Defined as rapid onset of encephalopathy and marked decrease in liver synthetic function within 28d of symptom onset in patient without chronic liver disease
Major etiologies are 1)acetaminophen OD, 2) idiosyncratic drug reaction, 3) Hep B, 4) Hep A, 5) others
Coagulopathy usually precedes encephalopathy, which may quickly progress to coma
It is important to determine the etiology, since specific causes may have specific treatments:
NAC for acetaminophen, penicillin for amanita mushroom poisoning, delivery for acute fatty liver of pregnancy, zinc/trientine for Wilson's.
Pts should be admitted to ICU and transferred to a transplant centre.
Supportive care includes:
glucose (may need d10 drip)
electrolyte replacement
fluids
reversal of coagulopathy
neurochecks >q6h
FFP (4u) may normalize coags for 6h (for procedure or bleeding)
Empiric abx for any sign of infection
Poor prognostic indicators predicting need for transplant:
pH below 7.3 after resuscitation
PTT over 100
Cr over 290
Gr 3 or 4 encephalopathy
Lactate over 3.3 4h post admission
Major causes of transaminases in the thousands:
1) Ischemia
-inflow (hypotension- shock liver, PV thrombosis)
-outflow (CHF, Budd-Chiari)
2) Viral
HAV, HBV (rarely HCV)
Others- EBV, HSV, CMV
3) Drugs/toxins
4) Autoimmune
5) Obstruction/stone
6) Acetaminophen and EtOH both (but rarely EtOH alone)
Link:
Click here for a NEJM case of fulminant hepatic failure from HSV infection that discusses management considerations
Click here for a paper on approach to increased liver enzymes
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