Skin & Subcutaneous Tissue

Atopic dermatitis: outpatient management

Clinical Overview and When to Suspect Atopic Dermatitis

— Affects ~15–20% of children and 7–10% of US adults

— 60% present by age 1, 90% by age 5; about one-third persist into adulthood

— Strong familial clustering; concordance ~80% in monozygotic twins

— Infant (0–2 yr): cheeks, scalp, extensor surfaces; diaper area spared

— Child (2–12 yr): flexural (antecubital, popliteal), neck, wrists, ankles

— Adolescent/adult: hand eczema, eyelid/periorbital, flexural lichenification, "head-and-neck dermatitis"

— Mild: <10% BSA, localized, minimal sleep impact

— Moderate: 10–30% BSA, recurrent flares, some sleep/QoL impact

— Severe: >30% BSA or refractory, sleep disruption, depression risk

Board pearl: Filaggrin (FLG) mutations are the strongest known genetic risk and also predict ichthyosis vulgaris and peanut allergy — a single mutation can connect three Step 3 stems.

Step 3 management: AD is fundamentally an outpatient longitudinal disease — frame visits around trigger avoidance, daily emollients, step-up anti-inflammatory therapy, and atopic-march surveillance, not one-time cures.

Definition: Chronic, relapsing, intensely pruritic inflammatory dermatosis driven by epidermal barrier dysfunction (filaggrin loss-of-function), Th2-skewed immune activation (IL-4, IL-13, IL-31), and cutaneous dysbiosis with Staphylococcus aureus overgrowth.

Epidemiology:

Atopic march: AD often precedes food allergy, allergic rhinitis, and asthma — anticipate and screen for these longitudinally in primary care.

When to suspect (Hanifin–Rajka simplified / AAD criteria): Must have pruritus plus eczematous dermatitis with typical morphology and age-specific distribution, chronic or relapsing course, and personal/family history of atopy.

Age-based distribution:

Triggers to elicit in outpatient visit: dry climate/winter, sweat, wool, soaps/detergents, fragrances, aeroallergens (dust mites, pollens), stress, infections.

Severity stratification (drives therapy ladder):

Presentation Patterns and Key History

— Acute: erythematous papules/vesicles, weeping, crusting, excoriation

— Subacute: scaly erythematous plaques

— Chronic: lichenification, hyperpigmentation, prurigo nodules

— Onset age, flare frequency, duration of current flare

— Distribution and whether it migrates with age (supports AD vs. fixed dermatoses)

— Trigger inventory: hot showers, harsh soaps, fragranced lotions, wool, sweat, stress, illness, seasonal change

— Bathing/skincare practices — frequency, soap type, moisturizer use and timing

— Personal atopy: asthma, allergic rhinitis, food allergy, conjunctivitis

— Family history of atopy in first-degree relatives

— Occupational/hobby exposures (wet work, latex, nickel) — overlapping contact dermatitis is common

— Prior treatments: potency, duration, response, steroid phobia

— Sleep quality, school/work absenteeism, mood symptoms — QoL is a treatment endpoint

— Sudden monomorphic vesicles/punched-out erosions → eczema herpeticum

— Honey-colored crust with fever → impetiginized AD

— Failure to thrive + diarrhea + severe early AD → consider immunodeficiency (Wiskott-Aldrich, hyper-IgE/Job, Omenn)

— Onset after age 50 with no atopic history → think cutaneous T-cell lymphoma (mycosis fungoides)

Key distinction: AD pruritus is chronic and relapsing in atopic distribution; scabies pruritus is worse at night with web-space burrows and household contacts itching — always ask "is anyone else at home itching?"

Board pearl: A POEM score ≥17 or itch NRS ≥7 on most days defines uncontrolled disease and justifies step-up to systemic therapy referral.

Cardinal symptom: Pruritus is required — "the itch that rashes." Scratching produces the visible lesions; ask specifically about nocturnal itch and sleep loss.

Lesion evolution:

Targeted history checklist for the outpatient encounter:

Quantitative tools used in practice: POEM (Patient-Oriented Eczema Measure), DLQI, or simple 0–10 itch NRS — document baseline and reassess at follow-up.

Red flags that change the differential:

Physical Exam Findings

— Lichenification: thickened skin with accentuated skin lines from chronic rubbing

— Post-inflammatory hyper- or hypopigmentation (more visible in skin of color)

— Prurigo nodules: firm, hyperkeratotic, intensely pruritic papulonodules

— Fissures, especially fingertips, retroauricular folds, and infra-auricular crease

— Dennie-Morgan infraorbital folds

— Periorbital darkening ("allergic shiners")

— Hertoghe sign — lateral eyebrow thinning

— Keratosis pilaris on extensor arms/thighs

— Palmar hyperlinearity (filaggrin marker)

— Pityriasis alba — hypopigmented scaly patches on cheeks

— White dermographism

— Anterior neck folds, "dirty neck" reticulated pigmentation

— Honey crust, pustules, regional adenopathy → bacterial superinfection (S. aureus)

— Grouped umbilicated vesicles, punched-out erosions, fever → eczema herpeticum (HSV)

— Molluscum dermatitis: eczematous halo around umbilicated papules

Step 3 management: At every follow-up, palpate lichenified areas and photograph or body-map distribution — objective tracking drives therapy escalation decisions and supports prior-authorization for biologics.

Board pearl: New punched-out monomorphic erosions in an AD patient = eczema herpeticum until proven otherwise → start oral acyclovir empirically and obtain HSV PCR.

