Lipodermatosclerosis L94.0

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 31.10.2023

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Dermatosclerosis; indurated cellulite; sclerodermatitis sclerodermiformis; sclerosing panniculitis

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Huriez, 1955

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Lipodermatosclerosis, also known as "sclerosing hypodermitis," is a chronic, inflammatory disease characterized by subcutaneous and cutaneous fibrosis of the lower extremities. The pathophysiologic mechanisms of this disease process are ultimately not yet definitively understood. A relationship between lipodermatosclerosis and chronic venous insufficiency is likely . Disturbances of fibrinolysis are discussed. It is likely that diffusion of capillary contents, including fibrinogen and other inflammatory mediators, into the dermis and subcutis is caused by increased pressure in the venous circulation of the lower extremities. Progressive fibrosing panniculitis eventually leads to the classic appearance of lipodermatosclerosis, characterized by a lower extremity shaped like an inverted champagne bottle. This classic description is representative of advanced stage lipodermatosclerosis. The diagnosis is usually made clinically, based solely on the characteristic features.

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Lipodermatosclerosis can be categorized according to the duration of the onset of symptoms:

  • acute (<1 month)
  • subacute (1 month to 1 year) and
  • chronic (>1 year). (Bruce AJ et al 2002).

The acute phase of the disease is typically associated with loculated, tender, poorly demarcated, erythematous plaques that may be mistaken for bacterial infection; therefore, many patients are treated with antibiotics(suspected erysipelas) during the acute phase. At the onset of the disease, the initial lesions and associated focal, dull pain are generally more severe on the medial side of the leg than on the lateral side, particularly above the medial ankle.

The chronic phase of lipodermatosclerosis is characterized by well-defined, circumferential, thick, darkly pigmented, nonpainful plaques. These plaques are often described as firm, "woody" indurations. The sclerosis results in circumferential narrowing of the distal lower leg. At the same time, proximal swelling develops, resulting in the appearance of an "upturned champagne bottle."

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Lipodermatosclerosis classically occurs preferentially in women; it is also associated with immobility and high body mass index. The incidence of lipodermatosclerosis is highest in middle-aged and older patients. While most cases of lipodermatosclerosis are diagnosed in women > 40 years of age, the disease process may also begin at a much later age.

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Lipodermatosclerosis usually develops in the context of chronic venous insufficiency, which may result from loss of venous valve function, obstruction of venous flow, or decreased functionality of the calf muscle pump. Risk factors most commonly associated with the development of chronic venous insufficiency and lipodermatosclerosis include obesity, physical inactivity, age, history of deep vein thrombosis, family history of venous insufficiency (CVI), and tobacco use .

Chronic venous insufficiency (CVI) is more common in patients whose occupation involves prolonged standing. Immobilization of the ankle (e.g., after trauma) can also lead to symptoms comparable to chronic venous insufficiency (Bergan JJ et al 2006).

In a recent study, venous Doppler ultrasound and air plethysmography revealed that most patients with acute lipodermatosclerosis had underlying venous insufficiency, even if they did not have obvious symptoms of chronic congestion. These findings support the prevailing theory that lipodermatosclerosis results from chronic venous disease. Although chronic venous insufficiency appears to be the driving force for the development of lipodermatosclerosis, other factors may also play a role. An association between abnormalities of fibrinolysis and hypercoagulable states, such as protein C and protein S deficiency, and the development of lipodermatosclerosis has been suggested. The relationship has not been fully established (Falanga V et al. 1990). Individuals who use tobacco products or have a high body mass index have an increased risk of developing chronic venous insufficiency and subsequent lipodermatosclerosis. Therefore, weight loss and smoking cessation are also recommended interventions.

