Stasis Dermatitis 

Updated: Jun 05, 2018
Author: Scott L Flugman, MD; Chief Editor: Dirk M Elston, MD 

Overview

Background

Stasis dermatitis is a common inflammatory skin disease that occurs on the lower extremities (see the image below). It is usually the earliest cutaneous sequela of chronic venous insufficiency with venous hypertension and may be a precursor to more problematic conditions, such as venous leg ulceration and lipodermatosclerosis.

This patient exhibits the classic hyperpigmentatio This patient exhibits the classic hyperpigmentation and varicosities of stasis dermatitis. There is inflammatory eczematous change overlying the medial ankle, with healed scarring from recent ulceration.

Accurate diagnosis is critical, as many patients admitted for the treatment of cellulitis actually have stasis dermatitis and lipodermatosclerosis.[1]

Stasis dermatitis typically affects middle-aged and elderly patients, rarely occurring before the fifth decade of life. An exception would be patients with acquired venous insufficiency due to surgery, trauma, or thrombosis.

Etiology

Stasis dermatitis is caused by venous hypertension resulting from retrograde flow related to incompetent venous valves, valve destruction, or obstruction of the venous system. The ensuing inflammatory process is mediated by metalloproteinases, which are up-regulated by ferric ion from extravasated red blood.[2]

Stasis dermatitis occurs as a direct consequence of venous insufficiency. Disturbed function of the 1-way valvular system in the deep venous plexus of the legs results in a backflow of blood from the deep venous system to the superficial venous system, with accompanying venous hypertension. This loss of valvular function can result from an age-related decrease in valve competency.[3]

Alternatively, specific events, such as deep venous thrombosis, surgery (eg, vein stripping, total knee arthroplasty, harvesting of saphenous veins for coronary bypass), or traumatic injury, can severely damage the function of the lower-extremity venous system. (See the image below.)

Patient with stasis dermatitis. The large scar on Patient with stasis dermatitis. The large scar on the calf resulted from military shrapnel. Injuries to the venous system due to trauma or surgery are common factors in the development of stasis dermatitis.

Causes of inflammation

The mechanism by which venous hypertension causes the cutaneous inflammation of stasis dermatitis has been extensively studied for decades. Several theories have been proposed.

Hypoxia/stasis theory

The earliest theories regarding the cause of cutaneous inflammation in venous insufficiency centered on oxygen perfusion of lower-extremity tissues. Originally, an incompetent venous system was thought to lead to pooling of blood in the superficial veins, with reduced flow and therefore reduced oxygen tension in the dermal capillaries. This pooling hypothesis led to the term stasis dermatitis. It was believed that the decreased oxygen content of pooled blood led to hypoxic damage to the overlying skin.

The hypoxia/stasis theory was refuted by evidence that instead of pooled, stagnant blood with low oxygen tension, leg veins in patients with venous insufficiency have increased flow rates and high oxygen tension. Arteriovenous shunting could have accounted for these findings, but no evidence of shunting in patients with venous insufficiency was found. The complete lack of evidence to support a hypoxia/stasis theory has led many investigators to advocate the abandonment of the term stasis dermatitis.

Fibrin cuffs

Subsequent research focused on the role of lower-extremity microcirculation in the pathogenesis of skin damage due to venous insufficiency. In the 1970s and 1980s, increased venous hydrostatic pressure was found to be transmitted to the dermal microcirculation. This rise in pressure leads to increased permeability of dermal capillaries.

This increased permeability enables macromolecules, such as fibrinogen, to leak out into the pericapillary tissue; then, polymerization of fibrinogen to fibrin results in the formation of a fibrin cuff around dermal capillaries. It has been hypothesized that this fibrin cuff serves as a barrier to oxygen diffusion, with resulting tissue hypoxia and cell damage.

