Acute liver failure



Background

  • Acute deterioration in liver function (often previously normal) leading to encephalopathy and encephalopathy
  • 50 % die or need transplant (less if acute on chronic dysfunction)
  • Most develop SIRS (early treatment significantly improves prognosis)
  • Very rapid progress (time jaundice to encephalopathy < 8 days) relatively better prognosis (if no cerebral oedema)

Aetiology

  • Paracetamol toxicity 50%.
  • Other drugs (esp. NSAIDs, anticonvulsants).
  • Acute viral hepatitis (incl. Hep A).

Initial assessment

Differential DDx hepatic dysfunction and antlered mentation

  • Acutely decompensated chronic liver disease.
  • Sepsis.

N-acetylcysteine?

  • Immediately indicate if ANY chance paracetamol toxicity.
  • Helps with repletion of hepatic glutathione and O2 delivery to cells.
  • Probably Indicated in most cases, irrespective of aetiology.

Transfer to liver unit?

  • Discuss potential cases early
  • Beware INR > 2 or encephalopathy
  • Extremes of age
  • Early transplant being considered
  • Beware HYPOGLYCAEMIA (continue 5% dextrose)
  • Beware airway (consider RSI and ETT in all) if encephalopathy

King’s College criteria for Liver Transplant in ALF

Paracetamol toxicity

  • Lactate > 3.5 4 hrs after resuscitation.

or

  • pH< 7.30 or lactate > 3.0 12 hrs after resusc.

or

  • INR > 6.5 (PT > 100 sec).
  • Creat > 3.4 mg/dl
  • Stage 3 or 4 encephalopathy

Non-paracetamol causes

  • Lactate > 3.5 4 hrs after resuscitation.

or

  • INR > 6.5 (PT > 100 sec).

or

  • any 3 of the following:
    • INR > 3.5 (PT > 50 sec).
    • Age <10 or > 40 years.
    • Serum bilirubin > 17.5 mg/dl.
    • Duration of jaundice > 7 days.
    • Aetiology: drug reaction.

Complications

  • SIRS and multiorgan failure often triggered by sepsis
  • Immunocompromise (side effect ALF)
  • Invasive lines, chest (bacterial or fungal), UTI (catheter)
  • Clinical signs sepsis may be lacking
  • Prophylactic antibiotics indicated in most ALF
  • Beware subtle, progressive airway compromise
  • ARDS occurs in 1/3
  • 1/4 develop cerebral oedema (? ammonia trigger)

Cerebral oedema

  • Oedema more common in hyper-acute ALF
  • Consider ICP monitoring
  • Nurse 30° head up
  • Prophylactic Lactulose & antibiotics to reduce ammonia
  • Opiate sedation relatively safe
  • Actively treat pyrexia
  • Monitor for and avoid hyponatraemia
  • Mannitol (1 g/kg body weight) if worse confusion, serum osmolality is <320 mOsm/l, or high osmolar gap
  • Seizures (atypical) very common in encephalopathy, Phenytoin unproven

Other complications

  • Vasodilation and hypoperfusion treated a per sepsis (response to crystalloid challenge ± early inotropes)
  • Beware adrenal failure
  • Despite coagulation factor deficit and thrombocytopenia, bleeding only really with invasive procedures
  • Prophylactic PPI (e.g. Zoton Fastab - MADE IN IRELAND). Variceal haemorrhage rare!
  • Acute renal failure (acute tubular necrosis +/or hepatorenal synd.) common (50%), esp. in paracetamol poisoning
  • Renal replacement therapy indicated for azotemia, volume overload, acidosis and electrolyte problems
  • All above aggressively treated to try to prevent cerebral oedema

Content by Dr Íomhar O' Sullivan 19/08/2009 Last review Dr ÍOS 1/04/19