A varicose ulcer is a deep lesion of the skin that results from impaired vein function, blood stasis and tissue inflammation.
Typical venous VU are located in the lower leg, preferentially in the lower calves. Ulcers may be rather extensive, but are usually not too deep. Moist granulation tissue that oozes blood upon manipulation may be visible at their base. Borders are irregular. The surrounding, not ulcered skin may show signs of chronic ischemia and dermatitis. Patients with venous VU often report mild pain that can, however, be alleviated by elevating the affected legs.
Of note, there are other types of ulcers that are sometimes deemed VU. In detail, these are arterial, neurotrophic and diabetic ulcers. They differ from venous VU in location and appearance.
While VU may be diagnosed after clinical examination, a thorough workup is necessary to identify the underlying disease and to evaluate tissue perfusion.
With regards to the former, many VU patients have already been diagnosed with heart insufficiency, diabetes mellitus or any of the afore mentioned diseases that may provoke varicose veins and ulcers. If this is not the case, laboratory analyses of blood samples and possibly imaging techniques may reveal the cause of VU.
There are different diagnostic measures to assess tissue perfusion. Doppler sonography may be applied to detect venous reflex . Sensitivity has been estimated to be > 75%. Ascending venography may provide detailed information regarding vein valve function and potential vessel occlusion.
Furthermore, contrast agents may be used to establish femoral arteriograms that display perfusion of the leg, even of distal parts if deemed necessary. Angiographic images may be obtained using X-rays, computed tomography or magnetic resonance imaging. Magnetic resonance angiography has been found particularly sensitive  .
Ulcer healing may be supported by interactive wound dressings, e.g. interactive hydrocolloid dressings. Other than conventional, passive dressings, these products release growth and migration factors and thus directly promote the healing cascade. Application of platelet-derived growth factor, epidermal growth factor or fibroblast growth factor, among others, aim at enabling the development of healthy granulation tissue and enhanced epithelial cell migration. This may be very valuable in VU patients whose healing process is delayed due to low tissue perfusion. Furthermore, in such a humid environment, formation of rigid eschar is significantly reduced. Of note, interactive hydrocolloid dressings may only be used to accelerate healing of uninfected wounds. Infected wounds require topical if not systemic antibiotic therapy. Silver sulfadiazine is often used to this end. Regular changes of wound dressings decrease the risk for infection .
Other therapeutic measures need to be adjusted to the overall condition of the patient and the disease that triggered varicose vein formation. In this context, compression dressings are usually applied to patients suffering from VU due to hypertension . Recently, it has been reported that compression hosiery yields better long-term effects than bandages . Moreover, it has been proposed to treat patients suffering from VU due to lymphedema with intermittent pneumatic compression . It has yet to be shown whether this technique may replace traditional compression methods.
Alternative therapeutic options for VU include low-intensity pulsed ultrasound and hyperbaric oxygen therapy. It could be proven that wound healing improves under ultrasonic stimulation. It has been speculated that ultrasound waves stimulate growth factor production and angiogenesis . According to current knowledge, hyperbaric oxygen therapy only improves wound healing in the short term .
Etiology of VU, overall condition of the patient and applicable treatment determine prognosis. If adequate treatment can be provided in a timely manner, prognosis for preservation of the affected leg and leg function is good. Prognosis is less favorable if the underlying disease is not curable. VU that are left untreated are likely to become infected and gangrenous. This stage of disease requires amputation.
Relapses are frequent. It has been estimated that half of all VU patients will suffer from recurrences within five years after termination of initial VU treatment.
In general, varicose veins develop due to venous insufficiency. This pathological condition, however, may result from a variety of factors and underlying diseases.
There is a genetic component that may predispose certain individuals for varicose veins. Thus, a family history of varicose veins or deep vein thrombosis augments the risk for varicose veins and subsequently VU. If no precise cause for varicose vein development can be identified, primary varicose veins are diagnosed. Moreover, genetic factors may also contribute to systemic diseases like hypercholesterolemia, hypertension, heart insufficiency and diabetes mellitus that render patients more prone to varicose veins. Furthermore, vascular and dermatological disorders, e.g., vasculitis, lupus erythematodes and scleroderma, may accelerate pathophysiological events leading to varicose veins or ulcers. Similar to blood stasis, lymphedema is associated with skin remodelling and susceptibility to injury. In isolated cases, other rare causes have been described . If any of these underlying diseases account for blood stasis or vein thrombosis, the respective patient will suffer from secondary varicose veins.
Patients that are maintained for prolonged periods of time in a lying position may also develop varicose veins and ulcers. Lack of physical activity not only facilitates formation of thrombi, venous blood flow from the legs back to the heart also depends directly on leg muscle activity. Thus, blood pools in leg veins and this condition, unfortunately, makes vein thrombosis even more likely.
Neoplasms are sometimes associated with VU.
Smoking has repeatedly been related to the individual risk for VU.
