NSAIDs — Adverse Effects & Contraindications
The same COX inhibition that relieves your patient's pain is simultaneously thinning the gastric mucosa, stressing the kidneys, and raising cardiovascular risk. Knowing which patient should never get an NSAID is the real test.
Core Concept
NSAIDs block cyclooxygenase (COX), reducing protective prostaglandins throughout the body — not just at the pain site. GI effects are the most common: prostaglandin depletion thins the gastric mucosal barrier, causing epigastric pain, ulceration, and GI bleeding. The client should take NSAIDs with food and report dark, tarry stools immediately. Renal effects matter next: prostaglandins maintain renal blood flow, so NSAIDs can precipitate acute kidney injury, especially in clients who are dehydrated, elderly, or already on ACE inhibitors or diuretics. Monitor BUN, creatinine, and urine output. Cardiovascular risk increases with prolonged use — COX-2 selective agents (celecoxib) carry a black-box warning for MI and stroke. NSAIDs also inhibit platelet aggregation (except celecoxib), increasing bleeding risk; they must be held before surgery (7–10 days for aspirin due to irreversible platelet inhibition; shorter holds for other NSAIDs based on half-life). Key contraindications: active peptic ulcer disease, third trimester of pregnancy (risk of premature ductus arteriosus closure), severe renal impairment, aspirin-sensitive asthma (cross-reactivity can trigger bronchospasm), and clients on anticoagulants without careful risk-benefit evaluation. Ketorolac (Toradol) deserves special attention — limited to 5 days maximum due to high GI and renal toxicity risk.
Watch Out For
Don't confuse NSAID-related GI bleeding (prostaglandin loss → mucosal erosion) with acetaminophen hepatotoxicity — completely different organ targets. Students assume celecoxib is 'safer' across the board, but it spares the stomach and platelets while carrying higher cardiovascular risk. Aspirin-sensitive asthma is a contraindication to ALL NSAIDs, not just aspirin — cross-reactivity through the COX pathway triggers bronchospasm with any agent in the class.
Clinical Pearl
Black stool, rising creatinine, or wheezing in an NSAID client — stop, assess, and call. GI, renal, respiratory: those are your three alarm systems.
Test Your Knowledge
3 quick questions — see how well you understood NSAIDs — Adverse Effects & Contraindications