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Multifactorial pathogenesis of lipodermatosclerosis is likely; chronic venous insufficiency plays a crucial role in the development of the main pathological changes. Chronic venous insufficiency and venous hypertension lead to blood pooling in the venous system of the lower extremities. The subsequent increase in capillary permeability leads to continuous exudation from the veins into the adjacent tissues. Migrating leukocytes are activated, releasing inflammatory mediators and cytokines, leading to chronic inflammation. Leakage of fibrinogen with formation of perivascular fibrin cuffs disrupts oxygen exchange and leads to subtoxic tissue hypoxia. The result is an increase in collagen synthesis affecting the subcutis and cutis (Kirsner RS et al 1993). Dysregulation of angiogenesis, increased activity of metalloproteinases predispose the affected lower extremity tissue to poorly healing ulcerations (Geist RS et al. 2023). Chronic lipodermatosclerosis exhibits septal sclerosis, increased proliferation of dermal fibroblasts, and increased expression of procollagen type 1 mRNA and transforming growth factor β1 (Ortega MA et al. 2021). Advanced stages of lipodermatosclerosis are associated with decreased inflammation, decreased plasma fibrinolytic activity, low levels of proteins C and S, and alterations in matrix turnover. Thus, the development of the characteristic manifestations of lipodermatosclerosis is based on a complex interplay of underlying pathophysiological mechanisms, with phasic progression of sclerosing inflammation. Further research is needed to further elucidate the primary factors causing the pathogenesis of this disease.

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Lipodermatosclerosis typically occurs in patients with a history of CVI and is often accompanied by signs of chronic venous insufficiency, such as persistent, painful, erythematous edema, venous varices, scarring from previous lower extremity ulceration. Hyperpigmentation is also common in individuals with lipodermatosclerosis and is attributed to hemosiderin deposition. Classically, lipodermatosclerosis occurs bilaterally on the lower extremities. However, in a study of 97 patients with lipodermatosclerosis, bilateral lower extremity involvement was noted in only 45% of cases (Bruce AJ et al 2002).

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Occurring mainly on the distal thirds of the lower legs.

Clinical features
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Unilateral or bilateral redness in the area of the distal lower leg, not overheated, flat reddening and initially doughy, firm, later brown-red, hard as a board, flat (not nodular), painful indurations which change with finger pressure or spontaneously. Always detectable signs of CVI with all possible complications (up to venous leg ulcer).

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In patients with suspected lipodermatosclerosis, laboratory, radiographic, or other diagnostic tests are usually not required. In cases where the clinic and biopsy are inconclusive or the patient has findings consistent with a more critical disease state, additional testing may be warranted.

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The histologic appearance of lipodermatosclerosis varies widely depending on the stage of development of the disease process. In the acute phase, there is often septal lymphocytic infiltration of the subcutaneous adipose tissue. This results in cystic fat necrosis and capillary hemorrhage accompanied by erythropocyte extravasation and hemosiderin deposition. Characteristic histopathologic features of more advanced lipodermatosclerosis generally include lobular panniculitis with a mixed cellular infiltrate, adipocyte depletion, and lipomembranous change leading to the formation of "pseudocysts" in the subcutaneous tissue (Walsh SN et al 2010). The lipomembranous changes are defined by adipocytes with thick, eosinophilic margins .In addition, chronic lipodermatosclerosis is associated with significant septal fibrosis and hyaline sclerosis that overlap (Walsh SN et al 2010).

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Medical history. In most cases, the diagnosis of lipodermatosclerosis can be made by clinical features alone and treated empirically without additional diagnostic tests.

However, in patients who do not respond to first-line therapy or who deviate from the expected clinical course, further investigation with biopsy and histologic evaluation should be considered.

In general, biopsy should be avoided initially if possible in lower extremity panniculitis, as this anatomic region characteristically has poor wound healing ability. The highest diagnostic yield from biopsy is the peripheral margin of the lesion of interest rather than the area of central involvement.

Differential diagnosis
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The differential diagnosis of lipodermatosclerosis includes several diseases depending on the stage of the disease.

In the acute stage of lipodermatosclerosis, diseases such as erysipelas, erythema nodosum, trauma-induced fat necrosis, and other forms of panniculitis must be differentiated.

In the subacute and chronic stages of lipodermatosclerosis, the differential diagnosis includes morphea, necrobiosis lipoidica , and (rarely) nephrogenic systemic fibrosis.

