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Acute liver failure is characterised by coagulopathy,
typically an INR of at least 1.5,
together with hepatic encephalopathy developing within 26 weeks in a patient without pre-existing cirrhosis.
Without encephalopathy it is acute liver injury, not failure.
The jaundice-to-encephalopathy interval sorts the syndrome.
Hyperacute failure, under seven days, follows paracetamol,
ischaemia and hepatitis A or E,
and carries the highest risk of cerebral oedema.
Acute failure, seven to 28 days, is typically hepatitis B.
Subacute failure, 28 days to 26 weeks, follows idiosyncratic drugs,
Wilson's disease and autoimmune hepatitis;
it swells the brain less but has the worst prognosis.
Two laboratory values deceive.
Alanine aminotransferase leaks from hepatocytes dying now
and says nothing about how many remain;
when necrosis is nearly complete, the enzyme falls while the patient worsens.
Ammonia does not track the grade of encephalopathy,
though a level above 150 micromol/L raises the risk of intracranial hypertension.
Severity is read instead from what the liver still does:
synthesis by the INR, excretion by bilirubin, and the grade of encephalopathy.
Fresh frozen plasma is therefore withheld unless the patient bleeds;
it hides the INR.
Acute liver failure is characterised by coagulopathy,
typically an INR of at least 1.5,
together with hepatic encephalopathy developing within 26 weeks in a patient without pre-existing cirrhosis.
Gluconeogenesis is hepatic,
because muscle lacks glucose-6-phosphatase and can only return lactate
and alanine to the liver through the Cori cycle.
When hepatocytes are exhausted, glucose falls and lactate accumulates,
which is why hypoglycaemia is watched hourly
and a lactate above 3.0 mmol/L after resuscitation is a transplant criterion.
Ethanol oxidation floods the cell with NADH and diverts pyruvate to lactate,
so the fasting drinker becomes hypoglycaemic and acidotic.
Paracetamol is the commonest cause worldwide, hepatitis B in Taiwan.
N-acetylcysteine, 200 mg/kg over four hours then 100 mg/kg over sixteen,
starts without delay and improves survival even in non-paracetamol failure.
Cerebral oedema is the leading killer, so the head is raised,
sodium held at 140 to 145 mmol/L,
and hypertonic saline or mannitol treats surges.
The King's College criteria for paracetamol are an arterial pH below 7.30 after resuscitation,
or an INR above 6.5 with creatinine above 300 micromol/L
and grade III or IV encephalopathy.
Once they are met, only transplantation changes the outcome.
A mutation in ATP7B stops copper entering ceruloplasmin and bile,
so copper accumulates in liver, lentiform nuclei and cornea.
Ceruloplasmin is low while free serum copper and urinary copper are high,
a direction examiners reverse.
Kayser-Fleischer rings and Coombs-negative haemolysis complete the picture,
and fulminant disease needs a new liver.
Mechanism before sequence governs bleeding too.
Shock kills before the lesion does, so the airway is secured,
two large cannulae placed and volume restored before any endoscope.
Early haemoglobin may be normal, because whole blood is lost before dilution.
Suspected variceal bleeding receives terlipressin or octreotide and intravenous ceftriaxone at once,
then band ligation within twelve hours; balloon tamponade bridges to TIPS.
Propranolol belongs to prophylaxis and is withheld during the bleed.
In mesenteric ischaemia, flow is restored with fluid and revascularisation;
vasoconstrictors are forbidden.
Acute liver failure is characterised by coagulopathy,
typically an INR of at least 1.5,
together with hepatic encephalopathy developing within 26 weeks in a patient without pre-existing cirrhosis.