This review outlines the pathophysiological mechanisms linking venous valvular stasis, hypoxia, and thrombosis within the framework of Virchow's triad.
No change to VTE prophylaxis; extends Virchow's triad framework for mechanistic trials.
This review focuses on the role of the venous valves in the genesis of thrombus formation in venous thromboembolic disease (VTE). Clinical VTE and the evidence for the valvular origin of venous thrombosis are reviewed. Virchow's triad is then used as a framework for discussion to approach the question posed regarding the link between venous valvular stasis-associated hypoxia and thrombosis. Thus, the effects of blood flow stasis, hypercoagulability of blood, and the characteristics of the vessel wall within the venous valvular sinus are assessed in turn.
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Bovill et al. (2011) studied this question.
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