Eczema (Atopic Dermatitis) — Causes, Symptoms, Triggers & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Eczema is a common, chronic inflammatory skin condition characterised by intensely itchy, inflamed, dry skin — occurring in episodes (flares) interspersed with periods of relative remission. Atopic dermatitis (AD) is the most common form (accounting for over 90% of eczema cases) and is part of the 'atopic march' alongside asthma, allergic rhinitis, and food allergy — 50-70% of children with AD develop asthma or allergic rhinitis. Atopic dermatitis affects approximately 15-20% of children and 3-10% of adults globally, making it one of the most prevalent non-communicable diseases worldwide — affecting an estimated 232 million people. Other forms of eczema include: contact dermatitis (allergic or irritant — from specific contactants); seborrhoeic dermatitis (scaly, greasy patches on the face, scalp, and chest); discoid (nummular) eczema (coin-shaped plaques); varicose (gravitational) eczema (on legs from venous insufficiency); and dyshidrotic eczema (vesicular eruption on palms and soles — pompholyx). Atopic dermatitis is driven by skin barrier dysfunction and Th2-mediated immune dysregulation — a complex interaction of genetic susceptibility (filaggrin gene mutations in 30% of patients), environmental triggers, and the microbiome. The condition carries significant burden — sleep disruption (from nocturnal itch), psychological impact (anxiety, depression, low self-esteem), time burden of treatment, and impact on school and work attendance.

The pathogenesis of atopic dermatitis involves two intersecting defects: skin barrier dysfunction and immune dysregulation. Filaggrin (FLG) gene loss-of-function mutations — present in 30% of patients with AD — cause impaired synthesis of filaggrin protein, which is essential for corneocyte maturation, stratum corneum integrity, and natural moisturising factor (NMF) production. FLG mutations result in a 'leaky' skin barrier that allows increased transepidermal water loss (TEWL — detectable before visible eczema develops), penetration of allergens and irritants, and susceptibility to Staphylococcus aureus skin colonisation. Immune dysregulation: Th2 cytokines (IL-4, IL-5, IL-13, IL-31) predominate in AD, suppressing antimicrobial peptide production, impairing barrier differentiation, and driving allergic inflammation and pruritus (IL-31 is a major driver of itch). Staphylococcus aureus colonises the skin of 90% of AD patients (versus 20-30% of healthy controls), releasing toxins and proteases that amplify inflammation and damage the barrier. Common triggers that provoke flares: irritants (soap, detergents, washing powder, swimming pool chlorine, wool clothing); aeroallergens (house dust mite, grass pollen, pet dander); heat and sweating; emotional stress; skin infections (Staphylococcus aureus, Herpes simplex virus — eczema herpeticum); teething in infants; and seasonal variation (worse in winter — dry air and cold). Food allergy (cow's milk, egg, peanut, wheat) may exacerbate AD in infants and young children — provocation by food is less relevant in older children and adults.

The hallmark symptom of eczema is pruritus (itch) — which can be intense, relentless, and sleep-disturbing. The itch-scratch cycle perpetuates inflammation — scratching releases histamine and cytokines, worsening the inflammatory response and creating lichenification (skin thickening). Clinical features: dry, scaly skin (xerosis — often the most prominent feature in chronic disease); erythematous (red) or pink-brown patches (less noticeable on darker skin tones — a common reason for delayed diagnosis); vesicles (tiny blisters) and oozing/weeping in acute flares; crusting and cracking; excoriations (scratch marks). Distribution by age: infants (below 2 years) — predominantly affects the face (cheeks), scalp, and extensor surfaces (outside of arms and legs); older children and adults — characteristically affects flexural areas (antecubital fossae — inside of elbows; popliteal fossae — behind the knees; wrists, ankles, around the neck). Severity classification: mild AD (areas of dry skin, infrequent itching with small areas of redness); moderate AD (areas of dry skin, frequent itching, redness with or without excoriations, localised skin thickening); severe AD (widespread dry skin, incessant itching, widespread redness with or without excoriations, extensive skin thickening, bleeding, oozing, cracking, and sleep disruption — significantly impacts quality of life). Eczema herpeticum: a medical emergency — sudden widespread vesicular eruption from Herpes simplex virus super-infection in a patient with AD; may be confused with severe bacterial infection.

