Acute liver failuređŸŽ„ {Free Video}

Acute liver failure

Introduction

Acute liver failure (ALF) is the rapid loss of hepatic function in a person without pre-existing cirrhosis, characterised by the triad of jaundice, an international normalised ratio (INR) ≄ 1.5 and any degree of hepatic encephalopathy developing within 26 weeks of symptom onset.

Epidemiology & Aetiology

  • UK leading cause: paracetamol toxicity (15 – 40 years).
  • Other causes: acute viral hepatitis (A, B, E), autoimmune hepatitis, drug-induced liver injury (e.g. isoniazid, sodium valproate, herbal remedies), ischaemic (“shock”) liver, pregnancy-related syndromes (AFLP, HELLP), Wilson’s disease, Budd–Chiari syndrome and malignant infiltration.
  • Incidence peaks vary by aetiology (see draft list above).

Clinical Features

Symptoms Signs
Fatigue, nausea, vomiting, right-upper-quadrant pain. Jaundice.
Progressive confusion, sleep–wake inversion. Asterixis → coma (grades I–IV encephalopathy).
Pruritus, dark urine, pale stools. Hypotension, tachycardia.
Easy bruising, bleeding. Ascites (late) or cerebral oedema features (papilloedema rare).

Investigations

Test Purpose / Typical Result
Bloods ↑ ALT/AST (often > 1000 IU L⁻Âč in paracetamol or ischaemia); ↑ bilirubin; ↓ albumin; prolonged PT/INR; thrombocytopenia; ↓ glucose; ↑ creatinine.
Specific assays Paracetamol level, viral serology, auto-antibodies, serum ceruloplasmin & copper, pregnancy test.
Venous/arterial blood gas Metabolic (lactic) acidosis common, guides transplant criteria.
Serum ammonia Correlates with encephalopathy and cerebral oedema risk.
Imaging Bedside abdominal ultrasound with Doppler (hepatic/portal flow, exclusion of Budd–Chiari); CT/MRI brain if focal neurology or to gauge oedema.
Culture screening Blood, urine, sputum on admission and twice weekly (high sepsis risk).

Complications

  • Cerebral oedema with raised intracranial pressure.
  • Hypoglycaemia, severe metabolic acidosis.
  • Sepsis and multi-organ failure.
  • Acute kidney injury / hepatorenal syndrome.
  • Coagulopathy with gastrointestinal or intracerebral bleeding.

Management (Critical-care Setting)

Initial steps

  • Admit to a level 3 ICU / regional liver unit and contact transplant centre early.
  • Secure airway if encephalopathy ≄ Grade II; monitor glucose and lactate hourly.

Treat the cause

  • Paracetamol: intravenous N-acetylcysteine (NAC) regardless of delay or level.
  • Autoimmune: high-dose IV corticosteroids once infection excluded.
  • Acute viral B: nucleos(t)ide analogue (tenofovir or entecavir).
  • Wilson’s disease: chelation (trientine) ± plasmapheresis but transplant usually required.
  • Pregnancy-related: expedite delivery after maternal stabilisation.

Supportive care

  • Maintain MAP > 65 mmHg (noradrenaline first line).
  • Target glucose 6 – 10 mmol L⁻Âč with 10 % dextrose infusion.
  • Encephalopathy: lactulose ± rifaximin; avoid sedatives where possible.
  • Coagulopathy: vitamin K 10 mg IV; use fibrinogen concentrate/cryoprecipitate or PCC for clinically significant bleeding or before procedures.
  • Cerebral oedema: head-up 30°, IV mannitol 0.5 g kg⁻Âč bolus; hypertonic saline if serum Na < 145 mmol L⁻Âč.
  • Renal support: continuous renal replacement therapy if Stage 2-3 AKI or severe acidosis/hyperkalaemia.
  • Infection prophylaxis: broad-spectrum IV antibiotics and antifungal (fluconazole) as per unit protocol.

Definitive therapy – Liver transplantation

  • King’s College Criteria (simplified):

    • Paracetamol ALF – arterial pH < 7.30 or (INR > 6.5 and creatinine > 300 ”mol L⁻Âč and Grade III/IV encephalopathy).
    • Non-paracetamol ALF – INR > 6.5 or any three of: age < 10 or > 40, jaundice → encephalopathy > 7 days, INR > 3.5, bilirubin > 300 ”mol L⁻Âč, drug-induced aetiology.

  • Early referral improves survival; extracorporeal albumin dialysis (MARS) may bridge to transplant.

FAQ from our users

What causes ascites in liver failure?
  • Ascites is caused by fluid accumulation in the abdomen.
  • Albumin, a protein made by the liver, maintains intravascular volume by drawing fluid into blood vessels.
  • When liver function declines, albumin production decreases, causing fluid to leak out of blood vessels and accumulate in the abdominal cavity.
What causes hepatic encephalopathy in liver failure?
  • The liver’s impaired detoxification ability can lead to a build up of ammonia.
  • Ammonia can cross the blood brain barrier & cause neurological symptoms.
What are the survival rates with and without a liver transplant?
  • Survival without transplant:

    • 50% for acetaminophen toxicity, viral hepatitis A, ischemic liver injury

    • <25% for other causes (Wilson’s, malignancy, autoimmune hepatitis)
  • Survival with liver transplant: 65-84% at 1 year
What are the causes of acute liver failure?
  • Drug-induced liver injury (e.g., paracetamol overdose, alcohol toxicity)
  • Viral hepatitis (Hepatitis A, B, E)
  • Pregnancy-related conditions (Acute fatty liver of pregnancy, HELLP syndrome)
  • Autoimmune hepatitis
  • Wilson’s disease
  • Ischemic liver injury (Budd-Chiari syndrome, shock liver)
  • Malignancy (e.g., lymphoma, metastases to the liver)

Common pitfalls in a clinical setting

Common pitfalls in a clinical setting
  • Liver function tests (LFTs) are not always an accurate representation of liver function.
    • Prothrombin time (PT/INR) and albumin are better indicators of synthetic liver function.
  • You may hear the term ‘Fetor hepaticus’.
    • This refers to a sweet, faecal-like breath odour seen in acute liver failure, which is a late sign of hepatic encephalopathy.
  • Remember that prothrombin time (PT) and albumin are the best markers of synthetic liver function.
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