Makindo Medical Notes

ALT is often below 300 IU/L in alcoholic hepatitis but this does not indicate a mild disease. Mortality is high, especially in severe cases with a Maddrey's score >32, which suggests the need for corticosteroids.

About

• Alcoholic hepatitis presents with fever, jaundice, and coagulopathy, often in a patient with a history of heavy alcohol use.
• Approximately 10-30% of long-term heavy drinkers develop this condition.
• There are similarities with Non-Alcoholic Steatohepatitis (NASH), but alcoholic hepatitis is distinct in its etiology and progression.

Aetiology

• Characterized by acute liver inflammation with raised AST and TNF-alpha levels.
• Occurs on a background of alcoholic steatosis (fatty liver) in many cases.
• While alcohol is hepatotoxic, not all heavy drinkers develop cirrhosis, highlighting genetic and environmental factors.

Host Characteristics

• Genetic differences in alcohol metabolism enzymes and inflammatory response genes.
• Additional risk factors: Obesity, iron overload, concurrent viral hepatitis, a1-antitrypsin deficiency, and certain medications or toxins.

Clinical Presentation

• Symptoms: Malaise, anorexia, fever (< 40°C), jaundice, and tender hepatomegaly.
• Chronic signs: palmar erythema, Dupuytren’s contracture, gynecomastia, malnutrition, and signs of hepatic encephalopathy.
• Patients may exhibit hepatic encephalopathy within 1-3 weeks in hospital, with symptoms like asterixis, disorientation, and coma.

Differential Diagnosis

• Other causes of liver failure (e.g., viral hepatitis, drug-induced liver injury).
• Acute cholecystitis.
• Acute hepatitis A or B infection.

Investigations

• Blood Tests: Anemia, thrombocytopenia, leukocytosis, and elevated IgA levels are common.
• Liver Enzymes: Elevated ALT but typically <300 IU/L, elevated AST, with an AST:ALT ratio >2:1.
• Prothrombin Time: Often prolonged and does not correct with vitamin K.
• Additional Tests: Elevated ammonia, low albumin, and elevated GGT.
• Imaging: Ultrasound can show fatty infiltration. A liver biopsy may reveal hepatocellular ballooning, Mallory bodies, and fibrosis, indicating progression toward cirrhosis.

Prognosis: GAHS and Maddrey's Score

• The Maddrey’s (Modified) Discriminant Function Score helps assess disease severity and the need for corticosteroids.
• GAHS (Glasgow Alcoholic Hepatitis Score) can also be used to gauge prognosis, with scores ≥9 indicating poor survival without treatment.

Glasgow Alcoholic Hepatitis Score

A GAHS score >9 suggests a poor prognosis and indicates that corticosteroid therapy may benefit the patient.

Management

• Alcohol Cessation: Abstinence is critical and offers significant benefits within 6-12 months.
• Supportive Care: Administer thiamine (200 mg/day) and IV Pabrinex, ensure adequate protein intake (1.5 g/kg) via enteral nutrition.
• Alcohol Withdrawal Management: Use chlordiazepoxide to prevent Delirium Tremens.
• Antibiotics: Prophylactic antibiotics to prevent bacterial infections from gut translocation.
• Electrolyte Management: Correct potassium and magnesium deficiencies.
• Encephalopathy Prevention: Lactulose and enemas to reduce ammonia levels.
• Nutrition: Provide NG or oral feeding and assess nutritional status.
• Severe Disease: For patients with MDF >32 or GAHS ≥9, corticosteroids (Prednisolone 30 mg/day for 30 days, then taper) or Pentoxifylline (400 mg TID for 4 weeks) can be beneficial. Pentoxifylline particularly reduces the risk of hepatorenal syndrome.
• Liver Transplantation: Consideration for end-stage liver disease but requires 6 months of abstinence and exclusion of active alcoholic hepatitis.
• Monitoring for Hepatocellular Carcinoma: 6-monthly serum alpha-fetoprotein and ultrasound for patients at risk.