Subsequently, the phenomenon of fibrin cuff formation was found in more severe disease, such as venous ulceration. Fibrin cuffs are not found in ulcers due to causes other than venous hypertension. Decreased cutaneous fibrinolytic activity has been proposed to contribute to the formation of fibrin cuffs.[4, 5, 6]

Formation of fibrin cuffs, coupled with decreased fibrinolysis, results in the dermal fibrosis that is the hallmark of advanced stasis dermatitis. Activated leukocytes become trapped in fibrin cuffs and the surrounding perivascular space, releasing inflammatory mediators that contribute to inflammation and fibrosis.[7] These leukocytes release transforming growth factor-beta1, an important mediator of dermal fibrosis.

Upregulation of vascular intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which are potent chemoattractants to keep leukocytes active in the perivascular environment, also occurs.[8]

The finding of leukocyte-mediated cytokine production, aided by fibrin cuff formation, provides a direct link between dysfunctional venous circulation and cutaneous inflammation with fibrosis.[9, 10]

Metalloproteinase

Herouy et al suggested that matrix metalloproteinases may be important in lesional skin remodeling in persons with stasis dermatitis.[11]

Epidemiology

Occurrence in the United States

Although not nearly as prevalent as skin cancer, dermatophytosis, or xerosis, stasis dermatitis affects a significant proportion of the elderly population. No conclusive investigations into morbidity and mortality in stasis dermatitis have been undertaken, but studies have estimated an approximately 6-7% prevalence of the condition in patients older than 50 years. This would translate into approximately 15-20 million patients older than 50 years with stasis dermatitis in the United States. This finding makes stasis dermatitis twice as prevalent as psoriasis and only slightly less prevalent than seborrheic dermatitis.[12, 13, 14]

International occurrence

In a cross-sectional population study on the prevalence of chronic venous insufficiency, carried out in 24 cities in northern, central, and southern Italy, Chiesa et al found that only 22.7% of the approximately 5900 participants (aged 18-90 years) demonstrated no visible signs of venous disease. Moreover, venous reflux, a sign of venous insufficiency, was found to some extent in about 53% of participants older than 50 years.[15]

Sex- and age-related demographics

A slight female preponderance has been reported in stasis dermatitis. This is most likely due to the fact that pregnancy results in significant stress on the lower-extremity venous system, with many women experiencing earlier and more severe derangement of lower-extremity valvular function.

The risk of developing stasis dermatitis steadily increases with each passing decade; when considering only adults older than 70 years, the prevalence of stasis dermatitis may be greater than 20%. The well-publicized aging of the population will undoubtedly result in a significant increase in cases of stasis dermatitis over the next few decades.

Prognosis

Complications of chronic stasis dermatitis include cellulitis and nonhealing venous ulcers. Direct consequences of stasis dermatitis include an increased incidence of allergic contact dermatitis, lower-extremity ulceration, lipodermatosclerosis, and id reaction (autoeczematization). (See Presentation, Treatment, and Medication.)[16, 17, 18, 19, 20, 21]

Patient Education

Patient education

Patients should be educated regarding the underlying cause of their stasis dermatitis and the permanent nature of venous valvular insufficiency.

For patient education information, see the Skin Conditions and Beauty Center, as well as Eczema (Atopic Dermatitis) and Deep Vein Thrombosis (Blood Clot in the Leg, DVT).

 

Presentation

History

Patient history may reveal the following:

  • Pruritus - Patients with stasis dermatitis typically present with an insidious onset of pruritus affecting 1 or both lower extremities

  • Discoloration - Reddish-brown skin discoloration is an early sign of stasis dermatitis and may precede the onset of symptoms

  • Ankle involvement - The medial ankle is most frequently involved, with symptoms progressing to involve the foot and/or calf

  • Edema - Stasis dermatitis patients may offer a prior history of dependent leg edema

Isoda et al reported a case of stasis dermatitis resulting from an artificial arteriovenous fistula that was created in the patient 33 years previously, during treatment for poliomyelitis.[22]

Factors that worsen peripheral edema (eg, congestive heart failure, long-standing hypertension with diastolic dysfunction) are often found in patients with stasis dermatitis. Some antihypertensive medications (such as amlodipine) may increase leg edema and trigger the onset of stasis dermatitis.[23]

Physical Examination

Physical examination in stasis dermatitis patients reveals erythematous, scaling, and eczematous patches affecting the lower extremity.

