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Dermatology
Primary Care
Paediatrics

Atopic Eczema

High EvidenceUpdated: 2025-12-22

On This Page

Red Flags

  • Eczema herpeticum (clusters of vesicles, fever, systemic illness)
  • Erythroderma (>90% BSA involvement)
  • Secondary bacterial infection (impetigo, cellulitis)
  • Severe widespread eczema unresponsive to treatment
  • Failure to thrive (children)
Overview

Atopic Eczema

1. Topic Overview

Summary

Atopic eczema (atopic dermatitis) is a chronic, relapsing inflammatory skin condition characterised by pruritus, dry skin, and eczematous lesions with age-dependent distribution. It affects 15-20% of children and 2-3% of adults, typically beginning in infancy. Atopic eczema is part of the "atopic triad" with asthma and allergic rhinitis. Management centres on regular emollients, topical corticosteroids for flares, and avoidance of triggers. Severe disease may require systemic therapy including dupilumab (anti-IL-4/IL-13) or JAK inhibitors.

Key Facts

  • Prevalence: 15-20% children; 2-3% adults
  • Age of Onset: 80% before age 5
  • Atopic Triad: Eczema, asthma, allergic rhinitis
  • Cornerstone of Treatment: Emollients (250-500g/week)
  • Flares: Topical corticosteroids (potency-matched to site)
  • Severe Disease: Dupilumab, JAK inhibitors (baricitinib, upadacitinib)

Clinical Pearls

"Emollients Are the Foundation": Even during flares, continue emollients. "Soak and seal" strategy.

"Treat the Itch": Breaking the itch-scratch cycle is key. The itch that rashes.

"Age Changes Distribution": Infants = face/extensors; Children = flexures; Adults = hands/face.

"Eczema Herpeticum is an Emergency": Widespread vesicles + fever = urgent aciclovir.

Why This Matters Clinically

Eczema profoundly impacts quality of life for patients and families (sleep disruption, social impact). Inadequate emollient use is the most common cause of treatment failure. New biologics offer hope for severe, refractory disease.


2. Epidemiology

Incidence & Prevalence

MeasureValue
Childhood Prevalence15-20%
Adult Prevalence2-3%
TrendIncreasing in developed countries

Demographics

FactorDetails
Age of Onset80% before age 5; 60% in first year
SexSlight female predominance
GeographyHigher in urban, developed countries

Risk Factors

Genetic:

  • Family history of atopy (strongest)
  • Filaggrin gene mutations (FLG)
  • Maternal history of eczema

Environmental:

  • Urban environment
  • Low birth weight
  • Reduced microbial exposure ("hygiene hypothesis")
  • Food allergens (in some)

3. Pathophysiology

Mechanism

Barrier Dysfunction:

  • Filaggrin deficiency → impaired stratum corneum
  • Increased transepidermal water loss
  • Allergen/irritant penetration

Immune Dysregulation:

  • Th2-predominant inflammation
  • IL-4, IL-13, IL-31 (itch cytokine)
  • TSLP from keratinocytes

Itch-Scratch Cycle:

  • IL-31 drives pruritus
  • Scratching damages barrier further
  • Self-perpetuating inflammation

Classification

TypeFeatures
IntrinsicNormal IgE, no sensitisation (20-30%)
ExtrinsicElevated IgE, allergen sensitisation (70-80%)

4. Clinical Presentation

Symptoms

Signs by Age

AgeDistributionMorphology
InfantFace, scalp, extensorsAcute: erythema, vesicles, oozing
ChildFlexuresSubacute: excoriations
AdultHands, face, flexuresChronic: lichenification

Red Flags

[!CAUTION] Red Flags:

  • Eczema herpeticum (vesicles, fever, malaise)
  • Erythroderma
  • Cellulitis
  • Failure to thrive

Pruritus (cardinal feature)
Common presentation.
Dry skin
Common presentation.
Sleep disturbance
Common presentation.
Skin pain (fissures)
Common presentation.
5. Clinical Examination

Structured Approach

  • Distribution pattern
  • Morphology (acute/subacute/chronic)
  • Signs of infection
  • Evidence of atopy (allergic shiners, Dennie-Morgan folds)

