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 (AV) fistulas for hemodialysis, or congenital AV 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.
●(See "Overview of lower extremity chronic venous disease".)
●(See "Clinical manifestations of lower extremity chronic venous disease".)
●(See "Approach to the differential diagnosis of leg ulcers".)
●(See "Pathophysiology of chronic venous disease".)
●(See "Diagnostic evaluation of lower extremity chronic venous insufficiency".)
●(See "Post-thrombotic (postphlebitic) syndrome".)
●(See "Medical management of lower extremity chronic venous disease".)
EPIDEMIOLOGY — Skin changes related to chronic venous insufficiency, including edema, hyperpigmentation, eczema, fibrosis, atrophy, and ulceration, are reported in 1 to 20 percent of women and in 1 to 17 percent of men [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.
The epidemiology of chronic venous insufficiency is discussed separately. (See "Overview of lower extremity chronic venous disease", section on 'Epidemiology and risk factors'.)
PATHOPHYSIOLOGY — Stasis dermatitis is caused by venous hypertension, which represents the final common pathway that leads to chronic venous disease [6]. In most cases, venous hypertension results from dysfunction of the venous valves, obstruction to the venous flow, or failure of the "venous pump" [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 changes in the dermis, including dilated capillaries with fibrin cuffs, leucocyte accumulation, 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 [7-9]. 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 Etiological Anatomical Pathological [CEAP] classification (table 1)) [10]. (See "Classification of lower extremity chronic venous disorders", section on 'CEAP classification'.)
Stasis dermatitis 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-D). Pruritus is variable but, when present, results in lichenification from chronic scratching or rubbing:
●Acute forms 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.
●Chronic forms are characterized by hyperpigmentation, due to dermal hemosiderin deposition, scaling, and potential development of lipodermatosclerosis.
Patients with stasis dermatitis may present with other signs of chronic venous insufficiency and related comorbidities, including (see "Clinical manifestations of lower extremity chronic venous disease"):
●Varicosities
●Secondary lymphedema
●Atrophie blanche (stellate, porcelain-white scarring areas resulting from microthromboses) (picture 2)
●Secondary cellulitis
●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].
Septal involvement of the subcutaneous fat, fat necrosis, microcyst formation, lipomembranous changes, elastosis, and calcification of adipocytes are typical features of lipodermatosclerosis [13,14].
COMPLICATIONS
Contact sensitization — Patients with stasis dermatitis and venous leg ulcers have a higher frequency of contact allergy than the general population. In case series, the prevalence of contact sensitization ranged from 17 to 82 percent [15-23]. (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 [15]. 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 [24-26]:
●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 and topical prescriptions or over-the-counter preparations, including [15-17,23,27-30] (see "Common allergens in allergic contact dermatitis"):
●Myroxylon pereirae (formerly called balsam of Peru) and fragrances.
●Lanolin (wool alcohol).
●Rubber and constituents of rubber, rubber accelerators, and latex products.
●Bandages, dressings, or adhesives (eg, colophony, epoxy resin, and formaldehyde resin). Modern hydrocolloid dressings are generally well tolerated. However, reactions to hydrocolloid gels have been reported and may be due to pentaerythritol ester of hydrogenated rosin, a tackifying agent that commonly cross-reacts with colophony [28,31].
●Topical antibiotics (eg, neomycin, bacitracin, and aminoglycosides) and antiseptics (eg, povidone-iodine, benzalkonium chloride, chlorhexidine, and clioquinol).
●Topical corticosteroids. A list of cross-reacting topical corticosteroids is provided in a figure (figure 1).
●Paraben preservatives.
Autosensitization — 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 [32]. Autosensitization has been reported in association with stasis dermatitis, contact dermatitis, and bacterial or fungal infections [33,34]. Typically, the autoeczematization develops one to two weeks after the primary inflammation and most frequently involves the forearms, thighs, trunk, and face [32].
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 cause of superficial (impetiginization) or deep (cellulitis and erysipelas) superinfection of stasis dermatitis [35]. (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 [35]. However, 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). (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 occurring on the lower limbs as a result of vascular hyperplasia secondary to hypostasis and elevated venous pressure [36,37]. 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 [36]. (See "Classic Kaposi sarcoma: Epidemiology, risk factors, pathology, and molecular pathogenesis".)
