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Background: During the past 18 years we have used a selective operative approach for variceal bleeders in whom endoscopic sclerotherapy failed or sclerotherapy was not indicated. Esophagogastric devascularization with splenectomy has been reserved for unshuntable patients and for those in whom a shunt was deemed inadvisable. The purposes of this study are to describe the surgical procedure technique and indications for esophagogastric devascularization and to report its long-term results., Methods: Thirty-two patients who underwent either a limited (n = 9) or extensive (n = 23) esophagogastric devascularization procedure without esophageal transection for variceal bleeding were retrospectively reviewed. Common indications were thrombosis of all splanchnic veins (n = 12), distal splenorenal shunt thrombosis (n = 7), generalized portal hypertension with isolated splenic vein thrombosis (n = 5), and symptomatic splenomegaly or severe hypersplenism (n = 6). Eighteen patients (56%) had cirrhosis, eleven (34%) received an emergency operation, and eighteen (56%) bled from gastric varices., Results: Three patients with Child's class C disease undergoing emergency surgery died during the early postoperative interval. Rebleeding occurred in nine surviving patients (31%) and was the cause of death in three. Rebleeding rates for the limited and extensive devascularization procedures were 50% and 24%, respectively. Only one of 11 patients with diffuse splanchnic venous thrombosis without liver disease has died. The 5-year survival rate of patients with liver disease was 51%. Only two patients experienced postoperative encephalopathy., Conclusions: When used in selected patients, esophagogastric devascularization without esophageal transection is a reasonably effective alternative to shunt surgery.

Background: The aims of this study were to determine the causes of recurrent upper gastrointestinal hemorrhage (UGH) after distal splenorenal shunting (DSRS) and to summarize our experience in the prevention and management of this complication., Methods: This study is based on a retrospective review of 145 consecutive patients undergoing DSRS from 1978 through 1991., Results: Recurrent UGH developed in 19 patients (13%), most frequently secondary to residual portal hypertension (84%). Eight patients had shunt thrombosis and 11 had patent shunts. The incidence of shunt thrombosis was significantly greater in patients whose splenic vein was less than or equal to 8 mm in diameter (44%) than those whose splenic vein was greater than 8 mm (7%, p less than 0.001). The frequency of shunt failure from 1985 through 1991 was significantly lower (2%) than from 1978 through 1984 (10%, p less than 0.05). Five patients, all with occluded shunts, underwent surgical treatment for recurrent UGH and three died (60%). Fourteen patients were managed nonoperatively, with a mortality rate of 38%., Conclusions: Recurrent UGH after DSRS occurs in patients with patent shunts and in those with occluded shunts; DSRS thrombosis is more frequent when the splenic vein diameter is less than or equal to 8 mm; DSRS thrombosis decreases with operative experience; and the mortality rate for this complication is high with both operative and nonoperative management.

Although total diversion of portal blood flow has been considered to be the main factor leading to encephalopathy following nonselective shunt (NSS), increased intestinal absorption of cerebral toxins secondary to mesenteric venous decompression could also play a role. Conversely, the low frequency of encephalopathy after the distal splenorenal shunt (DSRS) may be due to preservation of both hepatic portal perfusion and mesenteric venous hypertension. Portal hemodynamics, intestinal absorption of D-xylose, ammonia metabolism, and clinical encephalopathy were assessed preoperatively and in the early and late postoperative periods in cirrhotic patients selected for the DSRS (n = 12) and NSS (n = 10). Preoperatively, NSS patients had significantly less hepatopetal portal blood flow (P = 0.03) and lower D-xylose absorption (P = 0.004) than DSRS patients. DSRS resulted in no significant alterations in hepatic portal perfusion, portal pressure, D-xylose absorption, fasting blood ammonia (NH3), or tolerance to an oral dose of ammonium chloride. In contrast, NSS resulted in complete portal diversion and decompression and significant enhancement of D-xylose absorption on both the early (P = 0.02) and late (P = 0.03) postoperative evaluations. Early and late postoperative levels of MH3 were significantly higher in NSS patients. Encephalopathy was more frequent after NSS (80%) than after DSRS (17%, P = 0.003). When all patients were considered, preoperative to early DSRS (17%, P = 0.003). When all patients were considered, preoperative to early postoperative change in NH3 correlated with change in D-xylose absorption (r = 0.52, p = 0.02), and there were significantly more individuals with a greater than 2 gm increase in D-xylose absorption who developed encephalopathy (83%) than patients with no or minimal increase in D-xylose absorption (33%, P = 0.04). The results of this study suggest that altered intestinal absorption may be one of many factors determining postshunt cerebral function.