Popliteal entrapment syndrome results from extrinsic compression of the popliteal artery by the surrounding musculotendinous structures and is a rare cause of limb ischaemia. The purpose of this report is to highlight potential mistakes in the management of popliteal entrapment. In 2000, a 23 year old man underwent a popliteal to popliteal artery bypass surgery for what was initially diagnosed as a traumatic popliteal artery thrombosis. After being initially lost to follow up for 13 years, this “unspecified traumatic” thrombosis led to several inappropriate endovascular and open procedures misinterpreted as being caused by late graft failure. These included thrombectomy, aneurysmorrhaphy, polytetrafluoroethylene covered stent graft, a redo femoropopliteal bypass, and bypass thrombolysis. The diagnosis was reached 19 years after the initial surgery, when the patient underwent a redo bypass using a retrogeniculate approach. An abnormal lateral insertion of the gastrocnemius muscle medial head, and its accessory slip, constricted the artery, and also involved the popliteal vein (Type V), thus explaining previous revascularisation failures. Surgery consisted of resecting the accessory slip and the aneurysmal bypass. The artery was reconstructed with the cephalic vein. The patient was discharged on clopidogrel 75 mg, with no further complication, and a patent bypass at six months. Based on post-operative imaging (duplex ultrasound and magnetic resonance imaging), with forced plantarflexion and dorsiflexion, asymptomatic popliteal entrapment was also present on the contralateral side. The finding of an isolated popliteal artery lesion in a young individual should be considered to be caused by popliteal artery entrapment, unless proven otherwise. Definitive surgical release of the popliteal artery should be favoured over other strategies.

Background/Objectives: Germ cell tumors are the most common neoplasia in males < 50 y. In two case series, thromboembolic events (TEs) were reported in 8% and 13% of patients undergoing chemotherapy, whereas arterial thromboembolic events (ATEs) in other types of cancer treated with cisplatin had a frequency of 2% in a retrospective series and 0.67% in a meta-analysis. Recent data found a frequency of 2.4% for ATE in a large cohort of testicular cancer patients. Risk factors are not clearly identified, and given the severity of these events, further exploration is needed to determine appropriate preventive measures. Methods: We performed a retrospective cohort study of 171 patients undergoing chemotherapy for germ cell tumors in two centers in Switzerland and recorded the occurrence of ATE or venous thromboembolic events (VTEs) during chemotherapy or in the 3 months after its completion. Results: of 171 patients, 33.3% underwent adjuvant chemotherapy for stage I disease. Overall, 32 patients had a TE (18.7%, 95% CI 13.3–25.5%), 26 (15.2%, 95% CI 10.3–21.7%) had VTEs, and 11 (6.4%, 95% CI 3.4–11.5%) had ATEs. Five patients had both a VTE and ATE. VTEs were associated with disease stage (II, III, or relapse, with OR 15.6, p = 0.0002), retroperitoneal lymph nodes ≥ 3.5 cm (OR 3.2, p = 0.012), LDH > 500 UI/L (OR 5.3, p = 0.0025), and age > 35 y (OR 3.4, p = 0.005). The Khorana Score (KS) varied between 1 and 2 in 96% of the patients. ATEs were associated with active smoking (OR 6.5 p = 0.010), KS of ≥2 (OR 6.4 p = 0.004), and age > 35 y (OR 6.3, p = 0.01). Conclusions: Our findings show that ATEs are more frequent in our cohort than previous reports. We found a strong association between smoking and ATEs, which should be further assessed. Platinum-induced endothelial damage may be amplified by smoking in young patients in the absence of other risk factors and preventive medication.