- USES: Naproxen is a nonsteroidal anti-inflammatory drug (NSAID) used as a pain medication and in various inflammatory conditions. PHARMACOLOGY: Naproxen is a nonselective inhibitor of cyclooxygenases (COX-1 and COX-2), leading to decreased synthesis of prostanoids. Naproxen, like other NSAIDs, has anti-inflammatory, analgesic, and antipyretic properties. TOXICOLOGY: Prostaglandin inhibition is responsible for the gastrointestinal irritant effects and nephrotoxicity. EPIDEMIOLOGY: Poisoning with NSAIDs is not uncommon but rarely severe. Naproxen overdose is uncommon in the United States since other NSAIDs are used more often. MILD TO MODERATE POISONING: Gastrointestinal effects (eg, dyspepsia, ulceration, bleeding) are most commonly encountered. Renal dysfunction, most often in elderly patients, may occur. Mild CNS effects include altered cognition, drowsiness, headache, and mood changes, especially in the elderly population. SEVERE POISONING: Severe poisoning is rare but can include CNS depression, hallucinations, seizures, renal failure, gastrointestinal bleeding, and metabolic acidosis. ADVERSE EFFECTS: CNS effects include drowsiness, headache, fatigue, and cognition disturbances, especially in the elderly. Gastrointestinal effects (eg, dyspepsia, ulceration, bleeding) are as common as with other NSAIDs. Renal dysfunction, especially in the elderly population, may be seen. Instances of agranulocytosis, thrombocytopenia, and pancreatitis have been reported. Hepatotoxicity is rare.
Range of Toxicity:
- TOXICITY: Severe toxicity developed in an adolescent who ingested 13.75 g and another adolescent developed severe metabolic acidosis and refractory hypotension after ingesting naproxen 33 g and ibuprofen 10 g; both required aggressive management but recovered completely. An adult developed acute encephalopathy following an intentional ingestion of 90 g. THERAPEUTIC DOSE: ADULT: 250 to 500 mg orally twice daily. PEDIATRIC: 5 mg/kg orally twice daily.
- Support: MANAGEMENT OF MILD TO MODERATE TOXICITY: Primarily supportive care; activated charcoal may not be necessary given the fast gastrointestinal absorption of the drug and anticipated mild toxicity. Give benzodiazepines titrated to effect for anxiety and seizures. MANAGEMENT OF SEVERE TOXICITY: If significant CNS depression occurs, consider orotracheal intubation for airway protection before giving charcoal. Give benzodiazepines for anxiety, agitation, delirium, and seizures. Be aware of the risk of renal failure and gastrointestinal bleeding. Avoid nephrotoxic drugs.
- Decontamination: PREHOSPITAL: Not recommended because of potential for somnolence and seizures. HOSPITAL: Consider activated charcoal if patients present early after a substantial ingestion. However, be aware of fast drug absorption and the potential for significant CNS toxicity early in the clinical course.
- Airway management: Early orotracheal intubation in patients with signs of severe intoxication with CNS depression, seizures, or agitation.
- Antidote: None
- Monitoring of patient: Monitor vital signs and mental status. Naproxen plasma levels are not clinically useful or readily available. No specific lab work is needed in most patients. Obtain routine chemistry, blood gases, and CBC in case of severe toxicity.
- Enhanced elimination procedure: There is no role for repeat-dose activated charcoal. Hemodialysis is not useful given the high protein binding.
- Patient disposition: HOME CRITERIA: Asymptomatic children and adults with inadvertent ingestions can be managed at home. OBSERVATION CRITERIA: Symptomatic patients and those with deliberate overdose should be sent to a health care facility for evaluation. ADMISSION CRITERIA: Patients with serious CNS depression, agitation or seizures, renal failure, significant metabolic acidosis, and severe gastrointestinal toxicity (ie, bleeding) require admission. CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.