Lipodermatosclerosis

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Lipodermatosclerosis

Laurel M. Morton, Jennifer G. Powers and Tania J. Phillips

Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports

image

(Courtesy of Jeffrey Peterson. From Walsh, S.N., Santa Cruz, D.J., 2010. J Am Acad Dermatol 62(6), 1005–1012.)

Lipodermatosclerosis (LDS) consists of a progressive fibrotic process of the skin and subcutaneous fat induced by chronic venous insufficiency. It usually presents as an indurated fibrotic region surrounding venous ulcers above the medial malleolus on the lower leg. The diagnosis is based on clinical findings. LDS more often affects elderly women who have a high body mass index and venous insufficiency. Pain is the most consistent presenting symptom. Two stages of LDS have been described: acute and chronic. The acute form is usually painful, tender, and slightly indurated. Often, clinicians mistake the acute form for cellulitis, phlebitis, erythema nodosum, inflammatory morphea, or panniculitis. The chronic variant, which is strongly associated with venous insufficiency, is densely indurated and less painful than the acute form. In its late stages, chronic LDS alters the shape of the leg, making it look like an inverted bottle or bowling pin, with extreme fibrosis and sclerosis in the dermis and subcutaneous tissue. It may be associated with hyperpigmentation.

Management strategy

The current treatment of choice is the combination of stanozolol and compression therapy. Often patients with acute LDS find compression therapy painful: in this case stanozolol is used alone. Stanozolol is contraindicated in patients with uncontrolled hypertension and heart failure. Pentoxifylline is an alternative that stimulates fibrinolysis, but may adversely affect the gastrointestinal tract. Niacin has some fibrinolytic properties and has also been used. Other treatments, such as antibiotics, anti-inflammatory agents, antimetabolites, and long-term cimetidine, have been proposed. Intralesional triamcinolone, platelet rich plasma and topical capsaicin may be helpful. Surgical approaches include subfascial perforator endoscopic surgery (SEPS), perforator vein sclerotherapy, ultrasound therapy, and complete excision of LDS followed by split-thickness skin graft repair.

Specific investigations

First-line therapies

image Compression therapy A
image Stanozolol B
image Compression therapy plus stanozolol B
image HR (O-[betahydroxymethyl]-rutosides) B

Second-line therapies

image Pentoxifylline C
image Superficial venous surgery B

Third-line therapies

image Niacin E
image Subfascial perforator endoscopic surgery (SEPS) E
image Ultrasound D
image Excision of lipodermatosclerotic tissue D
image Antibiotics E
image Intralesional triamcinolone injections D
image Foam sclerotherapy E
image Intralesional platelet rich plasma E
image Topical capsaicin E
image Danazol E
image Oxandrolone E

[/level-membership-for-dermatology-category][not-level-membership-for-dermatology-category]

Lipodermatosclerosis

Laurel M. Morton, Jennifer G. Powers and Tania J. Phillips

Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports

image

(Courtesy of Jeffrey Peterson. From Walsh, S.N., Santa Cruz, D.J., 2010. J Am Acad Dermatol 62(6), 1005–1012.)

Lipodermatosclerosis (LDS) consists of a progressive fibrotic process of the skin and subcutaneous fat induced by chronic venous insufficiency. It usually presents as an indurated fibrotic region surrounding venous ulcers above the medial malleolus on the lower leg. The diagnosis is based on clinical findings. LDS more often affects elderly women who have a high body mass index and venous insufficiency. Pain is the most consistent presenting symptom. Two stages of LDS have been described: acute and chronic. The acute form is usually painful, tender, and slightly indurated. Often, clinicians mistake the acute form for cellulitis, phlebitis, erythema nodosum, inflammatory morphea, or panniculitis. The chronic variant, which is strongly associated with venous insufficiency, is densely indurated and less painful than the acute form. In its late stages, chronic LDS alters the shape of the leg, making it look like an inverted bottle or bowling pin, with extreme fibrosis and sclerosis in the dermis and subcutaneous tissue. It may be associated with hyperpigmentation.

Management strategy

The current treatment of choice is the combination of stanozolol and compression therapy. Often patients with acute LDS find compression therapy painful: in this case stanozolol is used alone. Stanozolol is contraindicated in patients with uncontrolled hypertension and heart failure. Pentoxifylline is an alternative that stimulates fibrinolysis, but may adversely affect the gastrointestinal tract. Niacin has some fibrinolytic properties and has also been used. Other treatments, such as antibiotics, anti-inflammatory agents, antimetabolites, and long-term cimetidine, have been proposed. Intralesional triamcinolone, platelet rich plasma and topical capsaicin may be helpful. Surgical approaches include subfascial perforator endoscopic surgery (SEPS), perforator vein sclerotherapy, ultrasound therapy, and complete excision of LDS followed by split-thickness skin graft repair.

Specific investigations

Magnetic resonance imaging as a diagnostic tool for extensive lipodermatosclerosis.

Chan CC, Yang CY, Chu CY. J Am Acad Dermatol 2008; 58: 525–7.

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