Dermatology · PANCE / PANRE

Atopic Dermatitis (Eczema)

Written & clinically reviewed by Ryan Busch, PA-C · Updated October 2026 · Report an error

Chronic relapsing pruritic inflammatory dermatosis driven by skin barrier dysfunction and Th2 immune skewing; part of the atopic march.

Also known as: atopic dermatitis, eczema, AD, atopic eczema, infantile eczema

Overview

A chronic, intensely pruritic, relapsing inflammatory skin disease characterized by age-dependent distribution of eczematous patches, often associated with personal or family history of atopy (asthma, allergic rhinitis, food allergy).

Epidemiology

Affects about 10-13% of US children (up to 15-20% in some high-income countries) and about 7% of US adults. Onset before age 5 in 85% of cases. Higher prevalence in urban populations and developed countries. Most childhood cases improve or remit by adolescence; a minority persist into adulthood, and adult-onset disease also occurs.

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Question 1DermatologyEasy
A 3-month-old infant has erythematous, scaly, weeping patches on the cheeks and scalp with intense itching. The rash spares the diaper area. Family history is positive for asthma and allergic rhinitis. Which of the following is the most likely diagnosis?
  • AContact dermatitis
  • BAtopic dermatitis
  • CSeborrheic dermatitis
  • DTinea capitis
  • EScabies infestation
Reveal answer & full explanation
Correct answer: B — Atopic dermatitis
  • AContact dermatitis
  • BAtopic dermatitis✓
  • CSeborrheic dermatitis
  • DTinea capitis
  • EScabies infestation

Why Atopic dermatitis is correct

  • Infantile atopic dermatitis presents with erythematous, scaly, weeping patches on the face and scalp
  • Intense pruritus is the hallmark feature
  • Sparing of the diaper area is characteristic and distinguishes it from seborrheic dermatitis
  • A family history of the atopic triad (eczema, asthma, allergic rhinitis) supports the diagnosis

Why the others are wrong

  • Contact dermatitis — requires a clear exposure and does not follow the infantile face/scalp pattern or correlate with atopic family history (premature closure on 'rash = irritant')
  • Tinea capitis — a fungal scalp infection with scaling and hair loss, not weeping facial patches, and rare at 3 months; confirmed by KOH or culture (buzzword-matching on 'scaly scalp')
  • Seborrheic dermatitis — involves the diaper area and scalp with greasy yellow scales and is not intensely pruritic (confused-with-AD trap; the diaper-area clue separates them)
  • Scabies infestation — infant scabies is intensely pruritic and, unlike scabies in adults, can involve the face and scalp, but it produces widespread papules, vesicles, burrows, and nodules that typically include the palms, soles, and axillae, and household contacts often itch too; weeping scaly patches confined to the cheeks and scalp in an infant with an atopic family history fit atopic dermatitis (buzzword-matching on 'intense itching')

Additional high-yield points

  • Treatment: emollients after bathing ('soak and seal'); low-potency topical corticosteroids for facial flares; topical tacrolimus or pimecrolimus for sensitive areas
  • Avoid fragrance, wool, and harsh soaps; dupilumab is approved down to 6 months for moderate-to-severe disease
Question 2DermatologyEasy
A 7-year-old has chronic, intensely pruritic eczematous patches on the antecubital and popliteal fossae. Family history is positive for asthma and seasonal allergies. Which of the following is the most likely diagnosis?
  • APsoriasis
  • BAtopic dermatitis
  • CContact dermatitis
  • DClassic scabies
  • ETinea corporis
Reveal answer & full explanation
Correct answer: B — Atopic dermatitis
  • APsoriasis
  • BAtopic dermatitis✓
  • CContact dermatitis
  • DClassic scabies
  • ETinea corporis

Why Atopic dermatitis is correct

  • Classic presentation: chronic, relapsing, intensely pruritic dermatitis with flexural distribution in older children and adults (antecubital fossa, popliteal fossa, neck); extensor surfaces and face are involved in infants.
  • Atopic triad: eczema, asthma, and allergic rhinitis — the family history of asthma and seasonal allergies supports this.
  • Pathogenesis: filaggrin gene mutations combined with a Th2-predominant immune response.
  • Diagnosis is clinical, based on morphology, distribution, chronic-relapsing course, and personal or family atopy.

Why the others are wrong

  • Tinea corporis — confused-with: fungal infection with annular scaly plaques and central clearing and a positive KOH preparation, not chronic flexural eczema with atopic history.
  • Contact dermatitis — right-concept-wrong-setting: distribution follows a linear or geometric pattern matching the exposure area and needs no personal or family atopic history.
  • Psoriasis — confused-with: well-demarcated plaques with silvery scale favor extensor surfaces rather than flexures, and associate with nail pitting and psoriatic arthritis.
  • Classic scabies — confused-with: an intensely pruritic, often eczematized eruption that can involve flexural skin, but scabies favors the finger webs, wrists, axillae, waistband, and genitals, may show burrows, and spreads to itching household contacts rather than following a chronic relapsing antecubital and popliteal course with family atopy.

