(See also Definition of Dermatitis.)
Contact dermatitis is caused by irritants or allergens.
ICD accounts for 80% of all cases of contact dermatitis. It is a nonspecific inflammatory reaction to substances contacting the skin; the immune system is not activated. Numerous substances are involved, including
Properties of the irritant (eg, extreme pH, solubility in the lipid film on skin), environment (eg, low humidity, high temperature, high friction), and patient (eg, very young or old) influence the likelihood of developing ICD. ICD is more common among patients with atopic disorders, in whom ICD also may initiate immunologic sensitization and hence allergic contact dermatitis.
Phototoxic dermatitis (see Chemical photosensitivity) is a variant in which topical (eg, perfumes, coal tar) or ingested (eg, psoralens) agents generate damaging free radicals and inflammatory mediators only after absorption of ultraviolet light.
ACD is a type IV cell-mediated hypersensitivity reaction that has 2 phases:
In the sensitization phase, allergens are captured by Langerhans cells (dendritic epidermal cells), which migrate to regional lymph nodes where they process and present the antigen to T cells. The process may be brief (6 to 10 days for strong sensitizers such as poison ivy) or prolonged (years for weak sensitizers such as sunscreens, fragrances, and glucocorticoids). Sensitized T cells then migrate back to the epidermis and activate on any reexposure to the allergen, releasing cytokines, recruiting inflammatory cells, and leading to the characteristic symptoms and signs of ACD.
In autoeczematization (id reaction), epidermal T cells activated by an allergen migrate locally or through the circulation to cause dermatitis at sites remote from the initial trigger. However, contact with fluid from vesicles or blisters cannot trigger a reaction elsewhere on the patient or on another person.
Multiple allergens cause ACD (see Table: Causes of Allergic Contact Dermatitis), and cross-sensitization among agents is common (eg, between benzocaine and paraphenylenediamine). Cross-sensitization means that exposure to one substance can result in an allergic response after exposure to a different but related substance. The Toxicodendron species of plant (eg, poison ivy, poison oak, poison sumac) account for a large percentage of ACD, including moderate and severe cases. The offending allergen is urushiol.
Causes of Allergic Contact Dermatitis
ACD variants include photoallergic contact dermatitis and systemically induced ACD. In photoallergic contact dermatitis, a substance becomes sensitizing only after it undergoes structural change triggered by ultraviolet light. Typical causes include aftershave lotions, sunscreens, and topical sulfonamides. Reactions may extend to non–sun-exposed skin. In systemically induced ACD, ingestion of an allergen after topical sensitization causes diffuse dermatitis (eg, oral diphenhydramine after sensitization with topical diphenhydramine).
In ACD, the primary symptom is intense pruritus; pain is usually the result of excoriation or infection. Skin changes range from transient erythema through vesiculation to severe swelling with bullae, ulceration, or both. Changes often occur in a pattern, distribution, or combination that suggests a specific exposure, such as linear streaking on an arm or leg (eg, due to brushing against poison ivy) or circumferential erythema (under a wristwatch or waistband). Linear streaks are almost always indicative of an external allergen or irritant.
Any surface may be involved, but hands are the most common surface due to handling and touching potential allergens. With airborne exposure (eg, perfume aerosols), areas not covered by clothing are predominantly affected. The dermatitis is typically limited to the site of contact but may later spread due to scratching and autoeczematization (id reaction). In systemically induced ACD, skin changes may be distributed over the entire body. The eruption usually begins within 24 to 48 hours after exposure to the allergen.
Contact dermatitis can often be diagnosed by skin changes and exposure history. The patient’s occupation, hobbies, household duties, vacations, clothing, topical drug use, cosmetics, and spouse’s activities must be considered. The “use” test, in which a suspected agent is applied far from the original area of dermatitis, usually on the flexor forearm, is useful when perfumes, shampoos, or other home agents are suspected.
Patch testing is indicated when ACD is suspected and does not respond to treatment, suggesting that the trigger has not been identified. In patch testing, standard contact allergens are applied to the upper back using adhesive-mounted patches containing minute amounts of allergen or plastic (Finn®) chambers containing allergen held in place with porous tape. Thin-layer rapid use epicutaneous (TRUE TEST®) patch testing is a simple, easy-to-use kit with the most common contact allergens that can be applied and interpreted by any health care practitioner. Skin under the patches is evaluated 48 and 96 hours after application. False-positive results occur when concentrations provoke an irritant rather than an allergic reaction, when reaction to one antigen triggers a nonspecific reaction to others, or with cross-reacting antigens. False-negative results occur when patch allergens do not include the offending antigen. Definitive diagnosis requires a positive test result and a history of dermatits in the area where the tested agent contacted the skin.
Common Allergens Used in Patch Testing
Resolution may take up to 3 weeks. Reactivity is usually lifelong. Patients with photoallergic contact dermatitis can have flares for years when exposed to sun (persistent light reaction).
Contact dermatitis is prevented by avoiding the trigger; patients with photosensitive contact dermatitis should avoid exposure to sun.
Topical treatment includes cool compresses (saline or Burow solution) and corticosteroids; patients with mild to moderate ACD are given mid- to high-potency topical corticosteroids (eg, triamcinolone 0.1% ointment or betamethasone valerate cream 0.1%). Oral corticosteroids (eg, prednisone 60 mg once a day for 7 to 14 days) can be used for severe blistering or extensive disease. Systemic antihistamines (eg, hydroxyzine, diphenhydramine) help relieve pruritus; antihistamines with low anticholinergic potency, such as low-sedating H1 blockers, are not as effective. Wet-to-dry dressings can soothe oozing blisters, dry the skin, and promote healing.
Contact dermatitis can be caused by irritants (eg, plants, soaps, chemicals, body fluids), comprising 80% of cases, or by allergens, comprising 20% of cases.
Symptoms can include predominantly pain (for irritant contact dermatitis) or pruritus (for allergic contact dermatitis).
Diagnosis is usually clinical.
Patch testing is helpful when allergic contact dermatitis is suspected and the trigger has not been identified.
Treatments commonly include cool compresses, topical corticosteroids, and systemic antihistamines as needed for pruritus.