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Hemofiltration in Treatment of multiple organ dysfunction syndrome the role of.doc

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Hemofiltration in Treatment of multiple organ dysfunction syndrome the role of

 PAGE \* MERGEFORMAT 19 Hemofiltration in Treatment of multiple organ dysfunction syndrome the role of Multiple organ dysfunction syndrome (multiple organ dysfunction syndrome, MODS) dangerous condition, a high fatality rate is the difficulty of ICU treatment. The plight of modern immunotherapy forcing people to look for new therapeutic approach, people will turn our attention to in vitro treatment, that is, removal of inflammatory mediators and cytokines, and circulating endotoxin, reduce the inflammatory response blocking systemic inflammatory response (SIRS) to continue to develop and the further deterioration in MODS. Hemofiltration (Hemofiltration, HF) in recent years in the treatment of SIRS / MODS has gradually developed in the field of theoretical and practical double the value of new technologies, more and more widely MODS application, showing good results. In this paper, hemofiltration in the treatment of MODS in recent years, the role, do a review. 1 MODS pathogenesis of MODS is a body subjected to severe trauma, shock, infection and major surgery such as acute damage to 24h, simultaneous or sequential emergence of two or more organ dysfunction, can not maintain a stable environment within the clinical syndrome, emphasizing the dynamics of disease and reversible [1]. The pathogenesis of MODS is not fully clear, is now a clear systemic inflammatory response syndrome (SIRS) is a key factor in MODS [2]. Mid-and late 20th century, 90 years, Bone [3] proposed compensatory anti-inflammatory response doctrine that a serious infection or trauma damage caused by acting on the body’s response after the response. SIRS, compensatory anti-inflammatory response syndrome (CARS) imbalance led to the development of MODS. A large number of inflammatory mediators released into the blood circulation, stimulate the release of inflammatory mediator cascade, leading to SIRS. SIRS, CARS imbalances led to runaway inflammatory response to changes in the protective effe

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