Protean Manifestations of Pylethrombosis

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Abstract
Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in 2 patients. Eight others (5 agnogenic and 3 with hypercoagulability) experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarction; survival was related to the promptness of operation and the extent of bowel ischemia. Of 5 patients with intraabdominal sepsis and pylephlebitis, only 1 survived. In the final 6 patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram) and computed tomography. Thirteen of 34 patients had ascites and, in 9 of 11 patients examined, protein concentration of ascitic fluid was extremely low (< 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxilliary venous collateralization and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia and malignancy. Improved imaging now allows early diagnosis.