Merck Manual

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Ischemic Hepatitis

(Acute Hepatic Infarction; Hypoxic Hepatitis; Shock Liver)

By

Whitney E. Jackson

, MD, University of Colorado School of Medicine

Last full review/revision Feb 2020| Content last modified Feb 2020
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Ischemic hepatitis is diffuse liver damage due to an inadequate blood or oxygen supply.

Etiology

Causes are most often systemic:

Focal lesions of the hepatic vasculature are less common causes. Ischemic hepatitis may develop when hepatic artery thrombosis occurs during liver transplantation or when thrombosis of the portal vein and hepatic artery develops in a patient with sickle cell crisis (thus compromising the dual blood supply to the liver). Centrizonal necrosis develops without liver inflammation (ie, not true hepatitis).

Symptoms and Signs

Symptoms may include nausea, vomiting, and tender hepatomegaly.

Diagnosis

  • Clinical evaluation and liver tests

  • Doppler ultrasonography, MRI, or arteriography

Ischemic hepatitis is suspected in patients who have risk factors and laboratory abnormalities:

  • Serum aminotransferase increases dramatically (eg, to 1000 to 3000 IU/L).

  • Lactic dehydrogenase (LDH) increases within hours of ischemia (unlike acute viral hepatitis).

  • Serum bilirubin increases modestly, only to 4 times its normal level.

  • Prothrombin time/international normalized ratio (PT/INR) increases.

Diagnostic imaging helps define the cause: Doppler ultrasonography, MRI, or arteriography can identify an obstructed hepatic artery or portal vein thrombosis.

Treatment

  • Hepatic reperfusion

Treatment is directed at the cause, aiming to restore hepatic perfusion, particularly by improving cardiac output and reversing any hemodynamic instability.

If perfusion is restored, aminotransferase decreases over 1 to 2 weeks. In most cases, liver function is fully restored. Fulminant liver failure, although uncommon, can occur in patients with preexisting cirrhosis.

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