Although there are no reliable data regarding the worldwide overall incidence of VU, this is not a rare condition. Approximately 2.5% of patients admitted to long-term care facilities in the United States show VU. In Northern Europe, almost 10% of people aged 70 years and older have suffered from VU at least once in their lives. In Europe and Australia, incidence of leg ulcers in general has been estimated to be around 1% and the vast majority of leg ulcers results from functional impairment of veins .
In large parts of the Western world, obesity is a major health problem. Overweight and obesity, in turn, are associated with a series of pathological conditions that facilitate VU development . This applies to hypercholesterolemia, hypertension, heart insufficiency and diabetes mellitus, for instance. Direct intra-abdominal vein compression may further aggravate venous pressure increase in obese patients. It would therefore be expected for VU incidence to diminish if these underlying diseases could be controlled better.
VU result from venous insufficiency and varicose veins that may either develop without any identifiable cause or subsequent to underlying, mainly cardiovascular diseases. Independent of their etiology, primary and secondary varicose veins are associated with blood stasis and increased venous pressure. There are different hypotheses regarding pathophysiological events that lead from augmented venous pressure to VU.
It has been shown that dilated veins are unable to prevent fluids from leaking into the surrounding tissue. Even molecules like fibrinogen may pass the damaged vascular wall and reach subcutis and dermis. Fibrinogen may be converted to fibrin and deposit around skin capillaries. This pericapillary cuff literally isolates dependent tissues from nutrient and oxygen supply. Hypoxic injury may then lead to ulceration. Any external lesion would accelerate this process because healing is severely delayed.
Elsewhere, it has been stated that venous wall damage triggers leukocyte activation and release of reactive oxygen species and proteolytic enzymes. These may then pass into the surrounding skin layers, trigger DNA damage and degrade structure proteins. Similar to the above described scenario, internal damage may lead to ulceration and may be exacerbated by external injuries.
Prevention of varicose veins and ulcers consists in avoiding risk factors and maintaining an active lifestyle. In this line, obesity, hypercholesterolemia, hypertension, heart insufficiency and diabetes mellitus as well as other predisposing conditions should be prevented or accordingly treated. Regular exercise contributes to weight control and avoids blood stasis. Prolonged periods of siting or standing should be interrupted by small breaks of exercise.
Venous blood flow largely depends on muscle activity and gravity; venous valves impede reflux inside the veins. However, if these valves do not close correctly due to venous insufficiency, blood will tend to follow gravity and flow back to lower body regions, particularly to feet and legs. The resulting blood stasis evokes elevated pressure on venous walls and triggers remodelling processes. Varicose veins develop.
Varicose veins are superficial and visible as dilated, protruding vessels. Patients suffering from varicose veins often report that minimal skin lesions result in poorly healing, painful ulcers . These varicose ulcers (VU) most commonly affect ankles and calves and are caused by extensive tissue inflammation and reduced oxygen supply to the skin surrounding varicose veins.
Blood is pumped throughout the body by the heart and, to a lesser extent, by arteries. However, reflux to the heart is largely dependent on the pumping action of muscles surrounding veins. In order to avoid blood pooling in the lower parts of the body, particularly in feet and legs, veins possess valves that impede backflow of blood once certain sections have been covered. If these valves do not close correctly, blood will tend to follow gravity and will accumulate in feet and legs. This blood stasis is associated with an increased venous pressure and favors development of varicose veins. Here, fluids are leaking from the intravascular space into the surrounding tissue. Pressure, fluids and its constituents may trigger skin remodelling processes. The latter reduce nutrient and oxygen supply to the skin which thus becomes much more susceptible to injury. Because the skin is deprived of its essential provisions, the healing process is severely slowed down and small lesions may rapidly develop into deep skin defects. These are called varicose ulcers (VU).
While genetic components play an important role in varicose vein and subsequent ulcer development, comorbidities and lifestyle decisions may further increase the individual risk. In this context, obesity, hypercholesterolemia, hypertension, heart insufficiency and diabetes mellitus as well as vascular and dermatological disorders, smoking and a sedentary lifestyle render patients more susceptible to VU.
Due to gravity, venous varicose veins typically develop in the lower parts of the leg, especially in the lower half of the calf. Here, they become visible as superficial, protruding vessels. The skin surrounding these vessels may turn bluish. Skin injuries take a very long time to heal or do not heal at all and turn into VU. These are extended, but not very deep skin defects. If manipulated, they may start to bleed. Patients often experience mild pain and find relief in elevating their legs.
Although VU may be diagnosed by means of clinical examinations, additional diagnostic measures will usually be applied to assess the extent of perfusion disturbances and to identify the underlying disease.
In order to visualize tissue perfusion, contrast agents may be injected into veins or arteries before magnetic resonance images are taken. This procedure is called angiography. In some cases, other techniques than magnetic resonance imaging will be utilized.
Analysis of blood samples may reveal valuable information concerning the underlying disease.
Intensive wound care is the mainstay of VU therapy. Patients suffering from certain pathological conditions, e.g., hypertension and lymphedema, may benefit from calf compression. Additionally, newer techniques such as low-intensity pulsed ultrasound and hyperbaric oxygen therapy may be applied.