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Chapter 92

Aortoiliac Disease

Loay S. Kabbani, Mitchell R. Weaver, and Alexander D. Shepard

Key Points

1 Aortoiliac occlusive disease is mainly the result of atherosclerosis.

2 Claudication is the most common presenting symptom of patients with significant aortoiliac

occlusive disease. Some patients may complain of erectile dysfunction. Physical examination

typically reveals diminished or absent femoral pulses.

3 Medical treatment of atherosclerotic aortoiliac occlusive disease is key to long-term success. This

includes risk factor modification (smoking cessation, control of hypertension, lipid abnormalities,

and diabetes mellitus), supervised walking programs and pharmacotherapy.

4 Smoking is the most important reversible risk factor for the development of lower extremity

atherosclerotic occlusive disease.

5 Percutaneous transluminal angioplasty, with or without stenting, has become the most common

therapy for aortoiliac occlusive disease.

6 Aortofemoral bypass is still the reference standard for reconstruction of advanced aortoiliac

occlusive disease.

INTRODUCTION

1 Peripheral arterial disease (PAD) is usually a manifestation of systemic atherosclerosis. It affects 3%

of the general population older than 40 years and 15% of those older than 70 years, with approximately

50% of patients with PAD being asymptomatic.1–3 Atherosclerotic occlusive disease of the aorta and iliac

arteries alone, or in combination with femoropopliteal or tibial occlusive disease, is the most frequent

cause of chronic lower extremity arterial insufficiency.

The wide availability of computed tomographic angiography (CTA) and magnetic resonance

angiography (MRA) has facilitated diagnosis, anatomic definition and subsequent intervention for

aortoiliac occlusive disease (AIOD). Selection of a patient-specific treatment from an increasing array of

treatment alternatives, although challenging, will frequently alleviate symptoms and reduce the risk of

disease progression. Endovascular and open reconstructive procedures for AIOD have become routine,

with low perioperative morbidity and mortality and excellent early and long-term outcomes.

ETIOLOGY

Anatomy and Pathophysiology

The arteries supplying blood to the lower extremities are frequently divided into abdominal, or

“inflow,” arteries (the aorta and iliac arteries) and infrainguinal, or “outflow,” arteries (the

femoropopliteal and tibial arteries).

Although atherosclerosis is a generalized disease, the earliest lesions tend to occur at arterial

bifurcations and in areas of relative fixation, where disruption of normal laminar flow is greatest, and

where eddy currents result in areas of low shear stress. Arteriopathies other than atherosclerosis, such

as Takayasu’s disease and radiation arteritis, can also involve the aortoiliac system. In slowly

developing aortoiliac occlusive lesions, hemodynamic alterations lead to the enlargement of a network

of auxiliary or collateral channels around the involved segments; this collateral network is usually

sufficient to provide enough blood flow to meet the resting metabolic needs of the lower extremities

(Figs. 92-1 and 92-2). These channels, however, do not have the capacity to increase blood flow to the

level necessary to meet exercise demands of the lower extremity musculature. The lumbar, hypogastric,

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femoral and profunda femoris arteries are interconnected with a large vascular collateral network.

Significant other collaterals join the internal mammary artery to the inferior epigastric artery and the

superior mesenteric artery (SMA) to the inferior mesenteric artery (IMA) and hemorrhoidal arteries.

The latter pathway gives rise to the Arc of Riolan (also known as the meandering mesenteric artery,

central anastomotic mesenteric artery, or Haller’s anastomosis) and the marginal artery of the colon

(also known as the Marginal Artery of Drummond) (Figs. 92-1 and 92-2). The Arc of Riolan connects the

proximal middle colic artery with a branch of the left colic artery. The Marginal Artery of Drummond

runs in the mesentery close to the bowel as part of the vascular arcade that connects the SMA and IMA.

PRESENTATION

Aortoiliac occlusive disease secondary to atherosclerosis is largely a disease of smokers. Other risk

factors include hypertension, lipid abnormalities, diabetes mellitus, male sex, older age, and genetic

predisposition. Smoking is the most important reversible risk factor for the development of lower

extremity atherosclerotic occlusive disease.4–6 Patients with symptoms of AIOD usually present in their

50s and 60s, whereas patients with infrainguinal disease or multilevel disease (AIOD + infrainguinal)

generally present in their 70s.7

2 Claudication (Latin claudicare = “to limp”) is the term used to denote the characteristic exerciseinduced, cramping pain in the muscles of the lower extremity that results from demand ischemia.

