At time of presentations, there were not acute symptoms of an OD, but after being admitted the patients liver enzymes dramatically increased to >6000 and INR rose to 3.8.
When liver enzymes are over 1000, always consider tylenol as one of the causes (the others include shock liver, autoimmune, viral hepatitis, and wilsons- although wilsons typically a chronic problem)
Acetaminophen pathway requires glutathione for the toxic metabolite (napq) to be metabolized. When glutathione runs out you are left with liver toxicity. NAC repeats it.
See this article for a good summary of acetaminophen pathway and treatment.
At presentation: high risk features include: pH <7.3. As well, elevated INR, encephaolopaty, Cr>300, high bili and hypoglycaemia are predictors of fulminent liver failure.
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