Stasis dermatitis

INTRODUCTION — Stasis dermatitis, or stasis eczema, is a common, inflammatory dermatosis of the lower extremities occurring in patients with chronic venous insufficiency, often in association with varicose veins, dependent chronic edema, hyperpigmentation, lipodermatosclerosis, and ulcerations (picture 1A-B). Stasis dermatitis may rarely involve the upper limbs in patients with artificial arteriovenous fistulas for hemodialysis or congenital arteriovenous malformations [1,2].

This topic will discuss the pathogenesis, clinical presentation, complications, and treatment of stasis dermatitis. The pathophysiology, clinical and diagnostic evaluation, differential diagnosis, and treatment of lower extremity chronic venous disease are discussed separately. The management of lower extremity venous ulcers is also discussed separately.

●(See "Pathophysiology of chronic venous disease".)

●(See "Clinical manifestations of lower extremity chronic venous disease".)

●(See "Diagnostic evaluation of lower extremity chronic venous disease".)

EPIDEMIOLOGY AND RISK FACTORS — Prevalence estimates of chronic venous insufficiency vary from 1 to 40 percent in females and 1 to 17 percent in males [3]. In a Turkish study, stasis dermatitis was reported in 6.2 percent of hospitalized patients over the age of 65 [4].

Established risk factors for varicose veins and chronic venous insufficiency include age, family history of venous disease, female sex, standing occupation, obesity, and history of deep vein thrombosis [3,5]. Heart failure and hypertension are aggravating factors. (See "Overview of lower extremity chronic venous disease", section on 'Epidemiology and risk factors'.)

PATHOPHYSIOLOGY — Stasis dermatitis is caused by venous hypertension, which in most cases results from dysfunction of the venous valves, obstruction to the venous flow, or failure of the calf muscle "venous pump" [6,7]. If the valves of deep or perforator veins are incompetent, the increased pressure generated during standing or calf muscle contraction causes blood to reflux into the superficial venous system, converting it into a high-pressure system. (See "Pathophysiology of chronic venous disease", section on 'Genesis and consequences of chronic venous hypertension'.)

Venous hypertension induces microcirculatory changes in the dermis, including dilated capillaries and increased permeability that lead to pericapillary fibrin cuffs and edema, leucocyte accumulation and adhesion to vascular endothelium, hemosiderin deposits, and hyperplastic venules. Ultrastructural and immunohistochemical studies of biopsies of skin affected by stasis dermatitis have shown thickening of basal lamina of capillaries; elevated numbers of macrophages, T lymphocytes, and mast cells; and upregulation of matrix metalloproteinases [6,8,9]. These findings support the hypothesis that chronic inflammation induced by venous hypertension is central in the pathogenesis of stasis dermatitis.

CLINICAL PRESENTATION — Stasis dermatitis is a late manifestation of chronic venous disease (stage C4 of the Clinical-Etiology-Anatomy-Pathophysiology [CEAP] classification (table 1)) [10] (see "Classification of lower extremity chronic venous disorders", section on 'CEAP classification'). It typically presents with erythematous, scaling, and eczematous patches or plaques on chronically edematous legs [2]. The medial ankle is most frequently and severely involved, although the skin changes may extend up to the knee and down to the foot (picture 1A-E). Pruritus is variable but, when present, results in lichenification from chronic scratching or rubbing.

Acute stasis dermatitis may present with severely inflamed, weeping plaques; vesiculation; and crusting. Impetiginized crusts and/or pustules due to bacterial or candidal superinfection may also be seen. Acute stasis dermatitis and acute flares on a background of chronic dermatitis are often misdiagnosed as cellulitis. (See 'Differential diagnosis' below.)

Hyperpigmentation due to dermal hemosiderin deposition and scaling are predominant features in chronic forms. Other signs of chronic venous insufficiency and related comorbidities are often present, including (see "Clinical manifestations of lower extremity chronic venous disease"):

●Varicose veins

●Secondary lymphedema

●Atrophie blanche (stellate, porcelain-white scarring areas resulting from microthromboses) (picture 2)

●Lipodermatosclerosis

●Ulceration

PATHOLOGY — Hyperkeratosis, parakeratosis, acanthosis, and mild spongiosis are the epidermal changes usually seen in uncomplicated stasis dermatitis. Spongiosis may be prominent in cases with a superimposed contact dermatitis. Dermal changes include proliferation of small blood vessels in the papillary dermis; variable dermal fibrosis; perivascular, lymphocytic infiltration; extravasated erythrocytes; and hemosiderin-laden macrophages [11]. A positive iron stain and the evaluation of the iron deposition pattern may be helpful to confirm the diagnosis [12].

