Darville T, Giroir B, Jacobs R
Dept. of Pediatrics, Arkansas Children's Hospital, University of Arkansas for Medical Sciences, Little Rock 72202-3591.
Infection. 1993 Sep-Oct;21(5):279-90. doi: 10.1007/BF01712446.
Despite widespread advances in intensive care practices, and more potent and effective antimicrobials, septic shock continues to have a mortality rate of greater than 40%. Although antimicrobials can treat the etiologic organism, they do not alter the host response. It is becoming clear that invading organisms and other insults induce the release of cytokines and secondary mediators by the host. These mediators produce alterations in cellular, metabolic and physiologic functions producing the clinical picture of septic shock. Recent advances in cellular and molecular biology have permitted the identification of some of the mediators involved in this inflammatory cascade. Potential therapies are being developed which block or interrupt their activity. Treatment populations must be meticulously defined if we are to extract useful information concerning the efficacy of these new treatment modalities. In the following, proposed definitions for clinical patterns seen in patients with sepsis, and their inherent problems when applied to pediatrics are discussed. The pathophysiology of sepsis is discussed, and specific therapies designed to interrupt the inflammatory cascade are examined.
尽管重症监护实践取得了广泛进展,并且有了更强大、有效的抗菌药物,但感染性休克的死亡率仍超过40%。虽然抗菌药物可以治疗病原微生物,但它们并不能改变宿主的反应。越来越清楚的是,入侵的生物体和其他损伤会诱导宿主释放细胞因子和继发性介质。这些介质会引起细胞、代谢和生理功能的改变,从而产生感染性休克的临床表现。细胞和分子生物学的最新进展使得能够识别参与这一炎症级联反应的一些介质。正在开发阻断或中断其活性的潜在疗法。如果我们要提取有关这些新治疗方式疗效的有用信息,就必须精心界定治疗人群。以下将讨论脓毒症患者临床模式的拟议定义,以及将其应用于儿科时存在的固有问题。还将讨论脓毒症的病理生理学,并研究旨在中断炎症级联反应的具体疗法。