An association between venous disease of the lower limb and ulceration at the ankle has been reported for more than 2000 years.
Ulcer formation is thought to be caused by venous insufficiency associated with venous hypertension and several factors may lead to venous incompetence;
- venous valve dysfunction (specially in the perforators) -
- may be due to trauma, congenital absence, venous thrombosis, or phlebitis
- retrograde blood flow due to valve dysfunction causes the vessels to distend and stretch to accommodate the additional blood flow which leads to venous hypertension
- calf muscle pump failure
- caused by paralysis, immobility, sleeping in a chair with legs dependant for long periods of time, and fixed ankle joints
- failure of the pump causes disruption of blood flow from the deep veins into the inferior vena cava leading to stasis of blood and increased venous pressure (1,2)
Three major theories have been described about ulcer development:
- fibrin cuff theory
- a pericapillary fibrin cuff is formed by the fibrinogens leaked from the dilated capillaries. This reduces oxygenated blood to the tissue
- leukocyte entrapment theory
- venous hypertension causes a reduction in blood flow within the capillaries and increases the adherence of blood cells to the endothelium. This results in release of inflammatory mediators (ICAM-1, VCAM-1) and reactive oxygen species causing obliteration of functioning capillary loops and aggravating ischemia
- microangiopathy theory
- occlusion due to microthrombi or long intracapillary stasis results in reduction of nutrition and oxygenation of the skin, predisposing to ulceration (1)
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