Allergic Contact Dermatitis
Definition, clinical characteristics. Allergic contact dermatitis (ACD) is generally more acute and more in flammatory than irritant dermatitis. It is a Type IV, delayed-type, T-cell mediated, hypersensitivity reaction. While ICD seems to occur on the palms (see Figure 3), ACD often in volves the dorsal fingers, web spaces (see Figure 4), and wrists. ICD and ACD may be clinically in distin guish able, however. In the acute phase, vesicles and edema are present (see Figure 5). In the chronic phase, lichenification (thickening of the skin) with scaling and fissuring are common (see Figures 6-7) (Belsito, 2000).
Clinical features. Patients with symptoms of ACD require a much more detailed history compared to those with most other dermatologic disorders. Individuals with ACD typically develop dermatitis within a few days of exposure in areas that were previously exposed to the allergen. However, certain allergens (for example, neomycin) penetrate intact skin poorly, and the onset of dermatitis may be delayed up to a week following exposure. A minimum of 10 days is required for individuals to develop specific sensitivity to a new allergen. Poison ivy is the classic example of acute ACD in North America. For example, an individual who never has been sensitized to poison ivy may develop only a mild dermatitis in the weeks following the initial exposure, but typically develops severe dermatitis within 1 to 2 days on the second and subsequent exposures (Hogan, 2006). ACD to workplace materials may improve initially on weekends and during holidays, but those with chronic dermatitis may not demonstrate the typical correlation of weekend and holiday improvement (Ingber & Merims, 2004; Wigger-Alberti, Iliev, & Elsner, 1999). ACD lesions are sharply demarcated, occurring at the site of allergen exposure (or contact) and develop over 48 hours. Initially there is redness and itching, followed by crusted vesicles and blisters, which becomes thickened skin with time (Warshaw et al., 2003).
Occupational factors. Wet work may potentiate development of ACD. When the protective capacity of the epidermis is disrupted by wet work exposure, the penetration of the allergen is facilitated; thus, the probability of sensitization may be increased (Warshaw et al., 2003). A common cause of workplace ACD on the hands is rubber sensitivity from chemical accelerators used in both natural rubber latex and non-latex synthetic gloves. Occupations most at risk for allergic contact dermatitis include hairdressers, cement workers, food processors, florists, printers, chefs, builders, nurses, motor mechanics, painters, laundry workers, animal handlers, and pharmaceutical factory workers (Ingber & Merims, 2004; Templet et al., 2004; Warshaw et al., 2003).
Diagnosis. Patch testing is the gold standard for diagnosis of ACD and is especially important for evaluation of recurrent hand dermatitis (Warshaw et al., 2003). The clinical appearance as well as the histology and the immunohistology of allergic and irritant contact dermatitis are indistinguishable. The development of the clinical dermatitis, the medical history, and the skin tests are diagnostic tools used in these cases. Patch testing involves application and occlusion of diluted antigens for 48 hours (see Figure 2). At that time, the patches are removed, the area marked, and the reactions read. At 72 to 96 hours, a second reading is performed (Bourke et al., 2001; Ingber & Merims, 2004). Patch testing is done on a skin site where the dermatitis is not apparent, usually on the upper back. In addition, no systemic steroids should be taken within 6 weeks prior to patch testing. Also, no topical steroids should be applied to the patch test area, and no antihistamines should be taken during the duration of the test. Common allergens causing ACD of the hands are listed in Table 4 .
Management. Management in cludes avoiding the implicated allergen and protecting skin with barrier creams (Warshaw et al., 2003). Allergen avoidance is imperative as contact allergy is usually life-long. Patients need to be aware of allergen sources in both the home and workplace to minimize the risk of flares. Patients should be provided with as much information as possible concerning the chemical to which they are allergic to aid in avoiding that chemical (Bourke et al., 2001). In formation regarding various chemicals is available to members on the American Contact Dermatitis So ciety Web site under "Contact Al lergen Replacement Database" at https://www.contactderm.org.
Topical corticosteroid creams are the mainstay of the acute treatment of ACD; however, oral steroids may be necessary in severe cases. Antibiotics may be helpful if the dermatitis is infected secondarily. Oral antihistamines are minimally helpful (Warshaw et al., 2003).
Contact urticaria. Contact urti caria is a rapid onset, localized urti caria, Type I, IgE mediated "wheal and flare" allergic reaction. This is often seen in kitchen workers who handle raw seafood and meat, dairy, fruits and vegetables, as well as health care workers due to natural rubber latex. Some common urti cants are listed in Table 5 . Symptoms range from urticaria, dermatitis, allergic rhinitis, and asthma to anaphylaxis. Diagnosis is made by prick testing, RAST (radioallergosorbent test), or use test (Kelly, Kurup, Zachariesen, Resnick, & Fink, 1993).
Dermatology Nursing. 2008;20(1):17-25. © 2008 Jannetti Publications, Inc.
The authors reported no actual or potential conflict of interest in relation to this continuing nursing education article.
All other Dermatology Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.
Cite this: Hand Dermatitis: A Review of Clinical Features, Diagnosis, and Management - Medscape - Feb 01, 2008.