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- W2886159127 abstract "The central role of the organ system gut for critically ill patients has not been acknowledged until the last decade. The gut is a crucial immunologic, metabolic and neurologic organ system and impairment of its functions is associated with morbidity and mortality. The gut has a central position in the cross-talk between organs and dysfunction of the gut may result in impairment of other intra-abdominal and extra-abdominal organ systems. The intestinal tract is the most important source of endogenous infections and determines the inflammatory status of the organism. Gut failure is an element of the multiple organ dysfunction syndrome (MODS). The leading mechanism in the evolution of endogenous infections is the intestinal translocation of microbes. A dysbiosis and damage of the intestinal mucosa leads to a disorder of the mucosal barrier function, increases the permeability and promotes translocation (leaky gut hypothesis). A further crucial mechanism of organ interactions is the increase in intra-abdominal pressure. Intra-abdominal hypertension promotes further injury of the gut, increases translocation and inflammation and causes dysfunction of other organ systems, such as the kidneys, the cardiovascular system and the lungs. Maintaining and/or restoring intestinal functions must be a priority of any intensive care therapy. The most important measure is early enteral nutrition. Other measures are the preservation of motility and modulation of the intestinal microbiome. Intra-abdominal hypertension must be reduced by an individually adapted infusion therapy, positioning of the patient, administration of drugs (abdominal compliance) and decompression (by tubes, endoscopically or in severe cases surgically)." @default.
- W2886159127 created "2018-08-22" @default.
- W2886159127 creator A5005648961 @default.
- W2886159127 date "2018-08-17" @default.
- W2886159127 modified "2023-10-13" @default.
- W2886159127 title "Intestinaler Crosstalk" @default.
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- W2886159127 doi "https://doi.org/10.1007/s00063-018-0475-1" @default.
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