Synopsis
Detect alcohol-related liver disease without stigma, manage withdrawal and decompensation safely, and recognise severe acute alcohol-related hepatitis requiring specialist treatment.
- Alcohol-related liver disease spans steatosis, steatohepatitis, fibrosis and cirrhosis; normal aminotransferases do not exclude advanced fibrosis.
- Ask about alcohol neutrally using beverage type, volume, strength, frequency, alcohol-free days and recent change, then convert to UK units and screen for dependence.
- A dependent patient can develop seizures or delirium tremens if alcohol stops abruptly; plan monitored withdrawal rather than simply advising immediate unsupported cessation.
- Acute alcohol-related hepatitis is a clinical syndrome of recent jaundice and systemic inflammation after sustained harmful drinking, not merely an AST higher than ALT.
- Exclude infection, biliary obstruction, viral hepatitis, drug injury, gastrointestinal bleeding and acute-on-chronic decompensation before attributing jaundice to alcohol-related hepatitis.
- Obtain a diagnostic ascitic tap promptly in anyone admitted with cirrhosis and ascites, including those without abdominal pain or fever.
- Nutrition and thiamine are active treatments: assess refeeding risk, provide dietitian-led energy and protein support, and use parenteral thiamine when Wernicke risk or features demand it.
- Corticosteroids are considered only for specialist-confirmed severe acute alcohol-related hepatitis after contraindications are addressed and benefit is reviewed early with a validated response score.
- Long-term outcome depends on integrated treatment of both liver disease and alcohol dependence, with relapse-prevention, mental-health, social and transplant pathways offered equitably.
Key red flags
New jaundice over days to weeks with anorexia, fever, tender hepatomegaly, leukocytosis and AST typically exceeding ALT after sustained drinking supports the syndrome once infection and obstruction are excluded.
Ascites, oedema, encephalopathy, variceal bleeding, spontaneous bacterial peritonitis, jaundice or hepatorenal dysfunction marks a major prognostic transition and requires structured acute care.
Tremor, sweats, anxiety, nausea, tachycardia, hypertension and insomnia can progress to hallucinations, seizures or delirium tremens, especially with previous complicated withdrawal or high dependence.
Confusion, ataxia or eye-movement abnormality may be incomplete and subtle; malnutrition, vomiting or withdrawal increases risk. Treat suspected disease promptly with parenteral thiamine rather than awaiting imaging.
Spontaneous bacterial peritonitis, pneumonia, urinary infection and bacteraemia may present without fever or leukocytosis. New kidney injury, encephalopathy or hypotension may be the only clue.
Very high aminotransferases, severe abdominal pain, shock, paracetamol exposure or biliary dilatation is atypical for alcohol-related hepatitis alone and should redirect the diagnostic work-up.
Investigation priorities
Quantify exposure, dependence, harms and withdrawal risk without judgement.
Management branches
Ascites, encephalopathy, gastrointestinal bleeding, jaundice with organ dysfunction or suspected infection.
- Use ABCDE and the current BSG–BASL admission bundle: obtain bloods and cultures, review medicines, assess bleeding and encephalopathy, monitor urine and identify the precipitant.
- Perform diagnostic ascitic tap without avoidable delay when ascites is present, start indicated infection or bleeding treatment and involve hepatology early.
- Assess alcohol withdrawal and Wernicke risk on arrival; prescribe the local symptom-triggered withdrawal and thiamine regimen with higher-observation care for previous seizures or severe dependence.
- Address nutrition, refeeding electrolytes, thrombosis and gastrointestinal prophylaxis individually, and review transplant suitability or ceilings of care rather than assuming alcohol exposure excludes escalation.