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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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Immediately surrounding the primary zone is an area of erythema,
edema, and ...