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Pathogenesis of liver injury in circulatory failure

Lawrence S Friedman, MD
Section Editor
Sanjiv Chopra, MD, MACP
Deputy Editor
Anne C Travis, MD, MSc, FACG, AGAF


The liver's complex vascular supply and high metabolic activity make it particularly vulnerable to circulatory disturbances. The severity and characteristics of hepatic injury depend upon the blood vessels that are involved and the degree to which injury is related to passive congestion or diminished perfusion [1].

There are several well-recognized forms of vascular injury to the liver including Budd-Chiari syndrome, sinusoidal obstruction syndrome (hepatic veno-occlusive disease), passive congestion due to heart failure, hepatic infarction, and ischemic hepatitis. This topic review will focus on the pathogenesis of passive congestion and ischemic hepatitis. Discussions on Budd-Chiari syndrome and sinusoidal obstruction syndrome are presented separately. (See "Budd-Chiari syndrome: Epidemiology, clinical manifestations, and diagnosis" and "Diagnosis of hepatic sinusoidal obstruction syndrome (veno-occlusive disease) following hematopoietic cell transplantation".)


The liver receives approximately 25 percent of cardiac output even though it makes up only approximately 2 to 3 percent of total body weight [2,3]. The portal vein provides approximately two-thirds of the blood supply while the hepatic artery provides the rest. Blood flowing through the liver is drained via the right, left, and middle hepatic veins into the inferior vena cava and then into the right side of the heart.

The composition of the portal venous and hepatic arterial blood supply differ. While portal venous blood is rich in basic nutrients (such as glucose, amino acids, and triglycerides) it is relatively deficient in oxygen. In contrast, the hepatic artery supplies oxygen-rich blood (accounting for more than 50 percent of the oxygen delivered to the liver and 100 percent to the major bile ducts) but contains fewer basic nutrients.

Despite its importance in providing oxygenated blood, ligation or occlusion of the hepatic artery in humans can be tolerated without adverse consequences. In most patients, collateral arterial flow combined with portal blood flow can provide adequate circulation [4]. In rare patients, disruption of the hepatic arterial flow can cause focal hepatic infarction.


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Literature review current through: Sep 2016. | This topic last updated: Dec 16, 2015.
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