Additional high-yield points

  • Treatment ladder: emollients (first step), topical corticosteroids (low to mid potency on body; low potency on face and skin folds), topical calcineurin inhibitors (tacrolimus), and trigger avoidance.
  • Severe or refractory disease: dupilumab (anti-IL-4 receptor monoclonal antibody).

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Risk factors

  • Family or personal history of atopy (asthma, allergic rhinitis, food allergy)
  • Filaggrin (FLG) loss-of-function mutations — strongest genetic risk factor
  • Low humidity climates, harsh soaps, frequent bathing without moisturizer
  • Aeroallergens, food allergens (in young children), Staphylococcus aureus colonization
  • Stress, sleep disturbance, sweating

Pathophysiology

Combination of (1) epidermal barrier dysfunction — filaggrin and lipid deficiency, increased transepidermal water loss — and (2) Th2-skewed immune response with IL-4, IL-13, IL-31 (pruritus), and IL-22 driving inflammation, epidermal hyperplasia, and impaired antimicrobial defense. Itch-scratch cycle perpetuates barrier disruption.

Clinical presentation

Symptoms

  • Intense pruritus — required feature; often worse at night, disrupts sleep
  • Chronic relapsing course with flares and remissions
  • Dry skin (xerosis) between flares

Signs / physical exam

  • Infants (0-2 yrs): erythematous, weeping, crusted patches on cheeks, scalp, extensor extremities; spares diaper area
  • Children (2-12 yrs): lichenified plaques in flexural areas — antecubital, popliteal fossae, neck, wrists, ankles
  • Adults: chronic lichenification of hands, neck, eyelids, flexures; nipple eczema; head-and-neck dermatitis (Malassezia)
  • Associated features: Dennie-Morgan infraorbital folds, allergic shiners, keratosis pilaris, ichthyosis vulgaris, palmar hyperlinearity, white dermatographism

Classic findings

Flexural eczematous patches with lichenification in a child or adolescent with personal/family atopy.

Differential diagnosis

  • Seborrheic dermatitis — Greasy yellow scale on scalp, eyebrows, nasolabial folds; less pruritic; infant cradle cap can mimic infantile AD
  • Allergic / irritant contact dermatitis — Sharply demarcated lesions matching exposure pattern; patch testing positive for contactant
  • Psoriasis — Well-demarcated thick silvery plaques on extensor surfaces, scalp, nails; Auspitz sign
  • Scabies — Intense nocturnal pruritus, burrows in web spaces/wrists, household contacts affected
  • Cutaneous T-cell lymphoma (mycosis fungoides) — Adult-onset 'eczema' refractory to therapy in non-sun-exposed areas; skin biopsy
  • Tinea corporis — Annular plaques with raised scaly border and central clearing; KOH positive
  • Nummular dermatitis — Coin-shaped well-circumscribed plaques on extremities; can overlap with AD

Diagnostic workup

Diagnostic criteria

Hanifin and Rajka criteria (3 major + 3 minor) or AAD simplified criteria. Essential features: pruritus + eczematous dermatitis in age-typical distribution + chronic/relapsing course.

Labs

  • Clinical diagnosis — no required labs
  • Serum total IgE often elevated; allergen-specific IgE or skin-prick testing only if clear allergic trigger suspected
  • Skin culture if secondary infection suspected
  • Skin biopsy reserved for atypical or refractory cases to exclude CTCL

Imaging

  • Not indicated

Diagnostic algorithm

Age GroupTypical DistributionLesion Features
Infant (0-2)Cheeks, scalp, extensor extremities; spares diaper areaAcute erythematous weeping crusted patches
Childhood (2-12)Flexural — antecubital, popliteal, neck, wrists, anklesSubacute scaly excoriated plaques, early lichenification
Adolescent / AdultFlexures, hands, eyelids, neck, nipplesChronic lichenified plaques, post-inflammatory pigment change
Age-dependent distribution of atopic dermatitis.

Treatment

First-line

  • Skin barrier repair: emollient/moisturizer (ceramide-containing, petrolatum-based) applied liberally ≥2x/day and immediately after bathing ('soak and seal')
  • Lukewarm short baths/showers with non-soap cleanser (e.g., syndet); pat dry
  • Topical corticosteroid potency tailored to severity and site — hydrocortisone 1-2.5% (low; face, folds, infants), triamcinolone 0.1% (mid; trunk/extremities), clobetasol 0.05% (super-high, class I; short courses of ≤2 weeks for thick lichenified plaques or palms/soles; not recommended under age 12 or on face/folds, so a child's mildly lichenified flexural patches get mid-potency triamcinolone)
  • Topical calcineurin inhibitors — tacrolimus 0.03-0.1% ointment, pimecrolimus 1% cream — steroid-sparing, especially face/eyelids/folds
  • Topical PDE4 inhibitors — crisaborole 2% ointment (≥3 months old), roflumilast cream (0.15% ages ≥6; 0.05% ages 2-5)
  • Topical JAK inhibitor — ruxolitinib 1.5% cream (mild-moderate AD, ages ≥2; short-term, non-continuous use); topical AhR agonist — tapinarof 1% cream (ages ≥2)
  • Trigger avoidance: harsh soaps, fragranced products, wool, sweating; address food allergies if proven
  • Proactive maintenance for recurrent flares at the same sites: once the skin clears, apply a medium-potency topical corticosteroid twice weekly to the usual flare sites (AAD 2023), or tacrolimus 2-3 times weekly, plus daily emollient to reduce relapse

