surface 186 system 167, 173, 182, 185, 189, 279, 339 technique 21 tip 70, 90, 167–9, 185, 189, 193 wire combination 55

Cauda equina 217 Caudal migration 416, 423, 440 Causalgia 206–7, 217 Cautery ablation 209 Cavagram 431, 434, 440, 443 Celiac artery 309, 314

origin 314 Central venous

catheter 295, 321 lesion 394 stenoses 390, 395

Cephalic internal carotid artery 348 Cerebral

cortical bullet injury 216 infarction 160 trunks 160 vascular accident 441

Cervical access 139, 144 approach 136–9, 146, 148, 160 spine injury 443

Chest, acute 308 Chest X-ray 208–9 Cholinergic fibres 206 Chronic

critical ischaemia 4, 7 limb ischaemia 1 pancreatitis 80, 99 thrombus 167, 399 venous insufficiency 360, 365, 369, 382, 387

Circumaortic renal vein 429–30 Clinical trials 164, 181, 197, 444, 459

Index 447

Clot 413 age 163, 189 disruption, mechanical 167 lysis 164–7 material 185, 188 transportation 182

Clot-free lumen 167, 179 Clotted haemodialysis grafts 195 Clotting factors 86, 164 Clotting of the graft 390 Coaxial catheter 168, 172–3 Coeliac 54, 78, 99

axis 99 Coeliac-shaped catheter 57 Colon ischaemia 290 Colonic disease 300 Colour-flow ultrasound 402 Colposuspension 223 Common carotid artery 116–7, 140–3, 147, 153, 157–9, 309, 316, 348 Common femoral

artery 12, 27, 33, 93, 108–9, 230, 251, 274, 286, 311, 323 artery bifurcation 108–9 vein 373, 377, 382, 429–30, 438, 456

Common iliac artery 2, 18, 274, 282, 296 lesions 4, 18 veins 431

Computed tomography 77, 136–9, 228, 234, 244, 271, 309, 317, 351, 428 contrast-enhanced 97, 229, 232, 281, 437

Congestive heart failure 10, 290, 411 Connective tissue disease 78 Contralateral

femoral artery 58, 82, 230–1, 252, 272, 276, 288 limb 231–2, 272, 277, 285–9

Conventional surgery 136, 228, 299, 304–5, 311 Coronary

angioplasty 77–9, 157, 391 arteries 164, 189, 347, 352 artery bypass 116, 207 artery disease 10, 116 bypass surgery 335 configurations 347 lesions 47 system 347 vessels 148, 345

Coumadin 163, 180, 412 associated necrosis 412 therapy 411

Index 448

Crural angioplasty 10 veins 374

Crush injury 207

Day-case basis 63, 112, 209 Deep vein thrombosis 163, 370, 373, 410–1, 440

progressive 413 recurrent 444

Deep venous system 337, 369, 383 valve surgery 369–70

Diagnostic angiography 14, 105, 452 arteriography 454 duplex ultrasound assessment 106 interventions 453 investigations 142 IVC catheter 430

Dialysis grafts 389, 391, 395, 398, 401–3 Diathermy 209–10, 364

ablation 209 coagulation 211

Distal embolization 4, 67, 77–8, 86, 99, 172, 177, 182–5, 188, 193–4, 232 Doppler systolic ankle pressure 457 Doppler 13, 79, 83–5, 108, 136–9, 145, 261, 324, 332, 348, 390, 430, 457 Duplex imaging accuracy 360 Duplex ultrasound 82, 97, 105–6, 114, 281, 341, 360, 457

Emergency bypass surgery 66, 71 Endarterectomy 160, 320, 348, 456 Endograft 229, 232, 271–4, 285–7, 291, 351

deployment 291 fabrication 351 limb 231

Endoscopic equipment 206, 361–3, 366 surgery 211, 335 sympathectomy efficacy 210 technique 360 thoracic sympathectomy 206, 209–12 venous valve surgery 369, 371, 374, 379

Endothelial damage 194, 329, 370, 379 Endovascular

procedures 77, 81, 235, 345, 356, 369, 452–4 treatment 14, 79, 102, 118, 134, 159, 227–30, 232, 238, 348, 398, 452

