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.
- Ask specifically about paracetamol in prescribed, combined cold-and-flu and over-the-counter products, deliberate or staggered ingestion, herbal products, recreational drugs, travel and viral exposures.
- Send a paracetamol concentration even when ingestion is denied or timing is unclear, and follow current TOXBASE advice because treatment is most effective when started early.
- Falling ALT is not always recovery: in massive hepatic necrosis it can fall while INR, bilirubin, lactate, creatinine and encephalopathy worsen.
- Ultrasound with portal and hepatic-vein Doppler looks for biliary obstruction, Budd–Chiari syndrome and chronic liver morphology, but normal imaging does not exclude severe hepatitis.
- Avoid sedatives and unnecessary correction of INR; frequent neurological, glucose and acid-base monitoring and early transplant-centre dialogue are more important than normalising laboratory numbers.
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.
Very high aminotransferases, early coagulopathy, metabolic acidosis, raised lactate and kidney injury with initially modest jaundice suggest paracetamol toxicity or hypoxic hepatitis; obtain the exposure and haemodynamic history urgently.
Acute jaundice can occur at any age and may have high IgG or autoimmune markers, but serology can be negative. Treatment and biopsy decisions require urgent hepatology input when severe.
A young person with haemolysis, low alkaline phosphatase relative to bilirubin, renal dysfunction or neuropsychiatric clues may have Wilson disease; routine copper markers are imperfect during acute failure and specialist assessment is urgent.
Painful hepatomegaly, ascites and hepatic-vein obstruction suggest Budd–Chiari; hypertension, haemolysis, thrombocytopenia or late-pregnancy illness raises HELLP or acute fatty liver and needs immediate obstetric-hepatology coordination.
Fever, hypotension, rising vasopressor need, worsening acidosis, seizures, unequal pupils or decreasing consciousness in liver failure may reflect sepsis or intracranial hypertension and require critical-care intervention.
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.
- Stop non-essential potentially hepatotoxic agents, send the structured aetiology screen and ultrasound with Doppler, and discuss severe injury early with hepatology.
- Admit and escalate when INR is prolonged, glucose falls, renal function worsens, lactate or acidosis persists, mental state changes, vomiting prevents hydration or diagnostic uncertainty is high.