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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Atopic eczema in infants and children

Dermatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
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Eczema herpeticum or invasive infection

Rapidly spreading painful monomorphic vesicles, punched-out erosions or crust with fever, lethargy or eye involvement suggests eczema herpeticum; rapidly advancing warmth, tenderness, purpura, systemic illness or shock suggests invasive bacterial disease rather than an ordinary flare.

Action: Arrange same-day urgent paediatric or dermatology care, obtain HSV PCR and bacterial samples without delaying systemic aciclovir or sepsis treatment, and obtain emergency ophthalmology advice for periocular or ocular symptoms.

Overview

Diagnose and grade childhood atopic eczema, teach families safe age- and site-specific topical treatment, recognise infection and allergy signals, and protect sleep, growth, education and wellbeing.

Atopic eczema arises from impaired epidermal barrier, immune dysregulation and environmental interaction. Itch drives scratching, which further damages barrier and sustains inflammation. Diagnosis is clinical: an itchy skin condition plus age-appropriate historical and examination criteria. Ask about onset, daily itch, sleep, triggers, infections, treatment quantities and beliefs, atopy, growth and family burden. Undress sufficiently to assess extent while preserving warmth, dignity and assent. Check cheeks, scalp, neck, flexures, hands, ankles, eyelids and behind ears, and look for napkin sparing in infants.

Severity is multidimensional. Clear disease has normal skin and no quality-of-life effect; mild disease has limited dry or infrequently itchy areas; moderate disease has more frequent itch, redness or colour change, excoriation and some sleep or activity effect; severe disease brings widespread dryness, relentless itch, bleeding, oozing, cracking, marked pigment or texture change and substantial sleep and function loss. Erythema may be subtle in richly pigmented skin, so palpate warmth and thickening and recognise follicular or papular eczema and post-inflammatory hyper- or hypopigmentation without treating pigment alone as active inflammation.

Practice

Two practice questions

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DermatologyOriginal SBA

Severe short facial flare

A 4-year-old with established atopic eczema has a severe inflamed facial flare without vesicles, crust, fever or eye symptoms. Emollient and a correctly used mild topical corticosteroid have not controlled it. Which plan best follows age- and site-specific guidance?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE atopic eczema in under 12sDiagnosis, severity, age- and site-specific topical therapy, infection, food allergy, referral and education.
  • BAD atopic eczemaClinical features, emollients, topical anti-inflammatory treatment, infection and practical self-care.
  • BAD eczema herpeticumRecognition of painful monomorphic lesions, emergency antiviral treatment and ocular risk.
  • NICE shared decision makingAge-appropriate involvement, treatment choices, risk communication and decisions with children and families.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Successful care depends on technique and shared priorities more than a growing prescription list. Demonstrate fingertip-unit dosing, separate emollient and corticosteroid applications by enough time to avoid dilution, and give a body-site map with potency and stop point. Observe a caregiver applying treatment when response is poor. Address steroid fears without dismissing them, prescribe enough emollient, and provide nursery or school instructions. Review environmental smoke, fragrance, overheating and occupational hand exposure, but avoid costly allergy claims unsupported by history.

Key points

  • Atopic eczema is an itchy relapsing inflammatory disorder: itch is essential, while dryness, excoriation, sleep loss and age-specific distribution support the diagnosis.
  • Infants often have cheek, scalp and extensor disease with relative napkin sparing; mobile children increasingly develop flexural, hand, ankle and eyelid eczema.
  • In brown or black skin, active eczema may look violaceous, grey, deep brown or follicular rather than bright red; warmth, texture, swelling and excoriation show activity.
  • Grade severity at the worst site and ask separately about night waking, mood, school or nursery, because visible area and life impact do not always match.
  • First-line maintenance is liberal unperfumed leave-on emollient used every day and as a soap substitute, with a written flare plan and fire-safety advice.
  • Match topical corticosteroid potency to severity and site: mild for mild disease, moderate for moderate disease and potent for severe disease, using extra caution on face and folds.
  • On face and neck use mild potency routinely; a clinician may prescribe moderate potency for only 3–5 days during a severe flare, while axillae and groin need short 7–14-day courses.

Aetiology

01

Inherited barrier susceptibility

Variants affecting filaggrin and other epidermal proteins increase water loss and allergen penetration, although eczema is polygenic and no single test diagnoses it.

