|Classification and external resources|
Venous ulcer on the back of the right leg.
|ICD-10||I83.0, I83.2, L97|
Venous ulcers (venous insufficiency ulceration, stasis ulcers, stasis dermatitis, varicose ulcers, or ulcus cruris) are wounds that are thought to occur due to improper functioning of venous valves, usually of the legs (hence leg ulcers).:846 They are the major occurrence 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.
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.
The exact cause 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, and 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.
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.
Compression stockings appear to prevent the formation of new ulcers in people with a history of the same.
The main aim of the treatment is to create such an environment that allows skin to grow across an ulcer. In the majority of cases this requires finding and treating underlying venous reflux and NICE (National Institute for Health and Care Excellence) recommends referral to a vascular service for anyone with a leg ulcer that has not healed within 2 weeks or anyone with a healed leg ulcer.
Most venous ulcers respond to patient education, elevation of foot, elastic compression and evaluation, called the Bisgaard regimen.
Non-elastic, ambulatory, below knee (BK) compression 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.
Regarding effectiveness, compression dressings improve healing. 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. Recently there have been clinical studies on a multi-functional botanical-based ointment in combination with compression therapy in the treatment of difficult-to-heal wounds, including venous leg ulcers.
Intermittent pneumatic compression devices may be used, but it is not clear that they are superior to simple compression dressings.
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 systematic review found that bilayer artificial skin with compression bandaging is useful in the healing of venous ulcers when compared to simple dressings.
Local anaesthetic endovenous surgery using the thermoablation (endovenous laser ablation or radiofrequency), perforator closure (TRLOP) and foam sclerotherapy showed an 85% success rate of healing, with no recurrence of healed ulcers at an average of 3.1 years, and a clinical improvement in 98% in a selected group of venous leg ulcers.
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. However treatment with local anaesthetic endovenous techniques suggests a reduction of this high recurrence rate is possible.
The current ‘best’ practice in the UK is to treat the underlying venous reflux once an ulcer has healed. It is questionable as to whether endovenous treatment should be offered before ulcer healing, as current evidence would not support this approach as standard care. EVRA (Early Venous Reflux Ablation) ulcer trial - A UK NIHR HTA funded randomised clinical trial to compare early versus delayed endovenous treatment of superficial venous reflux in patients with chronic venous ulceration opened for recruitment in October 2013. The study hopes to show an increase in healing rates from 60% to 75% at 24 weeks.
Research from the University of Surrey and funded by the Leg Ulcer Charity is currently looking at the effects that having a leg ulcer has on the relatives and friends of the affected person - and how this changes if the ulcer is permanently cured by endovenous surgery.
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