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09.20.03 (5 years ago)
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The classical presentation of a venous leg ulcer is an irregularly-shaped partial thickness wound with well-defined borders, surrounded by erythematous or hyperpigmented indurated skin (acute or chronic lipodermatosclerosis).
 Typical appearing venous ulcer of the gaiter area
A yellow-white exudate is commonly observed. Venous ulcers vary in size and location, but are usually found on the distal medial aspect of the lower leg ("gaiter" area). A lateral venous ulcer may be associated with short saphenous insufficiency. Varicose veins are often present in the venous ulcer patient. Typically there are telangiectatic veins of the medial ankle, so-called corona phlebectatica, indicative of chronic venous insufficiency. Edema of the ankle area is common, although in some patients the skin is brown, thickened and the ankle circumference is actually narrowed.
Other etiologies must be considered. Metabolic, neuropathic, neoplastic, vasculitic, infectious, hematologic and collagen vascular diseases should be considered. However, if arterial insufficiency is ruled out and the patient has normal pinprick sensation in the face of a typical appearing venous ulcer, then a venous etiology will be found in about 95% of cases.
The Calf Muscle Pump
The calf muscle pump of the leg is the primary mechanism the body has to return blood from the leg to the heart. The calf pump mechanism consists of the calf muscles, the deep venous compartment or pump chamber, a superficial compartment connecting the superficial veins to the deep veins via perforators, and an outflow tract (popliteal vein).
During systole (calf muscle contraction), blood in the pump chamber moves cephalad through the outflow tract. During diastole (calf muscle relaxation), blood fills the emptied pump chamber with flow from the superficial veins via perforators and from distal deep veins. Normal valvular function prevents reflux and permits one-way flow from superficial to deep and from distal to proximal.
Calf pump dysfunction may occur because of deep venous insufficiency (primary or post-thrombotic), deep venous obstruction, perforator insufficiency, superficial venous insufficiency, arteriovenous fistulas, neuromuscular dysfunction, or a combination of the above. The result of calf pump dysfunction is a failure to lower venous pressure in the distal veins of the leg; a condition referred to as ambulatory venous hypertension.
Macrocirculatory Misconceptions
As noted above, abnormalities of any of the components of the calf pump may contribute to calf pump dysfunction. Nonetheless, the main factor in calf pump failure is usually venous insufficiency. A common misconception is that a venous leg ulcer is pathognomonic of a post-thrombotic syndrome. It is true that a deep venous thrombosis may cause deep venous insufficiency and/or obstruction and lead to venous hypertension. However, it is not uncommon for venous leg ulcers to be due solely to superficial venous disease and/or perforator disease. The common final pathway to venous ulceration is venous hypertension, whether the overload comes from superficial, perforator, deep vein or combination disease.
Microcirculatory Abnormalities
It is unclear exactly how ambulatory venous hypertension causes ulceration, although recent research is shedding light on potential pathways. Chronic venous hypertension is associated with a number of microcirculatory abnormalities. These include extravasation of macromolecules (fibrinogen, albumin, a-macroglobulin and others) pericapillary fibrin cuff formation, abnormalities of fibrinolysis, leukocyte trapping and activation, lymphatic microangiopathy and abnormalities of the capillary network.
In attempting to explain the pathogenesis of venous ulceration, Browse and Burnand put forth the fibrin cuff theory. They suggest that pericapillary fibrin cuffs, typically but not exclusively found in patients with chronic venous insufficiency, act as an oxygen diffusion barrier. A number of publications have cast doubt on this premise. A more recent theory involves white cell rheology. With the reduction of capillary blood flow in venous hypertension, trains of white blood cells cause temporary plugging of capillaries. Glycoproteins cause leukocytes to become attached to capillary endothelium. These white cells become activated, releasing free radicals, proteolytic enzymes, and cytokines. Perhaps this chronic inflammatory state, if severe enough, leads to tissue damage and ulceration. Another hypothesis posits that fibrinogen and other macromolecules, which leak into the dermis as a result of venous hypertension and endothelial injury, "trap" growth factors and matrix proteins and render them unavailable for the maintenance of tissue integrity and repair processes. It is interesting to note that venous ulcer wound fluid, as distinguished from other acute wound fluid, inhibits in-vitro proliferation of cells involved in wound healing such as fibroblasts, endothelial cells, and keratinocytes. Bollinger states that the main factor in venous ulceration is focal microvascular ischemia secondary to the reduction of nutritive skin capillaries seen in chronic venous insufficiency. Obviously these theories are not mutually exclusive. As the pathogenesis of venous ulceration is elucidated, it is likely that therapeutic advances will occur.
The History and Physical
Details relating to the ulcer such as the duration and past treatment of the ulcer, the presence and characteristics of exudate, and the presence of pain and factors that aggravate and alleviate the symptoms should be sought. A history of similar lesions and their course and management is useful. In addition, a history of thromboembolic events, varicose veins, past vein treatment, tobacco abuse, history of arterial disease, diabetes, arthritis, ankle joint immobility, inflammatory bowel disease, and collagen vascular disease should be obtained. The patient's occupation and social situation should be determined.
Physical examination should include a careful inspection and palpation of the legs, from the foot to the groin, for varicose veins. The suprapubic area should also be inspected for varicosities, which might represent collateral bypass of an old ileofemoral thrombosis.
Suprapubic varices in a patient with a remote ileofemoral thrombosis
Percussion of veins helps to trace the origin and extent of varices. Examine for signs of chronic venous insufficiency such as ankle flare, eczema, hyperpigmentation, induration and atrophie blanche. Ankle and calf diameters should be recorded for both legs. The characteristics of edema (pitting vs. non-pitting) should be noted.
The ulcer(s) size, base, appearance and location, in addition to the condition of the surrounding skin, should be described. The presence and characteristics of exudate and signs of true tissue infection are noted. Note that acute lipodermatosclerosis, characterized by an erythematous tender area of induration, is commonly mistaken for cellulitis.
Acute painful lipodermatosclerosis
It is an inflammatory condition due to venous insufficiency, which does not cause fever and is unresponsive to antibiotics.
Signs of arterial insufficiency (cool skin, loss of extremity hair, shiny and atrophic skin, pallor on leg elevation) should be noted. Arterial pulses should be palpated. If there is suspicion of arterial insufficiency, an ankle brachial index (ABI; systolic pressure at the ankle divided by that at the brachial artery; normal > 0.9) should be done. Note that the ABI is unreliable in assessing arterial insufficiency in diabetes and other conditions where there may be arterial calcification. In such cases, metatarsal or toe pressures are more reliable. Ankle mobility and gait should be evaluated. Peripheral sensation should be checked.
Elucidate the Underlying Abnormal Hemodynamics
It is important to define the underlying abnormal hemodynamics of a venous ulcer patient because of the implications for treatment (see Individualize Treatment section below). In addition to a history and physical, a functional and anatomical test should be used to obtain a complete picture of the venous abnormality. Duplex ultrasound is a non-invasive approach that yields both anatomic and functional information about the venous system of the legs. Investigation of the greater saphenous vein, lesser saphenous vein, perforating veins, femoral vein, popliteal vein and deep veins of the calf should be done. Plethysmographic tests, such as photoplethysmography and air plethysmography, are functional tests that can be used to evaluate venous reflux, calf pump function and venous outflow. Utilizing tourniquets to occlude superficial veins, these plethysmographic tests can help assess the likelihood of hemodynamic improvement following treatment of superficial and perforator vein incompetence in a patient who also has deep vein disease. Invasive tests are generally not necessary.
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