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  • Nonsteroidal anti-inflammatory agents (NSAIDs) are relatively devoid of toxicity in the overdose setting.
  • Typically, patients who ingest NSAIDs exhibit only central nervous system (CNS) and/or gastrointestinal (GI) toxicity.
  • Long-term use of NSAIDs is associated with nephrotoxicity, including acute tubular necrosis, acute interstitial nephritis, and acute renal failure. Renal toxicity is not associated with acute overdose.
  • Infrequently, overdose of NSAIDs has been associated with an anion-gap acidosis. For patients with severe clinical symptoms, an arterial blood gas is indicated.
  • After the patient is stabilized, activated charcoal is administered

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There are many drugs in use today that are categorized as NSAIDs (Table 110–1). These drugs function largely by inhibiting cyclooxygenase,1 the enzyme needed to convert arachidonic acid to prostaglandin. NSAIDs are typically non-toxic in the overdose setting. The 2006 Annual Report of the American Association of Poison Control Centers listed one death secondary to ibuprofen, although there were more than 71 000 ingestions, of which more than 39 000 occurred in children younger than 6 years. There were 13 000 ingestions of other NSAIDs, resulting in one death.2

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Table Graphic Jump Location
Table 110-1. Currently Available NSAIDs
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Typically, patients who ingest NSAIDs exhibit only CNS and/or GI toxicity. Symptoms are generally seen within 4 to 6 hours of ingestion.

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Common symptoms of CNS toxicity can include drowsiness, dizziness, and lethargy.3 The mefenamic acid compound, Ponstel, has a propensity to cause seizures.4 Other NSAIDs associated with seizures include piroxicam, naproxen, and ketoprofen. Headache is more likely to occur after ingestion of indomethacin than other NSAIDs. Aseptic meningitis has been reported with NSAIDs, most typically with ibuprofen.5,6

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Symptoms of GI toxicity include nausea, vomiting, and epigastric pain, all of which can occur at therapeutic doses.3 The gastritis associated with NSAIDs probably occurs secondary to inhibition of prostaglandin synthesis.

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Cardiovascular complications of NSAID overdose are generally limited to tachycardia and hypotension, usually secondary to volume depletion.7 Respiratory complications include hyperventilation and apnea, which are rare.

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Long-term use of NSAIDs is associated with nephrotoxicity, including acute tubular necrosis, acute interstitial nephritis, and acute renal failure. Renal papillary necrosis has been reported in children being treated with NSAIDs for juvenile rheumatoid arthritis. Renal toxicity is not associated with acute overdose.

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Other long-term complications of NSAID use include hepatocellular injury and cholestatic jaundice.

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Assay procedures for measuring plasma ibuprofen levels are available. There is a poor correlation between the absolute level ...

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