STASIS DERMATITIS

 

Salient features

 

·       Often associated with other signs of venous hypertension

 

·       Can be complicated by allergic contact dermatitis

 

·       One of the most common causes of disseminated eczema (auto sensitization dermatitis)

 

Introduction

 

Stasis dermatitis is a common component of the clinical spectrum of chronic venous insufficiency of the lower extremities. It may arise as an early sign of chronic venous insufficiency, but can persist or recur throughout all stages and is often most prominent when ulcers are present. There is little doubt that chronic venous hypertension per se is the initial trigger for stasis dermatitis. Over time, additional etiological factors may act in concert, most importantly contact sensitization to ingredients of topical therapies. Stasis dermatitis is one of the most common causes of secondary dissemination of dermatitis, and is therefore a complex and multifactorial condition.

 

Epidemiology

 

Age

 

Venous eczema patients are usually middle‐aged or elderly.

 

Sex

 

There is an increased incidence in females, which may be due to hormonal effects and the tendency for deep‐vein thrombosis (DVT) to occur during pregnancy.

 

 

Pathophysiology

Schematic diagram showing the normal resorption of pericapillary fluid in response to pre capillary and post capillary pressure and interstitial pressure

 

Flowchart showing etiology of cutaneous manifestations of venous hypertension

Venous hypertension of the lower limbs is linked to the upright position and is caused by multiple factors, most importantly valvular incompetence of the deep leg veins. High ambulatory venous pressure within the calf muscle pump is transmitted to the capillary circulation in the skin and subcutaneous tissues of the calf. This distends the local capillary bed and widens the endothelial pores, thus allowing the passage of fluid and plasma proteins into the tissue (edema) and extravasation of erythrocytes (stasis “purpura” and hemosiderin deposition). These processes lead to microangiopathy, with serious consequences. As fibrinogen molecules escape into the interstitial fluid, they form a fibrin sheath around the capillaries. This layer of fibrin presumably forms a pericapillary barrier to the diffusion of oxygen and v other nutrients that are essential for the normal vitality of the skin.

 

PATHOGENETIC FACTORS IN STASIS DERMATITIS
Factor	Consequence
Chronic venous insufficiency and the microvasculature
Deposition of proteins, particularly fibrin, around vessels as hyaline cuffs	·       Deposits inhibit oxygen diffusion and metabolic exchange in combination with interstitial edema
Slow blood flow	·       Upregulation of ICAM-1 and VCAM-1 on endothelia   ·       Activation of neutrophils and macrophages   ·       Expression of L-selectin on neutrophils   ·       Neutrophils attracted into and trapped within affected areas, notably the medial supramalleolar region
Release of inflammatory mediators, free radicals, and proteases by neutrophils	·       Pericapillary inflammation
Free iron ions released from hemosiderin deposits	·       Increase in free radical production and lipid peroxidation   ·       Activation of matrix metalloproteinases
Platelet accumulation within the microvasculature	·       May trigger focal thrombosis
Fibrosis and tissue remodeling due to imbalances within the capillary network	·       Lipodermatosclerosis – dermal sclerosis and septal sclerosis that present as sclerosing panniculitis   ·       Lymphatic dysfunction   ·       “Atrophie blanche” – stellate sclerotic areas depleted of capillaries with the formation of peripheral giant capillaries   ·       May lead to the formation of venous ulcers
Elevated plasma levels of homocysteine	·       Hyperhomocysteinemia is associated with an increased risk of thromboses
Complicating factors
Allergic contact dermatitis	·       Sensitizers are often in topical agents used to combat pruritus, xerosis, and presumed infection   1.   Antibiotics, e.g. bacitracin, neomycin   2.   Lanolin derivatives   3.   Emulsifiers   4.   Antiseptics, e.g. iodine( More commonly causes irritant contact dermatitis).   5.   Preservatives, e.g. parabens   6.   Balsam of Peru and other fragrances   7.   Chemicals of plant origin   8.   Corticosteroids   9.   Wound dressing components   ·       Patients with chronic venous insufficiency often exhibit multiple contact allergies
Irritant contact dermatitis	·       The exudate from draining ulcers leads to maceration, increased inflammation, and bacterial colonization of surrounding skin   ·       Infectious eczematous dermatitis may occur

 

It has also been suggested that cutaneous inflammation in venous hypertension may result from increased sequestration of white cells in the venules, with a consequent release of proteolytic enzymes and free radicals which produce tissue damage. In normal subjects, white cells are sequestered in the limb when venous pressure is elevated, and in patients with venous insufficiency the effect is enhanced, with increased endothelial contact and adhesion of white cells. This effect may be related to an increase in expression of adhesion molecules intercellular adhesion molecule 1 (ICAM‐1) and vascular cell adhesion molecule 1 (VCAM‐1) on the vascular endothelium in affected skin.

