The most common cause of popliteal artery occlusion is athero-occlusive disease. Thrombosis of a popliteal aneurysm can also cause popliteal occlusion and acute leg ischemia. Claudication in a young, athletic individual with no risk factors for atherosclerosis and normal pedal pulses may suggest popliteal entrapment syndrome, popliteal adventitial cystic disease, trauma, or extrinsic compression by a Baker cyst.
Popliteal entrapment syndrome is a group of anatomic anomalies that leads to popliteal arterial compression. Type 1 (20% of patients) is produced by an abnormal course of the popliteal artery, passing medial to the medial head of the gastrocnemius muscle. Type 2 (25%) is caused by medial insertion of the medial head of the gastrocnemius muscle. The popliteal artery is compressed by an abnormal accessory slip of gastrocnemius muscle in type 3 (30%) or popliteus muscle in type 4 (8%). Almost 30% of patients have bilateral disease. Claudication symptoms may be atypical, such as pain with walking but not with running. Diagnosis is made by magnetic resonance angiography (MRA) or by positional angiography; the patent artery becomes impinged with passive dorsiflexion or active plantar flexion of the ankle.
Treatment is surgical and involves transection of the abnormal muscle; if the artery is injured or occluded, short-segment bypass with the greater saphenous vein is required.
Popliteal adventitial disease is a rare disorder of unknown cause characterized by formation of cysts within the wall of the popliteal artery. The cysts compress the arterial lumen, causing stenosis or occlusion. Their contents resemble synovial fluid, and some may be in continuity with the joint space. The disease most often affects healthy men 40-50 years of age. Larger cysts are amenable to ultrasound-guided aspiration, but most are small and appear only as a thickening of the popliteal artery wall on MRA. In these cases, bypass or interposition grafting is curative.
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Revision date: July 3, 2011
Last revised: by Tatiana Kuznetsova, D.M.D.