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25. Murphy TP, Cutlip DE, Regensteiner JG, et al; CLEVER Study Investigators. Supervised exercise

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results of a phase III multicenter trial. J Magn Reson Imaging 2010;31(6):1402–1410.

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40. Popma JJ, Satler LF, Pichard AD, et al. Vascular complications after balloon and new device

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42. Cao P, Eckstein HH, De Rango P, et al. Chapter II: diagnostic Methods. Eur J Vasc Endovasc Surg

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treatment of aortoiliac occlusive disease. J Vasc Surg 1986;3(3):421–436.

44. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major

vascular surgery. N Engl J Med 2004;351(27):2795–2804.

45. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 guidelines on perioperative

cardiovascular evaluation and care for noncardiac surgery: executive summary: a report of the

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48. Wong J, Lam DP, Abrishami A, et al. Short-term preoperative smoking cessation and postoperative

complications: a systematic review and meta-analysis. Can J Anaesth 2012;59(3):268–279.

49. Passman MA, Farber MA, Criado E, et al. Descending thoracic aorta to iliofemoral artery bypass

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50. Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction. Description of a new

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percutaneous transluminal angioplasty. Ann Surg 1987;206(4):403–413.

53. Tetteroo E, van der Graaf Y, Bosch JL, et al. Randomised comparison of primary stent placement

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occlusive disease. Dutch Iliac Stent Trial Study Group. Lancet 1998;351(9110):1153–1159.

54. Bosch JL, Tetteroo E, Mali WP, et al. Iliac arterial occlusive disease: cost-effectiveness analysis of

stent placement versus percutaneous transluminal angioplasty. Dutch Iliac Stent Trial Study Group.

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55. Goode SD, Cleveland TJ, Gaines PA. Randomized clinical trial of stents versus angioplasty for the

treatment of iliac artery occlusions (STAG trial). Br J Surg 2013;100(9):1148–1153.

56. Mwipatayi BP, Thomas S, Wong J, et al. A comparison of covered vs bare expandable stents for the

treatment of aortoiliac occlusive disease. J Vasc Surg 2011;54(6):1561–1570.

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58. Rzucidlo EM, Powell RJ, Zwolak RM, et al. Early results of stent-grafting to treat diffuse aortoiliac

occlusive disease. J Vasc Surg 2003;37(6):1175–1180.

59. Ali AT, Modrall JG, Lopez J, et al. Emerging role of endovascular grafts in complex aortoiliac

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occlusive disease. J Vasc Surg 2003;38(3):486–491.

60. Jongkind V, Akkersdijk GJ, Yeung KK, et al. A systematic review of endovascular treatment of

extensive aortoiliac occlusive disease. J Vasc Surg 2010;52(5):1376–1383.

61. Ozsvath KJ, Darling RC III. Renal protection: preconditioning for the prevention of contrastinduced nephropathy. Semin Vasc Surg 2013;26(4):144–149.

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64. Chang RW, Goodney PP, Baek JH, et al. Long-term results of combined common femoral

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66. Ichihashi S, Higashiura W, Itoh H, et al. Long-term outcomes for systematic primary stent

placement in complex iliac artery occlusive disease classified according to Trans-Atlantic InterSociety Consensus (TASC)-II. J Vasc Surg 2011;53(4):992–999.

67. Chiu KW, Davies RS, Nightingale PG, et al. Review of direct anatomical open surgical management

of atherosclerotic aorto-iliac occlusive disease. Eur J Vasc Endovasc Surg 2010;39(4):460–471.

68. Kakkos SK, Haurani MJ, Shepard AD, et al. Patterns and outcomes of aortofemoral bypass grafting

in the era of endovascular interventions. Eur J Vasc Endovasc Surg 2011;42(5):658–666.

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73. LoGerfo FW, Johnson WC, Corson JD, et al. A comparison of the late patency rates of

axillobilateral femoral and axillounilateral femoral grafts. Surgery 1977;81(1):33–38; discussion 38–

40.

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for aortoiliac occlusive disease. J Vasc Surg 1996;23(2):263–269; discussion 269–271.

75. Pursell R, Sideso E, Magee TR, et al. Critical appraisal of femorofemoral crossover grafts. Br J Surg

2005;92(5):565–569.

76. Valentine RJ, Hansen ME, Myers SI, et al. The influence of sex and aortic size on late patency after

aortofemoral revascularization in young adults. J Vasc Surg 1995;21(2):296–306.

