Fulminant Hepatic Failure (Acute Hepatic Failure)

Acute episode of severe liver dysfunction (jaundice, encephalopathy, coagulopathy) in a patient with a previously normal liver

Aetiology

  • Paracetamol - accounts for 50% of cases in the UK
  • Antibiotics
  • Viral - Hep. A-E, CMV, EBV, toxoplasmosis
  • Rare causes - AFLP, mushrooms, malignancy, Wilson’s, Budd Chiari, HAV

Pathophysiology

Paracetamol overdose

  • Accidental or non-accidental
  • Highly toxic intermediate (NAPQI) produced in paracetamol metabolism is normally immediately inactivated by glutathione
  • Toxicity can occur in normal doses if:
    • Patient has reduced glutathione stores (e.g. in anorexia)
    • Paracetamol has a longer half-life
    • Patient has increased P4502E1 (e.g. due to alcoholism) - bioactivate paracetamol to form toxins

Clinical presentation

  • Jaundice
  • Nausea
  • Stomach pain
  • Encephalopathy

Investigations

  • LFTs - ALT/AST > ALP, ↑ bilirubin, ↓ albumin
  • ↑ prothrombin time
  • USS
  • Virology
  • Rarely liver biopsy

Management

  • Supportive - inotropes, fluids, renal replacement, management of raised ICP
  • Transplantation