02

Immune dysregulation

Type-2-skewed cutaneous inflammation amplifies itch and barrier dysfunction and varies across age, disease stage and individual phenotype.

03

Environmental exposure

Soap, detergent, fragrance, heat, low humidity, saliva, friction and occupational wet work aggravate vulnerable skin without necessarily representing allergy.

04

Microbial interaction

Staphylococcal colonisation and viral susceptibility rise on broken skin, but colonisation alone does not mean that infection caused every flare.

Pathophysiology

  1. 1
    Barrier water loss

    Reduced lipid and structural integrity increases transepidermal water loss, dryness and penetration of irritants and antigens.

  2. 2
    Itch–scratch cycle

    Inflammatory mediators activate sensory nerves, scratching tears barrier and releases further alarmins, producing self-sustaining itch and lichenification.

  3. 3
    Inflammatory flare

    Cutaneous immune activation creates oedema, warmth, papules and exudation, while chronic rubbing thickens skin and exaggerates markings.

  4. 4
    Altered microbial ecology

    Barrier disruption and reduced antimicrobial defence favour staphylococcal density and HSV dissemination, especially during uncontrolled widespread inflammation.

  5. 5
    Pigmentary response

    Inflammation and scratching alter melanocyte activity, leaving post-inflammatory hyperpigmentation or hypopigmentation after active itch and texture have resolved.

Clinical features and red flags

Infant pattern

Itchy dry inflamed cheeks, scalp and extensor limbs appear in early life, often with relative protection of the moist napkin area; severe disease can become generalised.

Childhood flexural pattern

Antecubital and popliteal fossae, wrists, ankles, neck, eyelids and hands become prominent, with scratching, lichenification and painful fissures.

Activity across skin tones

Active skin can be pink, red-brown, violaceous, grey or darker than baseline and may show papules, follicular accentuation, oedema, warmth and roughness more clearly than redness.

Secondary bacterial change

New tenderness, rapidly worsening eczema, pustules, purulent exudate, honey crust, fever or malaise increases the probability of clinically important staphylococcal or streptococcal infection.

Eczema herpeticumRed flag

Painful clusters of similar vesicles evolve into sharply punched-out erosions and may disseminate with fever; periocular involvement threatens vision.

Food-allergy signal

Immediate reproducible urticaria, angioedema, wheeze, vomiting or collapse after a food, or moderate-to-severe refractory eczema with gastrointestinal symptoms or growth faltering, justifies targeted allergy assessment.

Treatment-burden signal

Empty small tubes, uncertainty about potency, intermittent emollient, fear of steroid, product stinging, school barriers or a complex family routine often explains apparent treatment resistance.

Red flags requiring action

Investigations

  1. 01
    Clinical diagnostic criteria and severity assessmentFirst step
    Why
    Confirm itchy age-patterned eczema and quantify skin and life impact.
    Interpretation and limitations
    Record extent and worst-site activity plus sleep, play, school and family burden; a photograph or score can monitor trend but does not replace the child's reported itch.
  2. 02
    Observed treatment review
    Why
    Distinguish inadequate delivery from genuinely refractory inflammation.
    Interpretation and limitations
    Check every product and potency, weekly amounts, fingertip units, sequencing, expired medicines and who applies them; observed technique frequently reveals underdosing or irritant products.
  3. 03
    Bacterial culture
    Why
    Guide antimicrobial selection in severe, recurrent, unusual or non-responsive suspected infection.
    Interpretation and limitations
    Swab purulent or crusted representative skin before antibiotics when feasible; colonisation is common, so interpret growth with pain, fever, spread and response rather than result alone.
  4. 04
    HSV PCR
    Why
    Confirm eczema herpeticum from a fresh vesicle or erosion.
    Interpretation and limitations
    Swab the lesion base, but do not postpone systemic aciclovir when morphology and systemic features are convincing; arrange eye assessment for periocular disease.

Differential diagnosis

01

Seborrhoeic dermatitis

Earlier greasy scalp, brow and fold scale with less itch contrasts with the dry itchy cheek and extensor or flexural eczema pattern.

02

Scabies

Household nocturnal itch, burrows, palms, soles and genital papules suggest infestation; infants may have scalp and widespread disease.

03

Allergic contact dermatitis

A sharply exposure-linked distribution, new treatment product or refractory eyelid, hand or footwear disease supports patch testing.

