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 and infected eczema
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Suspected eczema herpeticum
Painful rapidly spreading, similar-looking vesicles or punched-out erosions with fever or malaise can represent disseminated herpes simplex and may threaten the eye or systemic health.
Action: Arrange same-day paediatric or dermatology assessment and start systemic aciclovir without waiting for swab confirmation when clinically suspected. Admit young, unwell, extensive or immunocompromised children; obtain urgent ophthalmology review for eyelid, periocular, painful red-eye or visual involvement.
Overview
Assess childhood atopic eczema by impact and severity, restore the skin barrier with a practical emollient and anti-inflammatory plan, distinguish ordinary flares from bacterial infection and recognise eczema herpeticum before eye or systemic complications develop.
Atopic eczema arises from skin-barrier vulnerability and immune inflammation, producing itch, dryness and episodic erythema, oedema, papules, excoriation, weeping or lichenification. Distribution changes with age: infants often have cheeks and extensor surfaces, while older children commonly have flexures, hands, eyelids and neck. Ask about onset, itch, sleep, scratching, treatments, triggers, infection, asthma or rhinitis and family atopy. Examine all skin, growth and signs of another diagnosis.
Grade both clinical severity and life impact. Mild disease can still destroy sleep and family function; widespread visible disease may trouble one child less. Record itch, sleep nights, school or nursery absence, sport, swimming, bullying, parent exhaustion and treatment time. Urgent referral is warranted when severe disease is not responding, infection is recurrent, growth is affected or the diagnosis is uncertain. Allergy testing is not routine for every child with eczema.
Practice
Two practice questions
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Paediatrics and child healthOriginal SBA
Antibiotics for a crusted flare
A 6-year-old has an eczema flare with mild crusting but is afebrile, comfortable and not systemically unwell. There is no cellulitis. What is the best initial approach?
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 CG57 atopic eczemaSeverity, emollients, topical corticosteroid potency, eczema herpeticum, allergy and referral in under-12s.
Build a barrier plan that fits daily life. Offer a choice of unperfumed emollient ointment, cream, gel, lotion or combination and prescribe enough for whole-body frequent use. Smoother products may suit daytime or hairy areas; greasy ointment can reduce water loss in very dry skin but is unsuitable on actively weeping or infected areas. Apply gently in the direction of hair growth, decant from pots with a clean spoon or use pumps and recognise that paraffin residue increases fire risk on clothing and bedding.
During a flare, add a topical corticosteroid matched to current severity and site rather than waiting until the skin is raw. NICE supports once- or twice-daily application to active areas. Explain fingertip units and demonstrate the amount; vague instructions such as use sparingly produce undertreatment. Mild potency treats mild eczema. Moderate potency treats moderate disease. Potent corticosteroid is reserved for severe eczema and short, supervised courses, and is not used in a baby under 12 months without specialist oversight.
Use mild potency on face and neck, except a brief moderate-potency course for a severe flare under the plan. Avoid potent use on thin skin and occlusion without specialist direction. If a correctly used mild or moderate preparation has not controlled a flare within about one to two weeks, check adherence, quantity, infection and diagnosis before stepping up. Topical calcineurin inhibitors can reduce corticosteroid exposure in selected children over 2 years when second-line criteria are met and specialist advice supports initiation.
Bacterial colonisation is common, so a positive swab or yellow crust alone does not prove that antibiotics will improve a flare. Features include weeping, pustules, crust, rapid worsening, fever and malaise. If the child is not systemically unwell, NICE advises against routinely offering topical or oral antibiotics because benefit is limited and resistance risk is real. Continue emollient and anti-inflammatory treatment. Swab when infection is recurrent, worsening despite treatment or atypical, and consider nasal carriage or close-contact transmission selectively.
When an antimicrobial is needed, choose by extent and systemic state. A small localised infection may receive a short topical course such as fusidic acid 2% three times daily for 5 to 7 days. Widespread or severe infection, or systemic illness, usually requires oral flucloxacillin for 5 to 7 days using current child age or weight dosing; macrolide alternatives depend on allergy and local resistance. Cellulitis, sepsis or failure needs hospital assessment, microbiology and intravenous therapy.
Eczema herpeticum is primary or recurrent herpes simplex spreading through eczematous skin. Pain out of proportion to itch, clusters of similar vesicles, circular punched-out erosions, fever, malaise and rapid spread are key. Start systemic aciclovir on the same day through paediatric or dermatology care and admit if the child is young, unwell, widespread, immunocompromised or cannot take oral medicine. Eyelid or periocular involvement requires urgent ophthalmology because keratitis threatens sight.