The medial ankle is most frequently and severely involved, a result of the fact that it represents a watershed area with relatively poor blood flow compared with the rest of the leg. In advanced cases of stasis dermatitis, the inflammation may encircle the ankle and extend to just below the knee; this is sometimes referred to as stocking erythroderma. The dorsal part of the foot may be involved in severe cases.

A solitary, small patch of stasis dermatitis may mimic basal cell carcinoma or squamous cell carcinoma.[24]

Secondary infection can cause typical honey-colored crusting due to bacteria or can produce monomorphous pustules due to cutaneous candidiasis.

Eczematous changes

Involved skin in stasis dermatitis may exhibit changes seen in other eczematous conditions. Severe, acute inflammation may result in exudative, weeping patches and plaques. Underlying fat necrosis (lipodermatosclerosis) may be exquisitely painful; these cases of deep, acute inflammation may be difficult to differentiate from cellulitis or erythema nodosum. In fact, stasis dermatitis is the most frequent condition for which patients are admitted unnecessarily with the misdiagnosis of cellulitis.[25, 26, 27]

Chronic disease

In long-standing lesions, lichenification and hyperpigmentation may occur as a consequence of chronic scratching and rubbing. In addition, patients with chronic stasis dermatitis can show changes, such as skin induration, that may progress to lipodermatosclerosis (with the classic inverted champagne bottle appearance).[28]

Another unique feature sometimes seen in chronic stasis dermatitis is the development of violaceous plaques and nodules on the legs and the dorsal part of the feet. These lesions frequently undergo painful ulceration and can be clinically indistinguishable from classic Kaposi sarcoma. This clinical appearance has led this entity to be called pseudo–Kaposi sarcoma or acroangiodermatitis.

Signs of venous insufficiency

Stasis dermatitis frequently occurs along with a background of skin changes that are typical for patients with venous insufficiency (and that persist regardless of the activity of stasis dermatitis). These changes include the following (see the images below):

  • Edema

  • Varicosities

  • Hyperpigmentation

  • Atrophic patches (atrophie blanche)

  • Diffuse, red-brown discoloration representing deep dermal deposits of hemosiderin (from degraded, extravasated erythrocytes)

    This patient exhibits the classic hyperpigmentatio This patient exhibits the classic hyperpigmentation and varicosities of stasis dermatitis. There is inflammatory eczematous change overlying the medial ankle, with healed scarring from recent ulceration.
    This patient with chronic stasis dermatitis exhibi This patient with chronic stasis dermatitis exhibits classic features, such as erythema, hyperpigmentation, and dilated superficial veins reflecting poor function of the deep venous system. The condition is typically confined to the lower leg, particularly the medial portion of the leg.
 

DDx

 

Workup

Approach Considerations

Blood tests are generally not helpful in the management of stasis dermatitis, except in a patient in whom cellulitis and/or sepsis are suspected. An exception is the patient with stasis dermatitis due to venous thrombosis; such patients need a thorough hematologic workup to rule out underlying hypercoagulability states.

Doppler studies

Radiologic/Doppler studies may be helpful. In patients with acute new-onset stasis dermatitis or in a young patient, investigating the dynamics of the deep venous circulation is prudent. Venous Doppler studies may reveal deep venous thrombosis or severe valve damage due to past thrombosis. Of course, the consequences of an unrecognized acute or subacute deep venous thrombosis may be catastrophic.

Histologic Findings

Skin biopsy of stasis dermatitis, although rarely indicated, shows an acute or subacute dermatitis. Acute lesions may exhibit a superficial, perivascular lymphocytic infiltrate; epidermal spongiosis; serous exudate; scale; and crust. Chronic lesions may show epidermal acanthosis with hyperkeratosis. The dermis is characterized by deep dermal aggregates of siderophages due to uptake of hemosiderin from degraded erythrocytes. Dermal capillaries are frequently dilated; long-standing lesions show intimal thickening of small arterioles and venules along with dermal fibrosis.

