Saxena Sarah, Maze Mervyn
Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, UCSF; Department of anesthesia, Université Libre de Bruxelles, Belgium.
Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, UCSF.
Presse Med. 2018 Apr;47(4 Pt 2):e73-e81. doi: 10.1016/j.lpm.2018.03.011. Epub 2018 Apr 12.
The brain is both the orchestrator as well as the target of the innate immune system's response to the aseptic trauma of surgery. When trauma-induced inflammation is not appropriately regulated persistent neuro-inflammation interferes with the synaptic plasticity that underlies the learning and memory aspects of cognition. The complications that ensue, include postoperative delirium (POD) and postoperative cognitive dysfunction (POCD) at two poles of a constellation that is now termed perioperative neurocognitive disorders. While the relationship of acute POD to the more indolent POCD is not completely understood both can be further complicated by earlier-onset of dementia and higher mortality. How and why these disorders occur is the focus of this report. The innate immune system response to peripheral trauma signals to the brain through a regulated cascade of cellular and molecular actors producing a teleological defense mechanism, "sickness behavior," to curtail further injury and initiate repair. Sickness behavior, including disordered cognition, is terminated by neural and humoral pathways that restore homeostasis and launch the organism on a path to good health. With so many "moving parts" the innate immune system is vulnerable in clinical settings that include advanced age and lifestyle-induced diseases such as "unhealthy" obesity and the inevitable insulin resistance. Under these conditions, inflammation may become exaggerated and long-lived. Consideration is provided how to identify the high-risk surgical patient and both pharmacological (including biological compounds) and non-pharmacological strategies to customize care.
大脑既是机体对手术无菌创伤的固有免疫系统反应的协调者，也是该反应的目标。当创伤诱导的炎症未得到适当调节时，持续的神经炎症会干扰认知学习和记忆方面所依赖的突触可塑性。随之而来的并发症包括术后谵妄（POD）和术后认知功能障碍（POCD），它们是现在被称为围手术期神经认知障碍这一症候群两极的症状。虽然急性POD与较为隐匿的POCD之间的关系尚未完全明了，但两者都可能因更早出现痴呆和更高的死亡率而进一步复杂化。这些病症如何以及为何发生是本报告的重点。固有免疫系统对外周创伤的反应通过一系列受调控的细胞和分子因子级联反应向大脑发出信号，产生一种目的性防御机制——“疾病行为”，以减少进一步损伤并启动修复。包括认知紊乱在内的疾病行为通过恢复体内平衡并使机体走上健康之路的神经和体液途径而终止。由于有如此多的“运转部件”，固有免疫系统在包括高龄以及诸如“不健康”肥胖和不可避免的胰岛素抵抗等生活方式诱发疾病的临床环境中很脆弱。在这些情况下，炎症可能会变得过度且持久。文中探讨了如何识别高危手术患者以及如何采用药理学（包括生物化合物）和非药理学策略来定制护理方案。