COMPLICATIONS

Contact sensitization — Patients with stasis dermatitis and venous leg ulcers have a higher frequency of contact allergy than the general population. In a retrospective study of patients with stasis dermatitis referred for patch testing, 47 percent had a concurrent diagnosis of allergic contact dermatitis [13]. (See "Basic mechanisms and pathophysiology of allergic contact dermatitis".)

Superimposed allergic contact dermatitis may present as an acute dermatitis characterized by vesiculation, localized weeping, and the development or worsening of pruritus. It may also be relatively occult and diagnosed only with a high index of suspicion, meticulous history of exposures, and epicutaneous patch testing. (See 'Patch testing' below.)

Polysensitization is common. A multicenter study of 423 patients with leg ulcers found an average of four positive patch tests per patient [14]. The number of sensitivities increased with the disease duration.

The susceptibility to contact dermatitis in patients with stasis dermatitis and leg ulcers may be due to several factors, including [15-17]:

●Prolonged and repeated contact with topical preparations containing strong sensitizers

●Local hypervascularization

●Increased number of lymphocytes and Langerhans cells in the affected skin

●Impairment of the skin barrier function

The substances most frequently responsible for contact sensitization among patients with stasis dermatitis and/or leg ulcers are ingredients of many emollients, topical prescriptions, and over-the-counter preparations, including [13,14] (see "Common allergens in allergic contact dermatitis"):

●Fragrance mix

●Myroxylon pereirae (formerly called balsam of Peru)

●Topical antibiotics (eg, neomycin, bacitracin, and aminoglycosides)

●Antiseptics (eg, povidone-iodine, benzalkonium chloride, chlorhexidine)

●Preservatives (quaternium-15, diazolidinyl urea)

●Rubber and constituents of rubber, rubber accelerators, and latex products

●Bandages, dressings, or adhesives (eg, colophony, epoxy resin, and formaldehyde resin)

●Topical corticosteroids (a list of cross-reacting topical corticosteroids is provided (figure 1))

Autosensitization (autoeczematization) — Autosensitization (autoeczematization or "id" reaction) refers to an acute, pruritic, papulovesicular eruption that develops at cutaneous sites distant from a primary focus and is unrelated to the inciting cause of the primary inflammation [18]. Autosensitization has been reported in association with stasis dermatitis, contact dermatitis, and bacterial or fungal infections [19,20]. Typically, the autoeczematization develops one to two weeks after the primary inflammation and most frequently involves the forearms, thighs, trunk, and face [18].

The pathogenesis is not fully understood. Histologic findings are nonspecific and include spongiosis and a dermal, lymphohistiocytic infiltrate with eosinophils. Autosensitization due to stasis dermatitis may require treatment with topical and systemic corticosteroids.

Superinfection — In patients with acute stasis dermatitis, moist, exudative lesions are often extensively colonized by bacteria and fungi. The disruption of the epidermal barrier integrity by inflammation or scratching favors the secondary infection of eczematous lesions. Staphylococcus aureus and Streptococcus pyogenes are the most frequent causes of superficial (impetiginization) or deep (cellulitis and erysipelas) superinfection of stasis dermatitis [21]. (See "Impetigo" and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Lipodermatosclerosis — Lipodermatosclerosis is a chronic form of panniculitis resulting from chronic inflammation, fat degeneration, and fibrosis. In the acute phase, lipodermatosclerosis presents with a painful erythema of the medial perimalleolar region that mimics cellulitis [21]. In contrast with cellulitis, lipodermatosclerosis develops slowly (over weeks to months) and usually involves both legs. The chronic phase is characterized by hyperpigmented and indurated skin that constricts the ankle region, giving the legs an appearance of an inverted champagne bottle (picture 3). Histopathology shows septal involvement of the subcutaneous fat, fat necrosis, microcyst formation, lipomembranous changes, elastosis, and calcification of adipocytes [22,23]. (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Lipodermatosclerosis (C4b)'.)

