Pathophysiology of sepsis

Pathophysiology of sepsis
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DOI:
10.2353/ajpath.2007.060872
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发表时间:
2007-05-01
影响因子:
6
通讯作者:
Remick, Daniel G.
Remick, Daniel G.
中科院分区:
医学2区
文献类型:
--
作者:
Remick, Daniel G.

文献摘要

被引文献

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脓毒症仍然是一个严重的问题,严重的发病率和死亡率,即使在现代的重症监护管理。脓毒症中存在多种错乱,涉及几个不同的器官和系统,尽管它们在疾病过程中的个体贡献存在争议。脓毒症患者的凝血系统发生了重大的、危及生命的变化,目前,已有一种被批准的治疗方法使用凝血系统的一个组成部分(激活蛋白Q)来治疗严重脓毒症患者。以前,人们认为脓毒症仅仅代表了一种夸大的、高炎症反应,患者死于炎症诱导的器官损伤。最近的数据表明,脓毒症患者的炎症反应存在很大的异质性,一些似乎是免疫刺激的,而另一些似乎是抑制的。细胞变化延续了异质性的主题。有些细胞工作得太好了,比如中性粒细胞长时间保持激活。其他细胞变化会以一种有害的方式加速,包括淋巴细胞凋亡。新陈代谢变化明显,需要密切和个性化的监测。在这一点上,文献充分说明,没有单一的介质/系统/途径/病原体驱动脓毒症的病理生理学。这篇综述将简要讨论脓毒症的许多重要改变。
Sepsis remains a critical problem with significant morbidity and mortality even in the modern era of critical care management. Multiple derangements exist in sepsis involving several different organs and systems, although controversies exist over their individual contribution to the disease process. Septic patients have substantial, life-threatening alterations in their coagulation system, and currently, there is an approved therapy with a component of the coagulation system (activated protein Q to treat patients with severe sepsis. Previously, it was believed that sepsis merely represented an exaggerated, hyperinflammatory response with patients dying from inflammation-induced organ injury. More recent data indicate that substantial heterogeneity exists in septic patients' inflammatory response, with some appearing immuno-stimulated, whereas others appear suppressed. Cellular changes continue the theme of heterogeneity. Some cells work too well such as neutrophils that remain activated for an extended time. Other cellular changes become accelerated in a detrimental fashion including lymphocyte apoptosis. Metabolic changes are clearly present, requiring close and individualized monitoring. At this point in time, the literature richly illustrates that no single mediator/systenx/pathway/pathogen drives the pathophysiology of sepsis. This review will briefly discuss many of the important alterations that account for the pathophysiology of sepsis.