Inflammation of the epidermis and dermis caused by either irritant reaction (ICD) or allergic reaction from prior sensitization (ACD).

• ICD: Direct contact of dry skin with a chemical that removes water-binding/controlling lipids (ie, ceramides); causes impairment of keratinocyte-to-keratinocyte adhesion; results in an immediate inflammatory reaction; resolves after removal of offending chemical; may occur within minutes to 48 hours of exposure.
  
• ACD: Memory T-lymphocytes sensitized to an allergen activate immune response; requires a period of sensitization (days to weeks or longer); symptoms appear ~12 to 24 hours after reexposure to the offending allergen; triggers dermatitis lasting days to weeks after removal of causative allergen; severity of reaction varies with allergen varies; the more potent the allergen (ie, urushiol in poison ivy), the fewer exposures are required to sensitize T-cells and trigger a reaction.
  
• Variations: Photo-contact dermatitis, requires ultraviolet A irradiation (UVA) to transform a chemical into an irritant or allergen; associated with direct or immunological stimulation of mast cells. Phytophotodermatitis, requires contact with a photosensitizing chemical (furocoumarins, plant source) on the skin, UVA light chemically changes the preallergen to an allergen (eg, lime juice, celery juice).

Subtle variations in prevalence of certain allergens across regions of the world; the most common allergens (ie, nickel, neomycin, and lanolin) are common among developed nations; allergens can be natural or synthetic to include other metals (potassium dichromate used in leather); other topical medications (ie, bacitracin, triamcinolone); fragrances (ie, Balsam of Peru); preservatives (ie, formaldehyde and formaldehyde-releasing chemicals); other chemicals used in the diaper-, rubber-, and paper-making processes; propylene glycol.

• Irritant contact dermatitis (acute): Pink to red erythematous macules or patches with scale and sometimes fissures, crusts, or erosions; patches and plaques are well demarcated and may result in bullae, erosions, or ulcerations; common in diaper area because of contact with urine, feces, and sweat.
  
• Allergic contact dermatitis (acute): Pink to red erythematous and edematous papules and plaques with or without vesicles or bullae that may later crust over after rupturing; borders of the plaques are well defined but not as sharply as in ICD and the edematous plaques, vesicles and bullae may spill over the border.
  
• Subacute and chronic contact ICD/ACD: Similar to acute; pink to red erythematous macules, patches, and plaques, but often with lichenification.

Pattern of the dermatitis, especially when localized, can be helpful to identify a possible cause.

Serology and skin biopsy are of little value except to rule out viral or autoimmune disease.

Refer to a dermatologist/allergist for possible patch testing if the source is unclear.

• Identification and avoidance of offending irritant/allergen.
  
• Moisturization to reestablish the skin barrier function; sometimes wet wraps are used to augment.
  
• Flanders Buttocks Ointment (zinc oxide, white petrolatum, Peruvian Balsam) is an effective OTC product though Peruvian Balsam (Balsam of Peru) is, itself, a potential contact allergen.
  
• Topical mid-potency to high-potency topical steroids (triamcinolone, clobetasol respectively) and/or topical calcineurin inhibitors (for sensitive areas, such as the face and intertriginous areas); topical phosphodiesterase inhibitors (crisaborole).
  
• Prednisone 1 to 2 mg/kg/day for 7 to 10 days then tapered for 7 to 14 days if BSA >20%.
  
• Domeboro soaks (aluminum acetate solution, available OTC) to weeping or blistered areas may help dry the dermatitis.
  
• Consider bacterial culture if suspect secondary impetiginization.

Usually, pruritic hypopigmented to erythematous papules diffusely on sun-exposed skin; variants include vesicles, papulovesicles, nodules, lichenoid papules, targetoid lesions, and eczematous patches; African-Americans and Asians may present with pinpoint papules.

• Juvenile spring eruption (variant): Hypopigmented to erythematous papules on the sun-exposed ears, especially superior helix; 5- to 12-year-old boys; may evolve to vesicles and crusts and heal with scarring; develops hours to days after exposure; lasts up to a week if exposure is eliminated but in rare cases last for weeks.
  
• Actinic prurigo: Probably a hereditary variant of PMLE; one-third of patients are children under 10 years old; more common in native Americans; associated with itchy papules and nodules commonly on face, lips, and conjunctiva; often spreads to covered sites including the arms, legs, and buttocks.

