Abstract

Abstract Portal hypertension, defined as an increase in the hepatic venous pressure gradient above 5 mmhg, can be related to cirrhosis as well as non‐cirrhotic disorders. Based on the site of increased resistance, portal hypertension can be classified as presinusoidal, sinusoidal and postsinusoidal. Wedged hepatic venous pressure (WHVP) measurement distinguishes between presinusoidal (low WHVP reflecting normal sinusoidal pressure) and sinusoidal portal hypertension (high WHVP).According to the equation portal pressure = portal venous flow × portal venous outflow resistance, increase in pressure can result from an increase in inflow into the portal vascular system or by an elevated portal outflow resistance. Both, blood flow and resistance to flow can be estimated by means of Doppler ultrasound. The congestion index increases with the outflow resistance in the portal vein and the hepatic and splenic arterial resistance index reflects the outflow resistance in the downstream vascular region (i.e. the hepatic parenchyma or the whole portal vascular system).In cirrhosis, a sinusoidal form of portal hypertension, the hepatic venous pressure gradient (HVPG) is increased while portal blood flow is decreased. The congestion index of the portal vein as well as the resistance index of the hepatic artery and the spleen parenchyma are increased.Prehepatic portal hypertension due to an increased inflow through an enlarged spleen is characterized by an increased portal blood flow, a decreased splenic resistance index and an only slightly elevated HVPG. Vice versa, splenomegaly of portal hypertensive origin is characterized by a decrease in portal blood flow and an increase in the splenic artery resistance index. In idiopathic portal hypertension or non‐cirrhotic portal fibrosis, portal and splenic blood flow are increased and there is a gradient between elevated intrasplenic and normal or only slightly elevated wedged hepatic venous pressure. Schistosomiasis, the other presinusoidal intrahepatic form of portal hypertension, is characterized by a normal wedged hepatic venous pressure and portal blood flow seems to be preserved, too.Posthepatic portal hypertension, such as the Budd–Chiari syndrome, shows a very low HVPG due to an increase in both FHVP and WHVP together with a decrease in portal blood flow and sometimes a compensatory increase in hepatic artery flow.

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