Atopic dermatitis is a clinical diagnosis — no single diagnostic test exists. The UK Working Party criteria (modified Hanifin and Rajka) require: an itchy skin condition PLUS three or more of: onset below age 2 years (if the patient is over 4); history of flexural skin involvement; history of generally dry skin; personal history of other atopic disease (asthma or allergic rhinitis); and visible flexural dermatitis. Investigations are not routinely required for typical AD. Total serum IgE: elevated in the majority of AD patients (reflects atopic state but does not diagnose AD). Skin prick testing or specific IgE RAST testing: useful if food allergy is suspected as a provoking factor in infants or if aeroallergen sensitisation (house dust mite, pet dander) is suspected as a trigger — particularly when allergen avoidance or allergen immunotherapy is being considered. Patch testing: performed by a dermatologist when allergic contact dermatitis is suspected (occupational exposure, topical medication contact allergy). Bacterial swabs: if secondary bacterial infection (impetigo from Staph. aureus) is suspected. Skin biopsy: rarely needed but may help distinguish AD from psoriasis, cutaneous T-cell lymphoma (mycosis fungoides), or other skin conditions. Differential diagnosis includes: psoriasis (well-defined plaques with silvery scale, typically extensor surfaces and scalp, uncommon flexural involvement), contact dermatitis (pattern follows contactant exposure), seborrhoeic dermatitis, scabies (extremely pruritic, between fingers, genitals, wrists — scabies should always be excluded in a new or unusual eczema presentation), and ichthyosis.

Treatment follows a stepped-care approach (NICE NG190). Emollients — cornerstone and foundation of all eczema treatment regardless of severity: applied liberally at least twice daily (minimum 250-500 g per week for an adult) to hydrate the skin and restore the barrier. Applied immediately after bathing (within 3 minutes — 'soak and seal'). Emollient bath additives (oat-based, emollient oils): reduce skin colonisation and improve barrier. Key principle: emollients contain no anti-inflammatory agents and are used continuously — including during flares and remission. Step 1 (mild AD): emollients + mild to moderate potency topical corticosteroids (TCS) for flares — hydrocortisone 1% (mild) to clobetasone butyrate 0.05% (moderate) applied once daily during flares only (typically 5-7 days). Step 2 (moderate AD): moderate to potent TCS (fluocinolone acetonide 0.025%, betamethasone valerate 0.1%) for acute flares; topical calcineurin inhibitors (TCIs) — tacrolimus 0.03% or 0.1% ointment (Protopic) and pimecrolimus 1% cream (Elidel) — used for the face and flexures where TCS is risky (skin thinning and telangiectasia); TCS or TCI twice weekly maintenance therapy (proactive approach — proven to reduce flare frequency). Step 3 (severe AD): phototherapy (narrowband UVB — 3 sessions per week for 12-16 weeks — very effective, particularly for lichenified AD); short courses of oral ciclosporin (2.5-5 mg/kg/day — rapid onset but nephrotoxic with prolonged use); oral methotrexate (10-25 mg weekly); azathioprine; and systemic corticosteroids (short courses only — severe rebound on stopping makes these unsuitable for long-term use). Step 4 (moderate-severe refractory AD): dupilumab (Dupixent) — anti-IL-4 receptor alpha monoclonal antibody — subcutaneous injection every 2 weeks — transformative biologic treatment achieving 70-80% reduction in EASI (Eczema Area and Severity Index) in pivotal trials; approved by FDA and NICE for adults and children aged 6 months+ with moderate-severe AD; safe long-term profile. Tralokinumab (Adtralza — anti-IL-13) and lebrikizumab: alternatives to dupilumab. Abrocitinib and upadacitinib (JAK inhibitors — oral): also approved for adults with moderate-severe AD — highly effective, faster onset than dupilumab, but require monitoring for infections, thrombosis, and lipid levels. Antihistamines: sedating antihistamines (chlorphenamine 4 mg) may help nocturnal itch indirectly via sedation but do not treat the underlying inflammation.

