What is lipodermatosclerosis?
Lipodermatosclerosis refers to a skin change of the lower legs that often occurs in patients who have venous insufficiency. It is a type of panniculitis (inflammation of subcutaneous fat). Two-thirds of affected patients are obese. Affected legs typically have the following characteristics:
- Skin induration (hardening)
- Increased pigmentation
- “Inverted champagne bottle” or “bowling pin” appearance
Lipodermatosclerosis has also been called hypodermitis sclerodermiformis and sclerosing panniculitis.
What are the symptoms of lipodermatosclerosis?
The lower inner leg of one or both legs may be involved. Lipodermatosclerosis may present as an acute or as a chronic (longstanding) condition.
Acute lipodermatosclerosis generally occurs without any preceding illness or local injury. It presents as episodes of painful inflammation in the inner leg above the ankle, resembling cellulitis. The affected area is red, tender and warm, and may be scaly. Some thickening of the skin can be felt but this is not sharply demarcated as in chronic lipodermatosclerosis.
Patients with acute lipodermatosclerosis are mainly middle-aged.
Chronic lipodermatosclerosis may follow an acute episode or develop gradually. Common findings in chronic lipodermatosclerosis include:
- Hardening of the skin
- Localised thickening
- Moderate redness
- Increased pigmentation
- Small white scarred areas (atrophie blanche)
- Increased fluid in the leg (oedema)
- Varicose veins
- Leg ulcers
Chronic lipodermatosclerosis also predisposes to venous or stasis eczema.
What is the cause of lipodermatosclerosis?
The cause of lipodermatosclerosis is not well understood. It appears to relate to venous hypertension (raised pressure in the leg veins), venous incompetence (leaky valves) and obesity.
It has been proposed that there is an acute inflammatory stage of lipodermatosclerosis, which is followed in several months or perhaps even years by a chronic stage. This is characterised by extensive fibrosis or sclerosis (scarring) in the skin and subcutaneous tissue. However not all patients with chronic lipodermatosclerosis recall an acute stage.
The acute stage of lipodermatosclerosis can occur before there are obvious signs of venous disease. Back pressure in the capillaries results in the activation of cells and soluble factors which encourage inflammation.
In contrast, two-thirds of those with late fibrotic phase have obvious venous incompetence and venous hypertension.
Subtle changes in coagulation (blood clotting) may also be a factor.
Investigations in lipodermatosclerosis
- Early lesions show an infiltrate of lymphocytes (a type of white cell) and areas of tissue death in the fibrous tissue dividing the fat (septa).
- Intermediate lesions show a mixed infiltrate of white cells and new fibrous tissue in the septa. Fibrous zones are present in the fat.
- Late lesions show marked fibrosis in the fat with diminished or absent inflammatory cells. Changes in the dermis include a mixed inflammatory cell infiltrate, increased fibrous cells, atrophy, or both, and tortuous thick-walled veins. Fibrin cuffs are present around the capllaries by direct immunofluorescence.
The histology stages correlate well with the two stages seen clinically.
Blood tests are not usually required in lipodermatosclerosis but coagulation may be tested.
Ultrasound scans and magnetic resonance imaging may be used to define the extent of the disease and to determine whether there is a role for vascular surgery.
Management of lipodermatosclerosis
The most important part of management is compression therapy to correct venous stasis. Management may also include:
- Vein surgery, endovenous laser ablation or sclerotherapy
- Weight reduction
- Ultrasound therapy
- Fibrinolytic agents such as stanozolol
- Pentoxyfylline to increase blood flow
- Clobetasol propionate (ultrapotent topical steroid) or intralesional triamcinolone injections to reduce inflammation
- Capsaicin to reduce pain