Stasis
Most venous thromboses occur in the deep veins of leg, suggesting that the erect stance of humans produces
gravitational slowing of the blood flow in the veins. The seminal work of Sevitt and Gallagher showed that many thrombi developed in the valve cusps in patients who died of pulmonary embolism after fracture of the femur.
Sevitt suggested that packets of fibrin surrounded by platelets built up in the valve cusps where blood flow was relatively static. These gradually spread across the vessel lumen by a process of encrustation until flow was reduced or cut off, at which point thrombus extended up the vessel wall as loose propagated fibrin thrombus as far as the next collateral veins. Good flow through the proximal tributaries had the potential to maintain patency above the loose thrombus preventing further propagation, while poor flow through these
veins or compromise of their orifices might lead to further propagation to the next collateral inflow and so on up the vein.
The initial “white” thrombus has a coralline (coral-like) structure consisting of layers of platelets and white cells (lines of Zahn) broken up by red cells entrapped in a fibrin mesh. The propagated “red” thrombus is much more amorphous and consists predominantly of red cells bound by fibrin providing a much less adherent “loose” thrombus, which is more easily detachable.
Propagated thrombi are usually the source of pulmonary emboli, especially when they lie free in the vein with blood flow passing on either side preventing attachment. Even if embolism occurs, the fixed head of the thrombus is usually retained and may act as a source for further propagation.
Although some authors have suggested that thrombus can form in the valve cusp without endothelial attachment, this is probably rare, and the thrombus origin is usually the result of white cell and platelet attachment to some point on the endothelium. Occlusion of an isolated vein in an animal model fails to cause thrombosis, and it may be that slowing of blood flow is merely a facilitator rather than an initiator of thrombus formation.
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