Type IV Popliteal Arterial Entrapment Associated With an Osteochondroma

Abstract

Popliteal artery entrapment syndrome is a rare cause of peripheral vascular disease, often affecting young adults. Multiple studies have shown that osteochondromas can cause vascular injury. Intermittent compression, pseudoaneurysm, thrombosis, distal embolism, and venous thrombosis have all been described as possible complications. Here we present a case of popliteal arterial entrapment type IV with an associated tibial osteochondroma. (J Vasc Surg Cases and Innovative Techniques 2017;3:66-8.) Osteochondromas or exostoses are benign bone tumors that arise from the metaphysis of growth plates. These lesions are typically asymptomatic and found incidentally during adolescence or childhood. Osteochondromas may occur as solitary lesions or as familial multiple hereditary osteochondromas. Most often, the distal femur, proximal humerus, and proximal tibia are involved. The cartilaginous cap of this tumor is soft and pliable; however, over time, it will ossify, becoming rigid and firm. This bone protuberance can then cause vascular complications that include pseudoaneurysm, thrombosis, and popliteal entrapment.1-3 Here we describe a case of type IV popliteal artery entrapment syndrome (PAES), defined as the presence of the axial popliteal artery deep to the popliteus muscle or fibrous bands, that caused arterial thrombosis associated with a tibial osteochondroma. Informed consent for publication of this case report was obtained. CASE REPORTA 27-year-old man complaining of a several-month history of right lower extremity coolness was seen by his primary care physician. He works as a farmer and does not participate in long-distance running or heavy exercise; however, he tends his fields on the farm and commonly squats to milk cows. The The patient underwent angiography, which again demonstrated the occlusion of the anterior tibial, posterior tibial, and peroneal arteries. Catheters were then delivered to the anterior tibial and posterior tibial arteries to allow tissue plasminogen activator infusion (Fig 1). To rule out proximal embolization as a source of the embolization, cardiac evaluation was performed.Transthoracic and transesophageal echocardiography did not demonstrate any valvular masses, vegetations, or intracardiac thrombi, and there were no shunts. Results of hematology hypercoagulable laboratory workup, including antiphospholipid antibody, lupus anticoagulant, and cardiolipin antibody, were negative. On an 18-hour and 26-hour angiogram, after beginning of the arterial lysis, the posterior tibial artery remained occluded, and the anterior tibial artery opened up with good flow into the dorsalis pedis (Fig 1). With the posterior tibial artery remaining occluded in spite of increased dose, lysis was stopped, and the patient was started on anticoagulation. Further imaging was performed to look for potential causes of thrombosis.The patient underwent magnetic resonance angiography (MRA) with active dorsiflexion and plantar flexion to evaluateFrom the Marshfield Clinic.