Epidural anaesthesia 207, 362, 382 External atherosclerotic plaque 352

Index 449

External band valvuloplasty 369 carotid artery 140–3, 157 fibrosis 349 haemostatic valve apparatus 311 iliac arteries 19, 23–7, 122, 249, 274–6, 294–6

Extraluminal angioplasty 51, 53 Extraperitoneal

iliac incision 245 laparoscopic approach 299

Extravascular sealing devices 155

Fascial defects 364 Femoral

access 117, 125, 129, 141, 145, 160 angiography 456 approach 136–40, 147, 160, 416–8, 425, 434 artery 8, 12, 18, 20, 24, 27, 33–, 35, 40, 51–2, 58, 63–4, 69, 79, 82, 93, 108–11, 125–9, 185, 230–1, 251–2, 261, 272–6, 279, 286, 289, 311, 323, 457

catheterization 79 popliteal bypass 11 pseudoaneurysms 78 route 142–3, 154, 159, 427 vein 370–7, 382–3, 408, 423–5, 429–30, 438–40, 456

Femoropopliteal angioplasty 5–7, 10, 21, 352 bypass 27, 41, 299 disease 11 graft occlusions 170 interventions 5, 7, 10, 21 lesions 8 occlusions 5, 7, 51, 53, 65–6 segment disease 4 stenosis 7

Fibrinolysis 66, 86, 197 Filter

deployment 414, 423, 427, 432, 434 design 414–6, 422 evaluation 438 flexibility 418, 425

procedure 411, 430, 434 migration 408, 415, 438–43 misplacement 427, 434, 438 placement 411–3, 425, 431, 434, 438–40, 445

Fluoroscopy 180, 279, 286–7, 338–41, 348, 430 control 276–7, 342, 352 guidance 312, 335, 339

Fogarty

Index 450

balloon 339, 177, 193–5, 398–402 catheter 398–9, 402 technique 180, 194

Free-floating thrombus 412–3, 436

Gasless laparoscopic technique 301, 326 transperitoneal approach 325

Gastrocnemius veins 382 Gastroduodenal artery 79, 96, 99 General anaesthesia 51, 139, 154, 160, 222, 247, 274, 294, 311, 315, 326, 375 Gonadal vein 425, 427, 434 Graft catheter delivery system 274–7, 281 Graft declotting 398 Gravid uterus 434 Greenfield filter 408–10, 413–7, 422, 427, 434, 438–40, 442

Haematoma 66, 67–71, 86, 96, 143, 181–3, 299, 386–, 402, 438

formation 386 Haemobilia 80 Haemodialysis 164, 184–7, 190–1, 195, 389–90, 395

access 164, 191, 389, 395 failure 389 of choice 389

grafts 183–5, 190, 195 occlusions 187

machines 391 Haemodynamic

criteria 110 examination 136 injury 329 measurements 5 monitoring 295 patencies 66 success 53 tracing 22

Haemolysis 181, 185–91 Haemorrhage 79, 98, 164, 315, 412, 441

complications 164, 168 Haemostasis 79, 90, 110, 209, 279, 324, 434 Haemostatic

aortic anastomosis 324 valve 193, 311

Hand-assisted laparoscopy 294–6, 299–304 Heparin 10

anticoagulation 315 intravenous 10, 312, 324, 377 low dose 176, 413

Index 451

Hepatic artery aneurysm 78, 97 vein 425, 427

Iliac angioplasty 4 Iliac artery 19–27, 111, 122–5, 231, 240–54, 261, 264–7, 272–4, 277, 281, 289, 296–8, 320, 349–51

aneurysm 274 angulation 274 occlusion 122 occlusive disease 298, 320 tortuosity 275

Iliac disease 2, 12–, 18, 29, 32, 351 Iliac intervention 2–5, 12, 24, 27 Iliac occlusions 24, 51–2, 59, 67 Iliofemoral deep vein thrombosis 413 Inferior vena cava 194, 220, 408–11, 414–29, 433, 435, 438–45, 449 Infrainguinal

bypass grafting 2, 12, 129 vasculature 122

Infrapopliteal angioplasty 11 bypasses 11 data 11 PTA 10

Infrarenal abdominal aortic aneurysm 294 aorta 294, 305, 309, 323

Innominate vein 394 Inominate artery 140, 143, 148, 159 Internal carotid artery 143, 154, 348 Internal iliac artery 20, 229, 240, 241, 252, 264, 267 Interventionalist 1, 11, 13–, 43, 95, 100, 311, 392, 452–4, 456 Intracerebral