In chronic stasis dermatitis, biopsy may be necessary if acroangiodermatitis (pseudo–Kaposi sarcoma) has developed. The violaceous plaques and nodules of acroangiodermatitis may be clinically indistinguishable from classic Kaposi sarcoma, especially when they occur in an elderly man. Biopsy samples show changes typical of stasis dermatitis, along with a proliferation of capillaries and fibroblasts. However, the vascular slits and the atypical endothelial cells that are seen in classic Kaposi sarcoma are absent.

 

Treatment

Approach Considerations

Although extensive work has been completed in the study of venous ulcer treatment, no large, well-controlled trials have examined the treatment of stasis dermatitis. The overall mainstay of treatment has always been aimed at lessening the clinical impact of the underlying venous insufficiency and edema, a goal that is typically accomplished with high-level compression therapy.[29, 30]

Ligation

Stasis dermatitis related to an arteriovenous fistula or incompetent perforators may respond to ligation of the vessels.

Light

Combination therapy with autologous platelet-rich plasma and light-emitting diodes shows some promise in the treatment of refractory stasis ulcers.[31]

Stasis pigmentation, resulting from hemosiderin deposition, is notoriously difficult to treat and typically does not resolve even when the underlying stasis dermatitis is well controlled with topical therapy. However, some authors have reported improvement of stasis pigmentation after treatment with a noncoherent intense pulsed light (IPL) source.[32]

Compression Therapy

Assessing the patient's peripheral arterial circulation (clinically or with a Doppler study) before recommending compression therapy is important. Adding compression to a leg with compromised arterial circulation could increase claudication and put the patient at risk for ischemic damage.[33]

Compression accomplished by means of specialized stockings that deliver a controlled pressure gradient (measured in mm Hg) to the affected leg are suitable for long-term management of edema, but not for healing of stasis ulcers. Compression stockings should be applied early in the morning, before the patient rises from bed, in order to facilitate application when leg edema is at its lowest point.

High-level compression can be performed by using elastic wraps, compression (Unna) boots, and more sophisticated devices, such as end-diastolic compression boots. Most of these modalities require administration in a physician's office or wound care center. Frequent leg elevation is a necessary adjunct to leg compression.

Grafting

Allogeneic cultured dermal substitutes have been used, but are expensive. Most patients respond to high-level compression alone.[34]

Patient compliance

Counseling patients regarding the use of compression therapy is vital to the successful management of stasis dermatitis. Although the benefits of compression therapy are widely recognized, patient noncompliance with regard to compression stockings remains a major barrier to treatment. Difficulty in stocking application and patient concerns about appearance are among the reasons why patients may fail to comply with this therapy.[35]

In addition, patients frequently resist the idea of using compression dressings and/or stockings because these modalities may cause considerable discomfort when first applied to edematous, inflamed lower extremities. However, it is important to reassure patients that the discomfort lessens considerably as leg edema is reduced and to inform them that this therapy must be maintained permanently in order to prevent a recurrence of dermatitis and leg ulcers.

Topical Therapy

Topical treatment of stasis dermatitis has much in common with the treatment of other forms of acute eczematous dermatitis. Weeping lesions can be treated with wet to damp gauze dressings soaked with water or with a drying agent, such as aluminum acetate. Topical corticosteroids are frequently used to reduce inflammation and itching in acute flares; midpotency corticosteroids, such as triamcinolone 0.1% ointment, are generally effective.[36, 37]

Be wary of the use of high-potency topical corticosteroids in stasis dermatitis, because the chronically inflamed skin can increase the risk of systemic absorption and because steroid-induced cutaneous atrophy can predispose the patient to ulceration.[38, 39] Furthermore, prolonged use of topical steroids can cause their efficacy to decrease, a phenomenon known as tachyphylaxis. (Systemic corticosteroids are not part of stasis dermatitis treatment, although they may be required in very severe cases of widespread autoeczematization.)