77. Reed AB, Conte MS, Donaldson MC, et al. The impact of patient age and aortic size on the results of

aortobifemoral bypass grafting. J Vasc Surg 2003;37(6):1219–1225.

78. Nevelsteen A, Suy R. Graft occlusion following aortofemoral Dacron bypass. Ann Vasc Surg

1991;5(1):32–37.

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Chapter 93

Peripheral Arterial Disease

William P. Robinson III

Key Points

1 Chronic obliterative atherosclerosis of the infrainguinal vessels is the most prevalent manifestation

of peripheral arterial disease (PAD) encountered by the vascular surgeon.

2 The major risk factors for the development of PAD include smoking, diabetes, advanced age, male

gender, hypertension, dyslipidemia, and chronic kidney disease.

3 PAD is a powerful risk factor for cardiovascular morbidity and mortality.

4 The most common lesion seen below the inguinal ligament is that of a short-segment total occlusion

of the superficial femoral artery.

5 Typically half of patients proceeding to revascularization for arterial occlusive disease have

significant coronary artery disease; even more have hypertension, and almost 80% are current or

prior cigarette smokers.

6 The diagnosis of infrainguinal occlusive disease is generally made based on patient symptomatology,

physical examination, and noninvasive tests, such as ankle–brachial index (ABI), segmental pressure

measurements, and pulse volume recordings.

7 Percutaneous endovascular therapy is often applied as first-line therapy, particularly in patients with

more limited extent of anatomic disease and/or high operative risk.

8 Open surgical revascularization remains the gold standard for those patients with disabling

claudication, ischemic rest pain, and ischemic ulceration or gangrene.

9 Infrainguinal arterial bypass surgery remains the signature operation distinguishing vascular

surgeons from other specialists involved in the treatment of peripheral vascular disease.

10 Infrainguinal bypass surgery is best performed with autogenous vein conduit, preferably the

ipsilateral greater saphenous vein if available.

11 Many of the patients undergoing surgical reconstruction for critical limb ischemia (CLI) with tissue

loss will require one or more adjunctive operative procedures for salvage of their foot.

1 The term “Peripheral Arterial Disease (PAD)” broadly denotes stenotic, occlusive, and aneurysmal

diseases of the aorta and its branch arteries, exclusive of the coronary arteries. In common clinical

usage, PAD, which is defined as an ankle–brachial index (ABI) <0.9, denotes atherosclerotic stenosis or

occlusion of the arteries supplying the lower extremities.1 Atherosclerotic occlusive disease of the aorta

and iliac arteries is covered in Chapter 92. This chapter will cover PAD located in the femoropopliteal

and tibial (infrainguinal) arteries. PAD affects 12% of the U.S. adult population and almost 20% of U.S.

adults older than age 70 years.1–3 PAD involving the lower extremities is the third leading overall cause

of atherosclerotic morbidity worldwide after coronary artery disease and stroke.4 With the aging of the

American population, the prevalence of lower extremity occlusive disease has steadily increased in

recent decades. Not surprisingly, therefore, the clinical manifestations and complications of

atherosclerosis are the most common therapeutic challenges encountered and treated by vascular

surgeons.

The tendency for atherosclerotic lesions to develop at specific anatomic sites and follow recognizable

patterns of progression was first appreciated in the late 1700s by the British anatomist and surgeon

John Hunter. Considered one of the forefathers of vascular surgery, his dissections of atherosclerotic

aortic bifurcations are preserved at the Hunterian museum in London and presage the disease process

that Leriche would give his name to 150 years later.5 The modern era of surgical reconstruction for

complex atherosclerotic occlusive disease began in earnest in 1947, when the Portuguese surgeon J. Cid

dos Santos successfully endarterectomized a heavily diseased common femoral artery.6 Four years later,

building on the pioneering work of Alexis Carrel, Kunlin would report the first long-segment vein

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bypass in the lower extremity.7,8 It would be another 10 years before the initial efforts to extend vein

grafting to the tibial level were described by McCaughan.9 The last three decades have seen tremendous

advances in both the understanding of atherosclerosis biology and refinement in the techniques of

infrainguinal surgical revascularization that have greatly improved surgeons ability to preserve limbs

and improve quality of life in patients with femoropopliteal and tibial occlusive disease. Moreover, in

the last two decades, advances in percutaneous treatment have revolutionized the treatment of

infrainguinal occlusive disease. The concept of intravascular intervention was pioneered in the late

1960s by the radiologist Charles Dotter, and advanced greatly with the advent of the angioplasty

balloon by Gruntzig in the early 1970s.10,11 Nevertheless, endovascular intervention for infrainguinal

disease was not utilized significantly until the 1990s. The technology remains in rapid development and

surrounded by ongoing controversy as to its proper role.

