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• W2740565513 abstract "Summary: Background: Multiple organ failure (MOF) is not a disease, but the result of a series of events that in some cases may lead to the death of patients in the intensive care unit. Metl~ods: This is a review of pathophysiologic alterations that may occur after trauma. In this respect emphasis will be placed on mechanisms and significance of trauma-related ischemia/repeffusion, activation of eellular/humorat systems, bacteriJendotoxin translocation, and related mediators that can cause or perpetuate the development of MOE Results: In general, the body's response to trauma or stress is mediated by mediators derived by activation of humoral cascades, such as complement and coagulation systems and/or by a variety of cells, such as the monocytes/macrophages. Such a response, manifested as inflammation, should be beneficial to the host. From a certain threshold level of activation/inactivation, however, there might be an imbalance of the mediator system that could harm the host by leading to the development of MOF. Although the pathogenesis of MOF is most likely multifaceted, the cell's oxygen status, adherence of neutrophils to the endothelium with subsequent transmi~ation, gut barrier failure leading to the translocation of bacteria/endotoxin, and an initially hyperinflammatory state followed by delayed immunosupression that predispose to infection have recently been considered as key events in this scenario. Conclusions: The precise mechanisms, however, of the development of MOF have not been clearly understood. The relative importance of the cascades/mediators and their interrelationships remains to be defined." @default.
• W2740565513 created "2017-08-08" @default.
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• W2740565513 date "1998-01-01" @default.
• W2740565513 modified "2023-09-23" @default.
• W2740565513 title "Pathophysiology of Trauma- Multiple Organ" @default.
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