Popliteal Artery Entrapment Syndrome

Popliteal artery entrapment syndrome (PAES) is the most common cause of non-atherosclerotic claudication in young athletes. It is frequently missed, and left untreated, chronic PAES may progress to popliteal artery thrombosis, aneurysm formation, or even acute limb ischaemia requiring emergency revascularisation. Acute ischaemia is rare, but it is reported in late presentations with thrombosis.

Who. Patients are aged 15 to 40 years, peaking at 20 to 30, and the male-to-female ratio is approximately 2:1, although PAES is increasingly recognised in female athletes. Athletes are over-represented because of muscle hypertrophy. The typical patient is an athlete or military recruit with no diabetes, smoking or hyperlipidaemia.

How common. Anatomical variants are present in approximately 3 to 5 percent of cadaveric specimens. Imaging shows bilateral abnormality in 60 to 70 percent of patients, and the contralateral leg may be asymptomatic.

Why it is missed. Over 50 percent of patients are initially misdiagnosed, frequently as shin splints, CECS or lumbar radiculopathy, and the average delay from symptom onset to diagnosis is 12 to 24 months. A high index of suspicion and simple bedside provocative pulse testing can clinch the diagnosis.

The entrapment. The popliteal artery normally passes through the popliteal fossa without any musculotendinous compression. In PAES an anomalous relationship between the artery and gastrocnemius (most commonly the medial head), popliteus or fibrous bands leads to repeated arterial compression during plantarflexion and dorsiflexion. Functional PAES is the exception to the anomaly: a normal but hypertrophied gastrocnemius compresses a normally positioned artery during vigorous exercise.

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From compression to occlusion. Repeated compression damages the artery in a predictable sequence, and the end result is acute or chronic limb ischaemia:

1. External compression during exercise (functional)
2. Intimal irritation and fibrosis from repeated compression
3. Fibrous narrowing and post-stenotic dilatation
4. Thrombosis, aneurysm or complete occlusion

Why athletes. Progressive gastrocnemius hypertrophy narrows the popliteal space, and running, cycling and rowing put the artery through thousands of compression cycles. Higher training loads correlate with worse compression.

The Love-Whelan classification guides surgical planning. The anatomical types require resection of the anomalous structure, while functional entrapment responds to myotomy of the medial head of gastrocnemius.

History. The complaint is claudication: reproducible pain in the calf or foot on exertion, relieved promptly by rest. The foot may become numb, pale or cold during exercise, and calf pain on running, walking or dorsiflexion limits sport. Up to 30 percent report bilateral symptoms.

Examination at rest. The resting examination is often completely normal, with palpable pedal pulses. After exertion, look for pallor, delayed capillary refill or dependent rubor. Examine both legs even when the symptoms are unilateral, and feel the pulses in both the resting and the provoked positions.

Provocative pulse testing. This is the bedside hallmark. With the patient supine, palpate the dorsalis pedis and posterior tibial pulses before, during and after the manoeuvre: active plantarflexion against resistance, the examiner pushing against the forefoot, or passive dorsiflexion of the ankle to maximum. The test is positive when the pedal pulses diminish or disappear during the manoeuvre and return when the ankle comes back to neutral.

Reading the result. A positive provocative test in a young athlete with exertional calf pain is highly suggestive of PAES and mandates imaging. A negative test does not exclude the diagnosis, because sensitivity is imperfect, especially in functional PAES, where compression occurs only at higher forces.

A positive test is not the diagnosis. In Turnipseed's series, stress plethysmography was positive in 18 per cent of asymptomatic operated patients. Functional entrapment is therefore a diagnosis of symptoms plus a positive test plus normal compartment pressures, never of the test alone.

PAES or CECS. PAES is a vascular problem: claudication with pallor, a cold foot and diminished pulses on provocation, and the pain is ischaemic. Chronic exertional compartment syndrome is myofascial: burning, tight, bursting pain with normal pulses, no skin changes and a tense compartment after exertion, the pain coming from raised compartment pressure. Paraesthesiae and foot drop may occur in CECS from nerve compression within the compartment.

Duplex ultrasound first. Duplex is non-invasive, dynamic, done at the bedside and free of radiation. The resting scan assesses popliteal artery calibre, flow velocities and any aneurysmal change, and the scan is then repeated with active plantarflexion and passive dorsiflexion. A velocity increase of greater than 50 percent, or complete cessation of flow, with the provocative manoeuvres is the positive finding.

MR angiography is the gold standard. The popliteal fossa is imaged in the neutral position, then with the foot in active plantarflexion or passive dorsiflexion. It shows compression or occlusion of the artery, the anomalous musculotendinous structures and arterial wall changes such as thickening or aneurysm. There is no radiation, the soft-tissue characterisation is excellent, and muscle anatomy and arterial lumen are shown in one study.

CT angiography is the alternative when MRI is contraindicated (pacemaker, claustrophobia) or rapid assessment is needed in an acute presentation. It is performed in neutral and in plantarflexion. It is faster than MRI, gives excellent arterial detail and can assess calcification, at the cost of ionising radiation and less soft-tissue detail.

Conventional angiography is indicated if imaging suggests complete popliteal occlusion, or if endovascular intervention is being considered. It shows segmental occlusion, collateral formation and "spindle-shaped" post-stenotic dilatation, and it has a therapeutic role in catheter-directed thrombolysis for acute thrombosis.

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The principle. Surgical decompression is definitive for both functional and anatomical PAES. Release the offending structure, and reconstruct the artery only if it is diseased: a diseased segment needs an interposition vein graft or bypass. Plan bilateral surgery if the imaging abnormalities are bilateral.

Natural history. Untreated PAES follows the predictable course set out under pathophysiology, from compression to thrombosis or aneurysm. Young patients with anatomical PAES should be offered surgical decompression even if asymptomatic, because the natural history is one of progressive arterial damage. Functional PAES may be observed if symptoms are mild, but surgery is indicated for competitive athletes and for those with documented arterial wall changes.

Prognosis. The best prognosis belongs to functional PAES treated by myotomy alone, with a normal artery and a simple decompression. Anatomical PAES diagnosed early, before the arterial wall is damaged, does well; late presentation with thrombosis or aneurysm requiring bypass carries a guarded prognosis.

Warning signs. The poor prognostic indicators are delayed diagnosis over 12 months, acute limb ischaemia at presentation, and popliteal occlusion with poor run-off.

Symptom duration. Delayed diagnosis sits on that list, yet Sinha's systematic review found no relationship between duration of symptoms and the presence of irreversible arterial injury. Symptom duration alone should therefore not decide urgency.

Reconstruction fails often. The same review found a median failure rate of 27.5 per cent for arterial reconstruction, which is the argument for operating before the artery is damaged rather than after.