Weigand Markus A, Hörner Christian, Bardenheuer Hubert J, Bouchon Axel
Department of Anesthesia, University of Heidelberg, Im Neuenheimer Feld 110, Heidelberg 69120, Germany.
Best Pract Res Clin Anaesthesiol. 2004 Sep;18(3):455-75. doi: 10.1016/j.bpa.2003.12.005.
Sepsis and septic shock are the leading causes of death in intensive care units in developed countries despite recent advances in critical care medicine. Sepsis is the systemic inflammatory response to infection frequently associated with hypoperfusion followed by tissue injury and organ failure. The activation of monocytes/macrophages and neutrophils, with the consecutive release of pro-inflammatory mediators and activation of the coagulation cascade, seems to play a key role in the pathogenesis of sepsis. Elimination of the septic focus, anti-microbial therapy and supportive treatment are the cornerstones of sepsis therapy. In addition, the application of small doses hydrocortisone to patients with refractory septic shock and the treatment of patients with septic multiple organ failure with activated protein C are two adjunctive therapeutic strategies. Promising new experimental treatment options are interference with MIF, HMGB1, C5a or TREM-1 signal transduction pathways and an inhibition of apoptosis, which may further improve the prognosis of septic patients in the future.
尽管重症医学最近取得了进展，但脓毒症和脓毒性休克仍是发达国家重症监护病房的主要死亡原因。脓毒症是对感染的全身性炎症反应，常伴有灌注不足，继而导致组织损伤和器官衰竭。单核细胞/巨噬细胞和中性粒细胞的激活，以及随后促炎介质的释放和凝血级联反应的激活，似乎在脓毒症的发病机制中起关键作用。消除感染灶、抗菌治疗和支持治疗是脓毒症治疗的基石。此外，对难治性脓毒性休克患者应用小剂量氢化可的松以及用活化蛋白C治疗脓毒症多器官功能衰竭患者是两种辅助治疗策略。有前景的新实验性治疗选择包括干扰巨噬细胞移动抑制因子（MIF）、高迁移率族蛋白B1（HMGB1）、C5a或触发受体表达于髓样细胞-1（TREM-1）信号转导通路以及抑制细胞凋亡，这可能在未来进一步改善脓毒症患者的预后。