Maintenance prevents the next flare. Continue emollient when clear. For frequent flares at the same sites, a clinician may use proactive topical corticosteroid on two consecutive days each week after control, with review. Manage nails, cotton layers, overheating and sleep, but avoid restrictive unproven diets. Immediate food reactions, poor growth or persistent moderate-to-severe disease despite optimal treatment may justify allergy assessment; indiscriminate exclusion risks malnutrition.
Referral options include nurse-led education, dermatology, allergy, psychology and paediatric care. Wet wraps can enhance topical treatment but also increase steroid absorption and need instruction. Phototherapy, biologic and systemic immunomodulatory treatments require specialist selection, infection and vaccination planning and laboratory monitoring. At every review ask what the family actually applied, how much, where and why, because technique and corticosteroid fear are common remediable causes of treatment failure.
Key points
Atopic eczema is an itchy, relapsing inflammatory skin disorder; assess sleep, school, play, family burden and psychosocial impact separately from visible extent because impact may be severe with limited rash.
First-line maintenance is an unperfumed leave-on emollient used generously and frequently over the whole skin, with a suitable soap substitute and a product the child will actually tolerate.
Treat active inflammation with topical corticosteroid of appropriate potency: mild for mild disease, moderate for moderate disease and potent for severe disease, modified by age, site and specialist limits.
Apply topical corticosteroid once or twice daily only to active eczema and continue emollient; potent corticosteroid in a baby under 12 months requires specialist dermatological supervision.
Face and neck usually need mild potency, with a short moderate-potency course only for severe flare; axillae and groin need caution because absorption and adverse effects are greater.
Crusting, weeping, pustules and rapid worsening can reflect bacterial infection, but many non-systemically-unwell flares do not benefit from antibiotics; continue eczema treatment and reserve antimicrobials for the NICE-defined pattern.
Aetiology
01
Inherited barrier vulnerability
Filaggrin and other epidermal abnormalities increase water loss and allow irritants, allergens and microbes to enter more readily.
02
Type 2 immune inflammation
Cytokine-driven immune activity promotes itch, erythema and barrier disruption and links eczema with asthma and allergic rhinitis.
03
Irritant and environmental exposure
Soap, fragrance, heat, saliva, rough fabric, sweat and low humidity aggravate an already vulnerable barrier without representing true allergy.
04
Microbial and viral triggers
Staphylococcal overgrowth can intensify inflammation, while herpes simplex can disseminate through damaged skin as eczema herpeticum.
Pathophysiology
1
Transepidermal water loss
Defective lipids and structural proteins allow excessive water evaporation, producing xerosis, microfissures and increased irritant penetration.
2
Itch-scratch amplification
Inflammatory mediators trigger pruritus, and scratching further damages the barrier, releases cytokines and perpetuates nocturnal inflammation.
3
Altered skin microbiome
Reduced antimicrobial defence and barrier disruption favour staphylococcal colonisation, but colonisation alone does not establish antibiotic-responsive infection.
4
Herpes dissemination
HSV replicates across barrier-deficient epidermis, creating monomorphic erosions and potential ocular or systemic spread without prompt antiviral therapy.
Clinical features and red flags
Acute inflammatory flare
Intense itch accompanies erythema, papules, oedema, excoriation and sometimes weeping over the child's typical distribution.
Chronic lichenified eczema
Repeated scratching produces thickened skin, accentuated markings, pigment change and fissures, especially in flexures and hands.
Possible bacterial infection
New crust, pustules, weeping, pain, rapid worsening, fever or malaise raises infection probability beyond ordinary inflammation.
Eczema herpeticumRed flag
Painful monomorphic vesicles or punched-out erosions with fever or rapid spread requires same-day antiviral assessment.
Major life impact
Nightly waking, school loss, low mood, bullying or family exhaustion identifies severe burden even with modest visible extent.
Red flags requiring action
Monomorphic painful vesicles or punched-out erosions with fever suggests eczema herpeticum and needs same-day systemic antiviral treatment.
Periocular herpes lesions, painful red eye, photophobia or altered vision requires immediate ophthalmology involvement.
Rapidly spreading erythema, severe pain, fever, tachycardia or reduced responsiveness suggests cellulitis or sepsis.
Investigations
01First-line clinical diagnosis and severity assessmentFirst stepFirst line
Why
Confirm the age-patterned itchy dermatitis and document extent, intensity, sleep and quality-of-life impact.
Interpretation and limitations
Typical eczema needs no routine laboratory test; mismatch, systemic signs or failure despite correct treatment prompts reconsideration.
02Skin swab when infection is atypical or recurrent
Why
Identify bacterial pathogen and resistance when treatment fails, infection recurs or MRSA risk changes therapy.