Special Features

SignDescription
Dennie-Morgan FoldsInfraorbital creases
Allergic ShinersPeriorbital darkening
LichenificationThickened, leathery skin
XerosisGeneralised dry skin

6. Investigations
  • Usually clinical diagnosis
  • Allergy testing: SPT/specific IgE if food allergy suspected
  • Skin swab: If infection suspected
  • Patch testing: If contact allergy suspected

7. Management

See Management Algorithm above (Section 2)

Summary

SeverityTreatment
AllEmollients + trigger avoidance
MildMild topical steroid
ModerateModerate-potent steroid, TCI
SevereDupilumab, JAK inhibitors

8. Complications
ComplicationNotes
Eczema HerpeticumHSV dissemination — emergency
Bacterial InfectionS. aureus colonisation common
Skin AtrophyFrom prolonged potent steroids
Sleep DisturbanceMajor QoL impact
Growth RestrictionRare, from severe disease

9. Prognosis & Outcomes

Natural History

  • 60% clear by adolescence
  • 40% persist into adulthood
  • Adult-onset eczema also occurs

Atopic March

  • Eczema → Allergic rhinitis → Asthma
  • Screen for respiratory symptoms

10. Evidence & Guidelines

Key Guidelines

  1. NICE NG190: Atopic eczema in under 12s (2023)
  2. NICE CG57: Atopic eczema in adults (2007, updated)
  3. AAD Guidelines (2022-2023)

Landmark Trials

SOLO 1/2 (2016) — Dupilumab

  • Phase 3 RCTs showing significant EASI improvement
  • Established dupilumab as first biologic for AD

MEASURE UP 1/2 (2021) — Upadacitinib

  • JAK inhibitor vs placebo
  • Rapid, sustained responses

Evidence Strength

InterventionLevel
Emollients1a
Topical steroids1a
Dupilumab1a
JAK inhibitors1a

11. Patient/Layperson Explanation

What is Eczema?

Eczema is a common skin condition that makes your skin dry, itchy, and inflamed. It's not contagious and often runs in families with asthma or hay fever.

Why does it matter?

  • It can be very itchy and disrupt sleep
  • Skin can become infected if scratched
  • It affects quality of life

How is it treated?

  1. Moisturisers (emollients): Use lots, every day — the cornerstone of treatment
  2. Steroid creams: For flares — use as directed, not long-term on face
  3. Avoiding triggers: Soap, irritants, allergens
  4. Injection treatments: For severe eczema that doesn't respond to creams

When to seek help

  • Skin becoming infected (oozing, crusting, painful)
  • Clusters of blisters with fever (eczema herpeticum)
  • Treatment not working

12. References

Primary Guidelines

  1. National Institute for Health and Care Excellence. Atopic eczema in under 12s: diagnosis and management (NG190). 2023. nice.org.uk/guidance/ng190

Key Studies

  1. Simpson EL, et al. Two Phase 3 Trials of Dupilumab versus Placebo in Atopic Dermatitis (SOLO 1 and SOLO 2). N Engl J Med. 2016;375(24):2335-2348. PMID: 27690741

Reviews

  1. Wollenberg A, et al. European guideline (EuroGuiDerm) on atopic eczema. J Eur Acad Dermatol Venereol. 2022. PMID: 35980214


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances.

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22

Red Flags

  • Eczema herpeticum (clusters of vesicles, fever, systemic illness)
  • Erythroderma (>90% BSA involvement)
  • Secondary bacterial infection (impetigo, cellulitis)
  • Severe widespread eczema unresponsive to treatment
  • Failure to thrive (children)

Clinical Pearls

  • **"Emollients Are the Foundation"**: Even during flares, continue emollients. "Soak and seal" strategy.
  • **"Treat the Itch"**: Breaking the itch-scratch cycle is key. The itch that rashes.
  • **"Age Changes Distribution"**: Infants = face/extensors; Children = flexures; Adults = hands/face.
  • **"Eczema Herpeticum is an Emergency"**: Widespread vesicles + fever = urgent aciclovir.
  • - Eczema herpeticum (vesicles, fever, malaise)

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines