Popliteal artery entrapment syndrome

Overview
The popliteal artery entrapment syndrome is a rather uncommon pathology, which results into claudication and chronic leg ischemia. The popliteal artery may be compressed behind the knee, due to congenital deformity of the muscles or tendon insertions of the popliteal space. This repetitive trauma may result in stenotic artery degeneration, complete artery occlusion or even formation of an aneurysm.

History
The syndrome was first described in 1879 by Anderson Stuart, a medical student, in a 64-year-old male. Hamming and Vink in 1959 first described the management of the popliteal artery syndrome in a 12-year-old patient. The patient was treated with myotomy of the medial head of the gastrocnemius muscle and concomitant endarterectomy of the popliteal artery. They later reported four more cases and claimed that the incidence of this pathology in patients younger than 30 years old with claudication was 40%. Servello was the first to draw attention to diminished distal pulses observed with forced plantar or dorsiflexion in patients suffering from this syndrome. Bouhoutsos and Daskalakis in 1981 reported 45 cases of this syndrome in a population of 20,000 Greek soldiers. During the recent years the increasing frequency with which popliteal artery entrapment is reported, strongly suggests a greater awareness of the syndrome.

Etiology

 * 1) A development defect in which the popliteal artery passes medial to and beneath the medial head of gastrocnemius muscle
 * 2) A slip of the muscle with consequent compression of the artery.
 * 3) Rarely an anomalous fibrous band
 * 4) Popliteal muscle deep to the medial head of gastrocnemius compressing structure both artery and vein.

Types

 * Type I: Artery displaced in an exaggerated loop
 * Type II: Gastrocnemius muscle arise more lateral than its origin
 * Type III: Accessory slip of muscle compresses
 * Type IV: Entrapment by deeper popliteal muscle
 * Type V: Any of the above with vein involvement
 * Type VI: Functional type artery occludes with plantar flexion but no anatomical abnormality.

Clinical Findings

 * 1) Claudication in the calf and foot of a young man.
 * 2) Nine times more common in men
 * 3) Onset of symptoms is often sudden occurring during the episode of intense lower extremity activity such as during running.
 * 4) Symptoms correlate with the development of segmental occlusion of mid pop artery.
 * 5) Symptoms include cramping in the calf and foot and coldness, blanching, paresthesias, with walking and relieved with rest.
 * 6) Pedal pulses absent in 63%, diminished in 10% and palpable in 16% and in 11% disappear with  passive dorsiflexion or active planter flexion.
 * 7) Increased collaterals around knee.
 * 8) Geniculate arteries may be palpable over the anteromedial and anterolateral aspects of knee which is warm.
 * 9) PVR could be done before and after dorsiflexion and plantarflexion.
 * 10) Systolic bruit may be present.
 * 11) Distended superficial veins, edema and dependent cyanosis could suggest venous involvement.

Diagnosis
Two or more of the following finding on Femoral arteriography
 * 1.Medial deviation of the proximal pop artery.
 * 2.Segmental occlusion of the mid pop artery.
 * 3.Post Stenotic dilatation.

In addition stress angiograms with the leg actively planter flexed against resistance or passively dorsiflexed to show compression that may not be seen in neutral position.

Duplex scanning of the popliteal artery for compression. Baseline and then repeat with active planter flexion.

MRI or CT  to study anatomy in the popliteal fossa may be helpful.

Summary

 * 1) Rare but important cause of arterial insufficiency in younger patients.
 * 2) High index of suspicion combined with dynamic non invasive testing and stress arteriography should be performed.
 * 3) Medial deviation though diagnostic absence does not exclude it.
 * 4) Surgical exploration with relief of constricting lesion  and arterial reconstruction  if thrombosis should be done.