Atopic dermatitis (AD), also called eczema, is a chronic, pruritic inflammatory skin disease and the most common chronic skin inflammation worldwide. It often begins in infancy and is nicknamed "the itch that rashes" (itching leads to scratching and then rash). A defective skin barrier (often filaggrin gene mutations) and IgE-mediated immune activation (Th2 skewing) underlie its recurrent eczematous lesions with dryness and lichenification.
AD affects up to 20% of children (and ~10% of adults), causing significant morbidity (sleep disturbance, secondary infections). It can greatly impact quality of life for patients and families, and it frequently appears on exams due to its prevalence and classic presentations.
Infantile AD: onset by 6–12 months with an itchy, red, scaly rash on the cheeks (often spreading to extensor limbs) that spares the diaper area. Infants may rub their skin instead of scratching, and fussiness at night is common.
Childhood AD: chronic eczema localizes to flexural creases – especially the antecubital fossae (elbows) and popliteal fossae (knees) – with skin lichenification from repeated scratching. Often associated with other atopic conditions like asthma or allergic rhinitis.
Adult AD: may persist from childhood or begin anew (adult-onset). Commonly involves flexures or presents as hand eczema, eyelid dermatitis, or nipple eczema. The skin is chronically dry, thickened, and easily inflamed; stress or irritants can precipitate flares.
Diagnose clinically – recognize the age-specific distribution and chronic relapsing course. If features are atypical (absence of pruritus, very poor response to therapy), reconsider the diagnosis or look for another cause. Routine lab tests are usually not needed.
Identify and minimize triggers: practice gentle skin care (lukewarm baths, mild soap, soft cotton clothing) and avoid irritants (excess washing, wool) or allergens (dust mites, certain foods) that can flare eczema.
Treat superinfections promptly: signs like oozing or honey-colored crust suggest Staph aureus infection (impetiginised eczema) – use appropriate antibiotics. Monomorphic punched-out lesions or sudden worsening could indicate HSV (eczema herpeticum).
Consider allergy workup in refractory cases: e.g., patch testing for contact allergens if a localized persistent rash, or evaluating food allergies in severe infantile eczema.
intensely itchy (especially at night) with burrows; often involves family members (contagious mites)
Basic management for all: maintain skin hydration with daily emollients (moisturizers) applied liberally; use gentle bathing (lukewarm water, mild cleansers) and avoid known triggers (harsh soaps, wool clothing, allergens).
For flares: apply topical corticosteroids (low-potency for face, medium/high for body) twice daily to inflamed areas until lesions improve. For steroid-sparing maintenance or sensitive areas (face, skin folds), use topical calcineurin inhibitors (tacrolimus, pimecrolimus). Sedating antihistamines at bedtime may help break the itch–scratch cycle.
If signs of secondary infection (e.g. impetigo with honey-colored crusts), treat with antibiotics and consider bleach baths to reduce Staph colonization. Viral complications (eczema herpeticum) require prompt acyclovir.
Moderate-to-severe or refractory AD: consider phototherapy (narrow-band UVB) or systemic therapy. Options include short-term cyclosporine or methotrexate, or newer biologics like dupilumab (anti–IL-4α receptor antibody) which can dramatically improve severe eczema.
AD is called "the itch that rashes" – intense itching typically precedes the rash.
Many cases involve a filaggrin gene defect – a skin barrier protein – leading to chronically dry, barrier-impaired skin.
Eczema herpeticum: eruption of painful, monomorphic blisters or punched-out erosions with fever on eczematous skin – indicates HSV infection on eczema (medical emergency, start antivirals).
Erythroderma: generalized (>90%) redness and scaling of the skin (can occur in severe AD) – risk of dehydration, hypothermia, infection; requires urgent evaluation and management.
Severe eczema in infancy with recurrent infections or poor growth – consider an immunodeficiency (e.g. Wiskott–Aldrich syndrome or hyper-IgE syndrome) as an underlying cause.
Chronic pruritic dermatitis in typical locations (face/extensors in infants, flexural in older patients) + personal/family atopy history → suspect atopic dermatitis.
Start: avoid triggers (irritants, allergens) and begin daily moisturizer use; treat active lesions with topical steroids.
If poor control or frequent flares: check adherence and look for complications (infection, contact dermatitis); add steroid-sparing topicals (tacrolimus) or antihistamines for itch as needed.
Escalate therapy for severe cases: refer for phototherapy or systemic treatments (e.g. dupilumab or cyclosporine) when AD remains uncontrolled by topical therapies.
Infant with chronic facial rash (erythematous, scaly cheeks) sparing the diaper area + family history of atopy → atopic dermatitis (infantile eczema).
Toddler with an itchy, eczematous rash in the antecubital and popliteal fossae + history of asthma → atopic dermatitis (flexural eczema).
Patient with known eczema develops fever and uniform "punched-out" erosions in eczematous areas → eczema herpeticum (HSV superinfection).
Case 1
An 8‑month‑old infant has a 6-month history of an itchy, red rash on the cheeks, trunk, and extensor surfaces.
Illustration of how atopic dermatitis distribution varies with age: infant (facial/extensor), child (flexural), adult (possibly hand or localized).
