Acetaminophen toxicity may occur with acute ingestion or chronic ingestions over a longer time frame. In general, acute ingestions involve the consumption of immediate-release acetaminophen as a single dose of 200 mg/kg by children or 10 g by adults.
- Stage I occurs within 24 hours of ingestion. Patients may have nausea, vomiting, lethargy, and diaphoresis or they may be asymptomatic.
- Stage II occurs between 24 and 72 hours and is associated with evidence of hepatitis, including elevated aminotransferases and right upper quadrant tenderness.
- Stage III occurs between 72 and 96 hours and can present as hepatic encephalopathy, jaundice, coagulopathy, and acidosis.
- Stage IV is the recovery phase and occurs between 96 hours and 2 weeks; laboratories may take more weeks to normalize.
The threshold for toxicity varies based upon a number of factors. Advanced age and poor nutritional status increase the risk of acetaminophen toxicity. Concomitant chronic alcohol ingestion and use of medications and herbal supplements that affect CYP2E1 enzymes (eg, anticonvulsants, St. John's Wort) also predispose patients to hepatotoxicity.
Acute kidney injury may be present and is directly related to the severity of toxicity. As many as 10% of patients with acute hepatic failure will develop renal dysfunction secondary to acute tubular necrosis. In contrast, less than 2% of patients with any degree of acetaminophen toxicity will develop renal dysfunction.
Related topic: Acute liver failure
T39.1X4A – Poisoning by 4-Aminophenol derivatives, undetermined, initial encounter
70273001 – Poisoning by acetaminophen
- Acute alcoholic hepatitis – serum aminotransferases usually does not reach levels seen in acetaminophen toxicity
- Hepatotoxicity induced by other drugs, Reye syndrome – may present similarly, but history and serum acetaminophen levels help distinguish
- Ischemic hepatitis – more likely with history of hypotension, elevated lactate dehydrogenase (LDH)