Abstract
Multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality
in intensive care units. It is being encountered frequently in critically ill patients
owing to advancements in organ-specific supportive technologies to survive the acute
phase of severe sepsis and shock. It is now believed that MODS is the result of an
inappropriate generalized inflammatory response of the host to a variety of acute
insults. The pathologic mechanisms of MODS were reviewed, and factors determining
the sequence and severity of organ dysfunction were discussed in depth. In the early
phase of MODS, circulating cytokines cause universal endothelium injury in organs.
In the later phase of MODS, overexpression of inflammatory mediators in the interstitial
space of various organs is considered a main mechanism of parenchyma injury. The difference
in constitutive expression and the upregulation of adhesion molecules in vascular
beds and the density and potency of intrinsic inflammatory cells in different organs
are the key factors determining the sequence and severity of organ dysfunction. By
activating the intrinsic inflammatory cell in a distant organ, organ dysfunctions
are linked in a positive feedback loop through circulating inflammatory mediators.
Antagonists targeted at adhesion molecules may alleviate the severity of endothelial
damage. And nonsteroidial anti-inflammatory drugs or steroids administered judiciously
in the early phase of MODS may retard the progress of multiple organ failure.
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Article Info
Publication History
Accepted:
October 17,
2007
Received in revised form:
October 16,
2007
Received:
September 19,
2007
Identification
Copyright
© 2008 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
