NSAIDs block the synthesis of prostaglandins by inhibiting the enzyme cyclooxgenase. Through this mechanism, NSAIDs decrease inflammation and pain

Onset of action: analgesic: 30-60 minutes, anti-inflammatory < 7 days
Time to peak: 1-2 h
Plasma ½ life: 2-4 h
Absorption: PO rapid (85%)


  • Inflammatory disease: 400-800 mg/dose 3-4 times/day PO (maximum: 3.2 g/day)
  • Analgesia/pain: 200-400 mg/dose q4-6h PO (maximum 2.4 g/day)
  • 5-10 mg/kg q8-12h PO

Have patient take with food if possible to decrease GI upset


  • Dizziness
  • Headache
  • Fluid retention
  • Nervousness
  • Itching/rash
  • Dyspepsia
  • Nausea
  • Vomiting
  • Heartburn
  • Tinnitus
  • Abdominal pain


Many of the toxic effects of NSAIDs are related to their primary mechanism of action (the inhibition of prostaglandin synthesis)
Common adverse effects:

  • Gastrointestinal complications
    • Dyspepsia
    • Peptic ulcer disease
    • Gastrointestinal bleeding
  • Renal toxicities
    • Acute renal failure due to renal vasoconstriction
  • Cardiovascular
    • Possible increased risk of myocardial infarction, stroke, and new onset or worsening of hypertension
  • Tinnitus
    • Typically reversible after stopping NSAIDs
  • Antiplatelet effects
    • Inhibit platelet aggregation
    • Can increase risk of significant bleeding for patients undergoing surgery, thrombocytopenic patients (platelet count < 50,000), or patients on anticoagulant therapy such as warfarin
  • Respiratory
    • Can precipitate bronchospasm or worsen asthma in small percentage of individuals
  • NSAIDs should generally be avoided in pediatric patients with fever due to risk of Reye's Syndrome. Acetaminophen/paracetamol should be used instead.

In summary: NSAIDs are effective, inexpensive, antiinflammatory drugs that are well tolerated in most people and can provide significant pain relief. However, patients with significant gastrointestinal problems, bleeding risks, or renal or cardiac compromise should be carefully evaluated before beginning therapy with NSAIDs. May need to adjust dose and monitor renal function for patients with renal compromise.


This information is drawn from a number of sources (see below). The reader is encouraged to access these and other relevant literature for more detail. As always, sound clinical judgment should be used in individual clinical cases. In particular, it should be remembered that there may be significant variation in the pharmokinetics of a drug resulting from a number of factors, including the individual patient’s metabolism/disease status and how the medication has been formulated.


  1. Brunton LL, Lazo JS, Parker KL, editors. Goodman and Gilman’s: the pharmacological basis of therapeutics. 11th ed. McGraw-Hill Professional; 2006.
  2. Twycross R, Wilcock A. Palliative care formulary. 3rd ed. Radcliffe Medical Press Ltd; 2008.
  3. Repchinsky C, editor. Compendium of pharmaceuticals and specialties (CPS): the Canadian drug reference for health professionals. 44th ed. Canadian Pharmacists Association; 2009.
  4. Goldman A, Hain R, Liben S. Oxford textbook of palliative care for children. 1st ed. Oxford University Press; 2006.

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