The most frequent abnormality of circulation to affect the liver is congestive heart failure, which leads to reduced outflow of blood from the liver. Other causes of hepatic congestion include constrictive pericarditis, obstruction of the inferior vena cava and hepatic veins (Budd-Chiari syndrome) and occlusion of the small hepatic veins (veno-occlusive disease). Increased resistance to hepatic venous outflow results in congestive hepatomegaly, dilation of hepatic venules and sinusoids, and hypoxia. The hypoxia in turn leads to hepatocyte damage with possible fibrosis and cirrhosis, the latter termed cardiac cirrhosis.

The clinical features of congestive heart failure include tender hepatomegaly and abdominal discomfort. In tricuspid insufficiency, the liver may be pulsatile. Ascites, which may be present, often involves exudate with a high protein content. Characteristic biochemical abnormalities are mild hyperbilirubinemia with a moderate elevation of aminotransferases (<300) and a mild elevation of alkaline phosphatase, especially in acute congestion. In ischemic liver damage, aminotransferase can be quite high (from the necrosis), simulating hepatitis - hence the term ischemic hepatitis. The prognosis is directly related to the severity and the response to therapy of the underlying heart failure.

Hepatic vein thrombosis is a rare disorder that may occur alone or in association with inferior vena cava thrombosis. It may be associated with polycythemia vera, paroxysmal nocturnal hemoglobinuria, hypercoagulability, use of oral contraceptives or neoplasia, or it may be secondary to obstruction by a membranous web. The presentation may be acute, with rapidly developing hepatomegaly, ascites, and abdominal pain leading to liver failure and coma. The chronic presentation is usually that of progressive ascites. The degree of aminotransferase elevation is variable, depending on the rapidity of the onset. The liver biopsy shows large hemorrhagic areas with congestion, atrophy and necrosis around the center of the lobule. Diagnosis may be assisted by liver- spleen colloid scan showing decreased uptake in areas that are otherwise normally drained by the hepatic vein. The caudate lobe demonstrates a normal uptake in that it has a different drainage, that being directly into the vena cava. Hepatic vein Doppler studies clarify the impaired venous blood flow. The conclusive study is IVC hepatic venography revealing blocked hepatic veins. Assuming absence of a correctable lesion such as a membranous web, treatment by anticoagulants and streptokinase is rarely successful. With acute thrombosis, most patients die of liver failure and hepatic coma. Occasionally helpful is a portacaval or mesocaval shunt to allow decompression.

Veno-occlusive disease refers to the obstruction of small and medium-sized intrahepatic veins. Causal factors include pyrroline alkaloids, hepatic irradiation, azathioprine and graft-versus-host disease related to bone marrow transplantation. The presentation mimics the Budd-Chiari syndrome. In the acute form, presentation may include hepatomegaly, ascites and liver failure. The chronic form leads to cirrhosis and portal hypertension with esophageal varices. The liver biopsy characteristically shows intense congestion around the hepatic venule with thickened obstructive hepatic veins. There is no effective therapy available. Control of the ascites may be required. Some patients have a spontaneous recovery, while others develop cirrhosis with sequelae of portal hypertension, varices and ascites. Liver transplantation may be the only hope for many.

Thrombosis of the portal venous system may result from trauma, pancreatitis, neoplasia (e.g., hepatoma), neonatal umbilical sepsis, pylephlebitis or a complication of cirrhosis, or may be idiopathic. Patients usually present with massive hematemesis that is recurrent. Splenomegaly is present. Biochemical tests of the liver are normal or only mildly elevated. Because liver function is usually normal, ascites and encephalopathy are uncommon and bleeding episodes are better tolerated. Diagnosis may be confirmed by special Doppler ultrasound studies of the portal vein, splenoportogram and/or a venous phase of hepatic angiography. If treatment is required for recurrent hematemesis from esophageal varices, sclerotherapy may be necessary. Because of normal liver parenchyma, surgical approaches such as mesocaval shunt may be considered and are generally better tolerated than by patients with chronic liver disease.