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Clinical Summary

Allergic contact dermatitis occurs after previously sensitized skin is rechallenged with the same allergen and represents a delayed-type hypersensitivity reaction. Papules and vesicles first develop; they can become a generalized morbilliform eruption (autosensitization). Pruritus is a dominant feature. The most common causes are nickel, toxicodendrons (poison ivy, poison oak, and poison sumac), neomycin, fragrances, balsam of Peru (common in perfumes), formaldehyde, bacitracin, and rubber compounds.

Management and Disposition

Identification of the causative agent and prevention of further contact is critical. Supportive care is given with antihistamines and topical corticosteroids. Systemic corticosteroids may be needed for generalized eruptions. Refer patients to dermatology for further evaluation and possible patch testing.

FIGURE 13.78

Contact Dermatitis. Erythematous eruption in a waist-band distribution (elastic allergy from underwear). (Photo contributor: J. Matthew Hardin, MD.)

FIGURE 13.79

Contact Dermatitis. The erythematous, edematous base of the eruption corresponds to the posterior watch surface. Superimposed on the erythematous base are multiple vesicles with exudate and crust. (Photo contributor: Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

FIGURE 13.80

Contact Dermatitis. Allergy to tattoo pigment. Note erythema, scale, and erosions contained within the tattoo image. (Photo contributor: J. Matthew Hardin, MD.)


  1. Obtaining a complete history of all exposures is critical; pay attention to personal hygiene products.

  2. Toxicodendron allergic contact dermatitis (poison ivy, poison sumac, poison oak) requires a minimum 3-week taper of oral prednisone; a shorter course allows rash reappearance.

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