Primary lesions: Ill-defined erythematous papules and plaques, often with overlying scale, excoriations, and serous crusting. Vesiculation suggests acute flare or superinfection.

Secondary changes (chronicity markers):

Distribution mapping (age-dependent — see Chunk 1). In skin of color, erythema may appear violaceous, gray, or hyperpigmented rather than red — do not under-rate severity by relying on redness alone.

Associated stigmata of atopy (worth documenting):

Signs of complications to examine for at every visit:

Severity grading at exam: Estimate BSA (palm ≈ 1%), note intensity (erythema, edema, excoriation, lichenification), and document on a body map.

Diagnostic Workup — Initial Evaluation

— Suspected superinfection: bacterial swab with culture and sensitivity of weeping/crusted lesions; consider MRSA coverage empirically while awaiting results

— Suspected eczema herpeticum: HSV PCR or Tzanck/DFA from vesicle base; do not delay acyclovir

— Recurrent skin infections, FTT, severe early-onset disease: CBC with differential, quantitative immunoglobulins (IgE, IgG, IgA, IgM), HIV in adults — rule out immunodeficiency

— Persistent unexplained eosinophilia or systemic symptoms: consider hypereosinophilic syndrome, parasitic infection

— Suspected IgE-mediated food allergy with anaphylaxis history (not for chronic AD severity)

— Refractory AD where aeroallergen avoidance might help

— Counsel families that food elimination diets without proven allergy can cause growth failure and de novo anaphylaxis on reintroduction

Key distinction: Elevated IgE supports atopy but does not establish or grade AD; clinical morphology + distribution + chronicity is the diagnostic standard. Don't anchor on a lab.

CCS pearl: Order "wound culture, bacterial" before initiating cephalexin for impetiginized AD — culture sensitivity drives Step 3 management when MRSA prevalence is high.

AD is a clinical diagnosis. No lab or imaging is required to make the diagnosis in a typical case. Step 3 stems testing "next best step" often want you to start emollients and topical steroids, not order labs.

When to obtain targeted testing:

Serum total IgE: Elevated in 70–80% of AD but non-specific and not required for diagnosis or to start therapy. Do not order routinely.

Allergy testing (skin prick or specific IgE): Reserve for:

Patch testing: Indicated when allergic contact dermatitis is suspected as a comorbid driver — eyelid, hand, or treatment-resistant AD; common culprits include nickel, fragrances, preservatives, neomycin, and topical corticosteroid components.

KOH prep: If lesions are annular or scaly with central clearing — exclude tinea before applying steroids (steroids → tinea incognito).

Diagnostic Workup — Advanced or Confirmatory Studies

— Atypical morphology (asymmetric, fixed, indurated plaques)

— Failure to respond to optimized therapy

— Adult-onset eczematous eruption without atopic history → rule out cutaneous T-cell lymphoma (mycosis fungoides) with biopsy and possible TCR gene rearrangement

— Suspected bullous pemphigoid in elderly with intense pruritus → DIF for linear C3/IgG at BMZ

— Photodistributed → ANA, photopatch testing → lupus, photoallergic dermatitis

— Greasy scale on scalp, nasolabial, sternum → seborrheic dermatitis (often coexists)

— Sharply demarcated plaques with silvery scale → psoriasis biopsy

— Genital/perianal predominance → consider contact dermatitis, lichen sclerosus

— Baseline CBC, CMP, hepatitis B/C, HIV, TB screen (IGRA) prior to dupilumab, JAK inhibitors, or traditional immunosuppressants

— Pregnancy test in reproductive-age women starting systemic agents

— Lipid panel and pregnancy screening before JAK inhibitors (upadacitinib, abrocitinib)

— Ophthalmology baseline if dupilumab planned in patients with prior conjunctivitis

Board pearl: A 50-year-old with new "eczema" that won't clear on steroids → biopsy for mycosis fungoides. Step 3 loves this stem — adult-onset, fixed buttock/trunk plaques, no atopic history.

Step 3 management: Document EASI, IGA, and DLQI in the chart before referring for dupilumab — these scores are the gateway for insurance approval and the right Step 3 "next step."

Skin biopsy: Rarely needed. Reserve for:

Histopathology of AD (non-diagnostic but supportive): Spongiosis (acute), acanthosis and hyperkeratosis (chronic), perivascular lymphocytic infiltrate with eosinophils.

Differential workup decision tree by atypical feature:

Workup for severe/refractory AD before systemic therapy:

Asthma/atopic march co-evaluation: Spirometry if wheeze/exercise intolerance; specific IgE or skin prick for environmental allergens if perennial rhinitis.

Quality-of-life and severity tools (re-administer at advanced workup): EASI ≥16 or IGA ≥3 or DLQI >10 supports systemic therapy criteria and insurance authorization.

