Lipodermatosclerosis

Abstract: Venous leg ulceration is due to sustained venous hypertension, which results from chronic venous insufficiency. In the normal venous system, pressure decreases with exercise as a result of the action of the calf muscle pump. When the muscles relax, the valves in the perforating veins connecting the superficial to the deep venous circulation prevent reflux and the pressure remains low. The venous pressure remains high, however, in a system where the valves are incompetent. View this table: Risk factors for venous ulceration Up to 10% of the population in Europe and North America has valvular incompetence, with 0.2% developing venous ulceration. Forty to fifty per cent of venous ulcers are due to superficial venous insufficiency and/or perforating vein incompetence alone with a normal deep venous system. There are many risk factors for venous ulceration. Recurrent venous ulceration occurs in up to 70% of those at risk. Many venous ulcers are painful, so appropriate pain relief and advice should be given. ### Examination Ninety five per cent of venous ulceration is in the gaiter area of the leg, characteristically around the malleoli. Ulceration may be discrete or circumferential. The ulcer bed is often covered with a fibrinous layer mixed with granulation tissue, surrounded by an irregular, gently sloping edge. Ulcers occurring above the mid-calf or on the foot are likely to have other origins. Pitting oedema is often present and may predate the ulcer. It is often worse towards the end of the day. Extravasation of erythrocytes into the skin occurs, resulting in the deposition of haemosiderin within macrophages, which stimulates melanin production, pigmenting the skin brown. In long term venous insufficiency, lipodermatosclerosis occurs. This …

Abstract: The value of fibrinolytic enhancement with an anabolic steroid (stanozolol) combined with elastic stockings in treating venous lipodermatosclerosis was assessed in a six-month double-blind cross-over trial. Thirty-four legs of 23 patients in whom other treatments had failed were studied. The patients were randomly divided into two groups who were treated with either stanozolol plus elastic stockings or placebo plus elastic stockings for three months, and then vice versa. Treatment with or without stanozolol caused the area of lipodermatosclerosis to decrease, but the rate of healing when patients took stanozolol was double that when they took the placebo, and this was assumed to be biologically important. Stanozolol also reduced the incidence of extravascular fibrin detected in skin biopsy specimens. The elastic stocking with placebo produced significant decreases in leg volume, ankle circumference, and skin thickness. Stanozolol is valuable in treating intractable lipodermatosclerosis, giving relief of pain and reducing induration, inflammation, tenderness, and pigmentation.

Abstract: The distribution of venous reflux in patients with skin changes associated with chronic venous insufficiency presenting to a specialist clinic was assessed. A total of 300 limbs in 153 patients were examined by Doppler ultrasonography with colour-flow imaging for the presence of venous reflux in superficial veins, deep veins and medial perforating veins, both above and below the knee. Ninety-eight limbs had skin changes, which included hyperpigmentation, lipodermatosclerosis, atrophie blanche and ulceration. Of this group, 2 per cent had no evidence of venous reflux on duplex scanning, 39 per cent had deep vein incompetence, 57 per cent had superficial vein incompetence and 2 per cent had isolated medial perforating vein reflux. Of 25 limbs with ulceration, 13 had superficial and 12 deep vein reflux. A total of 202 legs, which included 20 normal control limbs, had no skin changes; 22.3 per cent of these had no venous reflux, 8.4 per cent had deep vein incompetence, 65.3 per cent had superficial incompetence and 4.0 per cent had isolated medial calf perforating vein incompetence.