the portosystemic gradient fell to 5 mmHg and the portogram demonstrated no flow to the gastric varices.
CommentsVarious portosystemic collateral pathways have been described, including esophageal and gastric varices via short and left gastric veins, perisplenic, mesenteric, and retroperitoneal veins, as well as via spontaneous splenorenal and gastrorenal shunts [1]. Other portosystemic collaterals originating from the left portal vein include recanalized umbilical and paraumbilical veins, located in and around the falciform ligament [2].The left portal vein consists of a proximal transverse and a more distal umbilical portion. The transverse portion supplies the caudate and quadrate lobes and the umbilical portion divides into superior and inferior branches to supply the segments II, III, and IVB. Unusual variceal communication between the right intraheaptic portal vein and the inferior vena cava has been described in man and experimentally induced portal hypertension in a canine model. Others include mucocutaneous peristomal collaterals at the junction of an ileostomy between submucosal vein and superficial abdominal wall vein [3]. The ileostomy varices are assumed to be secondary to an adhesion that develops as a result of postsurgical changes.Direct variceal communication between the distal branch of the left portal vein and gastric varices, however, has not been reported. We postulate that such unusual extrahepatic venous communication was most likely due to adhesion from a previous splenectomy. This unusual communication was probably responsible for the low portosystemic pressure gradient despite extensive hepatofugal flow, providing effective decompression of the portal system. evidence that stent fracture will be prevented. We are left with serious misgivings concerning the safety of both conventional and covered stents in this situation.
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