Clinical course of acetaminophen overdose

The majority of overdoses are of small quantities of acetaminophen and the patients are not unwell. Thus the presence of symptoms or signs should be treated as an indicator of hepatotoxicity. Nausea and vomiting occur within a few hours of ingestion, soon followed by diffuse abdominal pain and hepatic tenderness. Liver function tests start to become deranged from 12 h with the AST peaking at 72 h. Jaundice becomes biochemically apparent at 24 h and rapidly deepens. A coagulopathy can be demonstrated only a few hours after overdose, with the prothrombin time being prolonged and continuing to rise until day 3. Oliguric or polyuric renal failure occurs in 11 per cent of severe overdoses, with or without the presence of acute liver failure, and is best monitored with the plasma creatinine as urea production is impaired in hepatic dysfunction. The renal failure can result from prerenal hypovolemia as well as a direct nephrotoxic effect of the acetaminophen. Once acute liver failure has developed, renal failure will be present in 70 per cent of cases. From 72 h many patients develop encephalopathy which worsens until 5 days after ingestion. This may occur earlier in the case of severe overdoses and persist for many days, and can be complicated by the development of cerebral edema.

There is often a profound metabolic disturbance with hypophosphatemia, hypoglycemia, and a metabolic acidosis. Hypoglycemia can occur within the first 24 h after overdose as a result of decreased gluconeogenesis and glycogen mobilization as well as an increased insulin concentration. The metabolic acidosis can occur early within the first 12 h owing to a derangement in hepatic lactate metabolism. Over subsequent hours, this worsens because of a further reduction in hepatic lactate clearance and an increased peripheral lactate generation due to tissue hypoxia. Hypovolemia is often profound, secondary to vomiting and vasodilatation, and worsens the tissue hypoxia and peripheral lactate generation.

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