The eczematous dermatitides include a group of diseases which present with a common morphology: erythematous and papulovesicular when acute; erythematous and scaling (with or without fissures and lichenification) when chronic. Included under this rubric are atopic dermatitis, contact dermatitis, nummular dermatitis, seborrheic dermatitis and stasis dermatitis.
Atopic dermatitis is a common infantile eczema which affects approximately 10-20% of children in the United States. The disease has a strong association with allergic rhinitis and asthma and occurs in approximately one-third of children with a personal or family history of these disorders. Although IgE antibodies may be elevated in up to 80% of individuals with atopic dermatitis, the skin manifestations do not seem to be a purely IgE-mediated process. The etiology of atopic dermatitis is unknown. Current hypotheses have concentrated on the possibility that an aberrant T cell response, perhaps to staphylococcal superantigen, results in the activation of TH2 cells.
Clinically, atopic dermatitis (Figure 1) has been called the “itch that rashes”. Pruritus is a hallmark of the disease. Infants less than 18 months of age typically present with an acute to subacute dermatitis which may involve the scalp, the face (particularly the cheeks), the posterior neck, the trunk and the extensor aspects of the extremities. After approximately two years of age, most individuals will present with a more chronic, lichenified and scaling form of the disease distributed about the face, neck, trunk and especially the flexural aspects of the extremities (antecubital and popliteal fossae). The reason for the change in distribution of the dermatitis on the extremities is not clear. Individuals with atopic dermatitis are prone to develop secondary infection with staphylococcal organisms, as well as with viruses and fungi. When the disease is flaring, these secondary infections must be excluded. Acute, weeping dermatitis benefits from drying agents whereas chronic lichenified dermatitis requires emollients. Topical glucocorticosteroids or macrolide immunosuppressants canbe helpful in reducing inflammation. Topical antihistamines are best avoided because they may induce asecondary allergy. Phototherapy with ultraviolet B or psoralen plus ultraviolet A (PUVA) can also be beneficial but should be undertaken by trained specialists. Other therapeutic modalities are available for treating more resistant disease but again should be rendered by specialty care.
Contact dermatitis can be broken down into two main areas: irritant contact dermatitis and allergic contact dermatitis.
Irritant contact dermatitis is the direct result of injury to the skin caused by chemical exposure. Irritation can be further subdivided into acute corrosion (caused by a single exposure to strong acids and alkalis), acute irritation (caused by a single exposure to chemicals such as strong solvents and non-corrosive acids and bases), cumulative irritation (the most typical and caused by repeated exposures particularly to surfactants and emulsifiers) and phototoxicity (caused by exposure to irritating chemicals which require light for their activation). The clinical presentation of irritation can therefore vary from the acute onset of a third degree chemical burn (corrosion following phenol exposure) to the chronic scaling and xerotic dermatitis of “dishpan hands” (Figure 2). Because irritant contact dermatitis is a function of the chemical, it will occur in all individuals exposed to this chemical given sufficient exposure times and concentrations. Nonetheless, it is clear that the skin of some individuals is much more irritable than others. The determinants of hyperirritable skin are numerous and include age, genetics, ambient environment, underlying skin disease(s), and concomitant chemical exposure.
Treatment for irritant contact dermatitis rests upon avoiding the irritants by the use of barriers (gloves or other mechanisms) and/or by using less irritating materials as substitutes. In addition, treatment for corrosion and acute irritation should proceed as that for the appropriate level burn. Treatment for chronic, cumulative irritant contact dermatitis involves avoiding contact with the known irritants and the liberal use of non-sensitizing moisturizers (such as plain petroleum jelly) with or without topical glucocorticosteroids. Phototoxic dermatitis is similarly treated; in addition, broad spectrum, UVA-blocking sunscreens may be beneficial. The pruritus and/or discomfort of irritant dermatitis often requires systemic antihistamines and/or non-steroidal anti-inflammatory agents. Topical antihistamines are best avoided for fear of inducing a secondary allergic contact dermatitis.Allergic contact dermatitis (ACD) develops following exposure to chemicals to which the individual has previously become sensitized. It is a type IV or delayed-type hypersensitivity reaction of the skin. There are over 3,000 environmental allergens which have been reported to cause this condition. The prevalence of ACD varies with the allergen. Typically, the patient will develop an erythematous, scaling, papulovesicular dermatitis at the sites of contact with the allergen (Figure 3). Longstanding, low grade allergens can create a more subacute to chronic, scaling lichenified dermatitis. Diagnosis of allergic contact dermatitis is made by patch testing. Treatment is allergen avoidance. The acute disease can be managed with topical glucocorticosteroids, oral antihistamines and other modalities. Nummular Dermatitis
Nummular dermatitis is characterized by its “coin-shaped” lesions (Figure 4). As with other dermatitides, the acute form is papulovesicular whereas the chronic form is scaly and lichenified. Mild to severe pruritus accompanies the disease which most frequently affects men, typically in the sixth decade or beyond. The prevalence of the disease is unknown, but it would appear to be lower than that for most of the other eczemas. Treatment includes the use of systemic antihistamines and topical emollients. Glucocorticosteroids may also be used as indicated. Ultraviolet B and PUVA phototherapy can be beneficial for resistant disease.
Seborrheic dermatitis is one of the most common cutaneous diseases and affects from 3 to 5% of the population. One proposed etiology is overgrowth of Pityrosporum, a yeast that normally inhabits sebaceous skin (e.g., scalp, eyebrows, central face). The disease has two peaks, one in infancy and the other post-pubertal. Infantile seborrheic dermatitis typically occurs within the first months of life and affects the scalp (“cradle cap”) and intertriginous areas with scales and crust. The skin about the ears and the neck may also be involved. In contrast, seborrheic dermatitis in adults typically involves the scalp, face, neck, mid upper chest and intertriginous zones (axillae, groin, submammary, and in obese patients beneath the pannus). On the face, it particularly concentrates about the eyebrows, nasolabial folds and retroauricular areas (Figure 5). Treatment for seborrheic dermatitis includes keratolytic shampoos and gels, topical antifungals, topical metronidazole and/or topical glucocorticosteroids as indicated. Topical macrolide immunosuppressants can also be very effective for disease involving especially the face and neck, although such use has not yet gained FDA approval. Of note, seborrheic dermatitis can be particularly recalcitrant in individuals who are immunosuppressed (e.g., patients with AIDS) and may require phototherapy when resistant to topical therapies.
Stasis dermatitis is an eczematous process of the skin of the lower extremities which results from non-specific inflammation presumably induced by the leakage of serum secondary to venous hypertension (Figure 6). The disease is particularly common over the medial and anterior aspects of the shin and malleolar areas. When significant inflammation occurs, it can be accompanied by a secondary autosensitization dermatitis referred to as an “id”. Treatment should be geared towards improving blood return by surgical intervention or by the use of graduated compression support hose. However, it is important that the hose have a proper pressure gradient or the disease can be worsened. In addition, low potency topical glucocorticosteroids and oral antipruritics can be of benefit. Patients with stasis dermatitis seem to have an increased incidence of allergic reactions to ingredients in topical medicaments and, as much as possible, should avoid products containing lanolin, fragrances, neomycin, and other common sensitizers.