Mileski W J
University of Texas Southwestern Medical Center, Dallas.
Surg Clin North Am. 1991 Aug;71(4):749-64. doi: 10.1016/s0039-6109(16)45484-8.
Sepsis, shock, and resuscitation may result in various degrees of ischemia-perfusion injury that may produce widespread organ dysfunction through complex interactions and activation of host immunoinflammatory processes. As the pathophysiologic mechanisms of the inflammatory response are better defined, we may be able to modulate the generalized inflammatory state we know as sepsis and prevent the development of multiple organ failure syndrome. At present, however, the mainstay of therapy remains prompt resuscitation to eliminate regions of hypoperfusion and to limit as much as possible those factors that predispose to further organ injury while the source of inflammatory stimulation is being identified and controlled.
脓毒症、休克和复苏可能导致不同程度的缺血-灌注损伤,这种损伤可能通过复杂的相互作用和宿主免疫炎症过程的激活而引发广泛的器官功能障碍。随着炎症反应病理生理机制的进一步明确,我们或许能够调节我们所熟知的作为脓毒症的全身性炎症状态,并预防多器官功能衰竭综合征的发生。然而目前,治疗的主要方法仍然是迅速复苏,以消除灌注不足区域,并在确定和控制炎症刺激源的同时,尽可能限制那些易导致进一步器官损伤的因素。