Introduction
Background
Stasis dermatitis is a common inflammatory skin disease that occurs on the lower extremities in patients with chronic venous insufficiency with venous hypertension. The condition typically affects middle-aged and elderly patients. It rarely occurs before the fifth decade of life, except in patients with acquired venous insufficiency due to surgery, trauma, or thrombosis. Stasis dermatitis is usually the earliest cutaneous sequela of venous insufficiency, and it may be a precursor to more problematic conditions, such as venous leg ulceration and lipodermatosclerosis.
Pathophysiology
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 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. Alternatively, specific events, such as deep venous thrombosis, surgery (eg, vein stripping, harvesting of saphenous veins for coronary bypass), or traumatic injury, can severely damage the function of the lower-extremity venous system. The mechanism by which venous hypertension causes the cutaneous inflammation of stasis dermatitis has been extensively studied for decades. Several theories have been proposed.In this patient with stasis dermatitis, note the large scar on the calf that was caused by military shrapnel. Injuries to the venous system due to trauma or surgery are common factors that contribute to the development of stasis dermatitis.
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.
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 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.1,2,3
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.4 These leukocytes release the growth factor transforming growth factor-beta1, an important mediator of dermal fibrosis. Furthermore, 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, occurs.5 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.6,7
Herouy et al suggested that matrix metalloproteinases may be important in lesional skin remodeling in persons with stasis dermatitis.8
Frequency
United States
Although not nearly as prevalent as skin cancer, dermatophytosis, or xerosis, stasis dermatitis affects a significant proportion of the elderly population. Studies have estimated the prevalence of stasis dermatitis to be approximately 6-7% in patients older than 50 years. This finding makes stasis dermatitis twice as prevalent as psoriasis and only slightly less prevalent than seborrheic dermatitis.9,10
Mortality/Morbidity
No conclusive studies on morbidity and mortality in stasis dermatitis have been undertaken. However, a prevalence of 6-7% would translate into approximately 15-20 million patients older than 50 years with stasis dermatitis in the United States. Much of the morbidity stems from the complications of chronic stasis dermatitis, including cellulitis and nonhealing venous ulcers.
Sex
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.
Age
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.
Clinical
History
- Patients with stasis dermatitis typically present with an insidious onset of pruritus affecting one or both lower extremities.
- Reddish-brown skin discoloration is an early sign of stasis dermatitis and may precede the onset of symptoms.
- The medial ankle is most frequently involved, with symptoms progressing to involve the foot and/or the calf.
- The patient 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 33 years previously during treatment for poliomyelitis.11
- Factors that worsen peripheral edema (eg, congestive heart failure, long-standing hypertension with diastolic dysfunction) are often found in patients with stasis dermatitis.
Physical
Physical examination reveals erythematous, scaling, eczematous patches affecting the lower extremity.
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.
This patient exhibits the dermal sclerosis and hyperpigmentation typical of chronic stasis dermatitis. In addition, the patient has developed a venous ulcer, which is a common complication of stasis dermatitis.
- The medial ankle is most frequently and severely involved because of the fact that the medial ankle 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.
- Involved skin in stasis dermatitis may exhibit the same changes as seen in other eczematous conditions.
- Severe, acute inflammation may result in exudative, weeping patches and plaques.
- Secondary infection can cause typical honey-colored crusting due to bacteria or monomorphous pustules due to cutaneous candidiasis.
- In long-standing lesions, lichenification and hyperpigmentation may occur as a consequence of chronic scratching and rubbing. In addition to lichenification and hyperpigmentation, chronic stasis dermatitis can show changes, such as skin induration, which may progress to lipodermatosclerosis with the classic inverted champagne bottle appearance.12
- Another unique feature sometimes seen in chronic stasis dermatitis is the development of violaceous plaques and nodules on the legs and 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.
- Stasis dermatitis frequently occurs along with a background of skin changes that are typical for patients with venous insufficiency.
- These skin changes include edema, varicosities, hyperpigmentation, atrophic patches (atrophie blanche), and diffuse red-brown discoloration representing deep dermal deposits of hemosiderin (from degraded, extravasated erythrocytes).
- These chronic changes persist regardless of the activity of stasis dermatitis.
Causes
See Pathophysiology.
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| Multimedia: Stasis Dermatitis |
| References |
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References
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Further Reading
Keywords
stasis dermatitis, venous ulcer, venous eczema, chronic venous insufficiency, venous hypertension
