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 two 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 five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six 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 nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (less than 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary 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.

The spontaneous onset of a painful unilateral blue toe is usually caused by fibrinoplatelet microemboli arising from an upstream stenotic or occlusive lesion of the iliac or femoral artery. This constellation of findings is referred to as the blue toe syndrome (BTS). In 12 patients who experienced 14 spontaneous episodes of BTS, angiography demonstrated 15 proximal atherosclerotic arterial lesions, which were presumed to be the source of the microemboli. Fourteen of the 15 lesions were short-segment stenoses or occlusions distal to the aortic bifurcation. Six lesions were treated with antiplatelet or anticoagulant drugs followed by delayed percutaneous transluminal angioplasty (PTA) 6-12 weeks later. Three lesions were treated with surgical bypass, three with long-term anticoagulation, and one with transcatheter clot aspiration and immediate PTA. Two were treated with immediate thrombolytic therapy and had embolic complications. Antiplatelet and anticoagulant therapy followed by delayed PTA may be an effective alternative to surgery for treating BTS.

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