Acroangiodermatitis — Acroangiodermatitis, also called "pseudo-Kaposi sarcoma," is a rare, reactive, vasoproliferative disorder resembling Kaposi sarcoma that occurs on the lower limbs as a result of vascular hyperplasia secondary to hypostasis and elevated venous pressure [24,25]. It presents with purpuric macules and papules that may coalesce and form large, purple-brown plaques on the extensor surfaces of the legs and dorsa of the feet (picture 4A-B).

Acroangiodermatitis can mimic and complicate stasis dermatitis. Histologically, the lesions consist of a proliferation of small, dilated dermal capillaries lined by plump endothelial cells with minimal or no atypia that are positive for CD31 and CD34 but, in contrast with true Kaposi sarcoma, negative for human herpesvirus (HHV) 8 [24]. (See "Classic Kaposi sarcoma: Epidemiology, risk factors, pathology, and molecular pathogenesis".)

DIAGNOSIS

Clinical — The diagnosis of stasis dermatitis is usually clinical, based on:

●Clinical appearance of the skin lesions (picture 1A, 1C, 1F)

●History of venous insufficiency

●Presence of other signs of chronic venous insufficiency (eg, varicose veins, pitting edema, hyperpigmentation (figure 2))

Skin biopsy — A skin biopsy is generally not necessary for the diagnosis of stasis dermatitis. However, in patients in whom the diagnosis is uncertain or who have atypical features (eg, solitary lesion, lack of ankle involvement), biopsy and histopathologic examination may confirm the diagnosis and/or exclude other skin diseases, such as allergic contact dermatitis, asteatotic eczema, or cutaneous malignancies (particularly in patients with a solitary lesion) [26]. (See 'Pathology' above.)

A skin biopsy should be made with caution or avoided in patients with concomitant peripheral arterial insufficiency, which is not uncommon. These patients have an increased risk of developing a nonhealing wound at the biopsy site due to insufficient blood supply. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)

Additional evaluation

Vascular studies — Color Doppler assessment of the blood flow in the lower limbs is helpful in evaluating venous incompetence and/or diagnosing deep venous thrombosis in patients with skin findings but without obvious manifestations of venous insufficiency. Arterial study may be necessary to evaluate arterial disease in patients with trophic changes (eg, atrophie blanche or ulcerations). (See "Clinical features and diagnosis of lower extremity peripheral artery disease" and "Diagnostic evaluation of lower extremity chronic venous disease", section on 'Venous duplex ultrasound'.)

Patch testing — Patch testing for contact sensitization may be warranted for patients who experience a worsening of symptoms despite appropriate skin care and topical therapy. Standard series of allergens should be used in addition to other series selected on the basis of exposure history and clinical suspicion (eg, corticosteroids, rubber, preservatives, excipients, antioxidants, fragrances, textiles, and topical medicines or products used by the patient). The specific standard series may vary depending upon the location of the patch testing center [27]. (See "Patch testing" and "Common allergens in allergic contact dermatitis".)

DIFFERENTIAL DIAGNOSIS — Many common and uncommon skin disorders may mimic stasis dermatitis.

●Common conditions

•Cellulitis – Lower limb cellulitis develops as a result of bacterial entry via breaches in the skin barrier. Cellulitis is typically unilateral; has an acute onset of symptoms (eg, erythema, edema, warmth); and is often accompanied by lymphangitis, pain, fever, and other systemic signs of infection (picture 5 and figure 2). Of note, cellulitis and erysipelas may be a complication of stasis dermatitis. (See 'Superinfection' above and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

•Irritant or allergic contact dermatitis (picture 6). (See "Irritant contact dermatitis in adults".)

•Asteatotic eczema (eczema craquelé) (picture 7). (See "Overview of dermatitis (eczematous dermatoses)", section on 'Asteatotic eczema'.)

•Lichen simplex chronicus (picture 8).

•Psoriasis (picture 9). (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Chronic plaque psoriasis'.)

•Dermatophyte infection (tinea corporis) (picture 10), which may also be a complication of stasis dermatitis. (See 'Superinfection' above and "Dermatophyte (tinea) infections", section on 'Tinea corporis'.)

•Actinically damaged skin (multiple actinic keratoses). (See "Actinic keratosis: Epidemiology, clinical features, and diagnosis".)