Although a diverse range of technical skill is required of the contemporary vascular and endovascular

surgeon, it is worth noting that infrainguinal arterial bypass surgery remains the signature operation

distinguishing vascular surgeons from other specialists involved in the treatment of PAD. This

distinction stems primarily from the fact that the outcome of infrainguinal reconstruction is highly

dependent on the judgment and technical skill of the surgeon, with the end result often being either

successful limb salvage or major limb amputation. This chapter reviews the surgical and endovascular

management of femoropopliteal and tibial arterial occlusive disease and details standard and advanced

techniques underlying successful infrainguinal operative revascularization. Endovascular intervention is

introduced, though a comprehensive review of endovascular techniques used to treat femoropopliteal

and tibial occlusive disease is beyond the scope of the chapter.

INFRAINGUINAL ARTERIAL OCCLUSIVE DISEASE

Epidemiology and Risk Factors

Symptomatic PAD in the form of claudication affects more than 10 million Americans including 1% to

2% of those aged <50, 5% of those aged 50 to 70, and 10% of those aged >70. Of those aged >50

with PAD, 1% to 3% will have critical leg ischemia in the form of rest pain or gangrene.12,13 The

incidence of CLI ranges from 220 to 1,000 new cases per year in a European or American population of

1 million people.14

2 The risk factors for infrainguinal occlusive disease are the same as those for the development of

atherosclerosis in general and include age, male gender, hypertension, diabetes mellitus (DM), smoking,

dyslipidemia, family history, and homocysteinemia. Smoking and diabetes are the most powerful risk

factors. Smokers are at four times the risk of symptomatic PAD than nonsmokers while diabetics are

more than three times more likely to develop symptomatic PAD in comparison to nondiabetics.14 The

propensity for heavy smokers to develop superficial femoral artery disease and for diabetics to develop

tibial disease should be noted. More recent evidence indicates that nonwhite ethnicity, inflammatory

markers such as C-reactive protein, and perhaps chronic renal insufficiency (CRI) are also associated

with an increased risk of PAD.15–17

Presentation and Natural History

3 Chronic obliterative atherosclerosis of the infrainguinal vessels is the most prevalent manifestation of

PAD encountered by the vascular surgeon. Patients are classified into two broad categories depending

upon their symptomatology: claudicants and those with critical limb ischemia (CLI). Claudication, the

reproducible ischemic muscle pain resulting from inadequate oxygen delivery during exercise, is the

cardinal presenting symptom. Natural history studies indicate patients with claudication have increased

rates of cardiovascular mortality, but an overall low risk of limb loss.18,19 Seventy to eighty percent of

patients with claudication demonstrate a stable pattern of disease throughout their lifetime or have

improvement in their symptoms as a result of risk factor modification, whereas 20% to 30% undergo

operation within 5 years as a result of disease progression. Claudication will progress to CLI in only 5%

to 10% of patients over their lifetime. However, PAD leading to claudication is a marker of severe

systemic atherosclerotic burden and increased cardiovascular morbidity and mortality. Twenty percent

of chronic instance experience a nonfatal myocardial infarction or stroke and 10% to 15% died of

cardiovascular-related mortality at 5 years.13 The annual rates of mortality and limb loss in patients

with claudication are approximately 2% to 5% and 1%, respectively.13,20

4 The most common atherosclerotic disease pattern encountered distal to the inguinal ligament is that

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of a short-segment total occlusion of the superficial femoral artery. Isolated disease of this nature

typically presents as calf muscle claudication. It is not uncommon, however, for patients with significant

single-level lesions, even those with long-segment arterial occlusions, in the superficial femoral artery

or more distal arterial beds to be only minimally symptomatic or even asymptomatic. While this can

sometimes be the result of exercise limitations imposed by concomitant coronary arterial disease or

other physiologic impairments such as lung disease or arthritis, it is more often a result of compensatory

collateral flow. Collateral perfusion from the profunda femoral artery around a heavily diseased or

occluded superficial femoral artery frequently reconstitutes the distal superficial femoral artery or

popliteal artery with enough well-perfused arterial blood to ensure sufficient resting tissue perfusion.

