Atopic eczema across the life course

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

Atopic eczema is chronic, relapsing and heterogeneous. Distribution changes with age and activity. Inflammation on brown or black skin may be violaceous, darker, grey or mainly palpable, while follicular prominence, lichenification and post-inflammatory pigment change can dominate. Ask the patient or carer what new inflammation looks and feels like for them.

Make treatment usable. Select acceptable emollient textures and affordable quantities, demonstrate soap substitution, prescribe enough topical corticosteroid and map potency to sites. Face, flexures and infants usually need lower potency and shorter courses; thick lichenified adult palms may need stronger supervised treatment. Review response rather than encouraging indefinite unsupervised escalation.

Atopic eczema across the life course care should combine visible inflammation with itch, pain, sleep, occupation and treatment burden. Agree where each product goes, how much is used and when response will be reviewed; explain urgent features separately so normal fluctuation is not confused with infection or treatment failure.

Key points

Infants often have cheeks, scalp and extensor involvement; flexural eczema becomes common in older children, while adult disease often affects hands, face, neck and flexures.
Assess clear, mild, moderate or severe disease by signs, itch, sleep and daily impact; visible redness may appear purple, brown or grey in deeply pigmented skin.
Use leave-on emollient every day and as a soap substitute, then add a topical corticosteroid whose potency matches site, age and flare severity.
Apply topical corticosteroid to active inflamed skin, not as whole-body moisturiser; teach fingertip units and a written body-site plan to reduce underuse and overuse.
Do not order broad food tests or advise exclusion diets without a compatible immediate reaction, growth concern or specialist assessment.
Widespread weeping or crust does not automatically require antibiotics in a systemically well patient; look for severity, progression and alternative causes.
For Atopic eczema across the life course, document body sites, severity, sleep and function, recent treatment, infection features and what the patient can realistically apply each day.
In Atopic eczema across the life course, reassess the diagnosis when a well-used, correctly potent regimen fails rather than repeatedly intensifying treatment without examining adherence, exposure and mimics.

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

Atopic susceptibility

Polygenic immune and barrier susceptibility interacts with dry climate, irritants, microbes and other environmental exposures; family atopy increases probability but is neither required nor diagnostic.

Barrier-gene variation

Filaggrin and other epidermal-barrier variants increase transepidermal water loss and allergen penetration in some patients, while many affected people have no identified variant.

Flare modifiers

Heat, sweating, soaps, friction, infection, stress and insufficient treatment commonly aggravate disease; a specific food is an uncommon explanation for isolated chronic eczema.

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

1
Barrier leak
Reduced lipids and structural proteins allow water loss and irritant entry, creating xerosis, fissuring and heightened sensory exposure.
2
Type-two inflammation
Cytokines including interleukin-4 and interleukin-13 promote allergic inflammation and further impair epidermal differentiation, sustaining recurrent itch and erythema or pigment change.
3
Itch-scratch amplification
Neural itch drives rubbing, which damages barrier, releases inflammatory signals and produces excoriation and lichenification despite brief subjective relief.
4
Microbial dysbiosis
Staphylococcus aureus colonisation rises during flares and can amplify inflammation, yet colonisation alone does not establish bacterial infection requiring antibiotics.

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

Infant pattern

Cheek, scalp, trunk and extensor eczema with itch and dryness is common in infancy, often sparing the napkin area.

Child flexural pattern

Antecubital and popliteal folds, wrists, ankles and neck develop recurrent itch, excoriation and lichenification through childhood.

Adult and occupational pattern

Hand, eyelid, head-and-neck and flexural disease may reflect persistent atopy plus irritant or allergic contact exposures.

Pigmentation-aware activity

New warmth, roughness, swelling, itch or purple, grey and dark-brown change can identify active eczema when bright erythema is subtle.

Herpetic departureRed flag

Rapid painful monomorphic vesicles or circular punched-out erosions with fever are not an ordinary flare and require immediate antiviral action.

Red flags requiring action

Painful monomorphic erosions, eye symptoms, fever, rapidly spreading blistering, failure to thrive, erythroderma, recurrent deep infection or safeguarding concern requires urgent assessment.

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 history and whole-skin examinationFirst step
Why
Confirm age-patterned itchy dermatitis and map severity, burden and possible alternatives.
Interpretation and limitations
Diagnosis is clinical; normal examination between flares does not exclude disease, so consented patient photographs can show prior morphology.
02
Growth and nutritional assessment in children
Why
Identify faltering growth, restricted intake or severe disease requiring paediatric input.
Interpretation and limitations
Plot serial measurements rather than relying on one centile; do not start an exclusion diet without nutritional protection and a specific indication.
03
Bacterial or viral sampling when indicated
Why
Clarify severe, recurrent or treatment-resistant infection without delaying urgent therapy.
Interpretation and limitations
Skin swabs are not routine at initial impetiginisation; take HSV PCR from a fresh vesicle or erosion when possible, but start aciclovir immediately if suspected.
04
Patch testing for selected persistent disease
Why
Find allergic contact dermatitis when distribution, occupation or topical products make it plausible.
Interpretation and limitations
Testing is specialist delayed hypersensitivity assessment; positive sensitisation matters only if exposure and anatomical relevance are established.
05
Baseline tests before systemic or biologic therapy
Why
Meet treatment-specific safety requirements in specialist care.
Interpretation and limitations
No universal eczema blood panel exists; required infection, pregnancy and organ tests depend on the proposed medicine.

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

Allergic or irritant contact dermatitis

New site-specific, occupational or treatment-related eczema can coexist with atopy; exposure geometry and delayed patch testing may reveal a remediable contact cause.

