The host response to infection is a highly complex yet well-orchestrated process that involves an elaborate array of soluble mediators and cells. Normally, the host response prevails in containing and eliminating the pathogenic threat. When excessive or sustained, however, the host response may "turn on its bearer" and lead to organ dysfunction. Severe sepsis is invariably associated with activation of primary and secondary hemostasis. This article describes sepsis-associated changes in coagulation, discusses the putative role for these changes in pathogenesis of the sepsis syndrome, and outlines current diagnostic and therapeutic strategies.