Moderate-severe / refractory

  • Wet-wrap therapy with mid-potency topical steroid for acute flares
  • Phototherapy: narrowband UVB (preferred), UVA1
  • Biologics — dupilumab (anti-IL-4Rα; ages ≥6 months), tralokinumab and lebrikizumab (anti-IL-13; ages ≥12), nemolizumab (anti-IL-31 receptor; ages ≥12)
  • Oral JAK inhibitors — upadacitinib, abrocitinib (ages ≥12); boxed warnings for serious infections, mortality, malignancy, MACE, and thrombosis
  • Conventional systemics — cyclosporine, methotrexate, azathioprine, mycophenolate (off-label, narrow use)

Secondary infection

  • Staph impetiginization: cephalexin or dicloxacillin × 7-10 days; mupirocin if localized; bleach baths (0.005%) twice weekly for chronic colonization
  • Eczema herpeticum (HSV superinfection): rapid-onset monomorphic punched-out vesicles, fever — IV or oral acyclovir, ophthalmology if periocular

Second-line / adjunct

  • Sedating antihistamine (hydroxyzine, diphenhydramine) at night for sleep — does not treat itch directly
  • Non-sedating antihistamines have minimal benefit in AD
  • Address psychosocial impact — sleep, school/work, mental health

Complications

  • Bacterial superinfection (S. aureus) and impetiginization
  • Eczema herpeticum — disseminated HSV; dermatologic emergency
  • Atopic march: progression to allergic rhinitis and asthma
  • Sleep disturbance, ADHD-like inattention, depression, anxiety
  • Ocular: keratoconus, atopic keratoconjunctivitis, cataracts (long-term steroid use)
  • Growth impairment in severe pediatric disease
  • Skin atrophy and striae from prolonged potent topical steroids

PANCE pearls

  • Pruritus is required for diagnosis — 'eczema' without itch is not atopic dermatitis.
  • Use the fingertip unit (FTU) rule: 1 FTU = ~0.5 g, covers area of 2 adult palms.
  • Topical calcineurin inhibitors carry a boxed warning for theoretical malignancy risk, but long-term data have not substantiated this — they remain safe and effective for face/folds.
  • Bleach baths (1/4 to 1/2 cup household bleach in full tub) twice weekly reduce S. aureus burden and flare frequency.
  • Sudden monomorphic punched-out erosions and fever in a child with AD = eczema herpeticum until proven otherwise — start acyclovir immediately.
  • Avoid systemic corticosteroids in atopic dermatitis (AAD 2024 makes a conditional recommendation against them): the disease often rebounds, sometimes worse, after the course ends; use at most as a brief bridge to steroid-sparing systemic therapy.

References

  • AAD 2023 — Guidelines of Care for the Management of Atopic Dermatitis in Adults with Topical Therapies (Sidbury R, Alikhan A, Bercovitch L, et al., J Am Acad Dermatol 2023;89(1):e1-e20)
  • AAP 2014 — Atopic Dermatitis: Skin-Directed Management — American Academy of Pediatrics (Tollefson, Bruckner, Pediatrics 2014)
  • Hanifin-Rajka — Diagnostic Features of Atopic Dermatitis (Hanifin and Rajka, Acta Derm Venereol Suppl 1980)
  • AAD 2024 — Guidelines of Care for the Management of Atopic Dermatitis in Adults with Phototherapy and Systemic Therapies (Davis DMR et al., J Am Acad Dermatol 2024;90(2):e43-e56)
  • AAD 2025 — Focused Update: Guidelines of Care for the Management of Atopic Dermatitis in Adults (Davis DMR, Frazer-Green L, Alikhan A, et al., J Am Acad Dermatol 2025;93(3):745.e1-745.e7)

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Commonly confused with

vs Seborrheic Dermatitisvs Psoriasisvs Scabies

Related Dermatology diagnoses

Acne VulgarisRosaceaAllergic and Irritant Contact DermatitisSeborrheic DermatitisPsoriasisLichen PlanusPityriasis RoseaTinea Infections (corporis, capitis, pedis, cruris, versicolor)Cutaneous CandidiasisScabiesPediculosisImpetigoHerpes Zoster (Shingles)Verrucae (Warts, HPV)

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.