Similarly, the rich network of geniculate collaterals can sometimes compensate for a diseased popliteal

arterial segment to a sufficient degree to prevent rest pain or overt tissue loss, but will usually prove

insufficient to meet the increased metabolic demands of ambulation and forestall claudication.

CLI, which must be differentiated from acute limb ischemia, is the most severe form of PAD and

refers to the presence of either rest pain or tissue loss in the lower limb. Rest pain occurs when blood

flow is inadequate to meet resting metabolic requirements. In the lower extremity, ischemic rest pain is

localized to the foot, frequently in the metatarsals or the instep, and should be easily distinguishable

from benign muscle cramps in the calf commonly seen in older patients. Patients with rest pain are

often awakened by severe discomfort in the forefoot and hang the affected extremity over the edge of

the bed for temporary symptomatic relief. Trophic changes, such as muscle wasting, thinning of skin,

thickening of nails, and hair loss are frequently also seen in the distal affected limb. Rest pain is an

ominous symptom and usually requires revascularization given the tendency for progression to tissue

loss. Ischemia ulcerations usually begin as small, dry ulcers of the toes or heel area, and progress to

frankly gangrenous changes of the forefoot or heel with greater degrees of arterial insufficiency (Fig.

93-1). Patients with diabetes or renal failure are more susceptible to the development of ischemic pedal

ulcers. Disease progression can be very rapid, as up to 50% of patients with CLI are asymptomatic 6

months before onset of pain or ulceration.21 Such progressive disease, affecting multiple levels of the

peripheral vasculature tree, is more frequently encountered in the elderly.

The natural history of CLI is dismal as these patients are generally of advanced age and possess

significant comorbidities contributing to their advanced limb ischemia. Overall, approximately 25% of

patients with CLI will die at 1 year, 30% will undergo major amputation, and 45% will be alive with

two limbs.13,14 The rate of amputation is 10 times higher in diabetics than nondiabetics and 5- and 10-

year mortality in patients with CLI have been reported to be 60% and 85%, respectively.21 CLI

mandates revascularization for limb salvage when feasible, as limb salvage with medical therapy and

wound care is virtually futile; success rates for rest pain and tissue loss have been reported to be as low

as 27% and 5%, respectively.21

Several identifiable patterns of infrainguinal PAD are well recognized. It is important to note that

symptoms and signs of ischemia generally involve the limb one level distal to the level of

hemodynamically significant disease. Patients with an extensive history of cigarette smoking typically

have lesions limited to the superficial femoral artery and corresponding symptoms of calf claudication

(Fig. 93-2). Patients with rest pain or ischemic tissue loss typically manifest more extensive

involvement of the femoral, popliteal, or tibial arteries than patients with claudication. Those with

tissue loss also more commonly have multilevel disease involving the femoropopliteal system in

combination with occlusive disease of the aortoiliac vessels or the infrageniculate runoff.22Diabetes

often targets the tibial vessels, and patients may present with frank tissue necrosis in the presence of a

palpable popliteal pulse and no prior history of claudication. Alternatively, the so-called “blue toe

syndrome” is a situation in which atherosclerotic debris breaks free from a more proximal source, for

example, an aortoiliac or femoropopliteal plaque or a thrombus-lined aneurysm, and embolizes to the

distal vessels.23 Wire manipulation during coronary or peripheral angiographic procedures and

crossclamping across a calcific aortic plaque during cardiac surgery are common sources of such emboli.

The terminal target of the microembolic particles, whether cholesterol crystals, calcified plaque, and

thrombus or platelet aggregates, is typically the small vessels of the toes and heel.

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Figure 93-1. A–C: Examples of digital ischemic ulcerations resulting from progressive arterial insufficiency.

Figure 93-2. Long-segment total occlusion of superficial femoral artery in a patient with a long history of cigarette smoking and

severe claudication. Proximal sfa occlusion is demonstrated (A), followed by wire traversal of the occlusion (B), which will allow

endovascular treatment of the occluded segment of the sfa proximal to reconstitution of the above-knee popliteal artery (C).

A particularly virulent form of atherosclerotic arterial disease is often found in young female

smokers.24,25 Radiographic imaging in this subset of patients typically reveals atretic, narrowed

vasculature with diffusely calcific atherosclerotic changes. Such patients invariably have an extensive

smoking history, with or without other typical risk factors for atherosclerosis. Given the diminutive size

of the inflow and outflow vessels, the durability of endovascular intervention is generally inferior in

these patients, particularly in the face of continued cigarette use.

