Synopsis
Identify the cause and severity of acute hepatitis, recognise transition to acute liver failure, and escalate early for organ support and transplant-centre assessment.
- Acute hepatitis is hepatocellular injury developing over days to weeks; causes include viral infection, medicines and toxins, autoimmunity, ischaemia, vascular obstruction, Wilson disease and pregnancy-related syndromes.
- Aminotransferase height reflects hepatocyte injury, not remaining liver function. INR, glucose, lactate, pH, mental state, renal function and trajectory identify danger.
- Acute liver failure requires acute liver injury with coagulopathy and hepatic encephalopathy in a person without pre-existing cirrhosis; diagnostic and transplant criteria are specialist protocol decisions.
Key red flags
New confusion, altered sleep, asterixis, agitation, somnolence or coma with prolonged INR after acute injury signals failing synthetic and detoxification function and mandates transplant-centre contact.
Investigation priorities
Define injury pattern and assess hepatic synthetic function.
Management branches
New marked liver-test abnormality, jaundice or a compatible systemic illness.
- Assess ABCDE, mental state and asterixis; check bedside glucose, INR, blood gas, lactate, renal function and urine output alongside the liver panel.
- Take a time-anchored exposure history covering every medicine, paracetamol-containing product, supplement, toxin, alcohol or drug use, travel, food, sexual, blood and pregnancy risk.
Key medicines
Intravenous acetylcysteineStart and continue according to current TOXBASE, BNF and local weight-based protocol.
Intravenous glucoseTitrate concentrated or maintenance glucose to frequent bedside measurements and critical-care targets.