Atopic eczema (atopic dermatitis) causes significant complications beyond skin inflammation that can substantially impact quality of life and long-term health. Infection complications: the disrupted skin barrier in eczema significantly increases susceptibility to bacterial superinfection — Staphylococcus aureus colonises skin in up to 90% of eczema patients and triggers inflammatory flares through superantigen release; clinical infection (impetigo — golden crusting, increased warmth, tenderness, pus) requires antibiotic treatment. Eczema herpeticum: a potentially life-threatening complication from disseminated herpes simplex virus infection on eczematous skin — widespread painful punched-out erosions, fever, systemic upset; requires urgent systemic aciclovir and hospitalisation in severe cases. Atopic march: childhood eczema is the first manifestation of the atopic march — sequential development of food allergies, allergic rhinitis (hay fever), and asthma; 60-70% of children with eczema develop at least one other atopic condition. Sleep disturbance: nocturnal itch disrupts sleep in 60% of patients, impairing cognitive development in children and quality of life in adults; parental sleep is similarly affected. Psychological complications: depression and anxiety affect 30-40% of adults with severe eczema; children show behavioural difficulties and reduced academic performance. Topical corticosteroid side effects with prolonged inappropriate use: skin atrophy, striae, and telangiectasia.

Daily emollient use is the most evidence-based preventive measure for reducing flare frequency and severity — reduce TEWL, prevent barrier breakdown, and reduce allergen penetration. Early emollient use in high-risk infants (with FLG mutations or strong family history): some evidence for early emollient application from birth reducing AD development (the BEEP trial showed no reduction in AD but minimal harm; ongoing research). Trigger avoidance: identify and minimise individual triggers — house dust mite reduction measures (anti-allergen mattress covers, washing bedding at 60°C weekly, HEPA vacuum cleaners); avoid highly fragranced soaps and washing powders; choose cotton clothing; avoid wool directly against the skin; maintain cool bedroom temperature; use pH-neutral, fragrance-free skincare products. Preventing the atopic march: early diagnosis and optimal treatment of atopic dermatitis may reduce progression to asthma and allergic rhinitis — evidence emerging for allergen immunotherapy and dupilumab in preventing asthma in atopic children. Early introduction of peanut (LEAP trial) and egg (EAT trial) to atopic infants' diets has been shown to prevent food allergy — this should follow national guidance on age-appropriate complementary feeding.

See a GP urgently (same day) for: rapidly worsening eczema with fever, widespread painful blistering and punched-out erosions — possible eczema herpeticum (HSV super-infection — requires urgent systemic aciclovir); eczema with significant spreading redness, warmth, swelling, and yellow crusting — possible bacterial infection (impetigo, cellulitis) requiring antibiotics; or eczema in an infant under 6 months that is not improving with basic emollient treatment. See a GP for: eczema that is significantly affecting sleep or quality of life; eczema not responding to appropriate topical treatment after 2-4 weeks; and first presentation of eczema without a prior diagnosis. Seek specialist dermatology referral for: moderate to severe eczema not controlled by appropriate topical treatment; when phototherapy, systemic therapy, or biologic treatment (dupilumab) may be needed; diagnostic uncertainty; or occupational eczema (where specialist patch testing and occupational health input is needed). Children with severe eczema significantly affecting growth, sleep, behaviour, or school attendance should be referred promptly to a paediatric dermatologist.