angiogram 137 circulation 142–5 haemorrage 160, 315 vessels 142, 155

Intracranial haemorrhage 412 neoplasm 164 tumour 412

Intractable angina 207 Intractable diseases 366 Intrahepatic

aneurysms 97 pseudoaneurysms greater 98

Intraluminal approach 52, 73

Index 452

recanalization 52, 64 Intravascular ultrasound 117, 140, 286, 345–7, 351–4 Ipsilateral approach 12, 59–60 Ischaemic limbs 66–8, 116 Isolated crural intervention 10

Jugular approach 422–5, 434–5, 438 Jugular vein 193, 370, 423–7, 434, 438

Katzen infusion wire 173, 175 Kawasaki disease 79 Kensey catheter 185–6

Laparoscopic

access 296, 300, 304 aneurysm surgery 294 aorto-femoral bypass 320, 323, 326 aorto-ileofemoral bypass grafting 320 aorto-iliac surgery 294 camera 295 cholecystectomy 80, 306, 361 dissection 296 experience 222, 305 instruments 296, 299, 360, 365 intra-abdominal 320 observation 218 operation 299, 304 port 217, 320–1, 324, 363–4 port insertion site 364 procedure 298 retroperitoneal approach 324 surgery 294, 299, 304, 325–6 technique 294, 302, 305, 320 transperitoneal approach 325 vascular anastomosis 326 vascular clamp 322 vascular occluders 326 vascular procedures 320

Laparoscopy-assisted approach 223, 294–6, 300–5 Left subclavian artery 116, 309, 315–7 Left thoracotomy 311 Left-sided

approach 429 cava 428, 430 IVC 429–32

Leg ischaemia 456 ulcers 360

Index 453

venogram 375 Life expectancy 7, 95 Limb

ischaemia 1, 8, 12, 51–2, 62, 67, 73, 163, 172, 454 loss 7, 65, 77 perfusion 217 revascularization techniques 116, 119, 122, 126, 129, 133

Lipodermatosclerosis 360, 366, 382, 387 Lower leg bypasses 27 Lower limb

arteries 178, 181–2, 187–8 nerves 223 occlusive disease 216 venography 374

Lower renal vein 430–2 Lumbar vertebral bodies 217–20 Lysis efficacy 163, 167, 185

Magnetic resonance imaging 77, 105, 351, 390, 414–6, 439 Major amputations 10, 389 Mechanical clot removal, mechanical 398 Mechanical thrombectomy 177, 179–85, 188, 194–7, 398–401 Mini-incision

aneurysm resection 294 aortic surgery 305 cholecystectomy 306

Mini-laparotomy 294–6, 302–5 Multilevel disease 2, 10, 18, 28, 33 Multiple renal veins 429–31 Myocardial infarction 10, 66, 165, 290, 411, 456

Native fistulas 179, 181–2, 403 Neointimal hyperplasia 81, 90, 94, 391, 395, 403 Nifedipine 10, 24, 35 Nitinol 23, 91, 155, 160, 279, 310, 317, 331, 336, 410, 415, 424–5, 435 Nitroglycerin 10, 22, 24–8, 35, 37

intravenous 10 Nitroprusside infusion 312 Norephinephrine, constricting influence of 216

Obesity 105, 299, 327, 411 Obliterative arterial disease 207 Occluded

segment 52, 69, 73, 169, 177 superficial femoral artery 20 balloon 193, 402

Pancreatitis 80, 97, 99, 299

Index 454

Particulate embolization 188–9 Pelvic oblique angiogram 23, 40 Percutaneous

biopsy 83, 436–7 catheter embolization 98 catheter techniques 98 chemical ablation 217 injection 223 intervention 1–4, 356 management of dysfunctional 389 mechanical thrombectomy 177, 179, 182, 398 methods 403 placement 80, 408, 414, 438, 445 puncture 116–8, 452 recanalization 5 removal of thrombus: 177 revision 403 subintimal angioplasty 51, 61 technique 177, 180, 222, 342, 402 therapy 403 thrombectomy 177, 181–2 thromboembolectomy 177 transluminal angioplasty 51, 109, 117, 122, 131, 177, 182, 390 treatment 85, 389, 397, 402 ultrasound 197 vascular intervention 4

