Eczema — UKMLA Guide 2026

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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

The Bottom Line

Part of the atopic triad (eczema, asthma, allergic rhinitis). Affects ~20% of children and ~10% of adults
Distribution: flexural in children/adults (antecubital/popliteal fossae), extensor and facial in infants
Stepwise management: emollients (mainstay) → mild TCS → moderate TCS → potent TCS → specialist (calcineurin inhibitors, phototherapy, biologics)
Emollients are the cornerstone — use liberally (250–500 g/week), apply before steroids, avoid soap
Infected eczema (weeping, crusted, golden crust): flucloxacillin for S. aureus; eczema herpeticum (punched-out erosions) is a dermatological emergency → IV aciclovir

Overview

Atopic eczema is a chronic, relapsing inflammatory skin condition characterised by intense pruritus, dry skin, and a characteristic distribution. It is the most common inflammatory skin disease, typically beginning in early childhood. The pathogenesis involves skin barrier dysfunction (often with filaggrin gene mutations), immune dysregulation (Th2-dominant), and environmental triggers. It is part of the atopic march — many children develop asthma and allergic rhinitis subsequently.

Epidemiology

Affects approximately 20% of children and 10% of adults in the UK. Onset is before age 5 in 90% of cases. ~60% will improve or resolve by adolescence. Strong genetic component — filaggrin loss-of-function mutations are the strongest known genetic risk factor. Environmental factors include irritants (soaps, detergents), allergens (house dust mite), infections, stress, and climate. Prevalence has increased significantly over the past 50 years.

Clinical Features

Symptoms

Intense pruritus — the hallmark symptom (worse at night, disrupts sleep)

Dry, rough skin

Relapsing-remitting course with flares

Rapidly worsening, painful eczema with punched-out erosions (eczema herpeticum)

Signs

Infants: extensor surfaces and face (cheeks)

Children/adults: flexural distribution — antecubital fossae, popliteal fossae, wrists, neck

Erythema, papules, vesicles (acute). Lichenification, excoriation (chronic)

Xerosis (dry skin) — universal feature

Secondary infection: weeping, crusting, golden crust (S. aureus), pustules

Eczema herpeticum: monomorphic punched-out erosions, may have fever, systemic unwellness

Investigations

First-line

Clinical diagnosisDiagnosis is clinical — based on history and examination. No routine blood tests needed

Second-line

Skin swab (MC&S)If infected eczema suspected — identifies organism and sensitivities

Viral swabIf eczema herpeticum suspected — HSV PCR

Specialist

Patch testingIf contact allergy suspected (e.g. occupational eczema, localised pattern)

Skin prick testing / specific IgEIf food allergy suspected as trigger (particularly in severe childhood eczema)

Management

NICE NG190 (Atopic eczema), 2007 + NICE CKS

Step 1 — Emollients (ALL patients, ALL the time)

Complete emollient therapy: use as soap substitute, bath additive, and leave-on moisturiser
Apply liberally and frequently — 250–500 g/week for adults
Choose based on patient preference (thicker = more effective but less acceptable)
Apply emollient FIRST, wait 20–30 min, then apply topical steroid on top

Step 2 — Mild topical corticosteroid

Hydrocortisone 1% for face, flexures, children
Use for 7–14 days during flares, then stop (or step down)
Apply thinly to active areas only — fingertip unit (FTU) dosing guide

Step 3 — Moderate/potent topical corticosteroid

Moderate: betamethasone valerate 0.025% (Betnovate-RD), clobetasone butyrate (Eumovate)
Potent: betamethasone valerate 0.1% (Betnovate), mometasone (Elocon)
Short course during flares — use lowest potency that controls symptoms
Side effects of prolonged potent TCS: skin thinning, telangiectasia, striae, adrenal suppression

Step 4 — Specialist therapies

Topical calcineurin inhibitors (tacrolimus, pimecrolimus): steroid-sparing, safe for face and flexures
Phototherapy (narrowband UVB)
Systemic immunosuppression: methotrexate, ciclosporin, azathioprine, mycophenolate
Biologic: dupilumab (anti-IL-4/13) for moderate-severe adult atopic eczema (NICE TA534)

Infected eczema

Bacterial (S. aureus): flucloxacillin 500 mg QDS for 7 days (clarithromycin if penicillin allergic)
Eczema herpeticum (HSV): DERMATOLOGICAL EMERGENCY — IV aciclovir if systemic/periocular; oral aciclovir if mild and localised
Stop topical steroids and calcineurin inhibitors on infected areas until infection treated

Complications

Secondary bacterial infection: S. aureus colonises >90% of eczema skin — causes exacerbation and impetiginisation
Eczema herpeticum: HSV infection of eczematous skin — painful, punched-out erosions, can disseminate. Medical emergency
Sleep disturbance: Pruritus disrupts sleep — significant impact on quality of life and development in children
Psychological impact: Anxiety, depression, social isolation — particularly in visible areas
Steroid side effects: Skin atrophy, striae, telangiectasia from prolonged potent topical steroid use

UKMLA Exam Tips

1Emollients are the MAINSTAY of eczema treatment — more important than steroids. Use liberally, use constantly
2Eczema herpeticum = punched-out erosions + vesicles + systemically unwell in a patient with eczema → IV aciclovir. Do NOT give topical steroids
3Topical steroid potency: mild (hydrocortisone 1%) → moderate (clobetasone) → potent (betamethasone 0.1%) → very potent (clobetasol)
4Use MILD steroids on face/flexures. Use POTENT steroids on trunk/limbs for short courses only
5Fingertip unit (FTU): squeeze from adult fingertip to first crease = ~0.5 g — covers an area equal to two adult palms
6Tacrolimus (calcineurin inhibitor): steroid-sparing for face/flexures — important exam option when steroids are inappropriate