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综述文章:预防性镇痛:何去何从?

Review article: Preventive analgesia: quo vadimus?

机构信息

Department of Psychology, York University, and Department of Anesthesia and Pain Management, Toronto General Hospital, BSB 232, 4700 Keele St., Toronto, ON, Canada M3J 1P3.

出版信息

Anesth Analg. 2011 Nov;113(5):1242-53. doi: 10.1213/ANE.0b013e31822c9a59. Epub 2011 Sep 30.

DOI:10.1213/ANE.0b013e31822c9a59
PMID:21965352
Abstract

The classic definition of preemptive analgesia requires 2 groups of patients to receive identical treatment before or after incision or surgery. The only difference between the 2 groups is the timing of administration of the drug relative to incision. The constraint to include a postincision or postsurgical treatment group is methodologically appealing, because in the presence of a positive result, it provides a window of time within which the observed effect occurred, and thus points to possible mechanisms underlying the effect: the classic view assumes that the intraoperative nociceptive barrage contributes to a greater extent to postoperative pain than does the postoperative nociceptive barrage. However, this view is too restrictive and narrow, in part because we know that sensitization is induced by factors other than the peripheral nociceptive barrage associated with incision and subsequent noxious intraoperative events. A broader approach to the prevention of postoperative pain has evolved that aims to minimize the deleterious immediate and long-term effects of noxious perioperative afferent input. The focus of preventive analgesia is not on the relative timing of analgesic or anesthetic interventions, but on attenuating the impact of the peripheral nociceptive barrage associated with noxious preoperative, intraoperative, and/or postoperative stimuli. These stimuli induce peripheral and central sensitization, which increase postoperative pain intensity and analgesic requirements. Preventing sensitization will reduce pain and analgesic requirements. Preventive analgesia is demonstrated when postoperative pain and/or analgesic use are reduced beyond the duration of action of the target drug, which we have defined as 5.5 half-lives of the target drug. This requirement ensures that the observed effects are not direct analgesic effects. In this article, we briefly review the history of preemptive analgesia and relate it to the broader concept of preventive analgesia. We highlight clinical trial designs and examples from the literature that distinguish preventive analgesia from preemptive analgesia and conclude with suggestions for future research.

摘要

经典的超前镇痛定义要求两组患者在切口或手术前后接受相同的治疗。两组唯一的区别是药物给药时间相对于切口的不同。包括术后治疗组在方法学上是有吸引力的,因为如果出现阳性结果,它提供了一个观察到的效应发生的时间窗口,并由此指向效应的可能机制:经典观点认为术中伤害性冲动在更大程度上导致术后疼痛,而不是术后伤害性冲动。然而,这种观点过于局限和狭隘,部分原因是我们知道除了与切口和随后的伤害性手术事件相关的外周伤害性冲动之外,敏化还会被其他因素诱导。一种更广泛的预防术后疼痛的方法已经发展起来,旨在最大限度地减少有害的围手术期传入输入的即时和长期影响。预防性镇痛的重点不是镇痛或麻醉干预的相对时间,而是减轻与有害术前、术中和/或术后刺激相关的外周伤害性冲动的影响。这些刺激诱导外周和中枢敏化,增加术后疼痛强度和镇痛需求。预防敏化将减少疼痛和镇痛需求。当术后疼痛和/或镇痛使用减少超过目标药物的作用持续时间时,就可以证明预防性镇痛,我们将其定义为目标药物半衰期的 5.5 倍。这一要求确保观察到的效应不是直接的镇痛效应。在本文中,我们简要回顾了超前镇痛的历史,并将其与更广泛的预防性镇痛概念联系起来。我们强调了临床试验设计和文献中的例子,这些例子将预防性镇痛与超前镇痛区分开来,并对未来的研究提出了建议。

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