Perforating vein 338–9, 360, 363–6, 369, 373, 382 Peripheral circulation 79, 90, 347, 351 Peritoneal cavity 221, 296, 300 Peroneal artery 42, 61–4, 69, 85 Pigtail catheter 230 Plasminogen 78, 164, 172, 398, 411

disorders 411 Platelet 72, 427 Pneumoperitoneum 222, 294, 297, 302, 322, 326 Polyarteritis nodosa 79 Popliteal

aneurysm 77, 80, 351 artery 8, 12, 24, 29, 31, 37, 44, 51, 63, 69, 93, 111, 125, 129, 351, 457 artery intervention 24 artery level 129 fossa 456 occlusion 52, 61–3 vein 370–3, 377–9, 382

Posterior thoracic wall veins 209 Posterior tibial

angioplasty 47 arteries 63

Index 455

artery lesion 111 artery, diseased 46 vein 364, 382

Postoperative complications 290, 299, 326 Preulcerative lipodermatosclerosis 360 Profunda

artery 52, 58, 71 disease 71 occlusion 52 vein 369, 377

Profundafemoris 251 Pseudoaneurysm formation 90, 391 pseudoaneurysm neck 82–5 Pseudoaneurysms 4, 77–86, 89–90, 95–102, 403 PTFE graft 90, 178, 181–5, 188, 244–5, 250, 261, 263, 306, 389, 391, 401 Pulmonary

artery 185 emboli 164, 194–5, 438 embolism 164, 194–7, 402, 408, 411, 434, 438, 444 thrombendarterectomy 413 thromboembolism 164, 412

Quincke’s classic triad 80

Radiologist 136, 139, 164, 300, 316, 452–8 Radio-opaque markers 109, 171, 231, 277, 286–7, 312, 379 Radiotherapy-induced stenoses 159 Raynaud’s phenomenon 208, 216 Recanalization 5–7, 13–, 18, 51–3, 58–64, 67–72, 116–9, 122–5, 168, 177, 185, 189, 370–1, 397 Recombinant DNA techniques 164 Renal

artery 177, 274, 277, 289, 345, 349 catheter 453 cell carcinoma 434 compromise 191 damage 454 failure 105, 164, 233, 350 function 114, 137, 264 pedicle 220 replacement therapy 389 vein 194, 427–37, 443

thrombosis 429, 434 vessels 264

Reserpin 207 Restenoses 150, 160 Reteplase 165 Retrograde approach 5, 18, 25, 59, 118, 122–5, 153 Retroperitoneal

Index 456

aorta 312 approach 309, 326 balloon dissection 217 dissection 218, 306 external iliac artery 249 haemorrhage 441 incision 309 plane 219 space 217, 222, 252 structures 217, 300

Retroperitoneoscopic lumbar sympathectomy 216–23 Retroperitoneum 65, 217–20, 298 Retrospective study 172, 333, 390, 395 Rifampacin 251 Right femoral

artery 274, vein 425

Right gonadal vein 427 Right-sided ovarian vein thrombosis 435–7 Roadmapping 7, 43, 139–40, 145, 154, 257

Saccular aneurysms 97, 102 Saline jets 186, 191 Saphenofemoral junction 372, 383 Saphenopopliteal junction 383 Saphenous

nerve 363 vein 12, 41, 98, 129, 329, 332–41, 364, 373, 382–3, 456

Small bowel 305, 441 Sonic thrombolysis 195–7 Splenic artery aneurysms 78–80, 97 Stenosis 1, 5–8, 11, 20, 27, 38–43, 46, 52, 65, 81, 110, 116–20, 129–31, 140, 341, 345, 349–52, 373, 389–93, 397–402, 457–8 Stenotic

disease detection 348 lesions 29, 391 plaque 348

Stent endoskeleton 311 Stent graft 90–1, 288, 291, 298, 308–16, 345, 349, 453, 458

combinations 453 deployment 289, 312, 315 placement 308, 312–5 procedure 311, 314, 345, 350

Stereotactic thermocoagulation 206 Streptokinase 66, 163, 398

intravenous 163 Subarachnoid haemorrhage 441 Subclavian artery 93, 116–7, 309, 315–7, 349