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Data on the efficacy of different treatment approaches for lipodermatosclerosis come primarily from case studies, as only a limited number of larger clinical trials are available (Requena C et al. 2008). However, initial treatment options for lipodermatosclerosis usually include compression therapy in combination with elevation of the legs. These methods help to alleviate associated symptoms and disease progression. Mechanical compression therapy with compression stockings, as well as elevation of the lower extremities, is the basis for treatment of lipodermatosclerosis because it promotes venous blood flow, minimizes edema, and reduces pain .

See below chronic venous insufficiency.

In acute lipodermatosclerosis, topical corticosteroids have proven useful in relieving symptoms. Adjunctive treatments for lipodermatosclerosis include increasing physical activity and weight loss. Physical activity should be encouraged to improve calf muscle pump functionality, and weight reduction is particularly effective when obesity is present.

Systemic therapy with oral corticosteroids has been shown to be effective in chronic lipodermatosclerosis or in acute disease that does not respond to initial therapies. Interventional therapy may be an option for patients whose lipodermatosclerosis has proven refractory to systemic therapy options. Ultrasound treatment of lipodermatosclerosis is also an option.

Other adjunctive therapies, such as capsaicin cream, may relieve the chronic pain associated with lipodermatosclerosis but do not prevent disease progression. In addition, patients with lipodermatosclerosis who fail nonsurgical and systemic therapies may be referred to a vascular surgeon or interventional radiologist (Geist RS et al. 2023).

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If left untreated, lipodermatosclerosis usually takes a long and progressive course.

The symptoms of the acute phase can be treated adequately in all cases by compression bandaging.

After discontinuation of compression therapy, progression of the disease must be expected (Suehiro K et al. 2019).

The chronic stage of lipodermatosclerosis is often considered a distinct phase preceding ulceration, characterized by impaired wound healing due to the persistent inflammatory state and fibrosis. However, venous ulcers often occur concurrently with lipodermatosclerosis. Numerous studies have demonstrated a direct correlation between the extent of dermatosclerosis subsequent ulcer risk and healing potential. Even minor trauma such as scratching can lead to ulceration in individuals with severe induration.

Lower extremity pain is another potential complication of lipodermatosclerosis. The acute phase of lipodermatosclerosis is usually associated with severe, burning pain; individuals with advanced lipodermatosclerosis may experience chronic, aching pain.

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  1. Bergan JJ et al (2006) Chronic venous disease. N Engl J Med 355:488-498.
  2. Bruce AJ et al (2002) Lipodermatosclerosis: review of cases evaluated at Mayo Clinic. J Am Acad Dermatol 46:187-192.
  3. Falanga V et al (1990) Protein C and protein S plasma levels in patients with lipodermatosclerosis and venous ulceration. Arch Dermatol 126:1195-1197.
  4. Geist RS et al (2023) Lipodermatosclerosis. In: StatPearls. Treasure Island (FL): StatPearls Publishing PMID: 37603653.
  5. Greenberg AS et al (1996) Acute lipodermatosclerosis is associated with venous insufficiency. J Am Acad Dermatol 35:566-568.
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  8. Kaya Ö et al (2022) Stasis dermatitis: A skin manifestation of poor prognosis in patients with heart failure. Hippokratia 26:13-18.
  9. Kirsner RS et al (1993) The clinical spectrum of lipodermatosclerosis. J Am Acad Dermatol 28:623-627.
  10. Miteva M et al (2010) Lipodermatosclerosis. Dermatol Ther 23:375-88.
  11. Ortega MA et al (2021) Understanding Chronic Venous Disease: A Critical Overview of Its Pathophysiology and Medical Management. J Clin Med 10:3239.
  12. Requena C et al (2008) Sclerosing panniculitis. Dermatol Clin 26:501-504, vii.
  13. Suehiro K et al (2019) Compression Therapy Using Bandages Successfully Manages Acute or Subacute Lipodermatosclerosis. Ann Vasc Dis 12:77-79.
  14. Walsh SN et al (2010) Lipodermatosclerosis: a clinicopathological study of 25 cases. J Am Acad Dermatol 62:1005-1012.


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Last updated on: 31.10.2023