Infrainguinal Occlusive Disease

Updated: Apr 08, 2015
  • Author: Christian Ochoa, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
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Overview

Background

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. [1] Furthermore, therapeutic recommendations for a given population may not be applicable to individual patients with even slightly differing risk factors, comorbidities, or vascular anatomy. [2]

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Problem

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. [3]

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. [4] The vast majority of patients with intermittent claudication remain stable or improve with noninvasive management.

According to Baumgartner, Schainfeld, and Graziani, 25% of patients with claudication will eventually require revascularization and only 5% will develop critical limb ischemia. [5] 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. Thirty percent of patients with peripheral artery disease die within 5 years, and 40% die within 10 years. [4, 6]

Feringa et al observed a cohort of 2642 patients having ankle-brachial indices less than or equal to 0.9. [6] 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, ankle-brachial index 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.

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Epidemiology

Frequency

Chronic atherosclerotic lower-extremity disease is present in 20% of the population older than 55 years. [7] 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.

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Etiology

Commonly accepted risk factors for both the occurrence and the progression of atherosclerotic vascular disease include the following [8] :

  • Abnormal glucose tolerance
  • Cigarette smoking
  • Advanced age
  • Hyperlipidemia
  • Hypertension

Certain biochemical factors have also been shown to be independent risk factors for atherosclerotic peripheral vascular disease, including the following:

  • Increased plasma fibrinogen levels [9]
  • Hyperhomocysteinemia [10, 11]
  • High-sensitivity C-reactive protein [12]

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 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.

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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 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 6 Ps, as follows:

  • Paresthesias
  • Pain
  • Poikilothermia (coolness)
  • Pallor
  • Pulselessness
  • Paralysis

The anatomic level at which pulse loss occurs helps identify the location of the occlusion.

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Presentation

History

Most people harboring atherosclerotic disease of the lower extremities are asymptomatic; others develop ischemic symptoms. Some patients attribute ambulatory difficulties to old age, unaware of the existence of a potentially correctible problem.

Symptomatic patients may present with intermittent claudication, ischemic pain at rest, nonhealing ulceration of the foot (see the image below), or frank ischemia of the foot.

Pressure ulcer of heel exacerbated by infrainguina Pressure ulcer of heel exacerbated by infrainguinal arterial occlusive disease.

Cramping or fatigue of major muscle groups in one or both lower extremities that is reproducible upon walking a specific distance suggests intermittent claudication. This symptom increases during ambulation until walking is no longer possible, and it is relieved by several minutes of rest. The onset of claudication may occur sooner with more rapid walking or when walking uphill or up stairs.

The claudication of infrainguinal occlusive disease typically involves the calf muscles, whereas symptoms that occur in the buttocks or thighs suggest aortoiliac occlusive disease. [13]

Physical examination

Physical examination discloses absent or diminished peripheral pulses below a certain level. Although diminished common femoral artery pulsation is characteristic of aortoiliac disease, infrainguinal disease alone is characterized by normal femoral pulses at the level of the inguinal ligament and diminished or absent pulses distally.

Specifically, loss of the femoral pulse just below the inguinal ligament occurs with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse suggests superficial femoral artery occlusion, typically in the adductor canal. Loss of pedal pulses is characteristic of disease involving the distal popliteal artery or its trifurcation.

Importantly however, be aware that absence of the dorsalis pedis pulse may be a normal anatomic variant, noted in approximately 10% of the population. On the other hand, the posterior tibial pulse is present in 99.8% of persons aged 0-19 years. Hence, absence of both pedal pulses is a more specific indicator of peripheral arterial disease.

Other findings suggestive of atherosclerotic disease include a bruit heard overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis of the toes, ulceration or ischemic necrosis, and, after 1-2 minutes of elevation above heart level, pallor of the involved foot followed by dependent rubor (see the image below).

Cyanosis of first toe and dependent rubor of foot, Cyanosis of first toe and dependent rubor of foot, characteristic of arterial insufficiency.

Differential diagnoses

Pseudoclaudication

Although ischemic findings in the face of absent pulses clearly pinpoint arterial insufficiency as the culprit, intermittent claudication, even when associated with absent pulses, is not always due to arterial insufficiency.

If symptoms are not always reproducible (ie, if the patient sometimes has "good days" when ambulation is not limited by claudication) or if the symptoms are associated with low back pain or radiculopathy, the clinician should consider the possibility of pseudoclaudication, which occurs as a result of spinal stenosis or cauda equina syndrome.

In that case, the pulse deficit may be an incidental finding of asymptomatic atherosclerosis. Noninvasive vascular laboratory testing (see Lab Studies), lumbosacral imaging, and neurologic evaluation all may contribute to distinguishing between these possibilities.

Two rather unusual conditions, venous claudication due to extensive iliofemoral venous thrombosis and chronic compartment syndrome due to calf muscle hypertrophy in athletes, result in a bursting type of pain in the calf with ambulation, which subsides slowly with elevation. In each case, the etiology is impaired venous outflow.

Atheroembolism

Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses, suggest the possibility of atheroembolism of plaque fragments from ulcerated, although nonocclusive, proximal atherosclerotic plaques or from thrombus lining the wall of an infrarenal aortic aneurysm (see Abdominal Aortic Aneurysm). [14]

Thromboangiitis obliterans (Buerger disease)

Severe ischemia of the toes with absent pedal pulses but normal proximal pulses in a man aged 35-50 years who smokes cigarettes may be the result of thromboangiitis obliterans (Buerger disease). [15] Ischemia of the fingers may also be present. The digits are cool, moist, mottled, and sometimes have tender shallow ulcers. Migratory superficial phlebitis may occur.