Index 457

Subclavian vein valves 373 Subcutaneous

fascia 363 fatty tissue 363 tissue 281, 363–4, 383, 434

Subfascial endoscopic perforator surgery 360–1 Subfascial vein interruption 360 Subintimal angioplasty 51, 53, 58, 61–5, 68, 71–4, 111, 129 Subintimal recanalization 58, 71 Supraphysiological hydrostatic pressures 372 Suprapubic region 322 Suprarenal aorta 276–7 Suprarenal inferior vena cava 430, 434, 435 Suturing 305, 326, 377, 454 Sweat gland loss 209 Sympathetic nervous system 206, 216

Teflon catheter 173, 185, 193, 195 Temporary filters 410, 444, 445 Terumo 16, 29, 54, 62, 140, 254, 453 Thoracic aneurysmal disease 308, 311, 313, 316, 456 Thoracic aorta 231, 276, 287, 308–12, 315 Thoracic aortic aneurysm 308, 313318 Thoracic aortogram 312–3, 316 Three-dimensional reconstruction 346, 348, 351–2 Thrombectomy 165, 177–97, 299, 399–402

balloon catheter 398–9 device 182, 185–6, 193–4, 399–401 devices 165, 182, 186, 195–7, 401 time 178, 181–3, 188

Thrombi 163, 167, 172, 177–82, 186, 189, 193–5 Thromboaspiration 402 Thromboembolic

complications 349 disease 163, 197, 411–3

Thrombogenic 72, 372 Thrombolysis 70–1, 78, 155, 163–75, 179, 182, 186, 189, 193–9, 204, 391, 398, 402, 412, 457–8 Thrombolytic

procedures 402 success 402, 191 therapy 6, 14, 24, 79, 163–4, 168, 172, 176, 413

Thrombotic complications 315, 438 Tibial

angioplasty 8–10, 34, 47, 61 artery 8, 44, 46, 51–2, 61–4, 69, 73, 111

occlusion 51–2, 61, 69, 72 circulation 43 occlusion 61

Index 458

Tibioperoneal angioplasty 8, 34 Ticlopidine 35 Transaxillary sympathectomy 210 Transbrachial catheterization 128 Transcranial Doppler 136–9, 145, 261 Tumescent anaesthesia 382–6

Ulcerated limb 369 Ulcerative colitis 412, 436 Ultrasonography 116, 140, 145, 234, 345, 349, 360, 427 Ultrasound guidance 71, 82, 105, 109, 111 Urokinase 164–8, 171, 398

Valsalva manoeuvre 374 Valvuloplasty 370 Valvulotome 330, 334–7 Valvulotomy 330, 336 Van Andel catheter 54, 61, 254, 261 Vasa vasorum 329 Vascular

anastomosis 324–6 balloon dissector 1 361 bypass operations 12 clamps 294, 297, 324 control 323 damage 186, 352 disease evaluation 12 injury 177, 186, 195, 400 intervention 1, 4, 12 lumen 177 procedures 320, 326, 452 reconstruction 216 rupture 402 smooth muscle 216 specialist 1 surgery 222–3, 232, 299, 369, 454 system 274, 336, 442, 453 territory 129 tree 371, 453 wall 177, 185

Vein construction 377 surgery 360, 363, 367, 369, 373, 382, 385 transplantation 370

Vein-graft bypass 129 distal bypass 122 junction 395

Index 459

Venography 360, 374, 391, 412, 429 Venous

anastomosis 390–1, 395–8 anatomy 374, 403, 416, 435 anomalies 429, 433 hypertension 90, 365, 369, 382 system 337, 369, 373, 383, 398, 429, 444 thrombosis 78, 163, 370, 410–1, 440

Visceral aneurysm 77, 80, 85, 88, 91, 96, 99, 102

Wallstent 5, 8, 15, 39, 154, 160, 195–, 310, 346, 349, 371, 395–7, 402 Warfarin 374 Warfarinized 378 Wound complications 233, 332–5, 340, 360, 366 Woven polyester prosthesis 272

X-ray 114, 208–9, 247, 261, 268, 350, 377, 453, 457

Y-connector 187

Z-shaped elements 310 Z-stent endoskeleton 309

Index 460

Minimal access therapy for vascular disease

Health & Medicine

Transcript of Minimal access therapy for vascular disease