Ischemic Hepatitis

Causes are most often systemic:

• Impaired hepatic perfusion (eg, due to heart failure or acute hypotension)

• Hypoxemia (eg, due to respiratory failure or carbon monoxide toxicity)

• Increased metabolic demand (eg, due to sepsis)

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 may include nausea, vomiting, and tender hepatomegaly.

• 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.

• Hepatic reperfusion

Treatment is directed at the cause, aiming to restore hepatic perfusion, particularly by improving cardiac output and reversing any hemodynamic instability (1).

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.