Hepatitis, Alcoholic

In USA, 8.5% of adults met DSM-IV criteria for current alcohol use disorder; 30.3% of adults met DSM-IV criteria for lifetime alcohol use disorder. Approximately 10–15% of alcoholics will develop alcoholic hepatitis and cirrhosis.

Mortality rate of 60–100% of pts undergoing surgery during acute alcoholic hepatitis.

Poorer prognosis when accompanied by increased bilirubin, increased Cr, PT >1.5× control, ascites, or encephalopathy.

>10% of pts develop DTs without prophylaxis.

Abdominal surgeries are associated with higher risk due to reduced hepatic blood flow.

Anemia and coagulopathy

Pulmonary shunting leading to arterial hypoxemia

Altered mental status and/or hepatic encephalopathy

Cerebral edema and increased ICP with hepatic encephalopathy, which may progress to coma

Hemodynamic instability secondary to DTs

Hypoglycemia due to poor gluconeogenesis

Insulin resistance

Electrolyte abnormalities

Renal insufficiency, which means hypotension and nephrotoxic drugs should be avoided

Citrate toxicity with blood transfusion due to decreased citrate metabolism

Most common form of liver disease in USA.

Usually preceded by period of heavy alcohol consumption.

An intermediate stage between fatty liver and alcoholic cirrhosis.

Can vary from mild (with only elevated liver function tests) to severe liver inflammation (prolonged prothrombin time and liver failure).

Can be chronic (less severe) or acute (more severe).

Characteristic clinical features include fever, hepatomegaly, jaundice, anorexia, and abdominal bruit over liver (indicated in >50% pts).

10–20% mortality risk with each episode of acute alcoholic hepatitis.

Mortality is 50% within 30 d of onset, with pts having hepatic encephalopathy, derangement in renal function, hyperbilirubinemia, and prolonged PT.

A daily intake of >40 g of alcohol, (e.g., roughly 4 beers or 3.5 oz of 80-proof liquor) in men and >20 g (e.g., 2 beers or approximately 2 oz of 80-proof liquor) in women significantly increases the risk of alcoholic hepatitis.

Inflammatory process via leukocytic infiltration that leads to hepatocellular necrosis with intracellular deposition of Mallory Bodies (characteristic, not specific).

Repeated episodes are a precursor to cirrhosis after healing and scar tissue formation.