Role of RBC Transfusion Therapy in Sepsis View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1995

AUTHORS

W. J. Sibbald , G. S. Doig , H. Morisaki

ABSTRACT

Sepsis is a clinical syndrome that arises because of an inappropriate and excessive host inflammatory response. Recent work has demonstrated that this syndrome is also characterized by the development of quantifiable injury in both the lungs and extra-pulmonary organs. This process is clinically expressed as Multiple Organ Dysfunction Syndrome (MODS). Sepsis is also a hypermetabolic state, where tissue O2 needs may be markedly increased. In this context, research has linked the widespread tissue injury typical of this syndrome with an inability to match tissue O2 delivery (D02) with these elevated tissue O2 needs. Thus, the emergence of metabolic dysregulation of tissue O2 availability in sepsis may contribute to the genesis of MODS [1]. For example, mortality in septic patients has been positively correlated with elevated arterial lactates [2] and “pathologic” VO2/DO2 dependency has been demonstrated both in animal [3] and clinical [4] studies of sepsis. As short term increases in arterial lactate and evidence of “pathologic” VO2/ DO2 dependency are regarded as evidence for underlying tissue ischemia [1, 5], it seems probable that MODS complicating sepsis reflects, in whole or in part, the summative effects of tissue injury on a hypoxic-ischemic basis. More... »

PAGES

191-206

Book

TITLE

Clinical Trials for the Treatment of Sepsis

ISBN

978-3-642-79226-7
978-3-642-79224-3

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-79224-3_12

DOI

http://dx.doi.org/10.1007/978-3-642-79224-3_12

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43 schema:description Sepsis is a clinical syndrome that arises because of an inappropriate and excessive host inflammatory response. Recent work has demonstrated that this syndrome is also characterized by the development of quantifiable injury in both the lungs and extra-pulmonary organs. This process is clinically expressed as Multiple Organ Dysfunction Syndrome (MODS). Sepsis is also a hypermetabolic state, where tissue O2 needs may be markedly increased. In this context, research has linked the widespread tissue injury typical of this syndrome with an inability to match tissue O2 delivery (D02) with these elevated tissue O2 needs. Thus, the emergence of metabolic dysregulation of tissue O2 availability in sepsis may contribute to the genesis of MODS [1]. For example, mortality in septic patients has been positively correlated with elevated arterial lactates [2] and “pathologic” VO2/DO2 dependency has been demonstrated both in animal [3] and clinical [4] studies of sepsis. As short term increases in arterial lactate and evidence of “pathologic” VO2/ DO2 dependency are regarded as evidence for underlying tissue ischemia [1, 5], it seems probable that MODS complicating sepsis reflects, in whole or in part, the summative effects of tissue injury on a hypoxic-ischemic basis.
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