Triad of pruritus, chronic relapsing eczema, and typical morphology and distribution.

Skin

• Newborns and infants: Erythematous, scaly patches and plaques; cheeks, neck, ears, forehead, scalp, upper chest, occasionally more widespread but diaper area invariably spared.
  
• Older infants and toddlers: Same as young infants but also extensor surfaces of arms and legs.
  
• Preschoolers and older children: Neck, flexures of arms and legs, buttock creases; can be widespread with sparing of areas difficult to reach/scratch.
  
• Other associated findings: Pityriasis alba, ichthyosis vulgaris, keratosis pilaris, secondary impetiginization, linear excoriations, lichenification, postinflammatory pigment changes.
  
• Eyes: Pruritus, prominence of infraorbital folds, photophobia, conjunctivitis, posterior subcapsular cataracts, and keratoconus.

Moisturize, treat active flare-ups until clear, address secondary bacterial infection, then maintain by more moisturizing, and avoidance of possible triggers.

• Bathing practices: Crucial to hydrate the skin; immediate application of moisturizers to reduce transepidermal water loss; bathe for 5 to 10 minutes in warm water; nonsoap cleansers free of topical sensitizers; dye and perfume-free; dilute bleach bath therapy; 1/4 cup (2 oz) of liquid, unscented house hold bleach in a bathtub volume of water; 2 to 3 times per week to reduce bacterial colonization; moisturize immediately while skin is still wet to avoid drying effect of bleach.
  
• Moisturizers: Cornerstone of maintenance therapy; alone, without topical corticosteroids, can decrease symptoms of atopic dermatitis; as often as is necessary to protect skin; avoid moisturizers with fragrance or topical sensitizers; ointments are free of preservatives though are not as cosmetically elegant; use at bedtime with old pajamas may be a best routine; creams are more moisturizing than lotions or oils; added ceramides can help improve function of a moisturizer; “soak and smear” with both topical steroids and moisturizers will improve effectiveness of both; prolonged use of wet wraps has been associated with adrenal suppression when used with high-potency steroid or when large surface areas are treated.
  
• Topical corticosteroids: Consider them “fire extinguishers,” use when skin is flared, not at all when clear; mainstay of therapy for several decades; twice per day use, applying more than twice daily increases risk of systemic absorption and adverse effects (striae, atrophy, telangiectasias, steroid acne, hypopigmentation, and hypertrichosis); choice is based on potency, vehicle, location used, and insurance coverage/cost; relative potency is ointment>cream>lotion; solutions and foams are ideal for hair-bearing skin; lower potency on thinner skin (face, axillae, and genitalia), twice per day for 2 to 4 days then taper to 2 to 3 times per week as needed; mid- to high potency on thicker skin twice per day for 1 to 2 weeks then taper to as-needed.
  
• Topical calcineurin inhibitors: Tacrolimus, and pimecrolimus; nonsteroid, can be used at any site, 1 to 2 times per day, slower response than with steroids, transient stinging possible; long-term risk controversial but generally considered safe for topical use.
  
• Topical phosphodiesterase inhibitors: Crisaborole, nonsteroid, can be used at any site, 1 to 2 times per day, also slower response than with steroids, transient stinging also possible.
  
• Topical Janus kinase inhibitors: Ruxolitinib, nonsteroid, also used at any site twice per day, also slower response than steroids, cannot be used along with dupilumab or tralokinumab-ldrm.
  
• Phototherapy: NB-UVB, 2 to 3 times per week, can be inconvenient, each treatment usually requires insurance co-pay; natural sunlight exposure, 10 to 15 minutes of unprotected exposure 3 to 4 days per week can be helpful.
  
• Biologic therapy:
  
  
  
  • Dupilumab: Subcutaneous injection once every 2 weeks, approved for 6 months or older; IL-4Rα receptor blocker, alters IL-4 and IL-13 signaling; excellent efficacy and safety profile, possible conjunctivitis in some patients though not usually severe enough to stop the medication.
    
  • Tralokinumab-ldrm: Subcutaneous injection once every 2 weeks, approved for 18 years or older, binds to and inhibits IL-13.

Erythema, scaling, and mild-to-moderate pruritus over areas of the body with higher density of sebaceous glands.

Infantile

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