Risk Stratification and First-Line Management Logic

— Daily lukewarm bath or shower ≤10 minutes; pat dry

— Apply thick emollient within 3 minutes of bathing ("soak and seal") — ointments > creams > lotions

— Fragrance-free, dye-free synthetic-detergent cleansers (e.g., Cetaphil, Dove Sensitive); avoid true soap

— Cotton clothing; avoid wool and rough synthetics; wash new clothes before wearing

— Cool, humidified environment; trim nails; cotton gloves at night for scratchers

— Identify and remove specific triggers from history

— Mild: Emollients + low-potency topical corticosteroid (hydrocortisone 2.5%) to face/folds; medium-potency (triamcinolone 0.1%) to body for flares, 1–2 weeks

— Moderate: Medium-to-high potency TCS BID for flares + topical calcineurin inhibitor (tacrolimus, pimecrolimus) or crisaborole/ruxolitinib for maintenance; consider proactive twice-weekly TCS to recurrent sites

— Severe/refractory: Add phototherapy (NB-UVB) or systemic therapy — dupilumab, tralokinumab, lebrikizumab, JAK inhibitors (upadacitinib, abrocitinib); short courses of cyclosporine for crisis control

— Systemic corticosteroids except brief rescue (rebound on taper)

— Topical antihistamines (sensitization)

— Indiscriminate antibiotics without infection signs (drives resistance, dysbiosis)

Key distinction: Reactive therapy treats visible flares; proactive (maintenance) therapy applies low-frequency anti-inflammatories to historically affected sites to prevent flares — the latter halves flare frequency in moderate-to-severe AD.

Step 3 management: When a stem says "patient using emollients but still flaring," the next step is add a topical corticosteroid of appropriate potency for site, not jump to a systemic agent.

Treatment is a stepwise ladder anchored on three pillars at every level: skin hydration, anti-inflammatory therapy, and trigger avoidance.

Foundational measures for ALL patients (basic skin care):

Severity-based step-up:

"Wet-wrap" therapy: For severe flares — TCS under damp cotton layer × 2–3 days, dramatic short-term improvement.

Avoid in primary care:

Pharmacotherapy — First-Line Drug Regimen

— Potency matched to site and severity (US classes I–VII; I = superpotent)

— Face, eyelids, genitals, intertriginous: low potency (class VI–VII) — hydrocortisone 1–2.5%, desonide 0.05%

— Trunk/extremities, moderate: medium potency (class IV–V) — triamcinolone 0.1%, mometasone 0.1%

— Lichenified plaques, palms/soles: high to superpotent (class I–III) — clobetasol 0.05%, fluocinonide 0.05%

— Dose: BID during flares, typically 2–4 weeks, then taper to proactive 2×/week to prior sites

— Fingertip unit (FTU): ~0.5 g covers two adult palms — counsel quantity to combat steroid phobia and underdosing

— Atrophy, telangiectasia, striae, hypopigmentation, perioral dermatitis, acneiform eruption

— Tachyphylaxis is largely a myth — non-response usually = non-adherence or wrong diagnosis

— Systemic absorption (HPA suppression) only with prolonged superpotent use over large BSA or in infants

— Tacrolimus 0.03% (≥2 yr), 0.1% (≥16 yr), pimecrolimus 1% cream

— Steroid-sparing — ideal for face, eyelids, neck, genitals, intertriginous and for maintenance

— Side effects: transient burning/stinging; FDA boxed warning for theoretical malignancy risk is not supported by current evidence — counsel reassuringly

Board pearl: Eyelid AD flaring on hydrocortisone → switch to tacrolimus 0.1% ointment, not a stronger steroid (atrophy risk + glaucoma/cataract from periocular steroid).

Topical corticosteroids (TCS) — cornerstone:

TCS adverse effects (counsel and monitor):

Topical calcineurin inhibitors (TCI):

Topical PDE-4 inhibitor: Crisaborole 2% ointment (≥3 months) — mild-moderate AD, non-steroidal; main side effect application-site burning.

Topical JAK inhibitor: Ruxolitinib 1.5% cream (≥12 yr) — mild-moderate AD on ≤20% BSA; boxed warning class effect but minimal systemic absorption.

Adjuncts: Sedating antihistamines (hydroxyzine, diphenhydramine) only for sleep during severe nocturnal itch — non-sedating antihistamines don't help AD itch.

Advanced Pharmacotherapy — Phototherapy and Systemics

— Narrowband UVB (311 nm) is first-line; 2–3 sessions/week, response in 8–12 weeks

— Indications: moderate-severe AD refractory to topicals, large BSA, patient preference to avoid systemics

— Contraindications: photosensitivity disorders, prior skin cancer, immunosuppression; logistical burden limits use

— FDA-approved ≥6 months; SC loading 600 mg then 300 mg q2 weeks (adult)

— First-line systemic for moderate-severe AD; no lab monitoring required

— Adverse effects: conjunctivitis (10–20%), injection-site reactions, head/neck dermatitis flare, rare keratitis

— Safe in pregnancy data accumulating; no live vaccines while on therapy

— Rapid itch relief (within 1–2 days), high EASI-75 rates

— Boxed warning (class): MACE, malignancy, VTE, serious infection, mortality (extrapolated from tofacitinib RA data)

— Pre-treatment: TB screen, hepatitis panel, CBC, lipids, pregnancy test; ongoing CBC, LFTs, lipids

— Avoid in age >65, smokers, CV/VTE risk factors when alternatives exist

— Cyclosporine 2.5–5 mg/kg/day — fastest acting for crisis; limit to 1 year; monitor BP, creatinine

— Methotrexate, azathioprine (check TPMT), mycophenolate — steroid-sparing options

— Systemic corticosteroids — avoid for chronic control; rebound is severe

— Cephalexin or clindamycin (or TMP-SMX/doxycycline for MRSA) for impetiginized AD × 7 days

— Dilute bleach baths (¼–½ cup 6% bleach in full tub, 2×/week) reduce S. aureus burden in recurrent infection

Step 3 management: Moderate-severe AD failing optimized topicals + emollients → refer to dermatology for dupilumab (no lab monitoring, best safety profile) before JAK inhibitors.

Phototherapy:

Dupilumab (IL-4Rα mAb, blocks IL-4 and IL-13):

Tralokinumab (anti-IL-13) and lebrikizumab (anti-IL-13): Alternatives, similar efficacy profile, q2–4 week dosing.

Oral JAK inhibitors — upadacitinib, abrocitinib (adults), upadacitinib ≥12 yr:

Traditional immunosuppressants (largely supplanted by biologics):

Antimicrobials:

Special Populations — Elderly and Renal/Hepatic Impairment

— Increasingly recognized phenotype; often lacks classic childhood atopy

— Frequently presents with diffuse xerosis, head/neck involvement, paradoxical sparing of antecubital fossae

— Mandatory differentials to exclude: bullous pemphigoid (pre-bullous phase looks eczematous — check anti-BP180/230, DIF), cutaneous T-cell lymphoma (biopsy + TCR), scabies (crusted in nursing home outbreaks), drug-induced eczematous eruptions (calcium channel blockers, statins, ACE inhibitors)

— Polypharmacy review: ACEi-induced pruritus, diuretic xerosis

— Skin atrophy risk is higher → use lowest effective potency, shortest duration; favor TCIs and crisaborole on thin skin

— Adherence/dexterity issues → simplify regimen, enlist caregiver, use pump bottles for emollients

— Vision/cognitive impairment → written labeled action plan

— Dupilumab preferred — no lab monitoring, no MACE/VTE signal

— Avoid JAK inhibitors in age >65 when alternatives exist (boxed warning specifically flags this group)

— Cyclosporine: nephrotoxicity and hypertension worsen with age — monitor BP and creatinine q2 weeks initially

— Cyclosporine — dose-dependent nephrotoxicity; avoid if CrCl <60 or use lowest dose with strict monitoring

— Methotrexate — renal clearance; avoid if eGFR <30; reduce dose at 30–60

— Dupilumab and topicals — no renal adjustment needed

— Avoid nephrotoxic NSAIDs for AD-related discomfort

— Methotrexate — contraindicated in significant hepatic disease, ethanol use; check baseline LFTs, hepatitis serologies, consider FibroScan with cumulative dosing

— Azathioprine — check TPMT/NUDT15; reduce dose in hepatic dysfunction

— JAK inhibitors — dose adjust in moderate hepatic impairment, avoid in severe

Board pearl: Tense bullae or urticarial plaques on eczematous base in an elderly patient on diuretics or DPP-4 inhibitor → bullous pemphigoid, not "just eczema." Biopsy with DIF.

Elderly-onset AD (>60 yr):

Topical therapy considerations in elderly:

Systemic therapy in elderly:

Renal impairment:

Hepatic impairment:

Special Populations — Pregnancy and Pediatrics

— Initiate daily emollients from birth in high-risk infants (family history) — data suggest possible reduction in AD incidence is mixed but practice is safe

— Avoid superpotent TCS in infants; favor hydrocortisone 1–2.5% on face and low-medium potency on body

— TCIs (tacrolimus, pimecrolimus) approved ≥2 yr; crisaborole ≥3 months — useful in infants for steroid-sparing

— Dupilumab approved ≥6 months for moderate-severe AD — game-changer for pediatric quality of life

— Counsel on growth and development: severe AD itself impairs growth via sleep loss and inflammation, NOT topical steroids at appropriate doses

— Food allergy: Do not eliminate foods empirically; refer for evaluation if reproducible IgE-mediated reactions. Early peanut introduction (4–6 months) in infants with severe eczema/egg allergy per LEAP/USDA guidance reduces peanut allergy

— Live vaccines: hold during high-dose systemic immunosuppression; TCIs and topical steroids do not preclude routine vaccination

— AD course is variable — ~50% worsen, especially face/neck

— Safe in pregnancy: emollients, low-medium potency TCS (limit potent/superpotent to <300 g/month — high cumulative exposure linked to low birth weight)

— TCIs: category equivalent, minimal absorption — generally considered safe; limited human data

— Dupilumab: accumulating reassuring registry data; mAb, doesn't cross placenta significantly in T1 — continue if benefit outweighs risk per shared decision

— Avoid: methotrexate (teratogen, abortifacient — discontinue ≥3 months pre-conception in both sexes), mycophenolate (teratogen, REMS), JAK inhibitors (animal teratogenicity), oral retinoids

— Cyclosporine acceptable if needed; phototherapy NB-UVB safe but supplement folate

Step 3 management: Pregnant patient with severe AD flare → escalate topicals + NB-UVB first; if systemic needed, cyclosporine has the most pregnancy safety data among traditional systemics.

Pediatrics — infants and young children:

Adolescents: Address mental health — depression, anxiety, suicidality risk elevated; screen with PHQ-9. School accommodations for visible disease.

Pregnancy:

Lactation: Topicals safe; avoid applying TCS directly to nipple before nursing.

Complications and Adverse Outcomes

— Bacterial superinfection (impetiginization) — S. aureus (often MRSA), occasional Streptococcus pyogenes. Honey crust, pustules, weeping; treat with cephalexin/clindamycin/TMP-SMX × 7 days based on local resistance

— Eczema herpeticum (Kaposi varicelliform eruption) — disseminated HSV; monomorphic punched-out vesicles/erosions, fever, lymphadenopathy. Hospitalize if extensive, periocular, immunocompromised, or systemic symptoms; IV acyclovir 5–10 mg/kg q8h. Ophthalmology if ocular involvement. Can be fatal if untreated.

— Eczema coxsackium — atypical hand-foot-mouth with diffuse vesicular eruption in AD distribution

— Molluscum dermatitis — eczematous halo around mollusca; resolves with treating molluscum

— Tinea/dermatophyte colonization — particularly head/neck

— Atopic keratoconjunctivitis, keratoconus, anterior subcapsular cataracts (chronic disease and periocular steroid use), retinal detachment (rare)

— Dupilumab-associated conjunctivitis — manage with artificial tears, ophthalmic ciclosporin, fluorometholone drops; rarely requires drug discontinuation

— Chronic sleep fragmentation → fatigue, ADHD-like symptoms in children, depression

— Adults: 2-fold increased risk of depression and suicidality — screen with PHQ-9 and counsel

— Stigma, social withdrawal, school/work absenteeism

Board pearl: Sudden worsening with monomorphic punched-out erosions + fever = eczema herpeticum → start oral or IV acyclovir empirically before PCR returns; hold TCS on involved skin.

Infectious complications:

Ocular complications:

Sleep and mental health:

Growth and development: Severe poorly controlled AD → short stature from sleep loss/inflammation; not from appropriately used topical steroids.

Atopic march progression: Asthma in 30%, allergic rhinitis in 35%, food allergy in 15% of AD children.

Cardiovascular and metabolic: Severe AD modestly associated with cardiovascular disease, obesity, hypertension — likely shared inflammation.

Iatrogenic: Steroid atrophy, telangiectasia, perioral dermatitis, glaucoma (periocular), HPA axis suppression (rare).

When to Escalate Care — Referral and Inpatient Triage

— Diagnosis uncertain or atypical morphology

— Moderate-severe disease unresponsive to ≥4 weeks of optimized topicals

— Need for phototherapy or systemic therapy (dupilumab, JAK inhibitors, cyclosporine)

— Suspected superimposed contact dermatitis requiring patch testing

— Recurrent infections, eczema herpeticum, or hospitalized flare

— Pediatric severe AD with growth failure or developmental concerns

— Suspected IgE-mediated food allergy with reproducible reactions or anaphylaxis

— Severe perennial environmental allergy considered as flare driver

— Concern for primary immunodeficiency (recurrent deep infections, FTT, eosinophilia + elevated IgE → hyper-IgE/Job syndrome workup)

— Dupilumab-associated conjunctivitis refractory to lubricants

— Suspected keratoconus, cataracts, or HSV keratitis

— Periocular eczema herpeticum

— PHQ-9 ≥10, suicidality, severe QoL impact, parent-child stress

— Extensive eczema herpeticum, particularly with systemic symptoms, periocular involvement, immunocompromise, or inability to tolerate oral intake → IV acyclovir

— Severe impetiginized AD with cellulitis, bacteremia signs, or failed outpatient antibiotics → IV antibiotics

— Erythrodermic AD (>90% BSA) with fluid/electrolyte derangement, hypothermia, hemodynamic compromise → admit for IV fluids, warming, wet wraps, aggressive systemic therapy

— Severe pediatric flare with dehydration or inability to maintain oral intake

CCS pearl: For erythrodermic AD admit, order: IV access, isotonic IV fluids, ambient temperature control/blankets, CBC/CMP/blood cultures, dermatology consult, wet-wrap therapy with mid-potency TCS, dilute bleach baths, empiric coverage for S. aureus if febrile, and reassess vitals q4h.

Step 3 management: Eczema herpeticum + face/eye involvement + systemic symptoms → admit for IV acyclovir + ophthalmology consult — do not manage outpatient.

Refer to dermatology when:

Refer to allergy/immunology when:

Refer to ophthalmology when:

Refer to mental health when:

Hospital admission indications:

ICU rare but consider for erythroderma with hemodynamic instability or sepsis from skin source.

Key Differentials — Same-Category (Eczematous/Inflammatory) Causes

— Sharply demarcated to exposure pattern (rectangular under watchband, linear from plant, glove pattern)

— Often coexists with AD and worsens it

— Common allergens: nickel, fragrance, preservatives (MCI/MI), neomycin, rubber accelerators, topical corticosteroids themselves

— Workup: patch testing (not skin prick)

— Greasy yellow scale on scalp, eyebrows, nasolabial folds, sternum, postauricular

— Driven by Malassezia; treat with ketoconazole shampoo/cream, low-potency TCS short course

— In infants ("cradle cap") often coexists with AD

— Coin-shaped, well-circumscribed, intensely pruritic plaques on extremities

— Often in adults, may be AD variant or stand-alone; high-potency TCS, treat dry skin

— Deep tapioca-like vesicles on lateral fingers, palms, soles

— Triggers: stress, sweat, nickel ingestion; treat with high-potency TCS, soaks

— Lower legs, medial malleolus, hyperpigmentation (hemosiderin), edema, varicosities

— Frequently mistaken for cellulitis (bilateral, afebrile, no leukocytosis) — avoid antibiotics; compression + TCS + emollients

Key distinction: AD is poorly demarcated, flexural, itchy, with atopic stigmata; psoriasis is sharply demarcated, extensor, with silvery scale and nail changes; ACD is patterned to the contactant.

Allergic contact dermatitis (ACD):

Irritant contact dermatitis: Hand involvement in wet-work occupations (healthcare, food service, hairdressers); burning > itching; no immune sensitization.

Seborrheic dermatitis:

Nummular eczema:

Dyshidrotic eczema (pompholyx):

Stasis dermatitis:

Asteatotic eczema (eczema craquelé): Elderly, winter, "crazy-paving" cracks on shins; treat with emollients, gentle bathing.

Lichen simplex chronicus: Localized lichenified plaque from chronic scratching (nape, ankle, scrotum); itch-scratch cycle; high-potency TCS occluded, behavioral interruption.

Psoriasis: Well-demarcated salmon plaques with silvery scale, extensor surfaces, scalp, nails (pitting, oil drops). Auspitz sign. Histology and distribution distinguish.

Key Differentials — Other-Category Causes

— Intensely pruritic, worse at night, web spaces, wrists, axillae, waistband, genitals, periareolar

— Burrows pathognomonic; household members itching

— Diagnose by mineral oil scraping, dermoscopy ("jet trail")

— Treat: permethrin 5% cream (whole body, neck-down, repeat in 7 days) + treat all household contacts + wash bedding in hot water; oral ivermectin for crusted scabies or outbreaks

— Adult-onset "eczema" resistant to therapy, fixed buttock/trunk plaques, "bathing trunk" distribution

— Patch → plaque → tumor stages; Sézary syndrome if leukemic

— Diagnose: biopsy + TCR gene rearrangement; treat with topical TCS/nitrogen mustard, phototherapy, bexarotene, brentuximab depending on stage

Board pearl: "Adult-onset eczema not responding to steroids, fixed plaques on buttocks" → biopsy for mycosis fungoides, not stronger steroids.

Scabies:

Cutaneous T-cell lymphoma (mycosis fungoides):

Bullous pemphigoid (pre-bullous phase): Elderly with intense pruritus and urticarial/eczematous plaques; tense bullae develop; DIF: linear C3/IgG at BMZ; serum anti-BP180/230.

Dermatitis herpetiformis: Symmetric grouped vesicles on extensors (elbows, knees, buttocks, scalp); celiac association; DIF: granular IgA in dermal papillae; treat with dapsone + gluten-free diet.

Tinea corporis: Annular plaques with active scaly border and central clearing; KOH prep positive; topical antifungals. Steroid use creates tinea incognito — flat lesions without scale.

Cutaneous candidiasis: Beefy red intertriginous plaques with satellite pustules; risk in diabetes, obesity, antibiotics.

Drug eruptions: Eczematous drug eruptions (calcium channel blockers, statins, ACEi, allopurinol, DPP-4 inhibitors); review medication timeline.

HIV-associated eczematous dermatitis and immunodeficiency-related eczema (hyper-IgE, Wiskott-Aldrich, Omenn, IPEX): severe, early-onset, infections, FTT — check immune workup.

Zinc deficiency (acrodermatitis enteropathica): Periorificial and acral eczematous dermatitis in infants weaning from breast milk; check serum zinc.

Secondary Prevention and Long-Term Plan

— Emollient ≥twice daily, especially after bathing

— Gentle non-soap cleansers, lukewarm short showers

— Trigger avoidance personalized to patient

— Cotton breathable clothing; humidified environment in winter

— In moderate-severe disease, apply TCS or TCI twice weekly to historically flare-prone sites even when clear → reduces flare frequency by 50%

— Continue for months to years; periodic reassessment

— Green zone (clear/maintenance): emollients ± proactive TCI/TCS 2×/week

— Yellow zone (flare): step up to daily TCS appropriate to site, increase emollient

— Red zone (severe/infected): contact clinician, consider antibiotics/antivirals

— Mirror asthma action plan format — patient-friendly

— Routine vaccines including live ones safe on topicals

— Live vaccines contraindicated on high-dose systemic immunosuppression (cyclosporine, methotrexate >0.4 mg/kg/wk, prednisone ≥20 mg/day for ≥14 days)

— Dupilumab/tralokinumab: avoid live vaccines while on therapy; inactivated vaccines fine

— Annual influenza, COVID-19 boosters per schedule

— Zoster (recombinant Shingrix) appropriate even on immunosuppression

— Mental health (PHQ-9/GAD-7) annually

— Asthma symptoms, allergic rhinitis review

— Bone health if recurrent systemic steroid bursts

— Cardiovascular risk in severe AD adults

— Generic mid-potency TCS in large tubes — combat undertreatment from small prescription sizes

— Document EASI/IGA/DLQI for biologic prior auth

— Connect to patient assistance programs for dupilumab/JAK inhibitors

Step 3 management: Proactive 2×/week TCS or tacrolimus to flare-prone sites + daily emollient + written action plan = the longitudinal outpatient backbone, not endless reactive courses.

Foundational daily regimen (non-negotiable, lifelong):

Proactive maintenance anti-inflammatory therapy:

Written eczema action plan:

Vaccination considerations:

Comorbidity screening:

Anticipatory guidance for atopic march: Counsel infant caregivers on early allergen introduction (peanut by 4–6 mo per LEAP), recognize asthma symptoms, avoid unnecessary food eliminations.

Insurance and adherence:

Follow-Up, Monitoring, and Counseling

— New diagnosis or new regimen: 2–4 weeks to assess response and adherence

— Stable on topicals: every 3–6 months

— On systemic therapy: every 3 months, more frequently early in course

— Phototherapy: weekly during induction, then maintenance schedule

— Disease activity: POEM, itch NRS, IGA, BSA estimate

— QoL: DLQI/CDLQI, sleep, school/work absenteeism

— Mental health: PHQ-9/PHQ-A, screen for suicidality

— Adherence: how often, how much, where — quantify TCS tubes used

— Side effects: atrophy, telangiectasia, dupilumab conjunctivitis, infections

— Atopic march symptoms: wheeze, rhinitis, new food reactions

— Topicals only: no labs

— Dupilumab: no routine labs required

— JAK inhibitors: baseline TB/HBV/HCV/HIV/CBC/CMP/lipids/pregnancy; then CBC, LFTs, lipids at 4 and 12 weeks then q3 months

— Cyclosporine: BP and creatinine q2 weeks × 2 months, then monthly; magnesium, potassium, lipids, uric acid

— Methotrexate: CBC, LFTs, creatinine baseline and q1–3 months; consider folate supplementation

— Phototherapy: annual skin cancer screening once cumulative dose accrues

— Steroid phobia: Demonstrate FTU, set expectations on duration, normalize use; under-treatment is more common than over-treatment

— Adherence: Simplify regimen, use combination products if helpful, leverage school nurses for pediatric application

— Bathing myths: Daily bathing IS beneficial when followed by emollient

— Diet: Strict elimination diets harm growth and may unmask anaphylaxis on reintroduction — refer first

— School/work: Provide accommodation letter; AD is not contagious

Board pearl: Patient "fails" topical therapy → ask "how many tubes per month?" and "how long do you apply when it flares?" — most failures are undertreatment, not pharmacologic failure.

Follow-up cadence (outpatient longitudinal):

What to assess at every visit:

Lab monitoring by therapy:

Counseling priorities:

Patient education resources: National Eczema Association, AAD patient handouts, written action plan in chart and patient portal.

Ethical, Legal, and Patient Safety Considerations

— Parents/patients frequently misperceive TCS risks. Provide balanced counseling: appropriate-potency, appropriate-duration TCS are safer than uncontrolled disease. Document discussion. Refusal of treatment requires capacity assessment and shared decision-making — offer steroid-sparing alternatives (TCI, crisaborole, dupilumab) rather than no treatment.

— TCI boxed warning for malignancy is not supported by current epidemiologic data (15+ years post-warning)

— JAK inhibitor class warning (MACE, malignancy, VTE, mortality) is extrapolated from older RA population — relevant especially for age >65, smokers, prior CV/VTE/cancer. Document risk-benefit discussion and consider dupilumab first when possible

— Provide written information; allow time for questions

— Adolescents should participate in treatment decisions; assess capacity for biologic initiation

— Parental refusal of evidence-based therapy in severely affected child with growth failure or recurrent infections may rarely require child protective services consultation if neglect criteria met

— Pediatric-to-adult transition often loses dermatology follow-up — establish adult derm before age 18–21

— Discharge after eczema herpeticum admission: ensure outpatient acyclovir continuation, dermatology follow-up within 1 week, antiviral prophylaxis consideration for recurrent eczema herpeticum, and clear return precautions

— Med rec: confirm topical regimens, antibiotics, and biologic injection dates at every transition

— Erythema underrecognized in skin of color → use edema, lichenification, scale, and patient-reported symptoms, not redness alone, to grade severity

— Address insurance barriers to biologics; document failed prior therapies thoroughly

Step 3 management: When parents refuse TCS for moderate-severe pediatric AD, offer tacrolimus 0.03% + crisaborole or referral for dupilumab — never simply discharge without treatment; document shared decision-making.

Steroid phobia and informed consent:

Black box warnings — accurate risk communication:

Pediatric assent and parental decisions:

Transition-of-care risks (Step 3 favorite):

Telehealth and photo-based care: AD is well-suited to telemedicine; ensure adequate photo quality, document remote exam limitations, and have low threshold for in-person evaluation if atypical features or suspected infection.

Health equity:

Occupational considerations: Hand AD in healthcare/food workers — counsel on glove use, barrier creams, workplace accommodations; document for workers' compensation if work-aggravated.

High-Yield Associations and Rapid-Fire Clinical Facts

Board pearl: Severe eczema + thrombocytopenia + recurrent infections in a baby boy = Wiskott-Aldrich, not just AD — order CBC with platelet count and size, immunoglobulins, WAS gene testing.

Filaggrin (FLG) loss-of-function mutations → AD + ichthyosis vulgaris + peanut allergy + palmar hyperlinearity.

Hyper-IgE (Job) syndrome (STAT3 mutation): Severe eczema + recurrent cold staphylococcal abscesses + cyst-forming pneumonia + retained primary teeth + coarse facies + IgE >2000.

Wiskott-Aldrich syndrome (WAS, X-linked): Eczema + thrombocytopenia (small platelets) + recurrent infections in male infants.

Omenn syndrome: SCID variant with severe eczematous erythroderma, lymphadenopathy, hepatosplenomegaly, eosinophilia, elevated IgE.

IPEX syndrome (FOXP3): Immune dysregulation, polyendocrinopathy (early T1DM), enteropathy, X-linked; severe AD.

Netherton syndrome (SPINK5): Ichthyosis linearis circumflexa + atopy + bamboo hair (trichorrhexis invaginata).

Eczema herpeticum = Kaposi varicelliform eruption; monomorphic punched-out erosions; IV acyclovir if severe.

Dennie-Morgan folds, Hertoghe sign, palmar hyperlinearity, pityriasis alba, keratosis pilaris = atopic stigmata constellation.

Atopic march: AD → food allergy → asthma → allergic rhinitis (general sequence).

LEAP trial: Early peanut introduction (4–6 mo) in high-risk infants ↓ peanut allergy by ~80%.

