From the Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany.
Anesth Analg. 2020 Dec;131(6):1693-1707. doi: 10.1213/ANE.0000000000005175.
The immune system is an evolutionary hallmark of higher organisms that defends the host against invading pathogens and exogenous infections. This defense includes the recruitment of immune cells to the site of infection and the initiation of an inflammatory response to contain and eliminate pathogens. However, an inflammatory response may also be triggered by noninfectious stimuli such as major surgery, and, in case of an overshooting, still not comprehensively understood reaction, lead to tissue destruction and organ dysfunction. Unfortunately, in some cases, the immune system may not effectively distinguish between stimuli elicited by major surgery, which ideally should only require a modest inflammatory response, and those elicited by trauma or pathogenic infection. Surgical procedures thus represent a potential trigger for systemic inflammation that causes the secretion of proinflammatory cytokines, endothelial dysfunction, glycocalyx damage, activation of neutrophils, and ultimately tissue and multisystem organ destruction. In this review, we discuss and summarize currently available mechanistic knowledge on surgery-associated systemic inflammation, demarcation toward other inflammatory complications, and possible therapeutic options. These options depend on uncovering the underlying mechanisms and could include pharmacologic agents, remote ischemic preconditioning protocols, cytokine blockade or clearance, and optimization of surgical procedures, anesthetic regimens, and perioperative inflammatory diagnostic assessment. Currently, a large gap between basic science and clinically confirmed data exists due to a limited evidence base of translational studies. We thus summarize important steps toward the understanding of the precise time- and space-regulated processes in systemic perioperative inflammation.
免疫系统是高等生物的进化标志，可抵御入侵病原体和外源性感染。这种防御包括将免疫细胞募集到感染部位，并启动炎症反应以控制和消除病原体。然而，炎症反应也可能由非传染性刺激引发，如大手术，而在这种反应过度的情况下，其机制仍未得到全面理解，可能导致组织破坏和器官功能障碍。不幸的是，在某些情况下，免疫系统可能无法有效区分大手术引起的刺激，这种刺激理论上只需要适度的炎症反应，以及由创伤或病原体感染引起的刺激。因此，手术程序代表了全身炎症的潜在触发因素，可导致促炎细胞因子的分泌、内皮功能障碍、糖萼损伤、中性粒细胞的激活，最终导致组织和多器官系统的破坏。在这篇综述中，我们讨论并总结了目前关于手术相关全身炎症的机制知识、与其他炎症并发症的区分，以及可能的治疗选择。这些选择取决于揭示潜在的机制，可能包括药物治疗、远隔缺血预处理方案、细胞因子阻断或清除，以及优化手术程序、麻醉方案和围手术期炎症诊断评估。目前，由于转化研究的证据基础有限，基础科学和临床证实的数据之间存在很大差距。因此，我们总结了在理解全身围手术期炎症的精确时间和空间调节过程方面的重要步骤。
