• INTRODUCTION
    • Popliteal artery entrapment is an uncommon syndrome, caused by extrinsic compression of the popliteal artery by muscular or tendinous structures. It occurs mainly in young individuals, with no atherosclerostic risk factors, and a mean age of presentation of 20 to 40 years, and has higher prevalence in males (83% of patients). Clinical presentation depends on the degree of arterial lesion, the most common being intermittent claudication, with critical ischemia being frequent. Occasionally, it may present as acute ischaemia.
  • METHODS
    • A 40-year-old female patient, physical education teacher, presented with a history of left foot paresthesia and left calf muscle pain during jogging for one year. The patient used to previously run 10 kilometers, currently mentioning claudication at 500 meters. No other medical conditions were mentioned. Lower extremity arterial duplex ultrasound revealed left popliteal artery compression and occlusion during active plantar flexion and passive dorsal flexion. The patient was referred to a vascular surgery center. Physical examination revealed palpable bilateral lower extremity pulses, with left asymmetry. Lower limb angiography and magnetic resonance imaging (MRI) were performed which demonstrated left popliteal artery compression and occlusion during a resisted plantar flexion. MRI revealed no anatomic anomalies, pointing to a probable functional entrapment caused by calf muscle hypertrophy (typo VI).
  • RESULTS
    • Entrapment correction surgery was performed through a posterior approach and exposure. During the procedure, the artery showed no signs of significant fibrosis. Since compression by the medial head of the gastrocnemius muscle was observed, myotomy of its lateral fibers was performed. The patient was discharged on the second day post-surgery. After three months, the patient remained free of symptoms, having taken up sports practice with no limitations.
  • CONCLUSION
    • Continuous popliteal artery compression leads to its progressive fibrosis, which may cause thrombosis or post-stenotic aneurysmal dilation. Treatment should be performed as soon as possible as to avoid this course and the eventual necessity of interposition or bypass grafting. Futhermore, late intervention worsens the interposition/ bypass grafting prognosis5. In this sense, the possibility of this diagnosis should be considered in a young patient presenting with intermittent claudication. Diagnostic tests are often decisive for differential diagnosis and to establish the disease subtype and intervention strategy. In most patients, a culprit muscular or tendinous anomaly is detected before surgery, however, in some individuals, especially physically active ones, compression results from muscular hypertrophy.