Bilateral popliteal artery entrapment syndrome: case report / Síndrome do aprisionamento da artéria poplítea bilateral: relato de caso

Popliteal artery entrapment syndrome occurs due to an extrinsic compression of the popliteal vessels that results in vascular damage. It is one of the most frequent causes of intermittent claudication in young patients. The authors describe a case of bilateral syndrome by anomalous position of the gastrocnemius muscle, with abnormal slip of its medial head (Rich's type III). During the operation the occluded right side was reconstructed by autologous saphenous vein bypass from femoral superficial to peroneal artery and on the left side the slip muscle was transected by posterior approach. Popliteal artery entrapment syndrome should be treated by surgery despite the degree of symptoms. Surgical treatment technique has released the vessel by extracting the muscle that caused entrapment, and reconstructing the narrow lumen bypass grafting.

A síndrome do aprisionamento da artéria poplítea ocorre em função de compressão extrínseca dos vasos poplíteos, que resulta em lesão vascular. Trata-se de uma das causas mais freqüentes de claudicação intermitente em pacientes jovens. Os autores descrevem um caso de síndrome bilateral devida à posição anômala do músculo gastrocnêmio, com deslizamento de sua cabeça média (tipo III da classificação de Rich). Durante a cirurgia, o lado direito ocluído foi reconstruído por derivação da veia safena autóloga da artéria superficial femoral para a artéria peroneal e, do lado esquerdo, o músculo que sofreu o deslizamento foi secionado através de via posterior. A síndrome do aprisionamento da artéria poplítea deve ser tratada por cirurgia, independente do grau dos sintomas. A técnica de tratamento cirúrgico liberou o vaso, extraindo o músculo que causava o aprisionamento e reconstruindo o lúmen estreito por derivação.

Ischemic and reperfusion syndrome of hind limbs: functional and histological renal changes in rats

Ischemic and reperfusion injury of the extremities may result in a systemic, severe and complex metabolic syndrome, manifested by acute renal failure, myoglobinuria, metabolic acidosis, hipercalemia and free radicals releasing. We investigated the functional and histologic renal changes after ischemia and reperfusion of the hind limb skeletal muscles. Rats were submitted to the ligature of the infrarenal aorta for 6 and 12 h. The animals were then randomized into four groups of 10 rats: Group I, 6 h of ischemia and 24 h of reperfusion; Group II, 12 h of ischemia and 24 h of reperfusion; Group III, 6 h of ischemia and 10 days of reperfusion; and Group IV, Group sham with no ischemia or reperfusion. Blood samples at the end of the experiment and urine volume in the first 24 h of reperfusion in group I and II and in the last day in group III for functional analysis were collected. The following renal functional parameters were studied: creatinine plasmatic level, creatinine depuration and sodium urinary/creatinine urinary ratio. The kidneys were removed and a histological tubulo-interstitial lesional index was evaluated for each animal. We found higher plasma creatinine levels and morphologic changes in groups submitted to ischemia and reperfusion. Ten days after reperfusion, the histologic changes persisted despite the recovery of renal function.