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Nonsteroidal Anti-inflammatory Poisoning, Emergency Medicine

Basics

Description

- GI: - Nausea - Vomiting - Epigastric pain

- Cardiovascular: - Pulmonary: - Eosinophilic pneumonia - Apnea - Hyperventilation

- Renal: - Acute renal failure, hyperkalemia - Acute tubular necrosis - Acute interstitial nephritis

- Liver: - Hepatocellular injury - Cholestatic jaundice

- Hypersensitivity: - Aseptic meningitis - Asthma exacerbation - Angioedema, urticaria

- Electrolytes, BUN/creatinine, glucose: - Baseline renal function - Check for metabolic acidosis.

  • Inhibit cyclooxygenase (COX), thereby blocking the conversion of arachidonic acid to prostaglandin.
  • Typically morbidity is low when an NSAID is ingested
  • Most literature on nonselective NSAID toxicity involves ibuprofen exposure likely due to its OTC availability.
  • Fatalities have been reported with large ingestions.
  • Greater potential for toxicity with underlying CHF or renal failure:NSAIDs cause sodium and water retention and decrease renal blood flow.Little overdose experience with the COX-2 inhibitors (celecoxib); treatment should be the same as for the traditional NSAIDs.Patients may ingest rofecoxib and valdecoxib from stored supplies even though both are no longer available in US

Etiology

  • Nonsteroidal medications are available by prescription and over-the-counter.
  • NSAIDs include:DiclofenacDiflunisalEtodolacFenoprofenIbuprofenIndomethacinKetoprofenKetorolacMeclofenamateMeloxicamNabumetoneNaproxenOxaprozinPiroxicamSulindacTolmetin

Diagnosis

Signs and Symptoms

  • GI:NauseaVomitingEpigastric pain
  • CNS:DrowsinessDizzinessLethargyAseptic meningitisSeizures
  • Cardiovascular:
  • Pulmonary:Eosinophilic pneumoniaApneaHyperventilation
  • Renal:Acute renal failure, hyperkalemiaAcute tubular necrosisAcute interstitial nephritis
  • Liver:Hepatocellular injuryCholestatic jaundice
  • Metabolic:Mild, short-lived metabolic acidosis
  • Hypersensitivity:Aseptic meningitisAsthma exacerbationAngioedema, urticaria

Essential Workup

  • Generally, NSAID ingestion results in mild toxicity.
  • Exact identification of drug helpful:Subtle toxicologic differences among the NSAIDsAseptic meningitis more common with ibuprofen exposureLiver toxicity more common with diclofenac and sulindac exposure

Diagnosis Tests & Interpretation

Lab

  • Electrolytes, BUN/creatinine, glucose:Baseline renal functionCheck for metabolic acidosis.
  • CBC
  • Arterial blood gas for large overdoses
  • PT/PTT:False-positive bilirubin/ketone dipstick with etodolac ingestion
  • Acetaminophen and salicylate level " ”patients often confuse salicylate, acetaminophen, and NSAID products thinking they are all the same.
  • NSAID difficult to detect on toxicology screens and is not beneficial in management

Differential Diagnosis

Agents causing metabolic acidosis, altered mental status, and GI irritation: ‚

  • Salicylates
  • Isoniazid
  • Ethylene glycol
  • Methanol
  • Isopropanol

Treatment

Pre-Hospital

Collect prescription bottles/medications for identification in the ED. ‚

Initial Stabilization/Therapy

  • ABCs
  • Naloxone, thiamine, dextrose (or Accu-Chek) for altered mental status

Ed Treatment/Procedures

  • Supportive care
  • Administer activated charcoal.
  • Extracorporeal methods to enhance elimination are not beneficial due to high degree of plasma protein binding.

Medication

  • Activated charcoal slurry: 1 " “2 g/kg up to 90 g PO
  • Dextrose: D50W 1 amp (50 mL or 25 g; peds: D25W 2 " “4 mL/kg) IV
  • Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV or IM initial dose
  • Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or IM

Piroxicam, naproxen, ketoprofen, and mefenamic acid have caused seizures in children. ‚

Follow-Up

Disposition

Admission Criteria

  • Protracted vomiting, hematemesis
  • CNS depression, seizure activity
  • Metabolic acidosis
  • CHF, hypotension, hypertension
  • Renal failure

Discharge Criteria

Nontoxic ingestion in a patient who is asymptomatic 6 " “8 hr after ingestion ‚

Followup Recommendations

Psychiatry follow-up/referral for intentional ingestion. ‚

Pearls and Pitfalls

  • Investigate for coingestions for all NSAID overdoses.
  • Obtain acetaminophen and salicylate level on all patients who present with suspected NSAID ingestion.
  • NSAID poisoning is generally benign, except with massive overdoses; patients with underlying CHF, coronary artery disease may be at higher risk of toxicity

Additional Reading

  • Dajani ‚ EZ, Islam ‚ K. Cardiovascular and gastrointes " “tinal toxicity of selective cyclo-oxygenase-2 inhibitors in man. J Physiol Pharmacol. 2008;59(suppl 2):117 " “133.
  • Frei ‚ MY, Nielsen ‚ S, Dobbin ‚ MD, et al. Serious morbidity associated with misuse of over-the-counter codeine-ibuprofen analgesics: A series of 27 cases. Med J Aust. 2010;193:294 " “296.
  • Halen ‚ PK, Murumkar ‚ PR, Giridhar ‚ R, et al. Prodrug designing of NSAIDs. Mini Rev Med Chem. 2009;9:124 " “139.

Codes

ICD9

976.0 Poisoning by local anti-infectives and anti-inflammatory drugs ‚

ICD10

  • T39.391A Poisoning by other nonsteroidal anti-inflammatory drugs, accidental, init?
  • T39.392A Poisoning by other nonsteroidal anti-inflammatory drugs, self-harm, init?
  • T39.394A Poisoning by other nonsteroidal anti-inflammatory drugs, undet?, init?

SNOMED

  • 278023006 Non-steroidal anti-inflammatory poisoning (disorder)