Acute Traumatic Coagulopathy: Initiated by Hypoperfusion: Modulated Through the Protein C Pathway?
By K. Brohi, M. Cohen, M. Ganter, Michael A. Matthay, R. Mackersie, J. Pittet. Annals of Surgery, 2007
819 citations recorded by the source corpus.
Subfields: Critical Care and Intensive Care Medicine, Epidemiology, Hematology
View Paper: https://www.semanticscholar.org/paper/171c74a3ef8f5c9d6a2f0246793c71cd2c32e17a
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In Critical Care and Intensive Care Medicine
In Epidemiology
In Hematology
Citations in the corpus
- The coagulopathy of trauma: a review of mechanisms. (2008, methodology): “A base deficit greater than six was associated with coagulopathy in a quarter of patients in one large study.(20) Contrary to historic teaching, platelet counts are generally unaffected.”
- Management of bleeding and coagulopathy following major trauma: an updated European guideline (2013, background): “cit >6 mE/l) [9,309] and is characterised by an up-regulation of endothelial thrombomodulin, which forms”
- Management of bleeding following major trauma: an updated European guideline (2010, background): “Rationale Major trauma results not only in bleeding from anatomical sites but also frequently in coagulopathy, which is associated with a several-fold increase in mortality [3,5,8,9,245].”
- Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis. (2008, methodology): “When present in excess, activated protein C is a potent inhibitor of PAI-1(4) and we have previously shown that patients in shock have low levels of PAI-1 and a direct correlation between protein C and PAI-1 levels, suggesting that protein C activation leads to PAI-1 consumption.(3) It has previousl”