●Less common conditions

•Pigmented purpuric dermatoses – Pigmented purpuric dermatoses are a group of chronic, purpuric skin eruptions affecting the lower extremities in most cases and characterized by petechiae, red to purple macules and patches, and hyperpigmentation due to hemosiderin deposition (picture 11A-B). Pigmented purpuric dermatoses may be associated with chronic venous insufficiency [28,29]. (See "Pigmented purpuric dermatoses (capillaritis)".)

•Hypertrophic lichen planus (picture 12A-B). (See "Lichen planus", section on 'Clinical features'.)

•Necrobiosis lipoidica (picture 13A-B). (See "Necrobiosis lipoidica".)

•Pretibial myxedema (picture 14). (See "Pretibial myxedema (thyroid dermopathy) in autoimmune thyroid disease", section on 'Clinical features'.)

•Skin cancer (squamous cell carcinoma, basal cell carcinoma). (See "Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis" and "Basal cell carcinoma: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Clinical presentation'.)

MANAGEMENT — Our approach to the management of stasis dermatitis is illustrated in the algorithm (algorithm 1).

General measures

Lifestyle modifications — Patients with chronic venous disease and stasis dermatitis should undertake lifestyle changes aimed at decreasing venous hypertension, reducing edema, and preventing venous ulcers. These include exercise, frequent walks, avoiding prolonged standing, leg elevation whenever possible, and weight loss.

Skin care — Gentle skin cleansing with mild, fragrance-free liquid cleansers and frequent use of bland emollients are indicated for the symptomatic treatment of skin dryness and pruritus associated with mild or chronic stasis dermatitis. Emollients provide a film of oil to lubricate the skin, which limits dryness and itching. Petrolatum-based products are preferred to emollients containing lanolin or fragrances to reduce the risk of contact sensitization. White petroleum jelly is effective, inexpensive, and nonsensitizing. Emollients can be applied multiple times per day. Emollients are best applied when the skin is damp (ie, immediately after showering or bathing) and may be applied after wet dressings to seal in hydration.

Compression therapy — Compression therapy, either with compression bandaging systems or compression stockings, is the mainstay of conservative treatment for stasis dermatitis and the underlying chronic venous disease (algorithm 1) [30]. (See "Compression therapy for the treatment of chronic venous insufficiency".)

●Compression bandages – Compression bandages, such as multilayer compression bandages and Unna boots, are preferred to compression stockings for patients with acute stasis dermatitis. The Unna boot is a closed topical dressing consisting of a moist, zinc oxide-impregnated bandage that provides nonelastic compression and topical treatment and has drying and anti-inflammatory properties. Both types of compression bandages should be applied by trained health care personnel and changed by them once or twice a week. (See "Compression therapy for the treatment of chronic venous insufficiency", section on 'Multilayer compression bandages' and "Compression therapy for the treatment of chronic venous insufficiency", section on 'Unna boot'.)

●Compression stockings – Compression stockings are an alternative to compression bandages for patients with milder or chronic dermatitis. However, patients' adherence to the regular use of compression stockings is generally low due to multiple factors, including difficulty in donning, discomfort, overheating, itching, irritation, and financial concerns [31]. (See "Compression therapy for the treatment of chronic venous insufficiency", section on 'Compression hosiery'.)

Acute disease

Topical corticosteroids — We suggest topical corticosteroids for patients with stasis dermatitis who have erythema, pruritus, vesiculation, and oozing (algorithm 1). High- or mid-potency corticosteroids (groups 3 and 4 (table 2)) in an ointment formulation can be applied to the affected skin once or twice daily for one to two weeks. A prolonged use of high-potency corticosteroids should be avoided since they may induce skin atrophy and increase the risk of ulceration.

Corticosteroid preparations containing emulsifiers and additives should be avoided to minimize the risk of sensitization. Petrolatum-based topical corticosteroids (eg, triamcinolone ointment, fluocinolone ointment) are preferred because they do not contain any additives. Nonetheless, contact sensitization to topical corticosteroids may occur; a list of cross-reacting topical corticosteroids is provided in the figure (figure 1).

There are few low-quality studies evaluating topical corticosteroids for the treatment of stasis dermatitis [32,33]. In a small trial, patients treated with betamethasone valerate foam 0.12% or placebo twice daily for 28 days had similar improvement of edema, postinflammatory hyperpigmentation, or pruritus [32]. However, patients in the betamethasone group had greater improvement compared with baseline than those in the placebo group. It is not known whether stronger potency corticosteroids or an ointment preparation (rather than foam) would be more beneficial.

