The form of eczema known as contact dermatitis can be subdivided into irritant dermatitis, resulting from nonspecific injury to the skin, and allergic contact dermatitis, in which the mechanism is a delayed hypersensitivity reaction. Irritant dermatitis is more frequent in children, particularly during the early years of life.

Irritant contact dermatitis can result from prolonged or repetitive contact with various substances that include saliva, citrus juices, bubble bath, detergents, abrasive materials, strong soaps, and proprietary medications. Saliva is probably one of the most common offenders; it may cause dermatitis on the face and in the neck folds of a drooling infant or a retarded child. In older children who habitually lick their lips because of dryness, frequently without being aware, a striking, sharply demarcated perioral rash may develop (Fig. 647-1). Among the exogenous irritants, citrus juices, proprietary medications, and bubble bath preparations are relatively common. Excessive accumulation of sweat and moisture as a result of wearing occlusive shoes may also cause irritant dermatitis.

Figure 647-1 Perioral irritant contact dermatitis from lip licking.

Irritant contact dermatitis may be indistinguishable from atopic dermatitis or allergic contact dermatitis. A detailed history and consideration of the sites of involvement, the age of the child, and contactants usually provide clues to the etiologic agent. The propensity for development of irritant dermatitis varies considerably among children; some may respond to minimal injury, making it difficult to identify the offending agent through history. Irritant contact dermatitis usually clears after removal of the stimulus and temporary treatment with a topical corticosteroid preparation (Chapter 638). Education of patients and parents about the causes of contact dermatitis is crucial to successful therapy.

Diaper dermatitis can be regarded as the prototype of irritant contact dermatitis. As a reaction to overhydration of the skin, friction, maceration, and prolonged contact with urine and feces, retained diaper soaps, and topical preparations, the skin of the diaper area may become erythematous and scaly, often with papulovesicular or bullous lesions, fissures, and erosions (Fig. 647-2). The eruption can be patchy or confluent, but the genitocrural folds are often spared. Chronic hypertrophic, flat-topped papules and infiltrative nodules may occur. Secondary infection with yeast is common. Discomfort may be marked because of intense inflammation. Allergic contact dermatitis, seborrheic dermatitis, psoriasis, candidosis, atopic dermatitis, and rare disorders such as Langerhans cell histiocytosis (histiocytosis X) and acrodermatitis enteropathica should be considered when the eruption is persistent or is recalcitrant to simple therapeutic measures.

Figure 647-2 Severe, erosive diaper dermatitis.

Diaper dermatitis often responds to simple measures; some infants are predisposed to diaper dermatitis, and management may be difficult. The damaging effects of overhydration of the skin and prolonged contact with feces and urine can be obviated by frequent changing of the diapers. Over-washing should be avoided because it leads to chapping and a worsening of the dermatitis. Disposable diapers containing a superabsorbent material may help maintain a relatively dry environment. Frequent topical applications of a bland protective barrier agent (petrolatum or zinc oxide paste) may suffice to prevent dermatitis. Candidal infection is signified by red-pink tender skin that has numerous 1- to 2-mm pustules and papules at the periphery of the dermatitis. Treatment with a topical anticandidal agent may be helpful.

Juvenile plantar dermatosis is a common form of irritant contact dermatitis occurring mainly in prepubertal children. The dermatitis characteristically involves the weight-bearing surfaces, may be pruritic or painful, and causes a glazed appearance of the plantar skin (Fig. 647-3). Fissuring may become extensive, producing considerable discomfort. The dermatitis results from alternating excessive hydration and rapid moisture loss, which cause chapping of the skin and cracking of the stratum corneum. Affected children often have hyperhidrosis, wear occlusive synthetic footwear, and subject their feet to rapid drying without moisturization. Immediate application of a thick emollient when socks and shoes are removed or immediately after swimming usually minimizes this condition. Severe inflammatory cases may require short-term (1-2 wk) application of a medium- to high-potency topical steroid.

Figure 647-3 Red, scaly juvenile plantar dermatosis.

Allergic contact dermatitis is a T cell–mediated hypersensitivity reaction that is provoked by application of an antigen to the skin surface. The antigen penetrates the skin, where it is conjugated with a cutaneous protein, and the hapten-protein complex is transported to the regional lymph nodes by antigen-presenting Langerhans cells. A primary immunologic response occurs locally in the nodes and becomes generalized, presumably because of dissemination of sensitized T cells. Sensitization requires several days and, when followed by a fresh antigenic challenge, manifests as allergic contact dermatitis. Generalized distribution may also occur if enough antigen finds its way into the circulation. Once sensitization has occurred, each new antigenic challenge may provoke an inflammatory reaction within 8-12 hr; sensitization to a particular antigen usually persists for many years.

