Sports Medicine: Just the Facts

MECHANISM OFACTION

• The major pharmacologic effect of NSAIDs is to
  inhibit the enzyme cyclooxygenase (COX), thus
  decreasing prostaglandin production. The decreased
  prostaglandins produce decreased inflammation and
  promote analgesia in the injured tissue. There are at
  least two forms of the COX enzyme, COX-1 and
  COX-2.
  •COX-1 is important in the production of prostaglandins
  involved in the homeostasis of various tissues including
  renal parenchyma, gastric mucosa, and platelets.
  •COX-2 produces prostaglandins involved in pain and
  inflammation. Most NSAIDs inhibit both COX-1 and
  COX-2 at various levels, with newer agents (e.g., cele-
  coxib) developed to be more COX-2 selective.
  Theoretically, this enhances the desired effects while
  limiting the side effects.


• NSAIDs also have physiologic effects on tissue pre-
  sumably caused by prostaglandin inhibition. The
  effects include inhibiting articular cartilage synthesis
  of glycosaminoglycans, decreasing neutrophil adher-
  ence to endothelial cells (although neutrophil meta-
  bolic activity does not seem to be affected), and
  probably inhibiting colorectal tumorigenesis. They
  are among the few agents known to be chemopreven-
  tive (Stanley and Weaver, 1998).

USE INACUTEINJURIES

• Studies have been conducted looking at the efficacy of
  NSAIDs in treating acute injuries, with some studies
  showing no clinical benefit (Stanley and Weaver,
  1998) including studies on exercise induced quadri-
  ceps injury and acute hamstring injuries (Yamamoto,
  2003; Bourgeois et al, 1999).


• Other studies have shown a benefit: a meta-analysis
  reviewing 84 articles on ankle soft tissue injuries con-
  cluded that early use of NSAIDs relieved pain and
  shortened the time to recovery. Subjects had less pain,
  were able to return to training more rapidly, and had
  better exercise endurance compared to subjects
  treated with placebo, and had a decrease in the per-
  ception of soreness and improved muscular perform-
  ance after injury (Ogilvie-Harris and Gilbart, 1995).
  •Overall, judicious use of NSAIDs for pain control in
  the acute phase of an injury probably speeds return to
  sport while not delaying healing.

USE INCHRONICINJURIES

• Histopathologic studies of tendons involved in
  chronic overuse injuries have shown an absence of
  inflammatory cells, but rather show disorganized
  fibroblastic or myofibroblastic cells and prominent
  capillary cell proliferation, often with discontinuity of
  these cells. This suggests that chronic tendon injuries

should be called tendonosis, referring to a degenera-

tive process, instead of tendonitis since inflammation

is not a major factor. Although NSAIDs are com-

monly used in these injuries to treat the chronic

inflammation, judicious short-term use of NSAIDs to

control pain may still be warranted (Almekinders and

Temple, 1998). Treatment for chronic tendon injuries

should be directed at correcting the underlying bio-

mechanical cause and properly rehabilitating the

injury.

SIDEEFFECTS ANDCOMPLICATIONS

• Side effects of NSAIDs have a significant impact. It is
  estimated that over 100,000 hospitalizations occur
  each year due to NSAID toxicity.
  
  
  • The most common side effect is dyspepsia, occur-
    ring in about 15%.
  
  
  • The most common serious side effect is gastroin-
    testinal(GI) ulceration, which occurs in 2–4% of
    patients taking the medicine for a year.
  
  
  • The following risk factors place a patient in a high
    risk category: past history of upper GI bleeding, past
    history of ulcer, concurrent anticoagulant use
    (including aspirin), concurrent corticosteroid use,
    age over 50, and use of multiple or high-dose
    NSAIDs.
  
  
  • The annual incidence of serious NSAID-induced GI
    complications (i.e., perforation, obstruction, and
    bleeding) is approximately 0.5% in patients without
    risk factors.
  
  
  • GI bleeds are more common in elderly patients with
    history of ulcers, there is a four- to sixfold relative
    risk of a fatal GI bleed.
  
  
  • Coadministration of aspirin and celecoxib produces
    the same risk of serious NSAID-associated GI com-
    plications as coadministration of aspirin and conven-
    tional NSAIDs. Therefore if aspirin must be
    coadministered with NSAIDs (e.g., for prophylaxis
    against coronary artery disease), less expensive con-
    ventional NSAIDs should be used (Schoenfeld, 2001).
  
  
  • Chronic NSAID use has also been associated with
    the development of liver injury, chronic renal dis-
    ease, and rarely in acute renal failure.
  
  
  • In 10–15% of all asthmatics, NSAIDs have also
    been associated with nonimmunoglobulin E (non
    IgE) mediated asthma and has been termed aspirin-
    induced asthma(AIA).
  
  
  • Sometimes, platelet function may be impaired,
    resulting in prolonged bleeding times.
  
  
  • There may be an increased risk of thromboembolic
    events including Myocardial Infarction, especially in
    those taking COX-2 inhibitors. Patients who are at
    risk for such an event should be treated with low-dose
    aspirin whether they are treated with COX-2-specific
  
  
  
  

416 SECTION 5 • PRINCIPLES OF REHABILITATION