EMed

Acute liver failure

Background

  • Acute deterioration in liver function (previously normal) leading to 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

Common

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

Rare

  • Wilson disease
  • "Vascular" sepsis, ischaemia, veno-occlusive
  • Toxins (e.g. mushrooms)
  • Infiltration (fatty or malignant)
  • Budd-Chiari syndrome
  • Pregnancy/HELLP

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 4hrs after resuscitation
  • or
  • pH< 7.30 or lactate > 3.0 12hrs 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 4hrs 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

Common

  • 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 ↓perfusion 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 PP
  • Variceal haemorrhage rare
  • ARF (acute tubular necrosis +/or hepatorenal synd.) common in paracetamol poisoning
  • Renal replacement therapy indicated for azotemia, vol. overload, ↓pH & electrolyte problems
  • All above aggressively treated to try to prevent cerebral oedema

Content by Dr Íomhar O' Sullivan . Last review Dr ÍOS 26/02/24