Stasis dermatitis frequently presents with signs of CVI which persists regardless of the state of stasis dermatitis. This includes edema, atrophie blanche, varicosities and hyperpigmentation and reddish-brown discoloration due to deep dermal hemosiderin deposits. Most of these symptoms started in the medial ankle and gradually spread up the lower leg or down the foot. Patient may also complain of pruritis.
Along with these symptoms, patient may present with crusts, exudation and superficial ulcerations in acute cases of stasis dermatitis.
Chronically, physical examination may present with lichenification and hyperpigmentation from scratching and rubbing due to pruritis. There will also be gradual tightening of the skin as it becomes drier. Dermal fibrosis as discussed above will result to lipodermatosclerosis, scar-like changes in the fat and other soft tissues. This may also present with the classic inverted champagne appearance of the ankle.
In severe cases, ulceration occurs with oozing, crusted areas made worse with contact dermatitis and bacterial infection. Some chronic conditions develop violet plaques and nodules on the legs and dorsal foot that may undergo painful ulceration called pseudo-Kaposi sarcoma or acroangiodermatitis.
Acute lesions may present with:
Treatment for stasis dermatitis is more focus on the clinical effects of CVI since it directly causes the condition.
Compression therapy is referred for both edema and venous ulcers. Excessive edema can delay healing and risk infection. For venous ulcers, compression therapy is coupled with bland (zinc oxide paste) or colloid-type dressings. Even after the ulcers heal, compression therapy must be continued as a lifetime habit to prevent recurrence.
Arterial function must first be assessed through physical examination or ancillary procedures. Compression therapy, a treatment for CVI leg edema, can exacerbate the patient’s condition if patient also has arterial dysfunction. Compression therapy is done through:
Ligation of the arteriovenous fistula or incompetent perforators can be effective if directly related to stasis dermatitis.
Varicose vein stripping is used when severe signs of stasis dermatitis such as liperdermatosclerosis, ulceration, atrophie blanche or hyperpigmentaton is present. Allogenic dermal substitutes can be used for intractable venous ulcers but are expensive and not necessary if patient responds to high-compression therapy . Emergency surgery is also done if patient’s condition worsens to cellulitis to necrotizing fasciitis.
Autologus platelet-rich plasma (PRP) coupled with light-emitting diode (LED) was found to be effective in treating recalcitrant ulcerating stasis dermatitis . Pigmentation caused by stasis dermatitis was also found to be successfully treated with noncoherent intense pulsed light (IPL) .
Topical corticosteroids are used to alleviate pruritis and inflammation. Midpotency corticosteroids are used to avoid systemic absorption and induced cutaneous atrophy that may lead to ulceration. Tachyphylaxis is a phenomenon where the corticosteroid’s efficacy decreases due to prolonged used.
Nonsteroidal treatment do not carry the risks of corticosteroids such as cutaneous atrophy and tachyphylaxis. Calcineurin inhibitors such as tacrolimus and pimecrolimus may prove to be effective.
Topical antibiotics are used if venous ulcers became infected. Mupirocin and silver sulfadiazine are some of the antiobiotics used. Beware of contact dermatitis caused by multiple topical medications. Any antibiotic used must first be approved by a physician. Triclosan has been shown to have low risk for contact dermatitis .
When patient acquires cellulitis, oral antibiotics are often prescribed such as cephalosporins and dicloxacillin.
The use of drugs, pentoxyfylline and flavonoids, may act on leukocyte activation and diminish the inflammatory response that leads to stasis dermatitis and venous ulceration . However, even if these drugs prove to be effective, they may only be used on venous ulcer patients unresponsive to other treatments.
Chronic venous insufficiency (CVI) causes stasis dermatitis. Valvular dysfunction of the deep venous system causes venous hypertension and blood backflow into the superficial venous system. This results to swelling and later on, skin breakdown and irritation.
Aging, deep venous thrombosis (DVT), surgery and traumatic injury can directly cause valvular dysfunction that in time would result into CVI. Other factors that can affect the lower extremity venous system are varicose veins, hypertension (HTN), kidney failure, obesity, sedentary lifestyle, drugs and hear conditions such as congestive heart failure (CHF). Female gender, pregnancy and family history of venous disease are also established risk factors  . Amlodipine, an antihypertensive drug, can also trigger stasis dermatitis through its common side effect lower leg edema .
The risk of stasis dermatitis also increases with age as one study shows that stasis dermatitis prevalence in 6.2% of patients over 65 years of age . Another study shows that stasis dermatitis affects an estimate of 20% of people over 70 years of age .
In a comprehensive review in the prevalence of CVI and varicose veins, reports of CVI prevalence vary from < 1% to 40% in females and from < 1% to 17% in males. A higher prevalence of varicose veins was seen in reports varying from <1% to 73% in females and 2% to 56% in males . CVI and varicose veins are more prevalent in women due to the stress pregnancy puts on the veins of the lower extremities.
Stasis dermatitis is a direct cause of CVI. However, the mechanism behind venous insufficiency remains unclear. The most accepted theory is the fibrin cuff theory. This theory was derived in the 1970s and 1980s’ studies where it was found that increased venous hydrostatic pressure transmits to the dermal microcirculation. With the increased dermal capillary permeability, macromolecules such as fibrinogen, leak out to the pericapillary tissues.
Fibrinogen then polymerizes into fibrin which forms into a fibrin cuff around the capillaries, preventing oxygen diffusion and resulting to hypoxia and cell damage .
Fibrin cuffs alongside with decreased fibrinolytic activity are then hypothesized to cause dermal fibrosis, the hallmark of stasis dermatitis. Trapped activated leukocytes release not only inflammatory mediators but mediators such as transforming growth factor beta1, an important mediator for dermal fibrosis . This mechanism supports a direct relationship between venous dysfuntction and cutaneous inflammation with fibrosis .
Chemoacttractants that keep the leukocytes active are also present in the upregulation of vascular intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) .
Stasis dermatitis is an inflammatory cutaneous vascular disease due to chronic venous insufficiency. It is characterized by edema, erythema, pruritus and scaling of the skin. It commonly starts on the medial ankle on one or both lower extremities.
Lipodermatosclerosis, lichenification, ulceration and bacterial infection follow in severe cases. This condition is a direct consequence of chronic venous insufficiencyy (CVI) and affects women more than men aged 50 years and above.
Stasis dermatitis is skin irritation and breakdown due to fluid accumulation. Stasis causes leg swelling due to poor circulation and fluid buildup. Dermatitis is skin irritation with scaling, dryness, redness and itching.
It is caused by prolonged poor blood circulation on the veins commonly in the legs usually due to aging. This causes itching, redness, swelling and dry skin starting on the inside ankle of the foot and gradually spread to the lower leg or down the foot.
If not treated, the affected leg or foot may develop ulcers, skin hardening and discoloration which may lead to infection and hardening of tissues.
Stasis dermatitis is confirmed through physical examination and history. A blood test may be given if bacterial infection through ulcers is suspected.
Stasis dermatitis is treated by compression therapy and limb evaluation to decrease swelling. One recommended treatment is wearing of compressive stockings in the morning up to the end of the day. The compressive stocking may feel uncomfortable at first but the discomfort will lower as the edema lessens.
Skin and would care is also advised to prevent further ulceration of the leg through compression, topical medicine and wound dressing. Surgery may be prescribed in severe cases.