Acute Hypoxic Hepatitis and Hepatic Consequences of Acute Heart Failure Syndrome

Abstract

Acute hypoxic hepatitis, also termed shock liver, acute ischemic hepatitis, or liver hypoxia, is generally defined on the basis of histologic findings including liver cell necrosis and congestion predominating in centrilobular areas (1), both resulting from circulatory changes or profound hypoxemia. Most often, it results from severe circulatory failure. However, severe liver necrosis may occasionally follow mild circulatory and transient circulatory changes. Controversy remains about the respective roles of decreased hepatic blood flow (“forward failure”), venous congestion (“backward failure”), and hypoxemia in its pathophysiology. Whether or not two or more of these mechanisms have to coexist for acute hypoxic hepatitis to occur also represents an unresolved issue (2–4). The prognosis of hypoxic hepatitis is variable, depending on the severity of the underlying circulatory or respiratory disorder rather than the extent of liver cell damage.