• W J Mileski.
• University of Texas Southwestern Medical Center, Dallas.
• Surg. Clin. North Am. 1991 Aug 1;71(4):749-64.

AbstractSepsis, 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.

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