Collagen-vascular disease must be excluded. [16] Angiography reveals pathognomonic findings of "corkscrew" arteries. Treatment is discontinuation of smoking and good local wound care. Vascular surgery is rarely possible because of the poor quality of the distal arteries.

Complex regional pain syndromes

Complex regional pain syndromes (CRPSs; eg, posttraumatic pain syndromes, causalgia, mimocausalgia, Sudeck atrophy, reflex sympathetic dystrophy) have been classified by the World Health Organization into the following two variants:

  • CRPS II (ie, causalgia), which is associated with a demonstrable nerve injury
  • CRPS I (ie, mimocausalgia, reflex sympathetic dystrophy, Sudeck atrophy), which includes the remainder

Causalgia (from the Greek words kausos "heat" and algos "pain") was first described in patients with arterial and nerve injuries sustained during the American Civil War. Both variants of CRPS remain poorly understood and often misdiagnosed.

Although the exact pathophysiology is elusive, the sympathetic nervous system clearly plays a focal role. Therefore, surgical sympathectomy—perfected decades ago by vascular surgeons to manage nonreconstructible arterial disease (a common situation at the time)—was once the mainstay for treatment of the CRPSs.

Although surgical sympathectomy is now mostly notable only for historic purposes, sympathetic blockade is quite effective and is commonly performed for the CRPSs. Hence, currently the treatment of CRPSs is performed mainly by pain management specialists. Nonetheless, because the vascular surgeon has always been primarily responsible for the diagnosis of extremity symptoms, it is not uncommon for patients with CRPS to report to a vascular surgeon because of extremity pain.

Such pain may occur after extremity trauma but may seem disproportionate to the degree of injury. [17] Pain may also manifest after delayed revascularization of an acutely ischemic extremity. The diagnosis is often one of exclusion and thus requires a high index of clinical suspicion.

The diagnosis should be considered more strongly if severe superficial burning pain and agonizing hypersensitivity are present and are associated with vasomotor abnormalities such as edema, erythema, and hyperhidrosis. Radiographic studies may demonstrate relative and patchy osteopenia in the involved extremity.

In addition to symptomatic relief, management of the CRPSs requires sympathetic blockade. This is best performed during the early (acute) stage when the clinical course may be reversible. As the disease progresses, the erythema gives way to cyanotic mottling, the acute edema transforms to brawny edema, and the pain becomes unrelenting and disabling. These findings occur at approximately the third month and represent the second (dystrophic) stage. At this point, both plain radiographs and bone scans tend to demonstrate indicative findings.

Over time, disuse leads to atrophy, soft tissue fibrosis, and joint contractures. Radiographs confirm ankylosis and severe osteoporosis. This signals the third (atrophic) stage. Note that atrophy can also occur because of intentional disuse for anticipated secondary gain. Such patients reportedly do not respond to treatment until litigation has concluded.

Typically, the clinician does not even consider the diagnosis of a CRPS until the second stage. At that point, a dramatic clinical response to sympathetic blockade may confirm the diagnosis. Unfortunately, too much damage may have already occurred for sympathetic ablation to be effective and to break the vicious cycle of pain, sympathetic overactivity, and pain; the progression of the CRPS may be inexorable and irreversible.

One other caveat is that in the face of coexisting arterial disease, the vascular surgeon who may attribute the symptoms to ischemia and thereby may consider bypass should be aware that a surgical incision tends to exacerbate the pain in an extremity afflicted with a CRPS.

For more information, see Complex Regional Pain Syndrome in Emergency Medicine.

Popliteal artery entrapment syndrome

Intermittent claudication occurring in younger persons (from the teens to approximately age 45 years), particularly males, raises the possibility of popliteal artery entrapment syndrome. [18]

In this unusual condition, the artery follows an aberrant course around the gastrocnemius, usually medial to the medial head instead of between the two heads of this muscle. Ambulation causes the muscle to compress the artery and results in transient loss of distal blood flow. Over time, the artery may thrombose or become aneurysmal.

Before complete thrombosis, this condition can sometimes be confirmed clinically by noting loss of the pedal pulse upon active plantar flexion or passive dorsiflexion of the foot. Computed tomography (CT) or magnetic resonance imaging (MRI) can reveal the muscular abnormality, and angiography with stress views can confirm the diagnosis.

Treatment entails sectioning the aberrant muscle fibers. Bypass grafting is needed if the occlusion is chronic in nature. Assessing the contralateral side is important because one third of cases are bilateral.

Cystic adventitial disease of popliteal artery

Intermittent claudication of abrupt onset occurring in a relatively young male also may be the result of cystic adventitial disease of the popliteal artery. [19]

This rare congenital anomaly is the result of ganglionlike cysts, perhaps from an adjacent synovium, compressing the artery. This compression may eventually lead to thrombosis of the artery.

Prior to occlusion, pedal pulses may be found to disappear with flexion of the knee joint. Ultrasonography, CT, or MRI may demonstrate the cyst, whereas angiography may demonstrate a characteristic hourglass deformity, which has been termed the scimitar sign.

Cystic adventitial disease of the popliteal artery is treated surgically by removing the cyst. Vascular bypass is required if occlusion has occurred. [20]

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Indications

Indications for lower extremity revascularization include gangrene, pain at rest, nonhealing arterial ulcer, and disabling claudication.

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Relevant 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 somewhat 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 and, thus, 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 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 great saphenous vein make it ideally suited for use in infrainguinal bypass surgery.

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Contraindications

In nonambulatory patients with ischemic pain at rest, gangrene, or extensive nonhealing wounds, primary lower extremity amputation may be a better choice than vascular bypass surgery.

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