for signs of overuse, including atrophy and striae, is important while managing this chronic condition FIGURE 65.4 Dyshidrotic eczema (Reprinted with permission from Craft N, Taylor E, Tumeh PC, et al VisualDx: Essential Adult Dermatology Philadelphia, PA: Lippincott Williams & Wilkins; 2010.) FIGURE 65.5 Contact dermatitis from a softball glove Note the striking distribution of the dermatitis with a sharp cut-off on the third and fourth fingers corresponding to where the fingers contacted the inside of the glove Contact Dermatitis Contact dermatitis is an inflammatory reaction of the skin caused by an allergen (allergic contact dermatitis) or a primary irritant (irritant contact dermatitis) Acute eruptions have intense pruritus, severe erythema, edema, vesicles, and erosions with serous discharge and crusting ( Fig 65.5 ) A specific distribution with a sharp demarcation between involved and unaffected skin may be a clue to this diagnosis Subacute reactions have mild erythema, dry scale, less vesiculation, and mild thickening of the skin Chronic exposures may result in lichenification, fissures, scales, excoriations, and hyperpigmentation Itching, distribution, and the surface changes described above are key components that can help differentiate acute contact dermatitis from acute skin infections such as cellulitis Treatment of contact dermatitis includes avoidance of allergens or irritants and use of thick emollients and topical corticosteroids when needed When oral corticosteroids are needed for severe or widespread contact dermatitis, a longer treatment course with a slow taper over 14 days will decrease the risk for rebound dermatitis Allergic Contact Dermatitis Allergic contact dermatitis is caused by a classic delayed T-cell–mediated hypersensitivity reaction (type IV) Repeated exposure causes an allergic sensitization The eruption is delayed after the initial exposure for up to to 10 days Repeated exposures can cause the rapid appearance of an acute dermatitis (within 12 to 24 hours) Rhus dermatitis, caused by an oleoresin in the sap of poison ivy, poison oak, or poison sumac plants, is the most common cause of allergic contact dermatitis in the United States Delayed exposure may occur because of contact with objects that have had contact with the plants (e.g., shoe laces, dogs) Typical presentation includes pruritus and erythema followed by development of papules, vesicles, and bullae, sometimes in a linear arrangement ( Fig 65.6 ) Burning of plants leads to aerosolization of the allergen, and may cause a widespread and severe outbreak on exposed skin surfaces, including severe edema of the eyelids and lips in some cases “Black dot poison ivy” can occur when a concentrated amount of the oleoresin gets deposited on the surface of the skin and oxidizes, creating a central black eschar surrounded by an acute dermatitis This entity has been confused with a pigmented lesion or an insect bite If possible, the black eschar should be removed by soaking or debridement to minimize spread of the resin Other plants, flowers, pollens (especially ragweed), clothing, shoes, metals (e.g., nickel in jewelry), cosmetics, adhesive tape, and latex-containing products can also cause an allergic contact dermatitis Nickel dermatitis occurs on earlobes as a result of nickel-containing earrings and on the abdomen due to pant buttons or belt buckles Shoe dermatitis usually occurs on the dorsal surfaces of the feet, sparing interdigital spaces, in a symmetric manner FIGURE 65.6 Allergic contact dermatitis caused by poison ivy (Reprinted with permission from Stedman’s Medical Dictionary 28th ed Philadelphia, PA: Lippincott Williams & Wilkins; 2005.) Allergic contact dermatitis is rare in neonates because of their impaired ability to react to allergens By to years of age, children react to