A new understanding of coagulopathy in trauma: potential therapeutic implications

Reade, M. C. and Holley, A. D. (2012). A new understanding of coagulopathy in trauma: potential therapeutic implications. In Jean-Louis Vincent (Ed.), Annual update in intensive care and emergency medicine 2012 (pp. 689-698) Berlin, Germany: Springer.

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Author Reade, M. C.
Holley, A. D.
Title of chapter A new understanding of coagulopathy in trauma: potential therapeutic implications
Title of book Annual update in intensive care and emergency medicine 2012
Place of Publication Berlin, Germany
Publisher Springer
Publication Year 2012
Sub-type Chapter in textbook
DOI 10.1007/978-3-642-25716-2_62
Series Annual Update in Intensive Care and Emergency Medicine
ISBN 9783642257155
3642257151
9783642257162
ISSN 2191-5709
Editor Jean-Louis Vincent
Chapter number 62
Start page 689
End page 698
Total pages 10
Total chapters 75
Collection year 2013
Language eng
Abstract/Summary Exsanguination is the second commonest cause of death in trauma after central nervous system (CNS) injury [1]. Admission coagulopathy in trauma is associated with multiple organ failure, longer intensive care unit (ICU) stay, and mortality [2]. If this association is causative, prevention, rapid identification and appropriate management of coagulopathy may improve outcome. Until recently, the pathogenesis of the coagulopathy of trauma was thought to be a ‘triad’ of loss and dilution of procoagulant clotting factors, hypothermia and acidemia [3, 4], perhaps along with disseminated intravascular coagulation (DIC) [5]. However, there is emerging evidence that tissue hypoperfusion accompanying major trauma also causes hypo- (and later, hyper-) coagulation, as do endothelial dysfunction, inflammation, and possibly platelet dysfunction. More specific focus on these factors may be useful therapeutic targets in trauma. Here, we review evidence for and against the traditional model of traumatic coagulopathy and explore what is known of the interaction between traumatic coagulopathy and hypoperfusion, inflammation, and endothelial and platelet dysfunction. We conclude by suggesting potential therapeutic avenues to exploit these relationships.
Q-Index Code BX
Q-Index Status Provisional Code
Institutional Status Non-UQ
Additional Notes Chapter included in part XVIII "Trauma"

Document type: Book Chapter
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Created: Wed, 04 Jan 2012, 17:00:07 EST by Michael Reade on behalf of School of Medicine