Toward Defining the Analgesic Role of Nonsteroidal Anti-inflammatory Drugs in the Management of Acute Soft Tissue Injuries

Abstract

Abstract: Although nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed for the management of soft tissue injuries, much of the world literature defining their usefulness for this indication is conflictual, vague, and uninstructive. Although differences in methodology between studies is an important factor, pharmacological differences between NSAIDs may be more important in explaining the clinical results. The authors challenge the traditional view that the analgesic effect of NSAIDs can be universally attributed to their inhibitory effects on the synthesis of peripherally formed prostaglandins. Much of our understanding of postinjury pain, hyperalgesia, and allodynia has been derived from studies performed on skin. Such findings may not be appropriate to trauma in deeper tissue. Recent clinical evidence is reviewed which supports the concept that peripheral events alone cannot adequately account for the phenomena of hyperalgesia and allodynia following injury to joints and muscle. A corollary of these findings is that in the management of acute pain, pharmacological intervention may be less effective when aimed solely at peripheral events, such as prostaglandin synthesis. In our survey we critically review the results of 26 different studies which were conducted under double-blind conditions and included a placebo control group. Of these, 14 studies demonstrated a significant difference between NSAID and placebo for nine NSAIDs—azapropazone, clonixin, ketoprofen, naproxen, diclofenac, fenbufen, ibuprofen, indomethacin, and piroxicam. In those studies where concomitant physical therapy was administered, we identified four NSAIDs which were demonstrated unequivocably to provide additional benefit–azapropazone, clonixin, ketoprofen, and naproxen. In the light of these findings we discuss the emerging view that, at least for some NSAIDs, effects on nociceptive pathways independent of prostaglandin synthesis may explain their analgesic character.