Objectives: To examine the role of vascular bed-specific pathways in determining the hemostatic phenotype in sepsis.
Data sources/study selection: Published research and review articles related to hemostasis and endothelial cell biology.
Data extraction and synthesis: The results of published studies have been used to generate a hypothesis of vascular bed-specific hemostasis in sepsis.
Conclusions: In sepsis, coagulation is initiated by the extrinsic pathway and is amplified through the intrinsic pathway. In addition, the body's natural anticoagulant mechanisms are significantly dampened. Together, these changes result in a net imbalance of hemostasis. The nature of this imbalance varies from one vascular bed to the next according to the local set point of the endothelium. These concepts lay an important foundation for understanding the pathophysiology of sepsis.