Vulvar dermatitis falls into two main categories: eczema and seborrheic dermatitis. Eczema can be further sub-divided into exogenous and endogenous forms. Irritant and allergic contact dermatitis are forms of exogenous eczema. They are usually reactions to potential irritants or allergens found in soaps, laundry detergents, textiles, and feminine hygiene products. Careful history can be helpful in identifying the offending agent and in preventing recur-rences. Atopic dermatitis is a form of endogenous eczema that often affects multiple sites, including the flexural sur-faces of the elbows and knees, retroauricular area, and scalp. The lesions associated with these three forms of dermatitis can appear similar: symmetric eczematous lesions, with underlying erythema. Histology alone will not distinguish these three types of dermatitis. They all exhibit a spongi-otic pattern characterized by intercellular edema withinthe epidermis, causing widening of the space between the cells. Therefore, these entities must often be distinguished clinically.
Although seborrheic dermatitis is a common problem, iso-lated vulvar seborrheic dermatitis is rare. It involves a chronicinflammation of the sebaceous glands, but the exact cause is unknown. The diagnosis is usually made in patients com-plaining of vulvar pruritus who are known to have sebor-rheic dermatitis in the scalp or other hair-bearing areas of the body. The lesion may mimic other entities such as pso-riasis or lichen simplex chronicus. The lesions are pale red toa yellowish pink and may be covered by an oily appearing, scaly crust. Because this area of the body remains continuallymoist, occasional exudative lesions include raw “weeping” patches, caused by skin maceration, which are exacerbated by the patient’s scratching. As with psoriasis, vulvar biopsy isusually not needed when the diagnosis is made in conjunction with known seborrheic dermatitis in other hair-bearing areas. Thehistologic features of seborrheic dermatitis are a combina-tion of those seen in the acanthotic and spongiotic patterns.
Treatment for vulvar dermatitis involves removing the offending agent, if applicable, initial perineal hygiene and the use of a 5% solution of aluminum acetate several times a day, followed by drying. Topical corticosteroid lotions or creams containing a mixture of an agent that penetrates well, such as betamethasone valerate, in conjunction with crotamiton, can be used for symptom control. As with LSC, the use of antipruritic agents as a bedtime dose in the first 10 days to 2 weeks of treatment frequently helps break the sleep/scratch cycle and allows the lesions to heal. Table 42.2 summarizes the clinical characteristics of the common vul-var dermatoses.