Interpretation and limitations
Colonisation is common, so culture must be interpreted with pain, pustules, spread, fever and treatment response.
03HSV swab or PCR
Why
Support eczema-herpeticum diagnosis and type the virus while systemic antiviral treatment begins.
Interpretation and limitations
A result is confirmatory but must not delay aciclovir when the clinical pattern is convincing.
Sensitisation does not prove clinical allergy; history-guided specialist interpretation prevents unnecessary exclusion diets.
Differential diagnosis
01
Seborrhoeic dermatitis
Greasy scale on scalp, eyebrows and folds with less intense itch is common in infancy and usually follows a different course.
02
Scabies
Severe night itch, affected close contacts, burrows and lesions on hands, wrists, axillae or infant palms and soles suggest infestation.
03
Contact dermatitis
A sharply exposure-related distribution, new product or repeated hand irritant can produce allergic or irritant inflammation superimposed on atopy.
04
Immunodeficiency or nutritional disease
Unusual infections, diarrhoea, faltering growth, bleeding or treatment-resistant widespread dermatitis warrants broader systemic and immune assessment.
05
Psoriasis or tinea
Well-demarcated plaques, scalp or nail change, or an enlarging annular scaly edge should prompt reconsideration and fungal sampling where appropriate.
Additional chapter-specific clues
Alternative systemic disorder
Faltering growth, diarrhoea, bleeding or recurrent unusual infection with refractory dermatitis suggests immune, nutritional or genetic disease.
Management
01Daily barrier careMake emollient use achievableFirst stepThe child has dry atopic skin during a flare or between episodes.+
1Offer unperfumed leave-on products suited to skin, season and preference and prescribe enough for frequent whole-body use.
2Replace soap and detergent cleansers, demonstrate pump or clean-spoon technique and apply gently with hair direction.
3Review tolerance, nursery or school access and paraffin fire safety and switch texture rather than abandoning barrier treatment.
02Inflammatory flareMatch corticosteroid potency to skinActive itchy erythema, papules, thickening or excoriation persists despite emollient.+
1Select potency from severity, age and body site and explain fingertip units and once- or twice-daily application to active areas.
2Continue emollient separately and use the planned course until controlled, avoiding potent treatment in a baby under 12 months without specialist input.
Complications
01
Bacterial cellulitis or sepsis
Barrier breakdown permits invasive staphylococcal or streptococcal infection with pain, spreading erythema, fever and systemic deterioration.
02
Eczema herpeticum
Disseminated HSV can cause painful widespread erosions, keratitis, viraemia, encephalitis and death without rapid systemic antiviral treatment.
03
Sleep and developmental burden
Persistent itch fragments sleep, impairs concentration and behaviour and can exhaust caregivers and disrupt education and relationships.
04
Treatment adverse effects
Incorrect prolonged potent corticosteroid use can thin skin and suppress adrenal function, while undertreatment sustains inflammation and infection risk.
05
Nutritional restriction harm
Unsupported exclusion diets can cause protein, calcium and micronutrient deficiency and impaired growth without reliably improving eczema.
Monitoring and follow-up
Review itch, sleep, school or nursery participation and family burden as well as erythema and body-surface extent.
Ask the family to show what product, potency, quantity and technique they use rather than recording adherence as yes or no.
Track antibiotic courses, swab results and recurrent infection to reduce resistance and identify eczema herpeticum or immune red flags.
Inspect face, folds and treated skin for atrophy, striae, telangiectasia and persistent steroid adverse effects.
Plot growth and assess nutrition when food exclusion, severe disease or systemic therapy affects intake or development.
For specialist systemic therapy, monitor infection, vaccination, laboratory and organ-specific safety according to the exact medicine.
Provide a written flare and emergency plan and confirm carers, school and the child know the eczema-herpeticum pattern.
Special situations
Severity includes sleep
A small area that wakes a child nightly can be clinically severe and justify active escalation.
Colonisation is not infection
Staphylococci commonly live on eczematous skin, so a swab result cannot replace clinical evidence of bacterial disease.
Fingertip units reduce fear
Showing the correct amount helps families avoid both harmful overuse and ineffective undertreatment of topical corticosteroid.
Herpeticum is painful
Pain, monomorphic lesions and punched-out erosions distinguish disseminated HSV from a simply itchier bacterial flare.
Diet can cause harm
Food removal without a convincing history and dietetic plan can impair growth while leaving barrier inflammation untreated.
Common pitfalls
01
Judging severity only by visible body-surface area and ignoring sleep or school impact.
02
Prescribing a tiny emollient quantity that cannot cover whole skin repeatedly.
