|Classification and external resources|
Venous ulcer on the back of the right leg.
|ICD-10||I83.0, I83.2, L97|
Venous ulcers (stasis ulcers, varicose ulcers, or ulcus cruris) are wounds that are thought to occur due to improper functioning of venous valves, usually of the legs. They are the major cause of chronic wounds, occurring in 70% to 90% of leg ulcer cases. Venous ulcers develop mostly along the medial distal leg, and can be very painful.
The exact etiology of venous ulcers is not certain, but they are thought to arise when venous valves that exist to prevent backflow of blood do not function properly, causing the pressure in veins to increase. The body needs the pressure gradient between arteries and veins in order for the heart to pump blood forward through arteries and into veins. When venous hypertension exists, arteries no longer have significantly higher pressure than veins, blood is not pumped as effectively into or out of the area,
Venous hypertension may also stretch veins and allow blood proteins to leak into the extravascular space, isolating extracellular matrix (ECM) molecules and growth factors, preventing them from helping to heal the wound. Leakage of fibrinogen from veins as well as deficiencies in fibrinolysis may also cause fibrin to build up around the vessels, preventing oxygen and nutrients from reaching cells. Venous insufficiency may also cause white blood cells (leukocytes) to accumulate in small blood vessels, releasing inflammatory factors and reactive oxygen species (ROS, free radicals) and further contributing to chronic wound formation. Buildup of white blood cells in small blood vessels may also plug the vessels, further contributing to ischemia. This blockage of blood vessels by leukocytes may be responsible for the "no reflow phenomenon," in which ischemic tissue is never fully reperfused. Allowing blood to flow back into the limb, for example by elevating it, is necessary but also contributes to reperfusion injury. Other comorbidities may also be the root cause of venous ulcers.
It is in the crus that the classic venous stasis ulcer occurs. Venous stasis results from damage to the vein valvular system in the lower extremity and in extreme cases allows the pressure in the veins to be higher than the pressure in the arteries. This pressure results in transudation of inflammatory mediators into the subcutaneous tissues of the lower extremity and subsequent breakdown of the tissue including the skin.
Wounds of the distal lower extremities arising from causes not directly related to venous insufficiency (e.g., scratch, bite, burn, or surgical incision) may ultimately fail to heal if underlying (often undiagnosed) venous disease is not properly addressed.
Edema and fibrinous exudate leads to fibrosis of subcutaneous tissues with localized pigment loss and dilation of capillary loops. This is called atrophic blanche. This can occur around ankles and gives an appearance of inverted champagne bottle to legs. Large ulcers may encircle the leg. Lymphoedema results from obliteration of superficial lymphatics. There is hypertrophy of overlying epidermis giving polypoid appearance, known as lipodermatosclerosis.
A clinical severity score has been developed to assess chronic venous ulcers. It is based on the CEAP (clinical, etiology, anatomy, and pathophysiology) classification system developed by an expert panel. A high score gives a poor prognosis.
Distinction from arterial ulcer
An arterial ulcer tends to occur on lateral side of distal leg and leg is pulseless and cool. Venous ulceration is typically seen just above the medial malleolus. Arterial ulcers are seen distally and over bony prominences.
The main aim of the treatment is to create such an environment that allows skin to grow across an ulcer.
Most venous ulcers respond to a regimen called Bisgaard regimen for treating ulcers. It has four components: Patient education, elevation of foot, elastic compression and evaluation.
Non-elastic, ambulatory, below knee (BK) compression aggressively counters the impact of reflux on venous pump failure. Compression therapy is used for venous leg ulcers and can decrease blood vessel diameter and pressure, which increases their effectiveness, preventing blood from flowing backwards. Compression is also used  to decrease release of inflammatory cytokines, lower the amount of fluid leaking from capillaries and therefore prevent swelling, and prevent clotting by decreasing activation of thrombin and increasing that of plasmin.
Compression is applied using elastic bandages or boots specifically designed for the purpose. It is not clear whether non-elastic systems are better than a multilayer elastic system. Patients should wear as much compression as is comfortable. The type of dressing applied beneath the compression does not seem to matter, and hydrocolloid is not better than simple low adherent dressings.
A meta-analysis of randomized controlled trials by the Cochrane Collaboration found that "Pentoxifylline is an effective adjunct to compression bandaging for treating venous ulcers and may be effective in the absence of compression". It works by reducing platelet aggregation and thrombus formation.
Artificial skin, made of collagen and cultured skin cells, is also used to cover venous ulcers and excrete growth factors to help them heal. A meta-analysis of randomized controlled trials by the Cochrane Collaboration concluded "Bilayer artificial skin, used in conjunction with compression bandaging, increases the chance of healing a venous ulcer compared with compression and a simple dressing".
Surgical correction of superficial venous reflux
Terminal Interruption of Reflux Source Technique entails blocking off the veins that drain the ulcer bed using Sotradecol or Polidocanol foam, administered by ultrasound guidance.
Venous ulcers are costly to treat, and there is a significant chance that they will recur after healing; one study found that up to 48% of venous ulcers had recurred by the fifth year after healing.
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