Effect of portal venous blood flow diversion on portal pressure.

To anticipate the hepatic vascular response to portacaval anastomosis, we studied portal pressure during diversion of portal blood through a temporary extracorporeal umbilical vein to saphenous vein shunt. The relationship of portal pressure to shunted flow was approximately linear. In five schistosomiasis patients (controls) portal diversion to 1,250 ml/min gave portal pressure-shunted flow curve slopes ranging from 0.13 to 0.57 cm water/100 ml per min (0.31+/-0.18, mean+/-SD). In 17 cirrhotic patients with portal hypertension a continuum of slopes was observed from within mean+/-2 SD of control (type A) to larger slopes (type B) indicating failure of portal pressure regulation. When portal flow was augmented by shunting from saphenous vein to portal vein, cirrhotic patients who had slopes less than mean+/-2 SD of controls during diversion (type A) exhibited a compliant system with small increases in portal pressure, whereas type B patients had significantly greater pressure increases. Selective investigations suggested that changes in portal pressure provoked compensatory changes in hepatic arterial blood flow that tended to maintain portal pressure at a set point. Type B patients demonstrated failure of this mechanism to varying degrees.After end-to-side portacaval shunt, seven type A cirrhotic patients maintained residual intrahepatic venous pressure unchanged from prior portal pressure, whereas six type B patients had a significant decrease. Residual intrahepatic venous pressure was measured after portacaval shunt in 40 cirrhotic patients who were followed for as long as 9 yr (median survival 4.0 yr). The 13 patients who developed chronic encephalopathy had significantly lower pressure (21.1+/-4.4 cm, mean+/-SD) and shorter survival (median 0.6 yr) than the other 27 patients (32.6+/-5.3 cm, 5.0 yr). The preoperative estimation of portal pressure-diverted portal flow curve slope anticipates the hepatic vascular response to portacaval anastomosis and identifies a group of patients in whom loss of portal blood flow results in a low residual intrahepatic venous pressure that is associated with early death and chronic encephalopathy.