Wet dressings — For patients with exudative eczema, wet dressings may facilitate the removal of crusts and exudate and reduce pruritus. Wet dressings are applied using tap water, saline, or an appropriate anti-infective solution diluted from stock (eg, zinc and copper sulfate solution, acetic acid, potassium permanganate, or aluminum acetate [Burow solution] or subacetate).

Saturated, but not dripping, soft cotton dermatologic roll gauze or cloths are applied directly to affected areas and covered with dry cotton, which is light and air permeable. The wet dressing is left in place for two to three hours and may be applied two to three times daily or continuously in more severe cases and in motivated patients. Emollients may be applied after removal to moisturize and seal in attained hydration.

Wet dressings may be used in conjunction with topical corticosteroids. The addition of dermatologic wet dressings to topical corticosteroids may increase the penetration and absorption of the corticosteroids.

In patients with bacterial superinfection, antibacterial wet dressings may help clear secondary impetiginization and obviate the need for topical or oral antibiotic therapy.

Response assessment — In the absence of complications (eg, infection, contact sensitization), improvement is expected to occur in a few days of starting treatment. We typically re-evaluate patients at intervals of one to two weeks, depending on disease severity.

Recalcitrant disease — Patients with persisting or worsening symptoms despite appropriate initial therapy should be evaluated for concomitant allergic contact dermatitis or superimposed infection (algorithm 1). Referral to a vein specialist may be indicated for patients with unsatisfactory responses to initial therapy.

Assess and treat allergic contact dermatitis — Patients in whom stasis dermatitis does not improve or worsens after an adequate course of topical therapy should be evaluated for allergic contact dermatitis. (See 'Contact sensitization' above and 'Patch testing' above.)

For patients with confirmed concurrent allergic contact dermatitis, we suggest a short course of systemic corticosteroids (eg, prednisone 20 to 40 mg daily for five to seven days). An alternative is a single dose of intramuscular triamcinolone 40 mg.

Substitution with alternative topical and contact therapies is recommended. Strict allergen avoidance measures should be utilized when patch testing is not possible due to logistic or availability reasons.

Data on the efficacy of systemic corticosteroids for the treatment of recalcitrant stasis dermatitis are lacking. Their use is based upon indirect evidence of efficacy in severe allergic contact dermatitis and clinical experience. (See "Management of allergic contact dermatitis in adults".)

Assess and treat secondary infection — Bacterial cultures and/or mycologic studies (eg, potassium hydroxide [KOH] preparation) may be useful when bacterial or fungal superinfection is suspected. (See "Office-based dermatologic diagnostic procedures".)

●Superficial infection – We suggest topical antibiotic therapy for patients with stasis dermatitis and impetiginized lesions. Topical antibacterial ointments should be selected based upon the results of bacterial culture, if available, and risk of contact sensitization. Mupirocin is the topical antibiotic of choice for impetiginization of stasis dermatitis when Staphylococcus or Streptococcus is documented and as empirical starting treatment pending culture results or in cases in which culture is not available, as it is unlikely to cause cutaneous sensitization [34,35]. Topical erythromycin ointment is an alternative treatment when mupirocin is not tolerated [36]. (See "Impetigo", section on 'Topical therapy'.)

Bacitracin, neomycin, and aminoglycosides should be avoided, as they frequently induce contact sensitization in patients with stasis dermatitis [13]. Triclosan-based topical antimicrobial preparations are an infrequent cause of contact sensitization and may be used as an alternative to topical antibiotics. The topical use of triclosan has been restricted in the United States since December 2017 [37].

Direct chlorhexidine scrubs in the shower or diluted bleach baths (one-half cup in a bathtub half full of tepid water) are also useful to decrease the cutaneous bacterial load. Topical antibacterial wet dressings utilizing 1% glacial acetic acid solution or a white vinegar 1:8 dilution may also assist in decreasing surface bacterial content and removing crusted impetiginization [38].

●Cellulitis – For patients with clinical signs of cellulitis, such as acute worsening of erythema and edema (especially if unilateral), pain, and fever (figure 2), we suggest systemic antibiotics. Pending culture results, empiric therapy covering group B Streptococcus, methicillin-resistant Staphylococcus aureus (MRSA), and other beta-hemolytic streptococci can be initiated. The choice of oral or parenteral antibiotics is based on the presence and severity of systemic and local symptoms (algorithm 2). (See "Acute cellulitis and erysipelas in adults: Treatment".)

