VENOUS ULCERS

                                    VENOUS ULCERS

Venous Ulcers

Venous ulceration is the eventual result of venous hypertension. This has multiple causes, but the most common cause is venous valvular incompetence or insufficiency, which may be congenital or acquired. Failure of the venous or muscle pump or venous obstruction may also contribute to venous hypertension. The end result is transmission of elevated venous pressure from the deep to superficial system of the veins, with local effects leading to ulceration. Although it is accepted that venous hypertension plays a dominant role in the development of ulceration, there are multiple hypotheses attempting to explain the direct cause of ulceration.
The fibrin cuff theory, proposed by Browse and colleagues, has asserted that as a result of increased venous pressure, fibrinogen is leaked from capillaries. This results in the formation of pericapillary fibrin cuffs that serve as a barrier to the diffusion of oxygen and nutrients. This theory has lost favor as the sole cause, because fibrin is probably not as significant a barrier to diffusion as previously believed.
The trapping of white cells to capillary endothelium is another hypothesis. Venous hypertension results in decreased flow in the capillaries, resulting in the accumulation of white cells. These white cells may then release proteolytic enzymes, as well as interfere with tissue oxygenation.
A different trap hypothesis has been proposed. This suggests that venous hypertension causes various macromolecules to leak into the dermis and trap growth factors. These growth factors are then unavailable for repair of damaged tissue.