Scabies

Nocturnal household itch, finger-web burrows, genital papules or nodules and affected close contacts suggest infestation rather than an isolated atopic flare.

Psoriasis and seborrhoeic dermatitis

Sharper plaques, extensor or scalp distribution and nail change support psoriasis, while greasy scale in sebaceous zones supports seborrhoeic disease.

Immunodeficiency or nutritional disease

Severe early-onset eczema with growth faltering, unusual infection, diarrhoea, bleeding or hair abnormality warrants paediatric specialist assessment.

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

01Daily controlRepair barrier and treat active sitesFirst stepEczema is mild or moderate without infection, systemic illness or diagnostic red flags.

1Agree a fragrance-free leave-on emollient and soap substitute used frequently, with separate clean containers or pumps to reduce contamination.
2Apply an age- and site-appropriate topical corticosteroid once or twice daily according to its product and written plan until the flare is controlled.
3Review technique, quantity, sleep and trigger exposures; consider proactive intermittent anti-inflammatory treatment for repeatedly relapsing sites under guidance.

02Poor responseCheck use, contact and diagnosisInflammation persists despite a reported topical regimen or recurs immediately at unusual sites.

1Observe application, calculate quantities and confirm the correct product reached each site before labelling treatment ineffective.
2Assess infection, scabies, tinea, psoriasis and allergic contact dermatitis, including patch-test referral when exposure history supports it.
3EscalationEscalate moderate or severe refractory disease to dermatology for phototherapy or systemic options rather than serial unsupervised oral corticosteroids.

03Cannot-wait flareTreat herpes or systemic infection promptlyPainful monomorphic erosions, eye involvement, rapidly spreading cellulitis, fever or significant physiological illness occurs.

1Start systemic aciclovir immediately for suspected eczema herpeticum and arrange same-day specialist advice, admission when systemically unwell and ophthalmology near the eye.
2For bacterial infection, assess systemic severity, obtain cultures when severe or recurrent and use antibiotic treatment according to NICE NG190.
3Continue gentle emollient and appropriate eczema treatment unless specialist advice changes it, while monitoring pain, hydration, temperature and spread.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

A mild topical corticosteroid suited to short treatment of thin or sensitive sites when infection and stronger-treatment need have been considered.

Hydrocortisone 1% cream

Adults apply a thin layer once or twice daily to affected skin for no longer than seven days under this product licence; paediatric use follows age-specific guidance.

Avoid untreated infection, eyes and prolonged unsupervised use; minimise face, flexure and large-area exposure, review local atrophy, and remember formulations may contain sensitising excipients.

A potent topical corticosteroid for appropriately selected moderate or severe body-site flares where a mild preparation is insufficient.

Betamethasone valerate 0.1% cream

Apply a thin film to affected skin once or twice daily for up to four weeks, reducing frequency or potency when control is achieved.

Avoid face, flexures, genital skin, untreated infection and large-area or occluded use unless directed; children and pregnancy require greater caution, and rebound suggests review.

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

Eczema herpeticum

Herpes simplex can disseminate through barrier-impaired skin, causing painful uniform erosions, systemic illness, keratitis, encephalitis and rarely death without rapid antiviral treatment.

Bacterial infection

Impetiginisation causes crust, pustules or ooze, while cellulitis produces progressive pain, warmth and systemic illness; antibiotics are reserved for clinically meaningful infection.

Sleep and developmental burden

Night itch affects concentration, behaviour, school, work, family sleep and mental health and may be severe despite limited visible body surface.

Treatment-related harm

Undertreatment prolongs inflammation, while unstructured very-potent steroid use, occlusion or repeated antibiotics creates atrophy, systemic exposure or antimicrobial resistance.

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

Track weekly itch, sleep disturbance, visible inflammation, school or work impact and rescue-treatment days rather than surface area alone.
Review topical potency by body site and total quantity used, checking for atrophy, striae, persistent telangiectasia or steroid phobia causing undertreatment.
In children with severe disease, monitor growth, diet, recurrent infection and the family’s practical ability to deliver the plan.
At review of Atopic eczema across the life course, compare itch, sleep, fissuring or ooze, affected sites, function and treatment use with the agreed baseline.
For Atopic eczema across the life course, record adverse effects, new contact exposures and the safety-net for pain, fever, rapidly spreading disease, eye symptoms or systemic illness.

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

Distribution matures with age

A diagnosis can remain atopic eczema as inflammation shifts from infant cheeks and extensors to flexures, hands or adult head and neck.

Redness is not universal

Activity in deeply pigmented skin can be purple, grey, darker, raised or warm and should not be graded by redness alone.

Treatment quantity reveals adherence

Asking how long a tube lasted is often more informative than asking whether the patient used the prescribed cream.

Colonisation differs from infection

Staphylococcus commonly lives on eczematous skin; antibiotics target clinical infection rather than a positive swab by itself.

Food questions need precision

Immediate reproducible symptoms and growth effects warrant allergy evaluation, whereas eczema fluctuation alone rarely justifies broad exclusion.

11Common pitfallsFrequent interpretation and management errors.

01
Calling eczema mild because visible redness is limited despite nightly waking and major school or work impairment.
02
Prescribing a small tube with no body-site map and then assuming treatment failure.
03
Using repeated oral antibiotics for every wet flare without systemic illness or clinical infection.
04
Stopping all topical corticosteroid abruptly from fear while active inflammation continues to damage barrier.
05
Delaying aciclovir until HSV results return in a painful monomorphic febrile eruption.