DIAGNOSIS
Clinical — The diagnosis of stasis dermatitis is usually clinical, based upon the clinical appearance of the skin lesions, ranging from erythema, scaling, and hyperpigmentation to edema, erosions, and crusts (picture 1A, 1C, 1E); history of venous insufficiency; and other clinical signs of chronic venous insufficiency, including varicosities, pitting edema, and hyperpigmentation (figure 2).
Skin biopsy — In patients in whom the diagnosis of stasis dermatitis is uncertain or who have atypical features (eg, solitary lesion or 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) [38]. (See 'Pathology' above.).
However, 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 the 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 — Laboratory tests are not usually necessary for the diagnosis of stasis dermatitis. However, laboratory evaluation may be indicated in the assessment of chronic venous insufficiency, particularly prior to intervention (eg, vein ablation procedure) [39].
Bacterial cultures and/or mycologic studies (eg, potassium hydroxide [KOH] preparation) are useful when bacterial or fungal superinfection or primary tinea corporis are suspected. (See "Office-based dermatologic diagnostic procedures".)
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. Substitution using different topical and contact therapies or the strictest allergen avoidance measures possible may be utilized when patch testing is not possible due to logistic or availability reasons
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, preservative, excipients, antioxidants, fragrance, textiles, and topical medicines or products used by the patient). (See "Patch testing" and "Common allergens in allergic contact dermatitis".)
The specific standard series may vary depending upon the location of the patch testing center [40]. Descriptions of the test substances included in the most common standard series are available through DermNet NZ.
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 insufficiency".)
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). 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).
•Asteatotic eczema (eczema craquelé) (picture 7).
•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 "Epidemiology, natural history, and diagnosis of actinic keratosis".)
●Less common conditions:
•Hypertrophic lichen planus (picture 11A-B) (see "Lichen planus", section on 'Clinical features')
•Necrobiosis lipoidica (picture 12A-B) (see "Necrobiosis lipoidica")
•Pretibial myxedema (picture 13) (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 "Epidemiology, pathogenesis, clinical features, and diagnosis of basal cell carcinoma", section on 'Clinical presentation')
MANAGEMENT — The management of the patient with stasis eczema involves the treatment of the underlying chronic venous insufficiency; symptomatic treatment of skin dryness, pruritus, and inflammation; prevention of ulceration; and patient education.
Patient education — Patient education on a standardized basis at a level comprehensible to them is critical for the success of implemented treatment and prevention measures, improved outcomes, and decreased need for repeat clinician visits or recurrent hospitalization. One study demonstrated that the use of a standardized approach to hospitalized patients and regular application of expectation management and medical information modules resulted in fewer clinician referrals, a decrease in readmission to hospital rates, and improved outcomes [41].
Treatment of underlying chronic venous insufficiency — Treatment of the underlying venous hypertension is the mainstay of treatment of stasis dermatitis. It may involve:
●General measures to reduce edema and venous hypertension (eg, leg elevation, daily walking, exercise, weight reduction) (see "Medical management of lower extremity chronic venous disease", section on 'General measures')
●Continuous compression therapy (see "Medical management of lower extremity chronic venous disease", section on 'Compression therapy' and "Compression therapy for the treatment of chronic venous insufficiency" and "Compression therapy for the treatment of chronic venous insufficiency", section on 'Static compression therapy')
●Systemic therapy, including venoactive or phlebotonic drugs (eg, hydroxyethylrutoside, escin [horse chestnut extract], calcium dobesilate), flavonoids (eg, diosmin and hesperidin, diosmiplex), or pentoxifylline [42-44] (see "Medical management of lower extremity chronic venous disease", section on 'Pharmacologic therapy')
●Ablation therapy (see "Techniques for endovenous laser ablation for the treatment of lower extremity chronic venous disease" and "Techniques for radiofrequency ablation for the treatment of lower extremity chronic venous disease" and "Open surgical techniques for lower extremity vein ablation")
Skin care — Gentle skin cleansing and frequent use of bland emollients are indicated for the symptomatic treatment of skin dryness and pruritus associated with stasis dermatitis. Patients should gently wash their legs daily using mild nonsoap (synthetic) liquid cleansers to remove scale, bacteria, and crusts. Products without common preservative allergens or fragrance are less irritating and less likely to induce contact sensitization.
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.
