Practice Essentials
This article reviews chronic infrainguinal atherosclerotic arterial occlusive disease caused by atherosclerosis involving the femoral, popliteal, or infrapopliteal arteries. Because chronic atherosclerotic disease may result in acute circulatory compromise, acute arterial occlusion is also covered. Less common etiologies of lower-extremity arterial insufficiency, such as atheroembolism, thromboangiitis obliterans (Buerger disease), popliteal artery entrapment syndrome, and cystic adventitial disease, are briefly discussed.
Decision-making in the management of vascular disease changes frequently as new information becomes available and as new technologies emerge. Furthermore, therapeutic recommendations for a given population may not be applicable to individual patients with even slightly differing risk factors, comorbidities, or vascular anatomy. [1]
Although most patients with infrainguinal disease are treated nonoperatively, more than 100,000 vascular reconstructive procedures are performed each year in the United States alone. Unfortunately, intervention fails in as many as 50% of cases within 5 years. [2]
Of the symptomatic patients under medical care, approximately 25% develop progressive symptoms within 5 years, with 5-10% requiring surgical intervention and 1-2% undergoing major amputation within this same period. [3, 4] The vast majority of patients with intermittent claudication remain stable or improve with noninvasive management. Surgical or endovascular intervention is indicated for intractable and disabling claudication, for ischemic pain at rest, and for ischemic necrosis. Surgery also may be useful for nonhealing ischemic ulceration.
According to Baumgartner et al, 25% of patients with claudication will eventually require revascularization, and only 5% will develop critical limb ischemia (CLI). [5] (The term chronic limb-threatening ischemia [CLTI] is increasingly used in preference to CLI. [6] ) Within the first year after the initial diagnosis, 6-9% of patients require intervention. [5] Subsequently, 2-3% of patients per year require intervention. [5]
Because lower-extremity atherosclerosis is a marker for systemic atherosclerotic disease, these patients have significant systemic morbidities. About 30% of patients with peripheral artery disease (PAD) die within 5 years, and 40% die within 10 years. [3, 7]
Feringa et al observed a cohort of 2642 patients having ankle-brachial indices (ABIs) less than or equal to 0.9. [7] They discovered that the major factors associated with mortality in this group of patients included renal dysfunction, heart failure, ST-segment changes, age greater than 65 years, hypercholesterolemia, ABI lower than 0.60, Q-waves, diabetes, cerebrovascular disease, and pulmonary disease. They also found that the use of statins, aspirin, and beta blockers correlated with reduced 10-year mortality.
Anatomy
The inguinal (Poupart) ligament is a tough, fibrous band stretching from the anterior superior iliac spine to the pubic tubercle. The common femoral artery is a continuation of the external iliac artery, beginning just under the middle of the inguinal ligament. It is palpable as the femoral pulse and is well suited to both percutaneous and surgical access because of its relatively superficial position.
Approximately 2.5-5.0 cm distal to the inguinal ligament, the common femoral artery divides into the deep femoral (profunda femoris) artery, usually arising in the posterolateral position, and the superficial femoral artery.
The deep femoral artery gives rise to several very proximal branches that tend to maintain patency even in persons with extensive atherosclerotic disease, thus providing the major source of collateral circulation around an occluded superficial femoral artery.
The term superficial femoral artery is something of a misnomer, in that it is superficial for only a few inches until it courses under the sartorius and into the aponeurotic covering of the adductor (Hunter) canal.
When the superficial femoral artery emerges anterior to the adductor magnus, it becomes the popliteal artery. Because the popliteal artery is bounded posteriorly by the popliteal vein, nerve, and fascia and the semimembranosus, gastrocnemius, plantaris, and soleus muscles, it is the most difficult of the lower-extremity pulses to assess accurately.
The popliteal artery passes posterior to the knee joint and into the upper leg where, just distal to the popliteus, it divides into the anterior tibial artery and the tibioperoneal trunk.