Acute allergic contact dermatitis is an erythematous, intensely pruritic, eczematous dermatitis, which, if severe, may be edematous and vesiculobullous. The chronic condition has the features of long-standing eczema: lichenification, scaling, fissuring, and pigmentary change. The distribution of the eruption often provides a clue to the diagnosis. Volatile sensitizers usually affect exposed areas, such as the face and arms. Jewelry, topical agents, shoes, clothing, henna tattoo dyes, and plants cause dermatitis at points of contact.

Rhus dermatitis (poison ivy, poison sumac, poison oak) is often vesiculobullous and may be distinguished by linear streaks of vesicles where the plant leaves have brushed against the skin (Fig. 647-4). Fluid from ruptured cutaneous vesicles does not spread the eruption; antigen retained on the skin, under the fingernails, and on clothing initiates new plaques of dermatitis if not removed by washing with soap and water. Antigen may also be carried by animals on their fur. Black spot poison ivy is a rare variant that manifests as small discrete black lacquer-like glossy papules with surrounding erythema and edema. The saplike allergen (oleoresin) is present on live and dead leaves, and sensitization to one plant produces cross reactions with the others.

Figure 647-4 Linear lesions in poison ivy.

Nickel dermatitis usually develops from contact with jewelry or metal closures on clothing and is seen most frequently on the earlobes, such as when earring posts of nickel-containing metal rather than nonmetallic materials or stainless steel are used to keep a pierced tract open. Metal closures on pants frequently cause periumbilical dermatitis (Fig. 647-5). Some children are exquisitely sensitive to nickel, with even the trace amounts found in gold jewelry provoking eruptions.

Figure 647-5 Chronic periumbilical nickel dermatitis.

Shoe dermatitis typically affects the dorsum of the feet and toes, sparing the interdigital spaces; it is usually symmetric. Other forms of allergic contact dermatitis, in contrast to irritant dermatitis, rarely involve the palms and soles. Common allergens are the antioxidants and accelerators in shoe rubber and the chromium salts in tanned leather or shoe dyes. Excessive sweating often leaches these substances from their source.

Wearing apparel contains a number of sensitizers, including dyes, mordants, fabric finishes, fibers, resins, and cleaning solutions. Dye may be poorly fixed to clothing and so may be leached out with sweating, as are the partially cured formaldehyde resins. The elastic in garments is also a frequent cause of clothing dermatitis.

Topical medications and cosmetics may be unsuspected as allergens, particularly if a medication is being used for a pre-existing dermatitis. The most common offenders are neomycin, thimerosal, topical antihistamines, topical anesthetics, preservatives, and ethylenediamine, a stabilizer present in many medications. All types of cosmetics can cause facial dermatitis; involvement of the eyelids is characteristic for nail polish sensitivity.

Contact dermatitis can be confused with other types of eczema, dermatophytoses, and vesiculobullous diseases. Patch testing may clarify the etiology. The essential principle in treatment is elimination of contact with the allergen. Acute dermatitis responds to cool compresses and topical application of a medium- to high-potency topical corticosteroid ointment. An oral antihistamine may be useful. Massive acute bullous reactions or reactions that cause swelling around the eyes or genitals, such as those to poison ivy, may require treatment with a 2-wk tapering course of oral corticosteroids beginning with 1 mg/kg/day. If secondary infection has occurred, appropriate systemic antibiotic therapy should be given. Desensitization therapy is rarely indicated.

Nummular eczema is unrelated to other types of eczema and is characterized by more or less coin-shaped eczematous plaques. Common sites are the extensor surfaces of the extremities (Fig. 647-6), buttocks, and shoulders. The plaques are relatively discrete, boggy, vesicular, severely pruritic, and exudative; when chronic, they often become thickened and lichenified. The cause is unknown. Most frequently, these lesions are mistaken for tinea corporis, but plaques of nummular eczema are distinguished by the lack of a raised, sharply circumscribed border; the lack of fungal organisms on a potassium hydroxide (KOH) preparation; and frequent weeping or bleeding when scraped. Control of pruritus and inflammation is usually achieved with a potent topical corticosteroid preparation. Steroid-impregnated tapes may simultaneously treat and provide barrier protection to these circumscribed eczematous plaques. An antihistamine may be helpful, particularly at night. Antibiotics are indicated for secondary infection.

Figure 647-6 Discrete, boggy plaque of nummular dermatitis.