Portal hemodynamics, intestinal absorption, and postshunt encephalopathy.

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.