Platelet count and generation of contact factor XIIa, thrombin, and soluble fibrin were assessed.
The APTT assay is traditionally used for identifying abnormalities in the contact (factor XII, prekallikrein, and high-molecular-weight kininogen), intrinsic (factors XI, VIII, IX) and common (factors X, V and II and fibrinogen) pathways of coagulation [5].
Contact factor activation generates systemic synthesis of bradykinin, resulting in systemic hypotension and tissue hypoperfusion.
The contact factor pathway also functions to activate the fibrinolytic system, along with the proinflammatory cytokine TNF [ 46, 54].
C1-esterase inhibitor is the major regulator of the intrinsic or contact factor pathway of coagulation [ 1, 2, 131].
The intrinsic cascade (contact factor pathway) primarily serves an accessory role in amplifying the prothrombotic events that are initiated in sepsis.
Thrombin generation feeds back at the level of factor XI and, to a lesser degree factor VIII and factor V, to promote factor X conversion and thrombin generation via the contact factor system.
The aim of the present study was to investigate whether CVVH using cellulose triacetate filters causes activation of the contact factor pathway or of the tissue factor pathway of coagulation.
It is now recognized that this classical view of the coagulation activation via the contact factor system is not the primary pathway of thrombin generation and fibrin generation in most patients with sepsis.