Claudication is the most common presenting symptom of patients with significant aortoiliac disease.

Induced by ambulation and quickly relieved by rest, claudication is usually described as a cramping pain

or easy fatigability of the involved muscle groups. Although patients with aortoiliac disease classically

present with claudication of the thighs, hips, and buttocks, a significant number complain of calf

claudication or have significant overlap. Erectile dysfunction in men secondary to reduced hypogastric

perfusion is another common complaint and may be found in as many as 30% to 50% of men with

AIOD.8 The combination of bilateral lower extremity claudication, atrophy of the lower extremity

musculature, impotence, and diminished or absent femoral pulses is known as Leriche syndrome, after

the French physician René Leriche.9

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Figure 92-1. A,B: Major visceral and parietal collateral networks that may become prominent with aortoiliac occlusive disease.

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Figure 92-2. CTA with 3D reconstruction demonstrating severe aortoiliac occlusive disease with juxtarenal aortic occlusion. Note

the extensive collateral networks reconstituting the inferior mesenteric artery (red arrow: marginal artery) and femoral arterial

segments (blue arrow: inferior epigastric artery) (green arrow: subcostal arteries and superficial iliac circumflex artery collaterals).

Physical examination typically reveals diminished or absent femoral pulses. A bruit auscultated over

the groins or lower abdomen is not specific for critical stenosis. Severely diseased, calcified femoral

arteries may be palpable as firm, tubular structures in the groins. Normal femoral and distal pulses may

be palpable, even in the presence of hemodynamically significant aortoiliac stenosis. These pulses,

however, rapidly disappear following ambulation, as the increased flow demands of the exercising leg

muscles lead to lowered peripheral vascular resistance and reduced distal arterial pressure. Patients with

longstanding aortoiliac atherosclerosis may have disuse atrophy of the lower extremity musculature.

Other common signs of lower extremity arterial occlusive disease include trophic changes, such as hair

loss on the legs or toes, and thin, shiny skin on the feet; patients with severe reductions in pedal blood

flow may display pedal rubor on limb dependency, coupled with pallor on elevation.

Critical limb ischemia (CLI) symptoms manifest in the lower leg or foot as ischemic rest pain,

nonhealing wounds, or gangrenous changes. Such symptoms may be a manifestation of AIOD alone but

almost always occur in combination with more distal femoropopliteal/tibial disease (i.e., multilevel

arterial occlusive disease). In the absence of infrainguinal disease, aortoiliac collaterals are usually

capable of maintaining adequate resting distal tissue perfusion.

Acute arterial occlusions from emboli lodging at the aortic, iliac or femoral bifurcation do not allow

collateral pathways to mature and compensate for the sudden loss of blood supply. This situation leads

to the acute onset of symptoms, with the resulting 5 “Ps” of acute ischemia: pain, pallor, pulselessness,

paresthesia, and paralysis. Cholesterol crystal embolism, or “blue toe” syndrome, occurs when debris

breaks free from an aortic, iliac, or more distal plaque, releasing platelet microthrombi, cholesterol

crystals, and other atheromatous material into the arterial lumen.10 Downstream embolism into the

microcirculation of the lower extremities can produce dermal discoloration in a characteristic reticular

pattern (livedo reticularis), digital ischemia, or even gangrene (Fig. 92-3). Such patients usually have

palpable pedal pulses. Embolic events can occur spontaneously or can be induced by interventions, such

as guidewire manipulation (e.g., during angiographic procedures or placement of an intra-aortic balloon

pump) or clamping an artery with unstable plaque during open vascular surgery.

Clinical Pathologic Types of Aortoiliac Disease

Different patterns of AIOD have been classically identified on preoperative imaging studies.11 Disease

confined to the distal infrarenal aorta and common iliac arteries, classified as type I, accounts for only

10% of patients with inflow disease. Patients with type I disease are younger (in their 50s and 60s),

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