What is the pathogenesis of a thrombus in deep venous thrombosis (DVT)?

Updated: Jul 05, 2017
  • Author: Kaushal (Kevin) Patel, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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Answer

Thrombus usually forms behind valve cusps or at venous branch points, most of which begin in the calf. Venodilation may disrupt the endothelial cell barrier and expose the subendothelium. Platelets adhere to the subendothelial surface by means of von Willebrand factor or fibrinogen in the vessel wall. Neutrophils and platelets are activated, releasing procoagulant and inflammatory mediators. Neutrophils also adhere to the basement membrane and migrate into the subendothelium. Complexes form of the surface of platelets and increase the rate of thrombin generation and fibrin formation. Stimulated leukocytes irreversibly bind to endothelial receptors and extravasate into the vein wall by means of mural chemotaxis. Because mature thrombus composed of platelets, leukocytes and fibrin develops, and an active thrombotic and inflammatory process occurs at the inner surface of the vein, and an active inflammatory response occurs in the wall of the vein. [18, 19]


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