19 Sept 2026
Patient history
A 23-year-old woman has two days of nausea, vomiting and right upper quadrant pain. Three days ago, after an argument, she took an unclear number of over-the-counter painkillers over an evening and the next morning, feeling well at first. She drinks most evenings and eats poorly.
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Acetaminophen (paracetamol) overdose with acute liver failure
Intravenous N-acetylcysteine
An ALT above 7000 U/L is not something viral or alcoholic hepatitis does, since those rarely clear a few hundred. Figures in this range mean hepatocytes dying in sheets, and the near-normal alkaline phosphatase alongside only modest bilirubin places the injury in the cells rather than the bile ducts. That leaves toxic or ischemic damage, and the ultrasound has already closed off the ischemic route by showing a normal liver with patent hepatic veins. The history is the classic staggered ingestion: an initial asymptomatic period of roughly 24 hours, then nausea and right upper quadrant pain as hepatic necrosis develops. Chronic alcohol use and poor nutrition deplete glutathione and induce CYP2E1, both of which increase susceptibility. The key trap is the undetectable drug level: after a staggered or late presentation the parent compound has already been metabolised, so a negative level does not exclude toxicity and must never be used to withhold treatment. Rising INR, hypoglycemia, lactic acidosis and encephalopathy define acute liver failure, and the combination of pH below 7.30, INR above 6.5, creatinine above 3.4 mg/dL and grade III–IV encephalopathy forms the King's College criteria for transplant referral, which is why the transplant unit is already on the phone. Intravenous N-acetylcysteine replenishes glutathione and neutralises NAPQI, the reactive metabolite doing the actual damage. It works best within 8 hours of ingestion and she is three days past that, which changes nothing: the benefit persists once liver failure is established, and it improves outcomes even in acute liver failure of other causes.