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Eczema - atopic

SNOMED: 2385460051023 wordsUpdated 03/03/2026
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Exam Tips

  • In UK exams, itch is the anchor symptom: an eczematous rash without itch should prompt reconsideration of diagnosis.
  • Use age-pattern distribution to differentiate: infant face/extensor involvement vs later childhood/adult flexural disease; hand eczema may dominate in adults.
  • Recognize and act on red flags for eczema herpeticum (painful monomorphic vesicles, punched-out erosions, fever/malaise): this requires same-day urgent referral.
  • When prescribing topicals, state potency, site, duration, and safety counselling (fingertip units, steroid atrophy risk, emollient fire safety).
  • Differentiate infected flare from non-infected flare because antibiotics are not routine unless clear clinical infection is present.
  • Image cue for OSCE recall: compare classic age-distribution map and morphology progression (acute oozy erythema to chronic lichenification) in standard dermatology atlases.

Definition

Atopic eczema (atopic dermatitis) is a chronic, relapsing inflammatory dermatosis characterized by intense pruritus, xerosis, and age-dependent eczematous morphology and distribution. It usually begins in early childhood (often before age 5), but can occur at any age, and reflects a combined epidermal barrier defect and immune dysregulation within the wider atopic phenotype (for example asthma, allergic rhinitis, and food allergy).

Pathophysiology

The disease is driven by interaction between skin-barrier failure and type 2-skewed immune inflammation. Reduced barrier proteins (classically filaggrin loss-of-function variants) increase transepidermal water loss and permit penetration of irritants, allergens, and microbes, producing dry itchy skin and recurrent inflammation. Immune activation (predominantly Th2 cytokines such as IL-4, IL-13, and IL-5, with IgE-associated sensitization in many patients) amplifies itch and inflammation; scratching then worsens barrier damage (itch-scratch cycle). Staphylococcus aureus colonization/infection further aggravates inflammation and flares. Clinical pattern changes with age: infant facial/extensor disease, later flexural lichenification, and adult hand/flexural involvement.

Risk Factors

  • Family history of atopy (eczema, asthma, allergic rhinitis), especially affected parent(s)
  • Filaggrin and other barrier/immune susceptibility gene variants
  • Personal atopic comorbidity (asthma, hay fever, food allergy)
  • Early-life and ongoing irritant exposure (soaps, detergents, wool/rough fabrics)
  • Environmental exposures (pollution, tobacco smoke, aeroallergens, climate extremes)
  • Skin infection/colonization and psychosocial stress as flare triggers

Clinical Features

Symptoms

  • Persistent itch (diagnosis less likely if itch absent)
  • Dry skin with episodic flares and remissions
  • Sleep disturbance due to nocturnal pruritus
  • Trigger-related worsening (irritants, heat/cold, stress, allergens)
  • Soreness/stinging during acute inflamed flares

Signs

  • Erythematous eczematous patches/plaques with poorly defined margins in acute disease
  • Excoriations, oozing, crusting, and occasional vesiculation during flares
  • Lichenification, scaling, and fissuring in chronic disease
  • Age-pattern distribution: infants (face/scalp/extensor limbs, often nappy area spared), older children/adults (flexures; adults may have prominent hand eczema)
  • Xerosis and possible keratosis pilaris on extensor upper arms/thighs/buttocks
  • Infection clues: honey-colored crusting/pustules (bacterial), grouped vesicles and punched-out erosions with systemic upset (eczema herpeticum)

Investigations

Clinical diagnosis (history + examination using UK/NICE-style criteria):Itchy skin condition plus typical morphology/distribution and supportive atopic history; no routine confirmatory lab test required
Skin swab for microscopy/culture if suspected secondary bacterial infection:May identify Staphylococcus aureus or streptococcal superinfection
Viral swab/PCR if eczema herpeticum suspected:Herpes simplex virus detection; urgent same-day assessment needed
Patch testing (specialist) when allergic contact dermatitis is suspected:Relevant contact allergen sensitization in atypical, localized, or treatment-refractory eczema
Targeted allergy testing (specific IgE or skin-prick) only if immediate-type food/aeroallergen reactions are suspected:Sensitization pattern that must be interpreted with clinical history to avoid overdiagnosis

