The liver has a dual blood supply. The portal vein (which is rich in nutrients and relatively high in O2) provides two thirds of blood flow to the liver. The hepatic artery (which is O2-rich) supplies the rest. The hepatic veins drain the liver into the inferior vena cava. When portal vein blood flow increases, hepatic artery flow decreases and vice versa (the hepatic arterial buffer response). This dual, reciprocally compensatory blood supply provides some protection from hepatic ischemia in healthy people.
Despite its dual blood supply, the liver, a metabolically active organ, can be injured by
Ischemia results from reduced blood flow, reduced O2 delivery, increased metabolic activity, or all 3. Diffuse ischemia can cause ischemic hepatitis; focal ischemia can cause hepatic infarction or ischemic cholangiopathy. Hepatic infarction results from hepatic artery disorders.
Insufficient venous drainage may result from focal or diffuse obstruction. Obstruction can occur in the intrahepatic or extrahepatic veins (Budd-Chiari syndrome) or in the intrahepatic terminal hepatic venules and hepatic sinusoids (veno-occlusive disease) but often occurs in both. Cirrhosis is the most common cause of diffuse intrahepatic venous outflow obstruction. Diffuse obstruction results in congestion of the sinusoids, hepatomegaly, portal hypertension, reduced portal blood flow, ascites, and splenomegaly. Manifestations of focal venous obstruction depend on the location.
Specific vascular lesions may occur in the hepatic artery, hepatic vein, or portal vein. The hepatic artery may be occluded. Uncommonly, aneurysms develop. In peliosis hepatis, blood-filled cystic spaces develop in the sinusoids (microvascular anastomoses between the portal and hepatic veins).
Hepatic vein disorders can result in focal or diffuse venous obstruction.
Nearly all portal vein disorders obstruct portal vein blood flow and cause portal hypertension (see Portal Hypertension). Obstruction can be
Last full review/revision September 2013 by Nicholas T. Orfanidis, MD
Content last modified October 2013