Generic Name

Ketorolac tromethamine

Mechanism

Ketorolac tromethamine is a potent, short‑acting non‑steroidal anti‑inflammatory drug (NSAID) that exerts its effect primarily by selective inhibition of cyclo‑oxygenase‑1 (COX‑1) and COX‑2, thereby suppressing the synthesis of prostaglandins responsible for pain, fever, and inflammation.
• Rapid oral absorption and peak plasma concentration (1–3 h).
• Metabolized by conjugation and excretion via the kidneys.

Pharmacokinetics

• Absorption: Oral: > 90 % bioavailability, peak at 1–3 h; IM/IV: immediate systemic availability.
• Distribution: 92‑95 % protein bound (predominantly albumin).
• Metabolism: Conjugation in the liver (glucuronidation).
• Elimination: Renal clearance; half‑life 5–7 h (oral), 4–5 h (IV).
• Special populations: Dose reductions recommended in renal impairment (CrCl < 30 mL/min); use with caution in hepatic disease.

Indications

• Moderate to severe acute pain (post‑operative, dental, musculoskeletal).
• Pre‑operative analgesia up to 24 h prior to surgery.
• Not indicated for chronic pain management due to GI, renal, and bleeding risks.

Contraindications

• Absolute contraindications:
• History of hypersensitivity to NSAIDs or aspirin.
• Active peptic ulcer disease, GI bleeding, or severe gastritis.
• Severe renal impairment (CrCl  65 y with comorbidities.
• Warnings:
• Monitor for GI ulceration, renal dysfunction, and bleeding.
• Avoid prolonged use (>5 days).

Dosing

• Special instructions:
• Administer with food or milk to reduce GI irritation.
• Use a rescue dosing strategy for breakthrough pain.
• Consider alternative analgesics (opioids, paracetamol) if higher analgesic need persists.

Adverse Effects

• Common (≥ 1 %):
• Dysphagia, nausea, dyspepsia, dizziness, headache.
• Serious (≥ 0.1 %):
• Peptic ulcer, GI bleeding, renal tubular acidosis, anaphylaxis, hepatic injury, severe hypersensitivity reactions.
• Thromboembolic events (especially in patients with cardiovascular history).

Monitoring

• Clinical: Pain score, sedation level, renal function status.
• Laboratory:
• Serum creatinine and eGFR baseline, then every 48 h for > 30 days.
• Liver enzymes (AST/ALT) if therapy > 3 days.
• Other: Monitor for signs of GI bleeding (hematemesis, melena) and bleeding after minor procedures.

Clinical Pearls

• Short‑term, high‑dose use gives powerful analgesia but limits to 5 days to prevent GI/renal sequelae.
• Use with caution in geriatric patients; baseline renal function assessment essential.
• Switch to acetaminophen (paracetamol) once ketorolac therapy ends to maintain analgesia without overlapping NSAID toxicity.
• Avoid concomitant aspirin unless therapeutic benefit outweighs bleeding risk – ketorolac markedly enhances aspirin’s bleeding effect.
• In patients on anticoagulants, ketorolac can potentiate bleeding; consider alternative analgesics or temporary discontinuation.
• Pregnancy counseling: ketorolac should be avoided after 32 weeks gestation, as it may cause premature closure of the ductus arteriosus.

*Always consult the most recent prescribing information and institutional protocols before prescribing.*