T-cell-mediated delayed hypersensitivity reaction. Antigen penetrates skin and conjugates with cutaneous protein. Hapten-protein complex undergoes transport to regional lymph nodes via Langerhans cells. Sensitized T-cells disseminate systematically. Re-exposure provokes inflammatory reaction within 8-12 hours.
Urushiol from poison ivy, nickel, neomycin, fragrances, shoe rubber accelerators, chemical sunscreens, methylisothiazolinone.
Clinical Manifestations
Disease Phase
Irritant Contact Dermatitis
Allergic Contact Dermatitis
Acute Presentation
Erythematous, scaling, and fissured skin directly localized to exposure site.
Intensely pruritic, erythematous, edematous, and vesiculobullous lesions.
Chronic Presentation
Chronic hypertrophic flat-topped papules and infiltrative nodules.
Lichenification, profound scaling, fissuring, and post-inflammatory pigmentary changes.
Distribution
Strictly confined to irritant contact area. Spares protected skin folds.
Airborne sensitizers affect exposed areas like face. May disseminate systematically if antigen enters circulation.
Specific Clinical Variants
Irritant Variants
Dry Skin Dermatitis: Results from repetitive wet-to-dry behaviors including lip licking, thumb sucking, and frequent handwashing.
Diaper Dermatitis: Triggered by prolonged contact with feces and ammonia produced by urea-splitting organisms. Involves convexity of buttocks while sparing depth of genitocrural folds. Frequently complicated by superadded candidal infection.
Allergic Variants
Rhus Dermatitis: Caused by urushiol allergen in poison ivy, sumac, or oak. Manifests as linear streaks of vesicles where plant brushed against skin. Black spot variant presents as discrete black lacquer-like glossy papules due to urushiol oxidation.
Nickel Dermatitis: Triggered by jewelry or metal closures on clothing. Typically presents as periumbilical or earlobe dermatitis.
Shoe Dermatitis: Reaction to antioxidants, rubber accelerators, adhesives, or chromium salts leached by sweat. Involves dorsum or soles of feet while sparing interdigital spaces symmetrically.
Cosmetic And Medication Dermatitis: Common offenders include neomycin, topical antihistamines, chemical sunscreens containing oxybenzone, and methylisothiazolinone found in wet wipes and homemade slime.
Diagnosis And Management
Diagnostic Approach
Detailed clinical history evaluating environmental exposures, cultural customs, daily activities, and personal product usage remains paramount.
Patch testing provides diagnostic utility for identifying specific allergens in older children but remains unreliable in infants.
Therapeutic Protocols
Intervention Category
Specific Management Strategy
General Preventive Measures
Identify and completely eliminate offending environmental agent. Strictly avoid prescribing sensitizing topical anesthetics or topical antihistamines.
Irritant Dermatitis Management
Eliminate repetitive wet-to-dry behaviors. Apply thick cream or ointment-based moisturizers twice daily to decrease transepidermal water loss. Utilize low-potency topical corticosteroids temporarily for active inflammation.
Acute Allergic Management
Apply mid-potency topical corticosteroid ointment for 2-3 weeks. Utilize wet dressings to cool skin, remove exudate, and decrease pruritus for weeping lesions. Administer sedating oral antihistamines to facilitate sleep.
Severe Allergic Management
Initiate systemic corticosteroids if greater than 10 percent of body surface area involved. Administer 0.5-1.0 mg/kg prednisone up to 60 mg daily for 7-10 days, followed by slow 7-10 day taper.
Diaper Dermatitis Care
Keep diaper area clean and dry. Avoid disposable semiabsorbent occlusive diapers. Rinse washed cotton diapers in dilute lemon juice or vinegar. Apply barrier creams including zinc oxide or petrolatum. Utilize topical antifungals for secondary candidiasis.