Patients with acute stasis dermatitis
Topical corticosteroids — We suggest topical corticosteroids for patients with stasis dermatitis who have erythema, pruritus, vesiculation, and oozing. 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 a figure (figure 1).
There are few low-quality studies evaluating topical corticosteroids for the treatment of stasis dermatitis [30,45]. 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 [30]. However, patients in the betamethasone group had greater improvement compared with baseline than those in the placebo group. Whether stronger potency corticosteroids or an ointment preparation rather than foam would be more beneficial is not known.
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's 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 that 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 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.
Compression bandages — Compression bandages, such as multilayer compression bandages and Unna boots, are beneficial 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 that has drying and anti-inflammatory properties. Both types of compression bandages should be applied by trained personnel and changed by them once or twice a week. (See "Compression therapy for the treatment of chronic venous insufficiency", section on 'Compression bandages'.)
Patients with recalcitrant stasis dermatitis — Patients in whom topical corticosteroids do not adequately relieve symptoms of inflammation or who experience a worsening of symptoms despite appropriate skin care and topical therapy may have a secondary allergic contact dermatitis and/or autosensitization (see 'Complications' above). For these patients, a short course of systemic corticosteroids (eg, prednisone 20 to 30 mg daily for five to seven days) may be indicated. An alternative is a single dose of intramuscular triamcinolone (40 mg).
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".)
Treatment of superinfection
Impetiginized lesions — 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 [46,47]. Topical erythromycin ointment is an alternative treatment when mupirocin is not tolerated [48]. (See "Impetigo", section on 'Topical therapy'.)
Contact sensitivity to bacitracin, neomycin, and aminoglycosides is frequently seen in patch-tested patients with stasis dermatitis or contact dermatitis, and these agents should be avoided. 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 [49]. Direct chlorhexidine scrubs in the shower or dilute 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 [50].
Secondary cellulitis — For patients with more extensive infection and signs of cellulitis or other soft tissue infection, we suggest systemic antibiotics. Pending culture results, empiric therapy options for group B Streptococcus, methicillin-resistant Staphylococcus aureus (MRSA), and other beta-hemolytic streptococci include oral clindamycin, trimethoprim-sulfamethoxazole, tetracyclines, and linezolid (table 3). (See "Acute cellulitis and erysipelas in adults: Treatment".)
Treatment of lipodermatosclerosis — Compression therapy is widely accepted as first-line treatment for patients with chronic dermatosclerosis [51]. Compression therapy and pharmacologic therapy for patients with lipodermatosclerosis are discussed in detail separately. (See "Medical management of lower extremity chronic venous disease".)
Prevention of venous ulcers — Patients with stasis dermatitis should be educated about the importance of lifestyle changes and specific interventions to prevent venous ulcers, including [52]:
●Minimize prolonged standing, elevating legs
●Using compression hosiery
●Undertaking a program of regular physical activity
●Losing weight
●Avoiding local trauma
●Seeking early medical intervention if skin damage is noticed
Treatment of ulcers — The management of ulcers in patients with stasis dermatitis is discussed separately. (See "Medical management of lower extremity chronic venous disease", section on 'Ulcer care'.)
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 5th to 6th 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 10th to 12th 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 is a common complication 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. The most common contact allergens include balsam of Peru, fragrances, lanolin, and topical antibiotics and antiseptics. (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, 1E); 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:
•Treatment of venous insufficiency – Treatment of the underlying venous insufficiency is the mainstay of therapy for stasis dermatitis. Treatment of venous insufficiency is discussed separately. (See "Overview of lower extremity chronic venous disease", section on 'Summary and recommendations' and "Approach to treating symptomatic superficial venous insufficiency", section on 'Summary and recommendations'.)
•Skin care measures – Gentle skin cleansing and emollients are the initial treatment for skin dryness and pruritus in patients with stasis dermatitis. Petrolatum-based emollients are preferred to preparations containing lanolin or fragrances to avoid contact sensitization. (See 'Skin care' above.)
•Acute stasis dermatitis – For patients with acute 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. (See 'Patients with acute stasis dermatitis' above.)
•Recalcitrant disease – For patients in whom topical corticosteroids do not adequately relieve symptoms of inflammation or who have secondary allergic contact dermatitis, a short course of systemic corticosteroids (eg, prednisone 20 to 30 mg daily for five to seven days) may be indicated. (See 'Patients with recalcitrant stasis dermatitis' above.)
