Non Steroidal Anti-Inflammatory Drugs in the Treatment of Sports Injury

Warning: Always consult a doctor or pharmacist before using any medication. Do not exceed the stated dose of any medication. If your symptoms persist consult your doctor.

Non Steroidal Anti-Inflammatory Drugs (NSAIDs) are commonly used in the treatment of acute sports injuries (Almekinders, 1993). NSAIDs are used primarily for reducing the pain, heat, swelling and redness that is associated with inflammation. The three most commonly used NSAIDs are aspirin (salicylate), acetaminophen, and ibuprofen. Aspirin has many trade names by which it is also known. Acetaminophen is manufactured under the trade name Paracetamol, and also as Tylenol and Datril. Other NSAIDs used in sports medicine include Flurbiprofen (Ansaid), Indomethacin (Indocin), Ibuprofen (Advil, Motrin, Nuprin, Nurofen), Naproxen (Naprosyn) and Diclofenac (Voltaren).

Aspirin is one of the most mis-used drugs because of its wide availability (Davies et al, 1984). It has several modes of action. It interferes with pain signals to a part of the brain called the Thalamus. Aspirin also irreversibly inhibits chemical mediators of inflammation, which produce pain and further inflammatory reactions. These chemicals are released following tissue and cell damage. In addition, aspirin reduces fever by having an effect on the hypothalamus in the brain, which leads to vasodilation and sweating. The side effects of aspirin use include upset stomach, heartburn, nausea, tinnitus (ringing in the ears), headache, and diaorrhea.

Aspirin has an effect on the blood clotting system, which means that bleeding within the damaged tissue may increase. This can increase soft tissue swelling and therefore the duration required for rehabilitation after injury. Although it is an NSAID, Ibuprofen also has analgesic (pain relieving) and antipyretic (fever reducing) effects. It does not affect blood clotting to the same extent as aspirin. Paracetamol (Acetaminophen) does not have significant anti-inflammatory effects, but does have antipyretic and analgesic effects. It is effective in relieving mild pain without upsetting the stomach, which makes it useful for an athlete. Because of possible side effects, all NSAID use should be monitored under the strict supervision of a doctor. There are anecdotal reports that serious gastro-intestinal bleeding leading to hypovolemic shock (blood loss) and anaemia (reduced oxygen to the tissues), have occured in instances where poorly supervised athletes have continued long term use of NSAIDs.

The aim of NSAID use is to reduce the inflammatory response following soft tissue injury. Following an acute soft tissue injury, the inflammatory response is mediated by chemicals which are released by the damaged cells. These chemicals cause blood vessels to open (vasodilation) and blood and cellular fluid to leak into the tissues (extravasation). This causes swelling, pain, redness and a loss of function of the injured part. (Almekinders, 1993). NSAID treatment is an attempt to reduce this response in order that the total rehabilitation time can be reduced.

However, it should be remembered that the inflammatory or 'lag phase' is the first stage of the healing process and a degree of pain and loss of function may be helpful to prevent the athlete doing further damage to the injured part. The question of whether NSAIDs have an adverse effect on healing was examined by Obremsky et al (1994) and Almekinders (1986). Both studies showed no significant effect on tensile strength recovery following NSAID treatment for muscle strain injury, and Obremsky et al (1994) further demonstrated that muscular force was also unaltered. However, both studies showed histologic evidence of delayed healing with NSAID use, although it should be stated that both studies utilised animal models.

To conclude, NSAIDs can provide pain relief and a reduction in the signs of inflammation if used in the acute stage of soft tissue injury. However, the precise mechanism and optimum use of these drugs remains unclear. The general concensus is that NSAIDs prescribed by a doctor are appropriate in the early stages of inflammation, but their use should be discontinued as soon as possible, in order to negate any potential adverse effects on the healing process.

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References

Ceuppens JL, Rodriguez MA, Goodwin JS. Nonsteroidal antiinflammatory agents inhibit synthesis of IgM rheumatoid factor in vitro. Lancet 1986;1:52-58.

Wahl LM, Olsen CE, Sandberg LE, et al. Prostaglandin regulation of macrophage collagenase production. Proceedings of National Academy of Sciences of the United States ofAmerica 1977:74:4955-4959.

McCormack K, Brune K. Dissociation between antinociceptive and antiinflammatory effects of nonsteroidal antiinflammatory drugs: a survey of their analgesic efficacy. Drugs 1991 ;41:533-547.

McIlmsten CL. Prostaglandins, thromboxanes, and leukotrienes in inflammation. Am J Med 1986;80 (4BSuppt):11-17.

Davies P, Bailey P, Goldenburg MM, et al. The role of arachidonic acid oxygenation products in pain and inflammation. Ann Rev Immunol 1984;2:235-247.

Almekinders LC. Antiinflammatory treatment of muscular injuries. Sports Med 1993; 15(3): 139-145.

Almekinders LC. Muscles injuries and antiinflammatory treatment. Med Sci Sports Exerc 1991;23(Suppl):110S.

Almekinders LC, Gilbert JA. Healing of experimental muscle strains and the effects of nonsteroidal antiinflammatory medication. Am J Sports Med 1986; 14:303-330.

Obremsky WT, Seaber AV, Ribbeck BM, et al. Biomechanical and histologic assessment of a controlled muscle strain injury treated with piroxicam. Am J Sports Med 1994;22(4):558-561.

Almekinders LC, Gilbert JA. Healing of experimental muscle strains and the effects oi nonsteroidal antiinflammatory medication. Am J SportsMed1986;14:303-330.

Palder S, Huval W. Reduction of polymorphonuclear leukocyte accumulations by inhibition of cyclooxygenase and thromboxane synthetase in the rabbit. Surgery 1986;99:72-81.

Scheinberg M, Rueda H, Mathews P. The effect of piroxicam on neutrophil and monocytemacrophage function. Eur J Rheum Inflamm 1983:6:36-40.

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