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The understanding of postoperative pain has evolved greatly during the past decade. Many laboratory investigations have established that peripheral tissue injury during surgery can trigger a prolonged state of spinal cord excitation. A reduction in neuronal thresholds in the central nervous system (CNS) is thought to amplify pain in postsurgical patients. Preemptive analgesia is an antinociceptive treatment targeted to block CNS hyperexcitability, and thereby leads to a reduced postoperative pain state. Despite numerous investigations, the clinical relevance of such treatment is, at present, an issue of controversy.

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The concept of preemptive analgesia was postulated by George Washington Crile during the early 1900s.1,2 Crile proposed that trauma induced by surgery caused a “shock and exhaustion” to the CNS. He went on to advocate preincisional and intraoperative local anesthetic infiltrations in addition to general anesthesia. In this way, noxious stimuli could be prevented from reaching the brain, thus establishing the “shockless operation.” Rekindling of this idea was not to occur until the 1980s.

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Wall, based on laboratory data and several clinical studies, postulated in an editorial in 1988 that (1) a reduction in massive small-fiber input into the CNS during surgery would prevent a central sensitization, and (2) analgesia that is present preoperatively has the potential to render prolonged effects, well beyond the known time frame of drug action.3 Consistent with this proposal was experimental data by Wall and Woolf demonstrating that low doses of opioids, given prior to a painful stimulus, can effectively prevent central sensitization.4 In contrast, much higher doses of opioids are required to suppress an already sensitized spinal cord. Since the editorial by Wall, a large number of investigations have been carried out; the overall results are to date equivocal. Appreciation for the multiple variables that influence postoperative pain as well as limitations in outcome measures have become more evident.

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Peripheral Sensitization

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The establishment of sensitization in the periphery involves the transition of high-threshold nociceptors into ones of low threshold, as induced by the release of various chemicals soon after surgical incision.5 At the site of damage, a complex array of inflammatory mediators, as outlined in Table 41-1, are mobilized from injured tissue, while others are delivered by the circulation.6 Small-diameter primary afferent neurons, Aδ and C fibers innervating the region of insult, subsequently enter a state characterized by ongoing discharge, a lowered activation threshold, and excitation elicited by suprathreshold stimulation (hyperalgesia).7 The center of a surgical wound, which is the primary zone of injury, would be expected to demonstrate static mechanical hyperalgesia.

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Table Graphic Jump Location
Table 41-1 Biochemical Mediators that Induce Peripheral Sensitization
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Immediately surrounding the primary zone is an area of erythema, edema, ...

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