Management

Lifestyle Modifications

  • Explain chronic relapsing course and agree a written flare-maintenance plan
  • Use liberal leave-on emollients multiple times daily; avoid fragranced products and use emollient soap substitutes instead of standard soaps
  • Identify and reduce irritant triggers (detergents, rough fabrics, overheating, rapid temperature shifts); prefer cotton clothing
  • Reduce scratching burden (short nails, night-time cotton gloves in children where helpful, behavioural itch strategies)
  • Treat sleep disruption and psychosocial impact; screen for anxiety/depressive symptoms in moderate-severe disease
  • Escalate urgently for painful rapidly worsening rash, fever, clustered erosions, or eye symptoms (possible eczema herpeticum)

Pharmacological Treatment

Emollients (first-line baseline therapy)

  • White soft/liquid paraffin 50:50 ointment as leave-on emollient, applied frequently and after bathing
  • Cream/ointment emollients supplied in large quantities (typical adults often require 250-500 g/week; more if extensive disease)

Use even when skin is clear. Ointments are more occlusive for very dry skin; creams may be preferred in weepy areas/daytime use. Fire risk: paraffin-based products can impregnate clothing/bedding; keep away from flames/smoking.

Topical corticosteroids for flares (use lowest effective potency)

  • Hydrocortisone 1% ointment/cream: apply once daily (or as locally advised) for 7-14 days on face/flexures in mild flare
  • Clobetasone butyrate 0.05%: once daily short course for moderate flare
  • Betamethasone valerate 0.1% or mometasone furoate 0.1%: once daily short course for trunk/limbs in more severe flare

Match potency to site/severity/age. Avoid prolonged potent steroid use on face, flexures, and genital skin due to atrophy/striae risk. Use fingertip-unit guidance and step down once controlled. Consider weekend proactive therapy in frequent relapsers under specialist/experienced supervision.

Topical calcineurin inhibitors (steroid-sparing, sensitive sites)

  • Tacrolimus ointment 0.03% (children >=2 years) or 0.1% (adults): apply twice daily during flare, then maintenance twice weekly if needed
  • Pimecrolimus 1% cream: apply twice daily for mild-moderate facial/flexural disease

Useful for recurrent facial/flexural eczema or steroid-induced skin changes. Avoid on clinically infected skin. Common early burning/stinging. Advise sun protection and avoid excessive UV exposure.

Antimicrobials for infected eczema

  • Flucloxacillin 500 mg orally four times daily for 5-7 days (adult typical dose) when widespread/significant bacterial infection is present
  • Clarithromycin 500 mg twice daily for 5-7 days if penicillin allergy (adult typical alternative)
  • Aciclovir 400 mg orally five times daily for 5-10 days for suspected eczema herpeticum (urgent specialist input; IV aciclovir if severe/systemically unwell)

Do not use routine topical/oral antibiotics for non-infected eczema flares. Eczema herpeticum is a dermatological emergency, especially in young children; same-day referral required.

Systemic and biologic therapy for moderate-severe refractory disease (specialist initiated)

  • Ciclosporin initially about 2.5 mg/kg/day in divided doses, titrated up to around 5 mg/kg/day if needed
  • Methotrexate once weekly (commonly 5-25 mg weekly) with folic acid supplementation
  • Dupilumab 600 mg loading dose then 300 mg every 2 weeks (adult regimen)

Require specialist monitoring and shared-care protocols where applicable. Ciclosporin: monitor blood pressure and renal function; caution in hypertension/renal impairment. Methotrexate: teratogenic; strict contraception, FBC/LFT/U&E monitoring, and avoid daily dosing errors. Dupilumab: watch for conjunctivitis/eosinophilia. Routine long-term oral corticosteroids are generally avoided due to rebound flares and adverse effects.

Complications

  • Secondary bacterial infection (impetiginization/cellulitis), commonly Staphylococcus aureus
  • Eczema herpeticum (disseminated HSV) with fever, malaise, lymphadenopathy; potential ocular/CNS complications
  • Superficial fungal skin infection
  • Sleep disturbance and reduced quality of life
  • Psychological morbidity (anxiety, low mood, social withdrawal, bullying impact in children)
  • Progression within the atopic march (food allergy, asthma, allergic rhinitis)

Prognosis

Course is typically relapsing-remitting, with flare frequency varying from occasional to very frequent; a minority have near-continuous severe disease. Many children improve with age, and a substantial proportion remit by adolescence, though relapse can occur later and adult-onset disease is recognized. Earlier onset, greater severity, and persistent childhood disease increase likelihood of persistence and comorbid atopic disease.

Sources & References

💊BNF Drug References(10)

NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1641)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1683)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1634, 1635)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1825)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1845)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1629)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1623, 1624)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1682, 1683)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1627, 1628)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1646)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1634)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1661)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1634)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1635)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1634)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1636)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1636, 1637)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1635)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 167)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 166, 167)[context]

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