Bleach baths: ¼–½ cup of 6% household bleach in full tub, 2×/week — reduces S. aureus colonization.

Soak and seal: Apply emollient within 3 minutes of bathing.

Fingertip unit (FTU): ~0.5 g; covers two adult palms.

Dupilumab AE: Conjunctivitis (~10–20%), head/neck dermatitis flare.

JAK inhibitor boxed warning: MACE, malignancy, VTE — caution age >65, smokers.

TCI boxed warning for theoretical malignancy = not supported by data.

Topical steroids on the face >2 weeks → perioral dermatitis, atrophy, periocular cataract/glaucoma.

Stasis dermatitis = often misdiagnosed bilateral "cellulitis" in elderly — don't give antibiotics.

Adult-onset fixed "eczema" refractory to TCS → biopsy for mycosis fungoides.

Pregnancy: TCS safe (limit potent <300 g cumulative); avoid MTX, mycophenolate, JAK inhibitors.

Board Question Stem Patterns

Step 3 management: When a stem says "eyelid" or "fold" + steroids — answer is almost always switch to tacrolimus or pimecrolimus.

Stem 1 — Classic infant AD: 6-month-old with itchy red scaly cheeks and extensor surfaces, family history of asthma. Next step: daily emollient + low-potency hydrocortisone 2.5% on face during flares. Distractor: food allergy testing (not first-line without specific reactions).

Stem 2 — Eczema herpeticum: Child with known AD develops sudden fever and monomorphic punched-out vesicles clustered on face. Next step: start oral or IV acyclovir empirically + HSV PCR; admit if periocular/extensive.

Stem 3 — Steroid undertreatment: Adolescent with flexural AD "tried hydrocortisone with no improvement." Next step: upgrade to medium-potency TCS (triamcinolone 0.1%) to body, BID 2 weeks; reserve low-potency for face.

Stem 4 — Eyelid AD: Adult with chronic eyelid eczema worsened by topical steroids. Next step: tacrolimus 0.03–0.1% ointment; avoid further periocular steroids (cataract/glaucoma risk).

Stem 5 — Impetiginized AD: Honey-colored crusting and weeping. Next step: culture + cephalexin (or clindamycin/TMP-SMX if MRSA risk) × 7 days + continue TCS to underlying eczema.

Stem 6 — Adult-onset refractory "eczema": 55-year-old with fixed plaques on buttocks/trunk, no atopic history, no response to potent TCS. Next step: skin biopsy — concern for mycosis fungoides.

Stem 7 — Atopic march/peanut prevention: Infant with severe AD and egg allergy. Next step: early peanut introduction at 4–6 months under guided protocol (LEAP).

Stem 8 — Hyper-IgE clue: Child with eczema, "cold" staphylococcal abscesses, retained primary teeth, IgE >2000. Diagnosis: Job (STAT3) syndrome.

Stem 9 — Wiskott-Aldrich: Infant boy with eczema, petechiae, recurrent otitis, small platelets. Diagnosis: WAS.

Stem 10 — Dupilumab side effect: Adult on dupilumab develops bilateral red itchy eyes 8 weeks in. Next step: lubricant drops ± ophthalmic ciclosporin, continue dupilumab.

Stem 11 — Pregnancy with severe AD: Pregnant woman with widespread flare. Avoid: methotrexate, mycophenolate, JAK inhibitors. Use: emollients, mid-potency TCS, NB-UVB, cyclosporine if needed.

Stem 12 — Bullous pemphigoid masquerade: 78-year-old on DPP-4 inhibitor with intensely pruritic urticarial plaques and a tense bulla. Next step: biopsy for H&E + DIF, anti-BP180.

One-Line Recap

Atopic dermatitis is a chronic, relapsing, pruritic inflammatory skin disease of barrier dysfunction and Th2 inflammation, managed longitudinally in the outpatient setting with daily emollients, stepwise topical anti-inflammatory therapy (topical corticosteroids and calcineurin inhibitors), trigger avoidance, and biologic escalation (dupilumab) for moderate-severe disease, while screening for and preventing complications across the atopic march.

Board pearl: AD is a marathon of barrier repair and anti-inflammatory maintenance — the right Step 3 answer is almost always optimize the regimen and prevent the next flare, not chase a cure.

Diagnosis is clinical — pruritus + eczematous morphology in age-typical distribution + chronic/relapsing course + personal/family atopy; labs and biopsy are reserved for atypical or refractory cases (mycosis fungoides, bullous pemphigoid, immunodeficiency).

Foundational therapy for every patient: daily emollients (soak and seal), gentle non-soap cleansers, lukewarm short baths, trigger avoidance, written eczema action plan; proactive 2×/week TCS or TCI to flare-prone sites halves flare frequency in moderate-severe disease.

Step-up therapy ladder: low-potency TCS for face/folds and medium-potency for body → topical calcineurin inhibitors, crisaborole, ruxolitinib as steroid-sparing maintenance → NB-UVB phototherapy → dupilumab first-line systemic (no labs needed) → JAK inhibitors (boxed warning, avoid age >65/smokers when possible) or cyclosporine for crisis.

High-yield safety nets: recognize eczema herpeticum (monomorphic punched-out vesicles → empiric acyclovir), impetiginization (cephalexin/clindamycin + bleach baths), adult-onset refractory eczema (biopsy for CTCL), eyelid disease (TCI not stronger steroid), pediatric severe AD (early peanut introduction, dupilumab ≥6 mo), and mental health screening for depression and sleep disruption at every visit.