pioid analgesics are commonly used during the perioperative period because of their pre-0 dictable anesthetic-sparing and pain-relieving qualities. However, concerns regarding opioid-related side effects (e.g., nausea, vomiting, ileus, biliary spasm, urinary retention, respiratory depression, and the potential for abuse by health care professionals) have stimulated a search for analgesics devoid of these untoward effects. Not surprisingly, the nonsteroidal antiinflammatory drugs (NSAIDs) have become increasingly popular in the perioperative management of pain ( Fig. 1) (1-3).In this review article, we discuss the published literature relating to the clinical use of the NSAIDs for premedication, as adjuvants during general anesthesia and monitored anesthesia care (MoAC), as well as during the postoperative period. Although the perioperative use of NSAIDs has been increasing because of concerns regarding the side effects of opioid analgesics, their efficacy and safety during and after surgery has been questioned recently. Finally, we make recommendations regarding the use of currently available NSAIDs in the management of perioperative pain. Mechanisms of NSAIDs ActionThe tissue response to surgery-induced injury initiates a cascade consisting of nociception, inflammation, and hyperalgesia (4 -6). After a noxious stimulus, peripheral nerves release prostaglandins, substance P, and related nociceptive peptides. The resultant prostaglandin-mediated inflammatory process is characterized by vasodilation and increased vascular permeability, followed by hyperalgesia, an altered functional state of the nervous system with sensitization of nociceptors, and a resultant decrease in the pain threshold (6). Primary hyperalgesia describes the changes in pain threshold within the area of injury, while secondary hyperalgesia refers to changes in the surrounding uninjured tissue as a result of altered central processing of the nociceptive input from the periphery (5). These sensitization processes are followed by expansion of the receptive fields with a decrease in the threshold of the dorsal horn neurons and a disruption of the normal pattern of afferent processing within the central nervous system (CNS). Sensitization is thought to be mediated centrally by activation of N-methyhaspartate (NMDA) receptors in the dorsal horn of the spinal cord (7,8). Consequently, a "wind-up" phenomenon occurs which results in the formation of a positive feed-forward circuit in which afferent sensory input, central sensitization, and sympathetic outflow all contribute to the modulation of the pain response. As a result, a hypersensitivity state may result that can outlast the duration of the initial injury (6).Traditionally, the analgesic properties of the NSAIDs have been attributed to their effects on the peripheral synthesis of prostaglandins (Fig. 2). Inhibition of prostaglandin synthesis by NSAIDs decreases the inflammatory response to surgical trauma and, hence, reduced peripheral nociception and pain perception (9). However, recent in vivo ...

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SummaryOne hundred obstetric patients presenting for elective surgery who had refused regional anaesthesia were interviewed just prior to entering the operating room. In each case, the reason for refusing a regional technique was recorded. The most frequent reasons given were fear of backache (33%) and fear of the needle (28%). Anaesthetists should be aware of patients' concerns and be able to discuss the relevant issues.

Inflammation or injury often lead to chronic pain states such as hyperalgesia where the perception of a normally painful stimulus is significantly exaggerated. Interleukin-1beta (IL-1beta) is a cytokine that is an important mediator of the inflammatory response. In addition, IL-1beta has been implicated in the modulation of pain transmission in both the peripheral and central nervous systems. We evaluated the spinal effect of this cytokine in the presence and absence of a peripheral carrageenan inflammation in rats since the spinal cord is a major region of the central nervous system in which nociceptive input is processed and modulated. Our results indicate that intrathecal IL-1beta has no effect on the latency of paw withdrawal in response to a noxious thermal stimuluation in normal rats. In contrast, we have observed that IL-1beta produces significant antinociception when administered intrathecally in rats with peripheral inflammation (carrageenan model). The IL-1beta effect appears to be selective as it is reversed when IL-1beta is administered in the presence of an IL-1beta neutralizing antibody. We evaluated some putative mechanisms of this IL-1beta-mediated antinociception and found it to be non-opioid-dependent. Collectively, these data indicate that intrathecal IL-1beta has no effect on the processing of thermal nociceptive information in the absence of a peripheral inflammation. Therefore, the response to acute pain remains normal in these rats. In contrast, IL-1beta is antinociceptive when applied spinally during inflammation. These results indicate that IL-1beta reduces inflammatory hyperalgesia while sparing the protective functions of acute pain. This study offers new insights into the role of IL-1beta and nociceptive processing at the level of the spinal cord and suggests that development of IL-1beta agonists may be an alternative to opiate based therapies in the treatment of inflammatory pain.

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