Alcoholic Hepatitis
A life-threatening, acute inflammation of the liver caused by heavy alcohol use, presenting with rapid-onset jaundice and liver swelling.
Emergency Management: Suspected Spontaneous Bacterial Peritonitis (fever, abdominal pain in a patient with ascites) requires immediate diagnostic paracentesis and empiric IV Cefotaxime or Ceftriaxone to prevent fatal sepsis.
Alcoholic hepatitis is an acute, severe inflammatory liver disease caused by heavy, prolonged alcohol consumption. It is characterized by progressive jaundice, malaise, and tender hepatomegaly, often occurring in patients with underlying chronic alcoholic liver disease (cirrhosis or steatosis).
Detailed Overview
It represents a critical juncture in alcohol-associated liver disease. The metabolism of alcohol in the liver generates toxic byproducts (like acetaldehyde) and reactive oxygen species, which induce intense oxidative stress, lipid peroxidation, and a profound localized inflammatory cascade. This results in ballooning degeneration of hepatocytes, infiltration of polymorphonuclear neutrophils (PMNs), and Mallory-Denk body formation. Severe alcoholic hepatitis has a high short-term mortality rate (up to 30-50% at 1 month without treatment) due to liver failure, portal hypertension complications, and an extremely high susceptibility to bacterial infections.
Epidemiology & Demographics
Occurs in approximately 10-35% of heavy drinkers. The mean age of presentation is 40-50 years. While more total cases occur in men, women are at higher risk for developing the condition at lower doses of alcohol.
Etiological Mechanism
The direct cause is chronic, heavy alcohol consumption. The threshold is typically considered > 80g/day of ethanol for men and > 50g/day for women for at least 5 years, often with a recent period of increased consumption (a "binge").
Primary Causes
Heavy, sustained ethanol consumption
Genetic predisposition (e.g., PNPLA3 gene variants)
Co-existing liver disease (e.g., Hepatitis C, obesity) exacerbates injury
1. Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde (highly toxic) and then by ALDH to acetate. 2. Heavy use upregulates CYP2E1, which metabolizes alcohol but generates massive amounts of Reactive Oxygen Species (ROS). 3. Acetaldehyde binds cellular proteins forming neoantigens, triggering an immune response. 4. ROS cause lipid peroxidation and mitochondrial damage. 5. Damaged hepatocytes release damage-associated molecular patterns (DAMPs), and increased gut permeability allows endotoxins (LPS) into the portal vein. 6. LPS activates Kupffer cells via TLR4 to release massive amounts of TNF-alpha and IL-8. 7. This causes dense neutrophil infiltration, severe lobular inflammation, hepatocyte necrosis, and acute loss of synthetic liver function.
Diagnostic Criteria & Guidelines
Clinical diagnosis based on history of heavy alcohol use, recent onset of jaundice, AST > 50 but < 400 IU/L, AST:ALT ratio > 2, and serum bilirubin > 3.0 mg/dL. Liver biopsy is gold standard but reserved for cases with diagnostic uncertainty.
1. Absolute alcohol abstinence. 2. Nutritional support (high calorie/high protein via enteral feeding). 3. For Severe AH (mDF ≥ 32 or encephalopathy): Prednisolone 40 mg PO daily for 28 days (if no active infection or GI bleed). Assess response at day 7 using the Lille Model; if non-responder (Lille score >0.45), discontinue steroids.
Second-Line & Adjunctive Therapy
If steroids are contraindicated (e.g., active sepsis, GI bleeding, renal failure), Pentoxifylline 400 mg PO TID was historically used, but recent evidence shows limited efficacy. Early Liver Transplantation is increasingly considered for highly selected patients facing imminent death despite medical therapy.
Surgical & Procedural Management
Liver transplantation is the only definitive cure for failing livers, historically requiring a 6-month abstinence period, but recent protocols allow early transplant in highly selected patients with first-episode severe AH and strong psychosocial support.
Patient Counseling & Advice
Inform the patient that continuing to drink alcohol is almost certainly fatal. Provide resources for addiction medicine. Explain that steroids may help short-term survival but abstinence is the only long-term cure.
Follow-Up & Monitoring Schedule
Close inpatient monitoring for infections and renal failure. Outpatient follow-up requires monitoring of liver function tests and management of underlying cirrhosis complications (varices screening, HCC surveillance).
Preventive Strategies
Avoid heavy, prolonged alcohol use. Identify and treat alcohol use disorder early.
Poor for severe cases. The 28-day mortality for severe alcoholic hepatitis (mDF ≥ 32) is approximately 30-50%. Long-term survival relies entirely on sustained abstinence; if the patient continues drinking, 5-year survival is <30%.