Wort S J, Evans T W
Unit of Critical Care, Imperial College School of Medicine, Royal Brompton Hospital, London, UK.
Br Med Bull. 1999;55(1):30-48. doi: 10.1258/0007142991902286.
The majority of deaths amongst critically ill patients requiring intensive care are attributable to sepsis and its sequelae: septic shock, the systemic inflammatory response syndrome (SIRS) and the acute respiratory distress syndrome (ARDS). Patients within the ICU who develop these conditions and fail to survive succumb to multiple organ dysfunction syndrome (MODS). ARDS is considered to be the pulmonary component of MODS and is characterized by pulmonary hypertension, often in the setting of systemic hypotension. Endothelial cells, normally responsible for modulating vascular tone, becomes dysfunctional in sepsis. Pro-thrombotic, pro-inflammatory and vasoactive mediators are released including nitric oxide (NO), endothelins (ETs) and products of cyclo-oxygenase metabolism. It is probably the disordered production of these mediators in vascular beds that results in MODS. This review highlights recent research in this area with particular emphasis on possible therapeutic options.
在需要重症监护的危重症患者中,大多数死亡归因于脓毒症及其后遗症:感染性休克、全身炎症反应综合征(SIRS)和急性呼吸窘迫综合征(ARDS)。重症监护病房(ICU)内发生这些情况且未能存活的患者死于多器官功能障碍综合征(MODS)。ARDS被认为是MODS的肺部组成部分,其特征是肺动脉高压,通常发生在系统性低血压的情况下。内皮细胞通常负责调节血管张力,在脓毒症中会功能失调。会释放促血栓形成、促炎和血管活性介质,包括一氧化氮(NO)、内皮素(ETs)和环氧化酶代谢产物。可能正是血管床中这些介质的无序产生导致了MODS。本综述重点介绍了该领域的最新研究,特别强调了可能的治疗选择。