03
Saying use steroid sparingly without specifying potency, site, amount and duration.
04
Using potent topical steroid on an infant or face without specialist oversight.
05
Giving antibiotics for every weeping flare despite no systemic illness.
06
Waiting for an HSV swab before treating convincing eczema herpeticum.
07
Missing eye risk when herpetic lesions approach the eyelid.
08
Recommending broad exclusion diets without immediate-reaction history, growth review and dietetic support.
For a small localised non-systemic bacterial infection, topical fusidic acid 2% three times daily for 5 to 7 days is an option when an antimicrobial is judged necessary; widespread or systemic infection usually needs oral therapy selected by age and allergy.
Painful rapidly spreading monomorphic vesicles or punched-out erosions, fever or malaise suggests eczema herpeticum and needs same-day specialist assessment and systemic aciclovir.
Eczema herpeticum around the eye needs immediate ophthalmology involvement as well as systemic antiviral treatment; do not use topical antiviral alone.
Persistent poor control requires review of diagnosis, quantity and technique, infection, irritants, allergy clues, treatment fear and access before escalating to wet wraps, calcineurin inhibitors, phototherapy or systemic therapy.
A baby with widespread severe eczema, diarrhoea, infections or faltering growth may have immunodeficiency or another systemic disorder.
Repeated potent topical steroid use on face, folds or large areas raises skin and systemic adverse-effect risk.
Sleep loss, depression, school refusal or family breakdown is a treatment-escalation signal, not a cosmetic concern.
Immediate food reactions with airway, breathing or circulatory features require anaphylaxis care rather than eczema management alone.
05
Systemic and immune investigations
Why
Assess blood count, immunology, nutrition or genetics when infection, growth or phenotype suggests another disorder.
Interpretation and limitations
Testing is selected from red flags and is not routine for otherwise typical atopic eczema.
3EscalationIf response is poor, verify dose, technique, adherence, infection and diagnosis before escalation or referral.
03Possible bacterial infectionTreat the child, not colonisationCrusting, weeping or pustules appear during an eczema flare.+
1Assess extent, pain, fever and systemic state and continue emollient and anti-inflammatory therapy.
2Avoid routine antibiotic in a non-systemically-unwell flare; if antimicrobial treatment is justified, choose short topical local or oral widespread therapy under NG190.
3EscalationSwab recurrent or non-responsive infection, escalate cellulitis or sepsis and review hygiene without stigmatising the family.
04Herpetic emergencyStart antiviral treatment the same dayPainful monomorphic vesicles, punched-out erosions, fever or rapid spread suggests eczema herpeticum.+
1Contact same-day dermatology or paediatrics and start systemic aciclovir while taking HSV samples when readily available.
2Admit when young, unwell, extensive, immunocompromised or unable to take oral medicine and provide analgesia and fluid support.
3Obtain urgent eye assessment for periocular disease and teach recurrence recognition before discharge.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Reduces water loss, restores barrier lipids, decreases itch and lowers reliance on anti-inflammatory treatment over time.
Leave-on emollient
Apply generously and frequently to the whole skin, including when clear, using a cream, ointment, gel or lotion the child tolerates; prescribe quantities sufficient for repeated daily whole-body use and bathing substitution.
Avoid fragranced products, use pumps or a clean spoon, stop a product that stings persistently and warn that paraffin-soaked fabric ignites readily.
Suppresses cutaneous inflammation and itch so the damaged barrier can heal and sleep and function recover.
Topical corticosteroid
Apply a thin measured layer once or twice daily to active eczema for the planned flare course: mild potency for mild, moderate for moderate and potent for severe disease, modified for face, folds, age and specialist limits.
Do not use potent preparations in infants under 12 months without specialist supervision; avoid prolonged high-potency use on face or folds and demonstrate fingertip units.
Treats a limited staphylococcal bacterial component without exposing the whole body to an oral antibiotic.
Fusidic acid 2% topical
When an antibiotic is justified for a small localised secondary bacterial infection, apply three times daily for 5 to 7 days while continuing eczema treatment.
Do not use routinely for every crusted flare or repeat frequently because resistance develops; reassess rapid spread, systemic illness or failure.
Limits HSV replication and reduces ocular, neurological and disseminated complications when begun promptly.
Systemic aciclovir
Start oral or intravenous aciclovir on the same day at the current age-, weight-, severity- and renal-function-specific BNFC regimen for suspected eczema herpeticum; use IV treatment for severe, extensive or systemically unwell disease.
Do not delay for viral results, ensure hydration and renal dose adjustment, and involve ophthalmology immediately when the eye region is affected.