Stasis Dermatitis

Updated: Apr 17, 2017
  • Author: Scott L Flugman, MD; Chief Editor: Dirk M Elston, MD  more...
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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.

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Etiology

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. [7]

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. [8, 9, 10]

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. [11] 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. [12]

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. [13, 14]

Metalloproteinase

Herouy et al suggested that matrix metalloproteinases may be important in lesional skin remodeling in persons with stasis dermatitis. [15]

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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. [16, 17, 18]

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. [19]

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.

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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.) [2, 3, 4, 5, 6]

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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).

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