Nonsteroidal treatment

The nonsteroidal calcineurin inhibitors tacrolimus and pimecrolimus may prove to be useful tools in the management of stasis dermatitis. Although these topical medications are approved only for atopic dermatitis, they have been shown to be effective in many steroid-responsive dermatoses. Because the calcineurin inhibitors do not carry the risks of skin atrophy or tachyphylaxis, they have the potential to become valuable agents in the treatment of chronic dermatoses such as stasis dermatitis.

A single-arm, interventional pilot study by Maroo et all indicated that combination therapy with topical tacrolimus and oral doxycycline may be effective against stasis dermatitis. The study evaluated treatment results in 15 patients with stasis dermatitis resulting from chronic venous insufficiency in the lower limbs. The patients were treated for 4 weeks with topical tacrolimus 0.1% and oral doxycycline 100 mg.[40]

The investigators found that 86.6% of the patients demonstrated improvement of the dermatitis area, while 6.7% showed no improvement, and another 6.7% experienced worsened dermatitis. Two patients showed adverse effects.

The researchers also found that patients had significant improvement in pain, edema, erythema, pigmentation, and exudation, as well as a statistically significant reduction in ulcer size.

Long-term management

Patients with chronic, quiescent stasis dermatitis can be treated with bland topical emollients to maximize epidermal moisture. Plain white petrolatum is an inexpensive occlusive moisturizer that is very effective and, importantly, does not contain any contact sensitizers.

Also see the guideline for venous ulcer care from the Association for the Advancement of Wound Care.

Systemic Therapy

Based on theories regarding the pathogenesis of cutaneous inflammation in venous insufficiency, systemic therapies that have been hypothesized to have beneficial modulating effects on neutrophil function have been investigated.

Treatments that have been studied for venous ulcers, such as prostaglandin-E1 (PGE1) and pentoxifylline therapies, have been hypothesized to decrease cytokine-mediated neutrophil activation, leading to reduced inflammation.[41] However, even if these systemic therapies are proven to be unequivocally effective, it is unlikely that their use will extend beyond the scope of treatment of recalcitrant venous ulcers.

Prevention and Management of Infection

Be wary of infection in stasis dermatitis. This becomes more problematic when using topical corticosteroids, which make the patient more susceptible to infection. Open excoriations and erosions should be treated with a topical antibiotic, such as bacitracin or Polysporin. Obvious superficial impetiginization should be treated with topical mupirocin or a systemic antibiotic with activity against Staphylococcus and Streptococcus species (eg, dicloxacillin, cephalexin, cefadroxil, levofloxacin).

Culture with sensitivity testing is important when managing suspected superinfection, because community-acquired methicillin resistance is becoming increasingly prevalent. Expanded coverage may be necessary in patients who are immunocompromised.

Suspected deep cellulitis should always be treated with oral or intravenous antibiotics. Necrotizing fasciitis would be a rare complication but is a surgical emergency.

Treatment-Related Allergic Contact Dermatitis

The development of contact dermatitis is especially problematic in the treatment of patients with stasis dermatitis. Chronic inflammation of the skin, coupled with the use of multiple topical medications (prescription and over-the-counter), frequently results in contact sensitization as a complication of stasis dermatitis. In addition, patients may become sensitized to rubber products found in some wraps and stockings.

Some of the most frequent contact allergens complicating stasis dermatitis include the topical antibiotics neomycin and bacitracin. Patients should be instructed against applying over-the-counter antibiotics or other topical agents without the direction of a physician.

Products based on the antimicrobial agent triclosan have been shown to present a low risk for contact sensitization in patients with stasis dermatitis. These products may be a good alternative to decrease bacterial colonization, especially in patients who have a history of cellulitis or other cutaneous infections.[42]

Topical corticosteroid allergy, while uncommon, is a condition that can worsen stasis dermatitis despite seemingly appropriate prescription therapy.

Consider contact dermatitis in any patient with stasis dermatitis who becomes clinically worse despite appropriate topical treatment.