5 Typically half of patients proceeding to surgery for arterial occlusive disease have significant

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coronary artery disease, even more have hypertension, and almost 80% are current or prior cigarette

smokers.26,27 The low mortality and morbidity associated with operative intervention in recent years

are in large part a result of advances in the management of concomitant coronary disease. Specifically,

the importance and benefit of better preoperative identification of patients in need of initial coronary

revascularization, awareness of the benefit of waiting an interval period following coronary stenting

prior to proceeding with major noncoronary vascular surgery, improved perioperative pharmacologic

management of patients with impaired myocardium, and more focused efforts to tailor operative and

postoperative fluid administration to the individual patient’s myocardial reserve are all well

recognized.28,29 Appropriate beta blockade and the use of statins have been shown to reduce

cardiovascular events and improve survival after inpatients undergoing vascular surgery, including

infrainguinal bypass.30,31 General advances in postoperative management, including pulmonary care,

infection control, and blood product utilization, have further contributed to the progress seen.

Diagnosis

6 The diagnosis of infrainguinal occlusive disease is generally based on patient symptomatology,

physical examination, and noninvasive tests, such as segmental pressure measurements and pulse

volume recordings. Accurate history-taking and physical examination are crucial to clarifying the

diagnosis and guiding a treatment management aimed at maximizing symptom relief and limb

preservation. Intermittent claudication (IC) indicative of infrainguinal occlusive disease is typically a

cramping, aching discomfort consistently reproducible at a given distance and relieved soon after

cessation of ambulation. This must be differentiated from lower extremity pain secondary to nerve root

compression or spinal stenosis which, in contradistinction to vasculogenic pain, often develops when

patients maintain a stationary standing posture. Vasculogenic claudication must also be distinguished

from venous claudication, hip and ankle arthritis, symptomatic Baker cyst, and chronic compartment

syndrome. IC patients with isolated infrainguinal disease will likely have palpable femoral pulses but

diminished popliteal and/or pedal pulses.

As is true with claudication, ischemic rest pain must be carefully distinguished from other sources of

pain in the elderly population, most commonly arthralgia and neuropathy. Although tissue necrosis and

gangrene are usually self-evident when caused by critical ischemia, similar lesions associated with

venous stasis, severe anemia, decubitus ulcers, and diabetic neuropathy must be excluded.

Noninvasive physiologic arterial testing allows confirmation of infrainguinal occlusive disease when it

is suspected based upon history and physical examination. Measurement of the ABI is the most useful

diagnostic adjunct. A properly performed ABI in a claudicant without significant evidence for vascular

calcification would be expected to be between 0.5 and 0.9. Ischemic rest pain generally occurs at ABI

0.4 to 0.5, whereas an ABI less than 0.4 is generally associated with tissue loss. Segmental pressure

measurements at the level of the upper thigh, lower thigh, upper calf, ankle, and metatarsal level also

aid in localizing the level of hemodynamically significant disease. A drop in pressure greater than 20

mm Hg between levels indicates a hemodynamically significant stenosis in the intervening arterial

vasculature. In patients with DM or CRI leading to extensive vascular calcification, the ABI will often be

erroneously elevated due to medial calcinosis and subsequent noncompressibility of the vessels. In such

circumstances, pulse volume recordings, which ascertain the volume of blood flowing into segment of

the limb, remain a reliable indicator of perfusion to the various levels of the lower extremity.

Measurement of toe pressures also effectively quantitates distal perfusion as the digital arteries are

generally spared of calcium which inhibits compressibility. A toe–brachial index less than 0.7 is

considered abnormal. Absolute toe pressure less than 30 to 50 mm Hg generally indicates severe lower

extremity occlusive disease with inadequate perfusion to heal tissue loss, particularly in diabetics.14

Further anatomic mapping is warranted only after the diagnosis of hemodynamically significant

infrainguinal disease has been made based upon physical examination and noninvasive testing and the

decision to pursue intervention has been made. The goal of anatomic imaging is to determine if

adequate revascularization is anatomically feasible and to delineate the options for both endovascular

therapy and open surgical revascularization. Duplex ultrasonography, magnetic resonance angiography

(MRA), and computed tomographic angiography (CTA) are increasingly being utilized as first-line

modalities in planning the optimal revascularization approach, and have supplanted contrast

angiography as the initial imaging study of choice in many centers.32 Nevertheless, due to inherent

limitations with each of these techniques, digital subtraction angiography remains the gold-standard

technique for imaging of the vascular tree prior to intervention.33

Although a growing literature supports the use of duplex scanning as a stand-alone preoperative

2649