Coagulation in sepsis: all bugs bite equally

doi:10.1186/cc2816

Critical Care
Volume 8
Issue 2

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Commentary

Coagulation in sepsis: all bugs bite equally

Marcel Levi¹ and Tom van der Poll²

¹Professor of Medicine, Chairman, Department of Medicine, Academic Medical Center, University of Amsterdam, The Netherlands

²Professor of Medicine, Department of Internal Medicine and Laboratory of Experimental Medicine, Academic Medical Center, University of Amsterdam, The Netherlands

author email corresponding author email

Critical Care 2004, 8:99-100doi:10.1186/cc2816


Published:	10 February 2004

See related Research article: http://ccforum.com/content/8/2/R82

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.