04

Psoriasis

Sharply demarcated plaques, scalp margin, nail pits and family history can distinguish psoriasis, although flexural childhood lesions may have little scale.

05

Immune, nutritional or metabolic disease

Unusual infections, diarrhoea, alopecia, purpura, growth failure or a non-classic eruption requires paediatric assessment beyond an eczema label.

Management

01First-line daily careRepair barrier and reduce irritant exposureFirst stepFirst lineAtopic eczema is diagnosed at any severity.+
  1. 1Choose an acceptable fragrance-free leave-on emollient, prescribe a quantity sufficient for whole-body daily use and use it instead of soap and detergent washes.
  2. 2Demonstrate smooth application in the direction of hair growth, decant tubs with a clean spoon or use a pump, and provide bedding and clothing fire-safety advice.
  3. 3Create a written site-specific flare plan, continue emollient when skin is clear and review acceptability because the best formulation is the one used consistently.
02First-line flare controlMatch potency to site and severityFirst lineItch, inflammation, excoriation or sleep disruption signals an active flare.+

Complications

01

Sleep and developmental burden

Nightly itch disrupts child and caregiver sleep, concentration, mood, school attendance, learning, play and wider family function.

02

Bacterial and viral infection

Excoriated skin can develop impetigo or cellulitis, while eczema herpeticum can disseminate and threaten the eye and systemic health.

03

Treatment adverse effects

Inappropriate prolonged potent corticosteroid can cause atrophy and systemic absorption, while undertreatment sustains inflammation and usually causes greater cumulative burden.

04

Growth and nutritional harm

Severe disease, chronic sleep loss and unsupported food exclusion can impair energy intake, nutrient balance and physical growth.

05

Psychosocial and educational effect

Visible lesions, pigment change, teasing, messy treatments and school restrictions can produce stigma, anxiety and reduced participation.

Monitoring and follow-up

  • Check actual emollient and corticosteroid quantities against expected use and ask the caregiver or child to demonstrate application and identify each potency.
  • Examine colour, warmth, oedema, texture, excoriation, fissures and infection; record post-inflammatory pigment separately so treatment is not escalated solely for residual colour.
  • Plot growth when eczema is moderate to severe, food is being excluded or feeding is difficult, and ensure a paediatric dietitian reviews any prolonged staple-food avoidance.
  • Provide explicit emergency advice for painful same-shaped blisters, punched-out erosions, fever, eye symptoms or rapidly spreading redness and document where same-day care is available.
  • Refer when diagnosis is uncertain, face or sleep remains uncontrolled, recurrent infection or contact allergy is suspected, treatment is socially unmanageable or systemic therapy may be needed.

Special situations

Itch outranks colour

An itchy warm thickened eruption may be highly active even when redness is muted; pigment remaining after control does not by itself justify stronger treatment.

Face and folds change potency

Thin, occluded skin absorbs more corticosteroid, so severity alone cannot determine the prescription without anatomical site and duration.

Weeping is not a culture result

Inflamed eczema can ooze without clinically important infection, and bacterial colonisation can produce a positive swab without causing the flare.

Technique is a diagnostic test

Watching one application can expose underdosing, steroid–emollient mixing, wrong-site potency or a stinging formulation more efficiently than another prescription.

Common pitfalls

  1. 01

    Underestimating severe eczema because erythema is less conspicuous in brown or black skin.

  2. 02

    Giving several steroid tubes without a written map linking potency, site, frequency and stop date.

  3. 03

    Using moderate or potent corticosteroid on an infant's face or folds without the short site-specific plan.

  4. 04

    Calling every crusted or weeping flare bacterial infection and prescribing repeated antibiotics.

  5. 05

    Missing eczema herpeticum because painful uniform erosions are labelled excoriations.

  6. 06

    Ordering a broad food panel or excluding milk and egg without a coherent reaction history, allergy interpretation, dietetic input and growth monitoring.

  7. 07

    Escalating to systemic therapy before observing daily treatment technique and assessing contact allergy and family barriers.