The anterior tibial artery passes laterally through the interosseous membrane and lies on the interosseous membrane throughout much of the leg. As it reaches the lower leg, it lies on the tibia and then becomes superficial at the ankle joint, at which point it is called the dorsalis pedis artery and hence is palpable as the dorsalis pedis pulse.
The tibioperoneal trunk divides within approximately 2.5 cm of its origin into the peroneal artery and the posterior tibial artery.
The peroneal artery lies on the medial surface of the fibula and ends in terminal branches near the os calcis. The peroneal artery, which is too deep to be palpable as a pulse, often remains patent despite atherosclerotic occlusion of the anterior and posterior tibial arteries; thus, it may be a usable site for the distal anastomosis of bypass grafts in patients with advanced infrapopliteal occlusive disease.
The posterior tibial artery runs along the medial side of the leg and posterior to the medial malleolus, where it is superficial and palpable as the posterior tibial pulse.
The great (long) saphenous vein (GSV) originates on the medial side of the dorsum of the foot and runs anterior to the medial malleolus. It then runs posteromedially to the tibia, posteriorly to the medial condyle of the femur, and along the medial thigh, coursing anteriorly until it enters the femoral vein through the foramen ovale, just below the inguinal ligament. The length and relatively superficial course of the GSV make it ideally suited for use in infrainguinal bypass surgery.
Pathophysiology
Atherosclerotic occlusive disease
With atherosclerotic occlusion of a major lower-extremity artery, the limb is perfused via collateral pathways. Although this alternate pathway may be adequate at rest, it becomes inadequate as the oxygen demands of the leg musculature increase with activity. This inadequacy results in calf muscle pain or fatigue, a symptom known as intermittent claudication. As the degree of atherosclerotic occlusion worsens, blood flow, even at rest, may become impaired. This may cause ischemic pain at rest, ischemic ulceration, and gangrene.
Acute arterial occlusion
Acute occlusion of peripheral arteries commonly involves the infrainguinal segment. Underlying atherosclerotic disease may result in intraluminal strictures that impair blood flow and cause acute thrombosis. Emboli typically lodge at bifurcations and hence tend to occlude the distal common femoral artery (the most common site, accounting for 34% of all arterial emboli) or the distal popliteal artery (14%). Popliteal artery aneurysms may thrombose as a result of turbulent blood flow.
The clinical indications of acute occlusion of lower-extremity arteries are the classic six Ps, as follows:
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Paresthesias
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Pain
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Poikilothermia (coolness)
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Pallor
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Pulselessness
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Paralysis
The anatomic level at which pulse loss occurs helps identify the location of the occlusion.
Etiology
Commonly accepted risk factors for both the occurrence and the progression of atherosclerotic vascular disease include the following [8] :
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Abnormal glucose tolerance
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Cigarette smoking
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Advanced age
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Hyperlipidemia
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Hypertension
Certain biochemical factors have also been shown to be independent risk factors for atherosclerotic peripheral vascular disease, including the following:
These factors may also increase the risk of bypass graft stenosis and reocclusion.
When more than one risk factor is present, the cumulative risk is often greater than that posed by the individual risk factors combined. This is especially true of cigarette smoking, which, when accompanied by another risk factor (eg, hypertension or hyperlipidemia) increases the disease risk to more than twice the sum of the individual risks.
Epidemiology
Chronic atherosclerotic lower-extremity disease is present in 20% of the population older than 55 years. [13] Most affected persons are asymptomatic. In fact, it has been estimated that only about 20% of people with atherosclerotic lower-extremity disease present to a physician because of symptoms. Another 20% are symptomatic but do not seek medical attention.
Prognosis
Medical management
Infrainguinal arterial disease is associated with a risk of limb-threatening ischemia. However, most patients improve with medical treatment. Approximately 10% of patients with intermittent claudication develop findings necessitating vascular reconstructive procedures.