Follow-up

Stasis dermatitis is a chronic condition. Acute exacerbations of this disorder should be closely monitored with weekly office visits, with careful observation for signs of infection. However, patients with long-standing stasis dermatitis may be able to manage the disease on their own with the use of compression stockings, elevation, proper skin care, and short courses of topical steroids for inflammatory exacerbations. The clinician must be vigilant in treating any signs of cutaneous ulceration with close follow-up care to ensure that ulceration does not become a chronic problem.

Consultations

Uncomplicated stasis dermatitis is usually managed in the dermatologist's office. However, a consultation with a vascular surgeon may be required, especially when an underlying surgically correctable vascular abnormality is suspected.

A consultation with a hematologist may be needed when treating a patient with stasis dermatitis due to deep venous thrombosis; cases such as these may be secondary to congenital or acquired hypercoagulable states.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications. Midpotency corticosteroids, such as triamcinolone 0.1% ointment, are generally effective in reducing the inflammation and itching of acute flares of stasis dermatitis.[36, 37] However, the clinician should be wary of using high-potency topical corticosteroids in stasis dermatitis; the chronically inflamed skin can increase the risk of systemic absorption and steroid-induced cutaneous atrophy can predispose the patient to ulceration.[38, 39]

Infection is a particular concern in stasis dermatitis, since topical corticosteroids make the patient more susceptible to infection. Open excoriations and erosions should be treated with a topical antibiotic.

Corticosteroids

Class Summary

These agents elicit anti-inflammatory and immunosuppressive properties.

Triamcinolone topical (Oralone, Triderm, Zytopic, Kenalog)

Triamcinolone topical is a moderate-potency steroid with anti-inflammatory properties. It treats inflammatory dermatosis that is responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Antibiotics, Other

Class Summary

These are used to treat open excoriations and erosions. Obvious superficial impetiginization should be treated with topical mupirocin or a systemic antibiotic with activity against Staphylococcus and Streptococcus species (eg, dicloxacillin, cephalexin, cefadroxil, levofloxacin).

Bacitracin (Baci-IM, Baciguent)

Bacitracin prevents the transfer of mucopeptides into the growing cell wall, which causes inhibition of bacterial cell wall synthesis.

Bacitracin and polymyxin B (Polysporin, Polycin, AK-Poly-Bac)

Bacitracin prevents transfer of mucopeptides into the growing cell wall, which causes inhibition of bacterial cell wall synthesis. Polymyxin B damages the bacterial cytoplasmic membrane and alters permeability, causing intracellular constituents to leak. This agent is used to treat open excoriations and erosions.

Mupirocin (Bactroban, Centany)

Mupirocin inhibits bacterial protein synthesis by binding to isoleucyl transfer-RNA synthetase.

Dicloxacillin

Dicloxacillin is used in the treatment of infections caused by penicillinase-producing staphylococci. It may be used as initial therapy when staphylococcal infection is suspected.

Cephalexin (Keflex)

Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. It has primary activity against skin flora and is used for skin infections or prophylaxis in minor procedures.

Levofloxacin (Levaquin)

Levofloxacin inhibits DNA gyrase and topoisomerase IV, resulting in bactericidal activity. It is used as an alternative agent for MRSA infection.

Cefadroxil

Cefadroxil is a first-generation semisynthetic cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms, including S aureus, S pneumoniae, S pyogenes, Moraxella catarrhalis, E coli, Klebsiella species, and Proteus mirabilis.

Topical Immunomodulators

Class Summary

These agents modify immune processes that promote inflammation.

Pimecrolimus (Elidel cream)

Pimecrolimus is indicated for eczema and atopic dermatitis. It was the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Pimecrolimus is derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus.

This agent selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release.

Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids.

Tacrolimus ointment (Protopic) 0.1% or 0.03%

Tacrolimus reduces itching and inflammation by suppressing release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin (IL)–3, IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha (TNF-alpha), all of which are involved in the early stages of T-cell activation.

