Level 1 of 6Core
Acute liver failure
The core to-do list — diagnose and manage, at a glance
Diagnose— recognise it
- Make the diagnosis on the triad — all three required: rapid deterioration of liver function in a patient *without pre-existing liver disease*, with acute liver injury, coagulopathy with INR 1.5 or higher, and hepatic encephalopathy of any grade. Jaundice and coagulopathy without encephalopathy is severe acute liver injury — same causes, same vigilance; the appearance of encephalopathy is the cardinal event.Not available at your setup — Coagulation (PT/INR).
- Take the drug history obsessively: paracetamol — dose, timing, staggered ingestion, several proprietary preparations together, all frequently denied — plus antibiotics, antituberculosis drugs, antiepileptics, and herbal or dietary supplements. Send a paracetamol level in every case, but a negative level excludes nothing: it is undetectable in plasma in 50% of cases, particularly in those presenting already in liver failure.
- Grade the encephalopathy and write the time beside it: grade 1 poor concentration and slow mentation; grade 2 drowsy but rousable, flapping tremor; grade 3 marked delirium, responds to pain and voice; grade 4 unconscious. A single grade is nearly worthless — serial timed grades are the disease's own trend line. Use asterixis, constructional apraxia (five-pointed star), the trail-making test (normal 15–30 seconds) and fetor hepaticus.
- Check a capillary glucose immediately and at least 2-hourly in the acute phase — hypoglycaemia is common, often profound, is the commonest reversible cause of drowsiness in a child, and causes permanent injury if missed. Do not rely on jaundice: it may be absent early, particularly in paracetamol overdose, and death in hyperacute failure may precede it.
- Hunt actively for rising intracranial pressure: unequal or abnormally reacting pupils, hypertensive episodes, bradycardia, hyperventilation, profuse sweating, myoclonus, focal fits, decerebrate posturing — papilloedema is rare and late, so its absence excludes nothing. Focal neurological signs are NOT hepatic encephalopathy: they mandate CT of the brain, not more lactulose — subdural haematoma in a coagulopathic patient who has fallen is the classic trap.Not available at your setup — CT scan.
- Record the other red flags: progressive prolongation of the prothrombin time (the point where high-dependency or intensive care becomes necessary), arterial pH below 7.3, arterial lactate above 3.5 mmol/L, oliguria or rising creatinine — and any unexplained deterioration means infection until proved otherwise (it complicates up to 90% of cases, frequently without fever or leucocytosis). A large spleen, spider naevi or caput medusae mean the liver disease is chronic, not ALF.Not available at your setup — Arterial blood gas, Coagulation (PT/INR), Renal function (creatinine/urea).
Manage now— do this, in order
- Move the patient early: monitor and treat in a high-dependency or intensive care environment as soon as the PT is progressively prolonging or any encephalopathy is identified — not once they become unstable.Not available at your setup — ICU / HDU bed.
- Grade 3 or 4 encephalopathy means the airway is not safe — intubate for airway protection, and for inability to clear secretions or hypoxaemia despite high-flow oxygen. Nurse head-up at 30 degrees with the neck straight — the position that reduces both intracranial pressure and aspiration risk.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
- Preserve intravascular volume with isotonic crystalloid in repeated boluses with reassessment — never 5% dextrose or 0.45% saline as resuscitation or maintenance fluid in an encephalopathic patient, since hypotonic fluids worsen cerebral oedema; where dextrose is needed for hypoglycaemia give it as a concentrated solution through a dedicated line. If hypotension persists after adequate volume, noradrenaline is the preferred vasopressor; vasopressin may be added.Doctor / Nurse
- Prevent hypoglycaemia rather than merely treating it: capillary glucose immediately and at least 2-hourly in the acute phase, with a continuous glucose-containing infusion running.Not available at your setup — Infusion pump.
- Give N-acetylcysteine early to all patients in whom paracetamol toxicity is suspected — do not wait for a level: IV 150 mg/kg in 200 mL 5% dextrose over 60 minutes, then 50 mg/kg in 500 mL over 4 hours, then 100 mg/kg in 1000 mL over 16 hours (same mg/kg in children, but reduce the diluent — about 3, 7 and 14 mL/kg of 5% dextrose for a child under 20 kg — to avoid hyponatraemia). Anaphylactoid reactions are rate-related, not allergy: stop, give an antihistamine, restart slower.Doctor / NurseNot available at your setup — Infusion pump.
- Give vitamin K, and only vitamin K, for the coagulopathy: phytomenadione 10 mg slow IV once daily for up to 3 days (children 250–300 micrograms/kg, maximum 10 mg, once daily). Blood products only for active major haemorrhage or immediately before an unavoidable invasive procedure — fresh frozen plasma blinds the prothrombin time, the most valuable prognostic test and the basis of the transplant criteria.Doctor / Nurse
- Treat the cause where a treatment exists: stop the culprit drug and every non-essential drug in idiosyncratic DILI; give empirical IV aciclovir 10 mg/kg every 8 hours if herpes simplex hepatitis is suspected — treatable and lethal if missed; a nucleos(t)ide analogue for acute hepatitis B; delivery for acute fatty liver of pregnancy and HELLP.Doctor / Nurse
- Minimise intracranial pressure by general measures first — head up 30 degrees, neck midline, minimal handling, quiet dim environment, treat fever, pain, hypoglycaemia and seizures. For signs of intracranial hypertension: mannitol 20%, 0.5–1 g/kg IV over 15–20 minutes (adult and paediatric dose the same; great caution if oliguric without renal replacement), or hypertonic saline to a serum sodium of about 145–155 mmol/L.Doctor / Nurse
- Bowel-directed treatment — never orally to a patient with an unprotected airway: lactulose 30–60 mL every 2 hours until improved mental status or a first bowel movement, then titrate to 2–3 stools/day (paediatric: 1 month–1 year 2.5 mL, 1–5 years 5 mL, 5–18 years 10 mL, all twice daily); a phosphate or lactulose enema where the oral route is compromised; rifaximin 550 mg twice daily. Do not sedate — sedatives precipitate encephalopathy and a benzodiazepine can turn a grade 2 patient into a grade 4. Do not restrict protein (no less than 60–80 g/day); screen cultures on admission and give broad antimicrobial cover for suspected sepsis without awaiting confirmation.
| Encephalopathy grade | Signs |
|---|---|
| 1 | Poor concentration, slurred speech, slow mentation, disordered sleep |
| 2 | Drowsy but easily rousable, occasional aggression, flapping tremor |
| 3 | Marked delirium, responds to pain and voice — airway not safe |
| 4 | Unresponsive to voice, unconscious — intubation required |
| N-acetylcysteine (IV) | Adult diluent | Child < 20 kg diluent |
|---|---|---|
| 150 mg/kg over 60 min | 200 mL 5% dextrose | ~3 mL/kg |
| 50 mg/kg over 4 h | 500 mL 5% dextrose | ~7 mL/kg |
| 100 mg/kg over 16 h | 1000 mL 5% dextrose | ~14 mL/kg |
Refer / escalate
Refer to a transplant centre and intensive care early — as soon as the PT is progressively prolonging or any grade of encephalopathy appears, always before the King's College criteria are met (meeting them implies 90% or greater mortality without transplantation; one-year survival after transplantation is 80–90%); escalate immediately for grade 3–4 encephalopathy, signs of rising intracranial pressure, focal neurological signs, arterial pH below 7.25–7.3, lactate above 3.5 mmol/L, creatinine above 300 micromol/L or anuria, or any unexplained deterioration.
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