Both microangiopathy and chronic inflammation are likely to be responsible for stasis dermatitis. Stasis dermatitis typically occurs in the same (i.e. the medial supramalleolar) regions where microangiopathy is most intense, and the patches of dermatitis arise preferentially over dilated varicose veins. Also, dermal inflammation is known to induce epidermal dysfunction, including barrier impairment.

Sometimes, patients report intense pruritus that even develops before the eczema. Pruritus may be caused by repeated congestion and decongestion, as well as by the release of inflammatory mediators within the dermis. Scratching or rubbing worsens and perpetuates the dermatitis. In addition, patients often apply topical agents to combat the pruritus and xerosis, increasing the risk of contact dermatitis.

 

 

Clinical features

 

Stasis dermatitis may develop suddenly or insidiously. It may occur as a late result of DVT.

Stasis dermatitis presents as erythema and scaling and are most pronounced around the ankle and lower leg. Stasis dermatitis is markedly pruritic, as evidenced by multiple excoriations which lead to oozing and crusting. Episodes of vesiculation occur infrequently, always raising the suspicion of superimposed contact sensitization. Chronic lesions of stasis dermatitis invariably exhibit considerable lichenification. The eczema is often accompanied by other manifestations of venous hypertension, including dilatation or varicosity of the superficial veins, edema, purpura, haemosiderosis, lipodermatosclerosis and ulceration, or small patches of white, atrophic, telangiectatic scarring (‘atrophie blanche’). Leashes of dilated venules around the dorsum of the foot or ankle are particularly common. There may be a subepidermal vascular proliferation producing purple papules around the ankle, which may resemble Kaposi sarcoma. Once ulcers form, stasis dermatitis frequently becomes highly irritated, oozing, and erosive. Ulcer healing is inhibited by stasis dermatitis, in part due to chronic lower leg swelling.

 

Contact sensitization often leads to secondary dissemination. Patches of eczema arise in a strikingly symmetric distribution pattern, particularly on the anterior aspect of the contralateral leg even when it is not affected by obvious venous insufficiency, the anterior thighs and the extensor surface of the upper extremities; lesions may generalize to involve the trunk and face and occasionally this can progress to erythroderma.

 

CUTANEOUS SIGNS OF CHRONIC VENOUS HYPERTENSION

1.   Edema, often tender   2.   Varicosities, including venulectasias of the instep   3.   Petechiae superimposed on a yellow–brown discoloration due to hemosiderin deposits (stasis purpura)   4.   Stasis dermatitis   5.   Lipodermatosclerosis, acute and chronic   6.   Stasis ulcerations, in particular above the medial malleolus   7.   Acroangiodermatitis (pseudo-Kaposi sarcoma)   8.       Livedoid vasculopathy (“atrophie blanche”): porcelain-white scars surrounded by punctate telangiectasias and painful ulcerations (Need to exclude causes of hypercoagulability).

 

 

 

Complications and co‐morbidities

 

Allergic contact dermatitis

 

Clinically this may present as an eczematous eruption with a sharp, linear cut‐off matching to the application of a topical therapy, wound dressing, or compression hosiery. Allergic contact dermatitis is a common complication of venous eczema, possibly because of the large number of antigen‐presenting cells in the inflamed skin and also because of prolonged contact with topical therapies and compression hosiery. Allergens include topical antibiotics, topical steroids, preservatives, fragrances and rubber accelerators.

 

Secondary infection

 

This usually presents as a sudden worsening of eczema. If cellulitis ensues, the patient may experience pain and increased skin temperature and swelling of the affected area, as well as malaise and rigors if infection becomes systemic.

 

 

Disease course and prognosis

 

Venous eczema is a chronic condition that undergoes relapses and remissions. Long‐term improvement may be provided by effective lower limb compression, if tolerated, or in some cases by varicose vein surgery.

 

Investigations

 

Ankle brachial pressure index (ABPI) measurement is required prior to consideration of compression therapy. An ABPI of more than 0.8 indicates suitability for graduated compression bandages.

 

Treatment

 

Basic measures include the regular use of adequate compression bandages or stockings to improve venous return, lifestyle changes, and exercise of the calf muscles.  Obese patients should be urged to lose weight. The legs should be elevated as effectively as possible. If indicated, surgical strategies are undertaken. However, these surgical approaches do not replace the need for ongoing compression therapy.

Mild topical steroids may be used to relieve irritation, but the use of potent corticosteroids should be limited to a few days as they may cause cutaneous atrophy and increase the risk of ulceration. Topical tacrolimus has been reported to be effective. Bacterial infection must be treated where appropriate, but the risk of sensitization to topical antibiotics and antiseptics should be borne in mind, and systemic antibiotics may be preferable.

 

Therapeutic ladder

 

First line

·        Skin care, including leg elevation, emollients and topical corticosteroids

Second line

·        Compression hosiery

Third line

·        Referral to vascular surgeon to consider surgical intervention