Diffuse ischemia can cause ischemic hepatitis; focal ischemia can cause hepatic infarction or ischemic cholangiopathy. Hepatic infarction results from hepatic artery disorders.
(Acute Hepatic Infarction; Hypoxic Hepatitis; Shock Liver)
Ischemic hepatitis is diffuse liver damage due to an inadequate blood or O2 supply.
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 a sickle cell crisis is associated with portal vein thrombosis (thus compromising the dual blood supply to the liver). Centrizonal necrosis develops without liver inflammation (ie, not a true hepatitis).
Symptoms may include nausea, vomiting, and tender hepatomegaly.
Ischemic hepatitis is suspected in patients who have risk factors and laboratory abnormalities:
Diagnostic imaging helps define the cause: Doppler ultrasonography, MRI, or arteriography can identify an obstructed hepatic artery or portal vein thrombosis.
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 wk. In most cases, liver function is fully restored. Fulminant liver failure, although uncommon, can occur in patients with preexisting cirrhosis.
Ischemic cholangiopathy is focal damage to the biliary tree due to disrupted flow from the hepatic artery via the peribiliary arterial plexus.
Common causes of ischemic cholangiopathy include vascular injury during orthotopic liver transplantation or laparoscopic cholecystectomy, graft-rejection injury, chemoembolization, radiation therapy, and thrombosis resulting from hypercoagulability disorders. Bile duct injury (ischemic necrosis) results, causing cholestasis, cholangitis, or biliary strictures (often multiple).
Symptoms (eg, pruritus, dark urine, pale stools), laboratory tests, and imaging studies indicate cholestasis.
The diagnosis is suspected when cholestasis is evident in patients at risk, particularly after liver transplantation. Ultrasonography is the 1st-line diagnostic imaging test for cholestasis, but most patients require magnetic resonance cholangiopancreatography, ERCP, or both to rule out other causes such as cholelithiasis or cholangiocarcinoma.
Treatment is directed at the cause. After liver transplantation, such treatment includes antirejection therapy and possible retransplantation. Biliary strictures warrant endoscopic balloon dilation and stenting.
Last full review/revision December 2007 by Eldon A. Shaffer, MD