Abstract
Severely ill patients are usually admitted to an intensive care unit after medical catastrophes such as severe infection, trauma, surgery, burns or combinations of these. The early phase of their stay in the intensive care unit is frequently characterized by hypotension and reduced tissue perfusion. In this phase, massive infusions of either crystalloid or colloid solutions, or blood products are often needed to maintain a stable circulation. In many patients, a sequence of events evolves which is thought to be triggered by the release of a host of inflammatory mediators such as complement factors, cytokines or arachidonic acid pathway products. This generalized response, now defined as the severe inflammatory response syndrome (SIRS) [1], is, amongst others, characterized by decreased microvascular integrity. A prevalent and early complication of this state is non-hydrostatic pulmonary edema (adult respiratory distress syndrome, ARDS), which often necessitates institution of sedation, muscle relaxation and mechanical ventilation, involving the use of positive end-expiratory pressure (PEEP). In addition, the multiple organ dysfunction syndrome (MODS) may develop which can also involve the kidneys and lead to varying degrees of acute renal failure. Even after the initial insult has subsided, many patients in intensive care units continue to receive relatively large volumes of intravenous fluids for parenteral nutrition and administration of vasoactive or antibiotic agents.
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Boer, W.H., Koomans, H.A. (1998). Edematous states in the intensive care unit. In: Critical Care Nephrology. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5482-6_16
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DOI: https://doi.org/10.1007/978-94-011-5482-6_16
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