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This article is a review of chronic infrainguinal atherosclerotic arterial occlusive disease caused by atherosclerosis involving the femoral, popliteal, and/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, 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, co-morbidities, or vascular anatomy.
Although most patients with infrainguinal disease are treated nonoperatively, over 100,000 vascular reconstructive procedures are performed yearly in the United States alone. Unfortunately, intervention fails in up to 50% of cases within 5 years.
Chronic atherosclerotic lower extremity disease is present in 20% of the population older than 55 years. Most affected persons are asymptomatic. In fact, estimates indicate that only approximately 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.
Commonly accepted risk factors for both the occurrence and progression of atherosclerotic vascular disease include abnormal glucose tolerance, cigarette smoking, advanced age, hyperlipidemia, and hypertension.
Certain biochemical factors have also been shown to be independent risk factors for atherosclerotic peripheral vascular disease. Such factors include increased plasma fibrinogen levels, hyperhomocysteinemia and high-sensitivity C-reactive protein12 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 (such as hypertension or hyperlipidemia) increases the disease risk to more than twice the sum of the individual risks.
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, comprising 34% of all arterial emboli) or 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 following classic 6 "P"s:
The anatomic level at which pulse loss occurs helps identify the location of the occlusion.
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.
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, 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.
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).
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 Buerger disease (thromboangiitis obliterans).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 See the eMedicine article Buerger Disease (Thromboangiitis Obliterans). 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 (eg, posttraumatic pain syndromes, causalgia, mimocausalgia, Sudeck atrophy, reflex sympathetic dystrophy)
Complex regional pain syndromes (CRPSs) have been classified by the World Health Organization as CRPS II (ie, causalgia), which is associated with a demonstrable nerve injury, and as CRPS I (ie, mimocausalgia, reflex sympathetic dystrophy, Sudeck atrophy), which includes the remainder. Causalgia (ie, causos, heat; algos, pain) was first described in patients with arterial and nerve injuries sustained during the American Civil War. Both variants 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, or 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, or 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.
Popliteal artery entrapment syndrome
Intermittent claudication occurring in younger persons (from the teens to approximately age 45 y), particularly males, raises the possibility of popliteal artery entrapment syndrome.
In this unusual condition, the artery follows an aberrant course around the gastrocnemius muscle, usually medial to the medial head instead of between the 2 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.
Prior to 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. CT scanning or 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 the 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.
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 scanning, or MRI may demonstrate the cyst, while 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.
Indications for lower extremity revascularization include gangrene, pain at rest, nonhealing arterial ulcer, and disabling claudication.
Most patients with atherosclerotic lower extremity disease do not undergo surgical treatment. In fact, only 25% of patients presenting with intermittent claudication eventually require invasive treatment of limb-threatening ischemia or intractable symptoms, and only 5-10% do so within 5 years of the onset of claudication.
The cornerstones of medical management of intermittent claudication are walking and elimination or control of medical risk factors.27,28 For further reading, see the eMedicine articles Atherosclerosis and Coronary Artery Atherosclerosis.
Encourage walking.29 Regular walking of approximately 1 hour per day usually results in a significant increase in walking distance over time. This increase in walking distance has been noted to range from 80% to more than 200%. Improvement results from improved flow in collateral pathways.
Risk factor 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.
Before considering surgical intervention, the clinician must address the possibility of coexisting atherosclerotic heart and cerebrovascular disease, which are extremely common in patients with atherosclerotic peripheral arterial disease. One study found that only 14% of patients with peripheral arterial disease had normal coronary arteries, while 15% had severe coronary artery disease that required surgical correction. See the eMedicine article Atherosclerosis for the cardiologic workup.
Obtain appropriate imaging studies. Before surgical intervention, the exact extent of the atherosclerotic disease is mapped using high-quality contrast angiography (see Imaging Studies).
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