Endovascular management
Patency rates following endovascular treatment of infrainguinal occlusive disease vary significantly among published series. Overall, primary patency has been somewhat inferior to that of bypass surgery. Nonetheless, successful endovascular management improves quality of life and patient satisfaction. [14] Moreover, further endovascular or surgical management can often correct a failed endovascular intervention. [15, 16]
A 2023 review and meta-analysis of randomized controlled trials comparing bypass surgery with endovascular treatment for occlusive infrainguinal PAD found no significant differences between the two approaches with respect to major and minor amputation rates, amputation-free survival, or all-cause mortality. [17] Endovascular therapy was associated with a shorter procedural time and a reduced length of hospital stay; however, it was also associated with a higher risk of major adverse limb events and reintervention.
Surgical management
Graft patency rates vary widely among series. One study in which graft patency was assessed by means of magnetic resonance angiography (MRA) disclosed an 84% limb salvage rate and a 78% primary graft patency rate at 21 months' follow-up. Prosthetic grafts carry a primary 3-year patency rate of 39% and a 3-year secondary patency rate of 59%, with a 25% risk of amputation within 3 years. [18]
Limb salvage rates are lower among patients with insulin-dependent diabetes. [19] Infrainguinal reconstructive surgery is associated with a mortality of somewhat less than 5% despite the high-risk nature of these patients. [20] The likelihood of coexisting coronary artery disease is a major risk factor.
A British study reports that the major amputation rate after femorodistal bypass remains high, with adverse events occurring after approximately 38% of femoropopliteal procedures and nearly 50% of femorodistal bypasses. The main predictors of a poor outcome reportedly were diabetes and chronic renal failure. [21]
The overall survival rate for patients with lower-extremity arterial occlusive disease is approximately 50% over 10 years. For patients who require bypass surgery, the survival rate drops to approximately 50% over 5 years.
A study by Suckow et al explored associations between statin use and long-term mortality, graft occlusion, and amputation after infrainguinal bypass. [22] The investigators found that such therapy yielded a significant benefit with respect to 5-year survival but did not offer a significant advantage with respect to 1-year amputation or 1-year graft occlusion rates.
Khoury et al studied trends in mortality, readmissions, and complications after endovascular and open infrainguinal revascularization for PAD. [23] They found that open infrainguinal revascularization, though associated with lower rates of adverse events in comparison with endovascular therapy, was independently associated with increased risks of short-term (30 d) readmission, complications, and mortality.
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Pressure ulcer of heel exacerbated by infrainguinal arterial occlusive disease.
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Cyanosis of first toe and dependent rubor of foot, characteristic of arterial insufficiency.
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Contrast angiogram showing severe atherosclerotic disease in distal superficial femoral artery.
Tables
Rutherford Category |
Fontaine Grade |
Clinical Description |
Objective Criteria |
0 |
0 |
Asymptomatic – No hemodynamically significant disease |
Normal treadmill or reactive hyperemia test |
1 |
|
Mild claudication |
Completes treadmill exercise (5 min at 2 mph on 12% incline) AP* after exercise >50 mm Hg but at least 20 mm Hg lower than resting value |
2 |
I |
Moderate claudication |
Between Rutherford categories 1 and 3 |
3 |
|
Severe claudication |
Cannot complete treadmill exercise and AP after exercise < 50 mm Hg |
4 |
II |
Ischemic rest pain |
Resting AP < 40 mm Hg, flat or barely pulsatile ankle or metatarsal PVR**; TP † < 30 mm Hg |
5 |
III |
Minor tissue loss (nonhealing ulcer, focal gangrene with diffuse pedal ischemia) |
Resting AP < 60 mm Hg, ankle or metatarsal PVR flat or barely pulsatile; TP < 40 mm Hg |
6 |
|
Major tissue loss (extending above transmetatarsal level, functional foot no longer salvageable) |
Same as Rutherford category 5 |
*AP = Ankle pressure. **PVR = Pulse-volume recording. † TP = Toe pressure. |
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Lesion Type |
Description |
A |
|
B |
|
C |
|
D |
|