Topical calcineurin inhibitors are specialist-led second-line options from age 2 years when steroid adverse effects are a significant concern, especially at vulnerable sites.
  • Crust and weeping may reflect inflammation rather than bacterial infection; systemic illness, rapid worsening and infection extent determine whether antimicrobial treatment is needed.
  • Do not start broad food panels or exclusion diets for eczema alone; investigate allergy when there is a reproducible immediate reaction or moderate-to-severe disease with growth or gastrointestinal concern.
    • Painful monomorphic blisters or punched-out erosions, periocular disease, fever or lethargy, rapidly spreading cellulitis, poor feeding or dehydration, extensive skin failure, growth faltering, recurrent deep infection, treatment toxicity or a diagnosis that remains uncertain requires urgent specialist review.
  • 05
    Targeted allergy testing
    Why
    Investigate a specific immediate food reaction or selected refractory eczema with growth or gastrointestinal concern.
    Interpretation and limitations
    Choose skin-prick or specific-IgE testing from history and interpret sensitisation against clinical reaction; broad panels create false labels and unnecessary exclusion.
    • 1
    Apply prescribed mild steroid to mild eczema, moderate steroid to moderate eczema and potent steroid to severe eczema once daily unless the product plan states otherwise, treating active skin until controlled.
  • 2Use mild potency on face and neck, with clinician-directed moderate potency for only 3–5 days in a severe flare; restrict axilla and groin treatment to mild or moderate potency for 7–14 days.
  • 3If correctly used treatment fails after 7–14 days, reassess diagnosis, infection, adherence and contact allergy before increasing potency; do not use a very potent steroid without specialist supervision.
    • 03Step-up and preventionReduce recurrent flares safelyFirst lineFrequent flares, vulnerable-site disease or steroid adverse-effect risk persists despite correct first-line care.+
    1. 1Seek specialist advice for a topical calcineurin inhibitor from age 2 years at an appropriate site, explaining transient burning, sun protection and that it is not applied to active infection.
    2. 2For frequent recurrences, consider clinician-directed two-consecutive-days-per-week anti-inflammatory treatment at previously affected sites with review at 3–6 months.
    3. 3First lineUse wet wraps only after trained demonstration, generally for a limited period; do not start whole-body steroid wraps as first-line care or cover infected eczema.
    04Infection escalationSeparate colonisation from systemic riskEscalationPain, vesicles, punched-out erosion, purulence, rapid worsening, fever or malaise develops.+
    1. 1Assess urgently for eczema herpeticum, cellulitis and sepsis, sample fresh lesions where this will not delay treatment and admit an unwell child.
    2. 2Start same-day systemic aciclovir for suspected eczema herpeticum and obtain ophthalmology advice for eye or periocular involvement.
    3. 3Use topical or oral antibacterial treatment only when clinical severity and extent justify it, continue eczema therapy as advised and review early rather than treating every weeping flare as infection.
    Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
    Core daily barrier treatment and itch reduction at every disease severity.

    Unperfumed leave-on emollient

    Apply generously to dry skin at least twice daily and whenever needed, including when eczema is clear; use a prescribed quantity appropriate to body size and wash with an emollient soap substitute rather than detergent cleanser.

    Ointments can be slippery and occlusive, creams can sting because of preservatives, and all paraffin-containing or paraffin-free emollient residue on clothing and bedding increases fire intensity; keep away from flames and smoking and wash fabrics regularly.

    First-line anti-inflammatory treatment for flares and, when prescribed intermittently, prevention at repeatedly affected sites.

    Topical corticosteroid

    Apply a fingertip-unit-calculated thin layer to active eczema once daily unless the specific product directs otherwise: mild potency for mild, moderate for moderate and potent for severe disease, with the site and age restrictions in the written plan.

    Use mild potency on face and neck except a 3–5-day clinician-directed moderate course for severe flare; use mild or moderate in folds for 7–14 days; potent steroid under 12 months or very potent steroid at any child age requires specialist direction. Avoid untreated HSV and monitor atrophy and growth with repeated high-potency exposure.

    Time-critical antiviral treatment that limits dissemination, eye disease and systemic complications.

    Systemic aciclovir for suspected eczema herpeticum

    Use urgent weight-, age-, renal-function- and severity-adjusted oral or intravenous dosing through paediatric guidance; do not await PCR when widespread painful monomorphic vesicles or punched-out erosions make the diagnosis likely.

    Assess hydration and renal function, ensure adequate fluid, adjust for renal impairment and involve ophthalmology for periocular or ocular disease; severe or systemically unwell children need intravenous treatment and admission.