Drug interactions

Ibuprofen + Ketorolac

For healthcare professionals — reference only. This page is a brief summary, not medical advice and not a substitute for official labeling or clinical judgement. Always verify before prescribing or dispensing.

Overview

Severity: Contraindicated · Evidence level: High

Concomitant use is contraindicated due to markedly increased risk of serious gastrointestinal bleeding/ulceration, renal toxicity, and additive antiplatelet effects.

Mechanism of action

Additive pharmacodynamic inhibition of prostaglandin synthesis via COX-1/COX-2, reducing gastric mucosal protection, impairing renal perfusion, and decreasing platelet aggregation; no clinically meaningful pharmacokinetic interaction.

Clinical management

Do not coadminister. Discontinue one NSAID and use a non-NSAID analgesic (e.g., acetaminophen) if additional pain control is needed. If inadvertent co-use occurs, stop one agent and evaluate for GI bleeding and renal dysfunction.

Drug reference

References

  • Toradol (ketorolac tromethamine) Prescribing Information — FDA Label
  • Ketorolac: Drug Information — UpToDate
  • Drug Interactions: Ketorolac and Ibuprofen — Lexicomp

Frequently asked questions

Can I take Ibuprofen with Ketorolac?

The interaction is rated: Contraindicated. Concomitant use is contraindicated due to markedly increased risk of serious gastrointestinal bleeding/ulceration, renal toxicity, and additive antiplatelet effects.

How serious is the interaction between Ibuprofen and Ketorolac?

The interaction is rated: Contraindicated. Evidence level: High.

How is the interaction between Ibuprofen and Ketorolac managed?

Do not coadminister. Discontinue one NSAID and use a non-NSAID analgesic (e.g., acetaminophen) if additional pain control is needed. If inadvertent co-use occurs, stop one agent and evaluate for GI bleeding and renal dysfunction.

Why do Ibuprofen and Ketorolac interact?

Additive pharmacodynamic inhibition of prostaglandin synthesis via COX-1/COX-2, reducing gastric mucosal protection, impairing renal perfusion, and decreasing platelet aggregation; no clinically meaningful pharmacokinetic interaction.

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