Eczema

Common inflammatory skin condition characterised by pruritus, erythema, and dry skin. Encompasses atopic eczema (most common), contact dermatitis, discoid eczema, varicose eczema, and seborrhoeic dermatitis. Atopic eczema affects ~20% of children and ~5% of adults in the UK. Management follows a stepwise approach with emollients as the cornerstone.

Key Facts

Atopic eczema: most common type; part of the 'atopic triad' (eczema, asthma, hay fever); filaggrin gene mutations Prevalence: ~20% of UK children; ~5% of adults; increasing in developed countries Emollients are the cornerstone of management — use liberally and frequently (250–500g/week) Topical corticosteroids: stepped approach — mild (hydrocortisone 1%), moderate (clobetasone butyrate 0.05%), potent (betamethasone valerate 0.1%), very potent (clobetasol propionate 0.05%) Eczema herpeticum: secondary infection with HSV — widespread vesicles/punched-out erosions; EMERGENCY — treat with IV aciclovir NICE CG57/NG190: atopic eczema management in children and adults Tacrolimus (Protopic) and pimecrolimus (Elidel): topical calcineurin inhibitors for sensitive areas (face, flexures) — no skin atrophy Dupilumab: anti-IL-4Rα monoclonal antibody for moderate-severe atopic eczema (NICE TA534)

Overview

Key Facts

Eczema is one of the most common reasons for dermatology referral. The stepwise approach to treatment — emollients first, then topical steroids, then immunomodulators — is a frequent exam topic.

Epidemiology

  • Atopic eczema: 15–20% of children; 2–5% of adults
  • Peak onset: first year of life (~60% by age 1; ~90% by age 5)
  • Increasing prevalence in developed countries ('hygiene hypothesis')
  • ~50% resolve by teenage years; some persist into adulthood

Aetiology

  • Genetic: filaggrin gene (FLG) loss-of-function mutations — defective skin barrier; strongest genetic risk factor
  • Environmental: allergens, irritants, infections, stress
  • Part of 'atopic march': eczema → food allergy → asthma → allergic rhinitis

Pathophysiology

  • Filaggrin deficiency → impaired epidermal barrier → increased transepidermal water loss + allergen penetration
  • Th2-predominant immune response → IL-4, IL-13, IL-31 (itch mediator)
  • IgE sensitisation to environmental allergens
  • Skin microbiome disruption: S. aureus colonisation in >90% of atopic eczema

Clinical Presentation

Infants

  • Face, scalp, extensor surfaces
  • Erythematous, weeping, crusting

Children/Adults

  • Flexural distribution: antecubital fossae, popliteal fossae, wrists, neck
  • Dry, lichenified (thickened) skin
  • Excoriations from scratching
  • Sleep disturbance from pruritus

Variants

  • Discoid (nummular): coin-shaped, well-demarcated plaques
  • Seborrhoeic: scalp, nasolabial folds, eyebrows (Malassezia-related)
  • Varicose (stasis): lower legs with venous disease
  • Pompholyx: vesicles on palms/soles

Red Flags

  • Eczema herpeticum: widespread punched-out erosions, fever, malaise — dermatological EMERGENCY
  • Secondary bacterial infection: crusting, weeping, pustules (S. aureus)
  • Erythroderma: >90% BSA involved — risk of hypothermia, fluid loss

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
PsoriasisWell-demarcated, silvery scale, extensor distributionClinical, biopsy if uncertain
Contact dermatitisDistribution matches contactant; patch testing positivePatch testing
ScabiesBurrows, finger webs, intense nocturnal itchDermoscopy, skin scraping
Tinea corporisAnnular, advancing scaly edge, central clearingSkin scraping + KOH/culture
Seborrhoeic dermatitisScalp, nasolabial folds, greasy scaleClinical

Diagnosis / Investigation

Bedside

  • Clinical diagnosis in most cases — no investigations routinely needed
  • Skin swab: if secondary infection suspected (S. aureus, HSV)
  • Dermatoscopy: if diagnostic uncertainty

Bloods

  • Total IgE: often elevated in atopic eczema (non-specific)
  • Specific IgE / skin prick testing: if food allergy suspected (especially children <2 with moderate-severe eczema)

Special Tests

  • Patch testing: if allergic contact dermatitis suspected — apply allergen panels for 48 hours, read at 48 and 96 hours
  • Skin biopsy: rarely needed; spongiotic dermatitis on histology
  • SCORAD / EASI score: validated severity assessment tools

Management

Stepwise Approach (NICE NG190)

Step 1 — Emollients (ALL patients):

  • Liberal use: 250–500g/week; apply frequently (at least 3–4 times daily)
  • Leave-on emollients: Cetraben, Doublebase, Diprobase, Epaderm
  • Soap substitutes: use emollient as wash
  • Pat dry, apply emollient within 3 minutes of bathing

Step 2 — Topical Corticosteroids:

  • Mild: hydrocortisone 1% (face, children)
  • Moderate: clobetasone butyrate 0.05% (Eumovate)
  • Potent: betamethasone valerate 0.1% (Betnovate); mometasone furoate 0.1%
  • Very potent: clobetasol propionate 0.05% (Dermovate) — short courses only
  • Use fingertip unit (FTU) dosing; apply thinly once daily

Step 3 — Topical Calcineurin Inhibitors:

  • Tacrolimus 0.03% (children) or 0.1% (adults) — for face, flexures, steroid-sensitive areas
  • Pimecrolimus 1% — mild-moderate disease
  • No skin atrophy risk

Step 4 — Specialist Therapies:

  • Phototherapy: narrowband UVB
  • Systemic immunosuppressants: methotrexate, azathioprine, ciclosporin
  • Biologics: dupilumab 300mg SC every 2 weeks (anti-IL-4Rα) — NICE TA534
  • JAK inhibitors: baricitinib, upadacitinib, abrocitinib (NICE approved)

Infection Management

  • Bacterial (S. aureus): flucloxacillin 500mg QDS 7 days; topical fusidic acid 2%
  • Eczema herpeticum: IV aciclovir 5mg/kg TDS — EMERGENCY

Referral Criteria

  • Dermatology: moderate-severe eczema unresponsive to topical treatment
  • Allergy clinic: suspected food allergy trigger
  • Urgent: eczema herpeticum, erythroderma

Prognosis

  • ~50% of childhood eczema resolves by teenage years
  • ~20% have persistent disease into adulthood
  • Filaggrin mutations predict more severe and persistent disease
  • Quality of life significantly impacted (sleep, psychosocial)
  • Eczema herpeticum: mortality <1% with prompt treatment; can be fatal if untreated

Other Relevant Information

Topical Steroid Potency Ladder

PotencyExampleUse
MildHydrocortisone 1%Face, children, mild disease
ModerateClobetasone butyrate 0.05%Body, moderate disease
PotentBetamethasone valerate 0.1%Body, severe flares
Very potentClobetasol propionate 0.05%Palms/soles, short courses

Fingertip Unit (FTU) Guide

Body Area (Adult)FTUs per Application
Face and neck2.5
One arm3
One hand (both sides)1
Trunk (front)7
One leg6