Snapshot
- A 20-year-old woman presents to the emergency department for ingestion of acetaminophen. She reports that she has had suicidal ideation and had ingested an unknown quantity of acetaminophen in an attempt to end her life. An hour later, she began feeling nauseous. She regretted the ingestion and came to the hospital. In the emergency room two hours after ingestion, she has vomited twice. Serum labs reveal no abnormalities. She is given activated charcoal since the ingestion was within four hours of presentation.
Introduction
- Mechanism of action
- central reversible inhibition of cyclooxygenase (COX)
- inactivated peripherally
- central reversible inhibition of cyclooxygenase (COX)
- Clinical use
- used as an antipyretic and analgesic
- especially useful in the pediatric population to avoid a risk of Reye syndrome in children with viral infection
- not used for inflammation
- used as an antipyretic and analgesic
- Toxicity
- massive hepatic necrosis
- pathogenesis
- cytochrome P450 in the liver metabolizes acetaminophen into N-acetyl-p-benzoquinoneimine (NAPQI)
- NAPQI depletes glutathione, which forms toxic byproducts that result in hepatic necrosis
- clinical manifestations
- immediately after ingestion, nausea, vomiting, malaise, and lethargy are common
- early manifestations of overdose are nonspecific and are not reliable predictors of hepatotoxicity, so serum acetaminophen levels should be determined
- liver enzymes may rise at 8-12 hours if patients severely overdose
- 48-72 hours later, hepatitis progresses rapidly and patients may die from multi-organ failure, including acute renal failure
- immediately after ingestion, nausea, vomiting, malaise, and lethargy are common
- treatment
- N-acetylcysteine (NAC) is the antidote for acetaminophen toxicity
- useful for up to 24 hours after ingestion
- activated charcoal if ingested within 4 hours
- N-acetylcysteine (NAC) is the antidote for acetaminophen toxicity
- pathogenesis
- minimal gastrointestinal irritation
- massive hepatic necrosis