The specific contribution of splenic blood inflow to portal hypertension in patients with cirrhosis is still unclear. In this study, we investigated this contribution by assessing the hemodynamic effects of transient splenic artery occlusion. In 15 cirrhotic patients, portal pressure gradient (PPG) was measured just before inserting a transjugular intrahepatic portosystemic shunt (TIPS), in baseline conditions, for 15 minutes after splenic artery occlusion and 5 minutes after recovery. Splenic artery occlusion caused a significant decrease in PPG (range, Ϫ4% to Ϫ38%, median Ϫ20%, P Ͻ 0.001) which promptly returned to baseline values after recovery of the splenic inflow. The decrease in PPG showed a significant correlation with spleen volume (r ϭ 0.70, P Ͻ 0.005), liver volume (r ϭ Ϫ0.63; P Ͻ 0.01), and spleen/liver volume ratio (r ϭ 0.82, P Ͻ 0.001). Seven out of eight patients with a spleen/liver volume ratio greater than 0.5 had a marked decrease in PPG (Ͼ20%), whereas none of patients with a ratio lesser than 0.5 had a marked PPG response. In conclusion, in cirrhotic patients with portal hypertension, splenic artery occlusion causes a significant reduction in portal pressure (PPG). The drop in PPG is directly related to spleen volume and indirectly related to liver volume. The spleen/liver volume ratio accurately predicts the drop in PPG and may be used to identify patients who could obtain a significant advantage from surgical and nonsurgical procedures decreasing splenic inflow.
See Editorial on Page 1186In patients with chronic liver disease, portal hypertension is induced by the hemodynamic interaction of abnormally high portal blood inflow and increased intrahepatic vascular resistance. 1 The splanchnic hyperemia is sustained mainly by splanchnic vasodilation, with increased mesenteric and splenic artery blood inflow. 2 Splenomegaly is a common finding in patients with cirrhosis and portal hypertension and is associated with increased splenic 3-5 and portal blood inflow. 6 The importance of the splenic blood inflow in the context of the splanchnic hyperemia is suggested by the observation that, in patients with cirrhosis, the contribution of splenic flow can increase portal blood flow by up to 60%. 7 Based on these observations, ligation of the splenic artery and splenectomy were proposed for the treatment of portal hypertension in patients with cirrhosis and recurrent episodes of hemorrhage from esophageal varices. [8][9][10][11][12][13][14] However, these nonshunting procedures caused only a mild reduction in portal pressure (PP) 9,10 which was suggested to be due to compensatory increases in mesenteric blood inflow. 7 After whole-organ liver transplantation, despite the normalization of intrahepatic resistance and PP, portal blood inflow remains elevated for months, which has Abbreviations: PPG, portal pressure gradient; PP, portal pressure; CT, computed tomography; NS, not significant. Address reprint requests to