Portal posthepatic

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

In posthepatic portal hypertension (prevalence about 5%), the flow hindrance is in the region of the inferior vena cava or the right heart. Extrahepatic processes impede the efferent flow of venous blood from the... 

The most frequent cause of posthepatic portal hypertension is right ventricular insufficiency. The central venous pressure is transferred to the hepatic veins and the sinusoids. Constrictive pericarditis leads to a state of pronounced posthepatic portal hypertension with the early development of ascites. Severe tricuspid valve incompetence also culminates in this condition. A membranous obstruction of the inferior vena cava was likewise described in 1968 as a genetically determined cause of posthepatic portal hypertension (S. Yamamoto et al.). Three variants can be distinguished by angiography, depending on the different ways in which the hepatic veins are involved or whether they are affected at all. Thrombosis of the inferior vena cava can develop either from thrombosis of the pelvic veins or independently in the presence of predisposing factors. 

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