INDICATIONS FOR REFERRAL — Patients with stasis dermatitis that does not improve with compression therapy and optimal topical therapy (after exclusion of secondary contact dermatitis or infection) should be referred to a vascular specialist for further evaluation and treatment. Infection disease consultation is warranted for patients with atypical or severe infection.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic venous disorders".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Varicose veins and other vein disease in the legs (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Pathophysiology – Stasis dermatitis, or stasis eczema, is a common, inflammatory dermatosis of the lower legs caused by venous hypertension, which results from dysfunction of the venous valves, obstruction to the venous flow, and failure of the "venous pump." Venous hypertension induces changes in the dermis, including dilated capillaries with fibrin cuffs, deposition of hemosiderin, and accumulation of macrophages and other inflammatory cells, resulting in chronic inflammation and changes in the overlying skin. (See 'Pathophysiology' above.)

●Clinical presentation – Signs and symptoms of stasis dermatitis include edema, inflammatory and trophic skin changes, pruritus, and hyperpigmentation. Manifestations of more advanced venous disease include lipodermatosclerosis (picture 3), lymphedema, and ulceration. (See 'Clinical presentation' above.)

●Complications – Contact sensitization and secondary infection are common complications of stasis dermatitis. Contact sensitization should be suspected in patients with atypical presentations and in patients failing to respond to appropriate treatment for stasis dermatitis. (See 'Contact sensitization' above.)

●Diagnosis – The diagnosis of stasis dermatitis is based upon the clinical appearance of the skin lesions (ranging from erythema, scaling, and hyperpigmentation to edema, erosions, and crusts) (picture 1A, 1C, 1F); history of venous insufficiency; and other clinical signs of chronic venous insufficiency, including varicosities, pitting edema, and hyperpigmentation (figure 2). In patients with atypical presentations or solitary lesions, biopsy and histopathologic examination may confirm the diagnosis and/or exclude other dermatoses or skin cancer. (See 'Diagnosis' above.)

●Management (algorithm 1)

•Compression therapy – Compression therapy, either with compression bandaging systems or compression stockings, is the first-line, conservative treatment for stasis dermatitis and the underlying chronic venous disease. Compression bandages and Unna boots applied by trained health care personnel are beneficial for patients with acute, severe disease in conjunction with topical therapies. (See "Compression therapy for the treatment of chronic venous insufficiency".)

•Acute disease – For patients with stasis dermatitis who have erythema, pruritus, vesiculation, and oozing, we suggest topical corticosteroids (Grade 2C). High- or mid-potency corticosteroids (groups 3 and 4 (table 2)) in an ointment formulation may be applied once or twice daily for one to two weeks to the affected skin. Wet dressings may be used in conjunction with topical corticosteroids in patients with exudative eczema and crusting. Emollients with low sensitizing potential (eg, petroleum jelly) can be used multiple times per day to improve skin dryness and pruritus. (See 'Topical corticosteroids' above.)

•Recalcitrant disease – Patients with persisting or worsening symptoms despite appropriate initial therapy should be evaluated for concomitant allergic contact dermatitis or superimposed infection. (See 'Recalcitrant disease' above.)

-Patients with concurrent allergic contact dermatitis – For patients with confirmed concurrent allergic contact dermatitis, we suggest a short course of systemic corticosteroids (eg, prednisone 20 to 30 mg daily for five to seven days) (Grade 2C). (See 'Assess and treat allergic contact dermatitis' above.)

-Patients with secondary infection – For patients with superficial superinfection (impetiginization), we suggest topical mupirocin, as it is unlikely to cause cutaneous sensitization (Grade 2C). (See 'Assess and treat secondary infection' above and "Impetigo", section on 'Topical therapy'.)

For patients with clinical signs of cellulitis (eg, acute worsening of erythema and edema, pain, and fever (figure 2)), systemic antibiotics are administered. Pending culture results, empiric therapy should cover group B Streptococcus, methicillin-resistant Staphylococcus aureus (MRSA), and other beta-hemolytic streptococci. (See "Acute cellulitis and erysipelas in adults: Treatment".)

•Indications for referral – Referral to a vascular specialist is indicated for patients with stasis dermatitis that does not respond to appropriate dermatologic therapy and compression. Infection disease consultation is warranted for patients with atypical or severe infection. (See 'Indications for referral' above.)