Additionally, tacrolimus may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of the high-affinity IgE receptor (FCeRI) on Langerhans cells.

Tacrolimus can be used in patients as young as 2 years. It is more expensive than topical corticosteroids. This agent is available as ointment in concentrations of 0.03% and 0.1%.

 

Questions & Answers

Overview

What is stasis dermatitis?

Which condition can be confused with stasis dermatitis?

Which group is at highest risk for stasis dermatitis?

What is the role of venous insufficiency in the pathogenesis of stasis dermatitis?

What is the role of venous hypertension in the pathogenesis of stasis dermatitis?

What is the hypoxia/stasis theory for the pathogenesis of stasis dermatitis?

What is the role of lower-extremity microcirculation in the pathogenesis of stasis dermatitis?

What is the role of fibrin cuffs in the pathogenesis of stasis dermatitis?

What is the role of adhesion molecules in the pathogenesis of stasis dermatitis?

What is the role of cytokines in the pathogenesis of stasis dermatitis?

What is the role of metalloproteinases in the pathogenesis of stasis dermatitis?

What is the prevalence of stasis dermatitis in the US?

What is the global prevalence of stasis dermatitis?

How does the prevalence of stasis dermatitis vary by sex?

How does the prevalence of stasis dermatitis vary by age?

What are the complications of stasis dermatitis?

What information about stasis dermatitis should patients receive?

Presentation

What medical history suggests stasis dermatitis?

Which physical findings suggest stasis dermatitis?

Which are of the body is most frequently and severely involved in stasis dermatitis?

Which conditions have a similar presentation to stasis dermatitis?

What may result from secondary infection of stasis dermatitis?

Which eczematous conditions should be included in the differential diagnoses of stasis dermatitis?

How are the lesions of chronic stasis dermatitis characterized?

What are dermatologic signs of stasis dermatitis?

DDX

What are the differential diagnoses for Stasis Dermatitis?

Workup

What is the role of lab testing in the diagnosis of stasis dermatitis?

What is the role of imaging studies in the diagnosis of stasis dermatitis?

Which histologic findings are characteristic of acute stasis dermatitis?

Which histologic findings are characteristic of chronic stasis dermatitis?

Treatment

What is the goal of treatment for stasis dermatitis?

How is ligation used in the treatment of stasis dermatitis?

How is light used in the treatment of stasis dermatitis?

What must be assessed prior to initiation of compression therapy for stasis dermatitis?

How is compression therapy performed in the treatment of stasis dermatitis?

What is the role of allogeneic cultured dermal substitutes in the treatment of stasis dermatitis?

Which factors contribute to patient compliance with compression therapy for stasis dermatitis?

What is the role of topical treatments for the management of stasis dermatitis?

What are risks of topical treatments for the management of stasis dermatitis?

What is the role of nonsteroidal calcineurin inhibitors in the treatment of stasis dermatitis?

Which combination therapies are effective in the treatment of stasis dermatitis?

What are the options for long-term management of stasis dermatitis?

Which systemic therapies are used in the treatment of stasis dermatitis?

How are secondary infections prevented during the treatment of stasis dermatitis?

What is the role of culture with sensitivity testing in the management of stasis dermatitis?

How are complications of stasis dermatitis treated?

What causes contact dermatitis secondary to stasis dermatitis?

What are the most frequent contact allergens that complicate stasis dermatitis?

Which agents have a low risk of contact sensitization during the treatment of stasis dermatitis?

What is topical corticosteroid allergy during the treatment of stasis dermatitis?

When should contact dermatitis be considered in patients with stasis dermatitis?

What monitoring is required following the treatment of stasis dermatitis?

Which specialist consultations are needed for the management of stasis dermatitis?

Medications

What medications are used in the treatment of stasis dermatitis?

Which medications in the drug class Topical Immunomodulators are used in the treatment of Stasis Dermatitis?

Which medications in the drug class Antibiotics, Other are used in the treatment of Stasis Dermatitis?

Which medications in the drug class Corticosteroids are used in the treatment of Stasis Dermatitis?