Atopic eczema in infants and children

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

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.
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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

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.

Immune dysregulation

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

Environmental exposure

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

Microbial interaction

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

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier water loss
Reduced lipid and structural integrity increases transepidermal water loss, dryness and penetration of irritants and antigens.
2
Itch–scratch cycle
Inflammatory mediators activate sensory nerves, scratching tears barrier and releases further alarmins, producing self-sustaining itch and lichenification.
3
Inflammatory flare
Cutaneous immune activation creates oedema, warmth, papules and exudation, while chronic rubbing thickens skin and exaggerates markings.
4
Altered microbial ecology
Barrier disruption and reduced antimicrobial defence favour staphylococcal density and HSV dissemination, especially during uncontrolled widespread inflammation.
5
Pigmentary response
Inflammation and scratching alter melanocyte activity, leaving post-inflammatory hyperpigmentation or hypopigmentation after active itch and texture have resolved.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

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

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

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.
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.
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.
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.
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.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Seborrhoeic dermatitis

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

Scabies

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

Allergic contact dermatitis

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

Psoriasis

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

Immune, nutritional or metabolic disease

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

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line daily careRepair barrier and reduce irritant exposureFirst stepFirst lineAtopic eczema is diagnosed at any severity.

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.
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.
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.

1Apply 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.

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.
2For frequent recurrences, consider clinician-directed two-consecutive-days-per-week anti-inflammatory treatment at previously affected sites with review at 3–6 months.
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.

1Assess urgently for eczema herpeticum, cellulitis and sepsis, sample fresh lesions where this will not delay treatment and admit an unwell child.
2Start same-day systemic aciclovir for suspected eczema herpeticum and obtain ophthalmology advice for eye or periocular involvement.
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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Sleep and developmental burden

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

Bacterial and viral infection

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

Treatment adverse effects

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

Growth and nutritional harm

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

Psychosocial and educational effect

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

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

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.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

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.

11Common pitfallsFrequent interpretation and management errors.

01
Underestimating severe eczema because erythema is less conspicuous in brown or black skin.
02
Giving several steroid tubes without a written map linking potency, site, frequency and stop date.
03
Using moderate or potent corticosteroid on an infant's face or folds without the short site-specific plan.
04
Calling every crusted or weeping flare bacterial infection and prescribing repeated antibiotics.
05
Missing eczema herpeticum because painful uniform erosions are labelled excoriations.
06
Ordering a broad food panel or excluding milk and egg without a coherent reaction history, allergy interpretation, dietetic input and growth monitoring.
07
Escalating to systemic therapy before observing daily treatment technique and assessing contact allergy and family barriers.