Popliteal Artery Entrapment Syndrome

Popliteal artery entrapment syndrome is compression of the popliteal artery by the medial head of the gastrocnemius, an aberrant muscle slip or a fibrous band. It causes exertional calf claudication in young, active people and can progress to arterial stenosis, occlusion or aneurysm.

Anatomical entrapment is found in about 3.5% of young adults on imaging, and in many it never causes symptoms. Symptomatic disease is rarer. Men are affected about 15 times more often than women, and it is usually diagnosed between ages 20 and 40. About 25 to 60% of cases are bilateral.

Anatomical types are:

• Type I: the artery runs medially around a normally attached medial head of gastrocnemius.
• Type II: the medial head attaches abnormally and laterally on the femoral condyle, with a medially displaced artery.
• Type III: an accessory slip of gastrocnemius passes around the artery.
• Type IV: the artery lies deep to popliteus or a fibrous band.
• Type V: any type with involvement of the popliteal vein.
• Type VI (functional): normal anatomy with hypertrophied gastrocnemius or popliteus that compresses the artery during plantar flexion.

Complications are fibrosis and stenosis, post-stenotic aneurysm, thrombosis, distal embolisation and acute limb ischaemia. Delay in diagnosis is common because the examination at rest is normal.

Pathophysiology.

Repeated compression during active plantar flexion or forced dorsiflexion traumatises the arterial wall. This produces intimal injury, fibrosis, stenosis and post-stenotic dilatation.

Thrombus forms in the damaged segment or in an aneurysm and may embolise to the calf and foot arteries. Chronic compression can occlude the vessel, and collaterals are usually poor in young patients, so symptoms are marked.

Venous involvement (type V) causes swelling and deep vein thrombosis. Functional entrapment causes symptoms with no structural arterial damage, so early surgery may prevent progression.

Exertional calf or foot pain (claudication), often with cramping, coldness, paraesthesia or numbness, in a young person who is athletic or who has recently increased training. Pain eases with rest, usually within minutes. Pain during running that is relieved by rest, with a normal examination at rest, is typical.

Signs are often absent at rest. Foot pulses may disappear or weaken on active plantar flexion or passive dorsiflexion of the knee in extension. A bruit, a pulsatile popliteal mass (aneurysm), or distal embolisation with blue toes or acute ischaemia may be present. Leg swelling suggests venous involvement.

Stepwise workup:

• Resting ankle brachial index is usually normal, so measure it again after exercise and with provocative manoeuvres. A fall of 50% or more with active plantar flexion against resistance, or with passive dorsiflexion, supports the diagnosis.
• Duplex ultrasound with provocative manoeuvres: loss of the popliteal waveform and flow during plantar flexion, plus structural detail such as aneurysm and thrombus.
• MRI or MR angiography with the knee in neutral position and with stress positions: shows muscle and band anatomy, arterial compression, and fat plane loss between artery and muscle. This is the best test for classification.
• CT angiography for arterial detail, occlusion or aneurysm when MRI is unavailable. Catheter angiography with provocative positions confirms the diagnosis when other tests are unclear, and is used before surgery or thrombolysis.
• Blood tests: full blood count, glucose, lipids, ESR and C-reactive protein, thrombophilia screen in unexplained thrombosis.
• Examine both legs because disease is often bilateral.

Differential diagnosis.

• Chronic exertional compartment syndrome, medial tibial stress syndrome and stress fracture.
• Cystic adventitial disease of the popliteal artery and popliteal aneurysm.
• Premature atherosclerosis, Buerger disease, fibromuscular dysplasia and vasculitis.
• Deep vein thrombosis, Baker cyst, and lumbar spinal stenosis.

Definitive treatment is surgical. Observation is acceptable only for anatomical entrapment without symptoms or arterial damage.

Release.

• Division of the medial head of gastrocnemius or the fibrous band, with restoration of the normal anatomy of the popliteal fossa. Release alone is enough when the artery is normal or has minimal damage, and gives relief of symptoms in most patients.
• Popliteal exploration through a posterior or medial approach, usually bilateral when both sides are affected (staged or same sitting).

Arterial reconstruction for stenosis, occlusion, aneurysm or thrombus.

• Resection with an interposition graft or bypass using reversed great saphenous vein (preferred in young patients).
• Cefazolin 2 g intravenously within 60 minutes before incision (3 g when weight is over 120 kg); heparin 70 to 100 units/kg intravenously before clamping, reversed with protamine 1 mg for each 100 units given in the previous 2 to 3 hours (maximum 50 mg, given slowly).
• Patency is good after vein grafting. Endovascular stenting or angioplasty alone is not used because compression persists and stents fracture.

Acute limb ischaemia from thrombosis or embolism.

• Unfractionated heparin 80 units/kg intravenous bolus (usual 5000 units), then 18 units/kg/h, aPTT 1.5 to 2.5 times control at 6 hours.
• Catheter directed thrombolysis for a viable or marginally threatened limb: alteplase 0.5 to 1 mg/h (usual total up to about 40 mg) with low dose heparin 500 units/h, with fibrinogen and clinical review every 6 hours. Absolute contraindications are previous intracranial haemorrhage, ischaemic stroke in the last 6 months, intracranial neoplasm, active bleeding, and major surgery or trauma in the last 3 weeks.
• Surgical thrombectomy with release and reconstruction for an immediately threatened limb. Fasciotomy for tense compartments or prolonged ischaemia. Monitor potassium, creatinine and creatine kinase for reperfusion injury.

Functional entrapment. A test injection of botulinum toxin into the medial head of gastrocnemius can confirm the diagnosis and give temporary relief, with dose and sites set by the specialist. Surgery is offered for persistent symptoms.

Antithrombotic therapy.

• After release alone: aspirin 75 to 100 mg orally once daily for 3 months.
• After arterial reconstruction: aspirin 75 to 100 mg daily lifelong, with anticoagulation for 3 months after thrombosis or embolism (apixaban 5 mg twice daily, 2.5 mg twice daily if two of age 80 or over, weight 60 kg or under, creatinine 133 micromol/L or over; or warfarin to INR 2.0 to 3.0).
• Atorvastatin 40 to 80 mg daily when atherosclerosis coexists.

Return to sport. After release alone, graded return from 6 to 12 weeks. After reconstruction, from 3 to 6 months, once duplex confirms patency.

Monitoring. Duplex with provocative positioning at 1 month, 3 months, 6 months and 12 months, then yearly for 3 years (vein graft surveillance). Ankle brachial index before and after exercise at each visit. Imaging of the other leg.

Referral and escalation. Refer every suspected case to a vascular surgeon with experience in the condition. Same day referral for acute limb ischaemia, a pulsatile popliteal mass, or distal embolisation.

Special groups.

• Pregnancy: avoid elective surgery; for thrombosis use low molecular weight heparin (enoxaparin 1 mg/kg subcutaneously every 12 hours), and avoid warfarin and direct oral anticoagulants.
• Athletes: counsel that continued training after the arterial damage can cause occlusion, so training is stopped until the diagnosis is settled.
• Kidney impairment: limit contrast volume, and give enoxaparin 1 mg/kg once daily when creatinine clearance is under 30 mL/min.
• Region specific: where MRI is unavailable, duplex with provocative positioning and CT angiography are the usual tools.