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Chapter Objectives

After reading this chapter, the student will be able to:

  1. History of anti-inflammatory medications

  2. Basic mechanism of action

  3. Practical and theoretical advantages of cyclooxygenase-2 (COX-2) inhibitors over other nonsteroidal anti-inflammatory drugs (NSAIDs)

  4. Indications for use of NSAIDs and corticosteroids in acute and chronic conditions

  5. Common adverse effects of NSAIDs

Chapter Outline

  • The Inflammatory Response

    • Leukotrienes

    • Prostaglandins

  • Anti-inflammatory Medications

    • Aspirin

    • Effects of Aspirin

    • Aspirin-Sensitive Asthma

    • Acetaminophen

  • NSAIDs

    • Overview of Selected NSAIDs

    • Topical NSAIDs

    • NSAID Indications

    • Adverse Effects

    • What to Tell the Athlete

  • Glucocorticosteroids

    • Physiology of Adrenal Corticosteroids

    • Adverse Effects

  • Scenario From the Field

  • Discussion Topics

  • Chapter Review

Athletic trainers administer therapeutic modalities such as ultrasound, ice, and electrical stimulation daily. The goal of treatment is to bring about a rapid and complete resolution of injuries to expeditiously return athletes to competition. The treatment for each injury is typically devised and agreed on by the athletic trainer and the team physician, with each drawing on their experience and knowledge to develop the most beneficial rehabilitation plan and treatment. This treatment plan often includes prescription or over-the-counter (OTC) nonsteroidal anti-inflammatory drugs (NSAIDs).


Inflammation is the response of vascular tissue to physiological damage and can be divided into three components: acute inflammation, the immune response, and chronic inflammation (Fig. 3–1). The acute inflammatory cascade is set into motion by the initial tissue insult. Acute inflammation is recognized by the classic and familiar signs of pain (dolor), heat (calor), erythema (rubor), swelling (tumor), and loss of function (functio laesa).

Figure 3–1

The inflammatory response.

Inflammation signals the initiation of the healing process that includes (1) the acute vascular inflammatory phase, (2) the repair-regeneration phase, and (3) the maturation phase. Typically, within 48 hours of the initial trauma, fibroblasts begin the process of wound repair and collagen synthesis. The response prevents the extensive spread of injury-causing agents to nearby tissues, disposes of cellular debris, and sets the stage for the repair process.

Cellular injury signals the release of chemical mediators, such as histamine, serotonin, anaphylatoxins, bradykinin, thromboxane, leukotrienes, and prostaglandins, after a short period of vasoconstriction. These chemical mediators increase cellular and capillary permeability and stimulate capillary vasodilation and blood flow. The changes in vascular permeability directly result in edema, caused by the flow of proteins and fluid into the interstitial space. There is also activation of the immune system and humoral response mechanisms. The increased blood flow and vessel permeability allow neutrophils to migrate to the site of injury and allows the leukocytes to target specific areas.

Activation of neutrophils at the injury site by lysosomal enzymes results in the generation of high concentrations of oxygen free radicals.35 These free radicals are ...

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