Coagulation in sepsis: all bugs bite equally
- PMID: 15025767
- PMCID: PMC420035
- DOI: 10.1186/cc2816
Coagulation in sepsis: all bugs bite equally
Abstract
Sepsis almost invariably leads to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation. There is compelling evidence from clinical and experimental studies that disseminated intravascular coagulation is involved in the pathogenesis of microvascular dysfunction and contributes to organ failure. Data from the PROWESS phase III clinical trial of recombinant activated protein C in patients with severe sepsis confirm this notion and demonstrate that the vast majority of patients with severe sepsis have increased markers for systemic coagulation activation, decreased physiological anticoagulant proteins and depressed fibrinolysis. There is no correlation between the type of microorganism that has caused the infection and the presence or severity of the coagulation disorder.
Comment on
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Universal changes in biomarkers of coagulation and inflammation occur in patients with severe sepsis, regardless of causative micro-organism [ISRCTN74215569].Crit Care. 2004 Apr;8(2):R82-90. doi: 10.1186/cc2459. Epub 2004 Feb 10. Crit Care. 2004. PMID: 15025782 Free PMC article. Clinical Trial.
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