Causes

In classical terms, occlusion is acquired by abnormalities in one or added of the afterward (Virchow's triad):

The agreement of the claret (hypercoagulability or thrombophilia)

Quality of the barge bank (endothelial corpuscle injury)

Nature of the claret breeze (stasis, turbulence)

editHypercoagulability

Main article: Thrombophilia

Hypercoagulability is acquired by, for example, abiogenetic deficiencies or autoimmune disorders. Recent studies announce that neutrophils play a cardinal role in abysmal venous thrombosis, mediating abundant pro-thrombotic accomplishments 345

editEndothelial corpuscle injury

Causes of abrasion to the vessel's bank cover trauma, surgery, infection or agitated breeze at bifurcations. The capital apparatus is acknowledgment of tissue agency to the claret agglomeration system.6

editDisturbed claret flow

Further information: Claret flow

Causes of abashed claret breeze cover stagnation of claret breeze accomplished the point of injury, or venous antithesis which may action in affection failure6 or afterwards continued periods of desk behavior— for example, sitting on a continued aeroplane flight. Also, atrial fibrillation, causes brackish claret in the larboard atrium (LA) or larboard atrial addendum (LAA), and can advance to a thromboembolism.6 Cancers or malignancies such as leukemia may could could cause added accident of occlusion by e.g. alien compression on a claret barge or (more rarely) addendum into the vasculature (for example, renal corpuscle cancers extending into the renal veins).6 Also, treatments for blight (radiation, chemotherapy) generally could could cause added hypercoagulability