Lucan · Conditions

Atopic eczema

Australian guidance: eTG Dermatology — Atopic Dermatitis + ACDA

1. Definition and epidemiology

Atopic eczema (atopic dermatitis) is a chronic, relapsing, inflammatory skin condition characterised by intense pruritus, disrupted epidermal barrier function, and immune dysregulation. It is the most common inflammatory skin disease in childhood, affecting approximately 15 to 20 percent of Australian children and 2 to 5 percent of adults. Corrected 2026-09-22: the captured RCH eczema CPG states that eczema affects 30% of children and often develops before 12 months of age, with some children developing lifelong eczema. The 15 to 20 percent figure understated the captured paediatric prevalence; the source's 30% is now stated alongside it rather than in place of it, since the earlier figure may describe a narrower or older sample. Not carried by either captured source: the 2 to 5 percent adult figure and the atopic triad prevalence trend. It is strongly associated with the atopic triad of asthma and allergic rhinoconjunctivitis, and the prevalence of all three conditions has risen over recent decades in high-income countries including Australia.

2. Pathophysiology

The central defect in atopic eczema is a breakdown of the epidermal barrier, driven largely by loss-of-function mutations in the filaggrin gene (FLG). Filaggrin is a structural protein essential for keratinocyte cornification and the formation of the stratum corneum. Its absence leads to increased transepidermal water loss, a raised skin pH, and enhanced penetration of allergens and microbes through the epidermis.

Barrier disruption triggers a predominantly Th2-polarised immune response. Keratinocytes release thymic stromal lymphopoietin (TSLP), IL-33, and IL-25, which activate dendritic cells and type 2 innate lymphoid cells. This promotes Th2 differentiation and overproduction of IL-4, IL-5, and IL-13. IL-4 and IL-13 both signal through the IL-4 receptor alpha subunit (IL-4Ralpha) and suppress filaggrin expression further, creating a self-amplifying cycle of barrier failure and Th2 inflammation. IgE levels are elevated in most patients, and sensitisation to environmental and food allergens is common, though not universally causative. In chronic lesions, a Th1 and Th22 component also develops, with interferon-gamma and IL-22 contributing to epidermal hyperplasia and lichenification. Staphylococcus aureus colonisation, present in greater than 90 percent of affected skin, amplifies inflammation through superantigen-mediated T-cell activation and direct barrier injury.

3. Clinical presentation and diagnostic criteria

Diagnosis is clinical, based on the Hanifin and Rajka major and minor criteria, or in practice the simplified UK Working Party criteria. Essential features are a pruritic skin condition with a chronic or chronically relapsing course. Supporting features include onset before age two, personal or family history of atopy, and typical morphology and distribution: in infants, erythematous weeping plaques on the face and extensor surfaces; in older children and adults, lichenified plaques in the flexural creases (antecubital and popliteal fossae, neck, wrists). Partly carried and partly corrected, 2026-09-22: the captured RCH CPG gives the infant distribution as the cheeks, scalp and extensor surfaces in infants under 18 months, not "onset before age two", and the older-child distribution as flexural dermatitis of the antecubital fossae, popliteal fossae, neck, front of the ankles and periorbital area; the front of the ankles and periorbital sites were missing from this note. The captured RCH page also carries a severity definition set this note lacks, in its own words: clear is normal skin with no active atopic eczema; mild is areas of dry skin with infrequent itching, with or without small areas of redness; moderate is areas of dry skin with frequent itching and redness, with or without excoriation and localised skin thickening; and severe is widespread dry skin with incessant itching and redness, with or without excoriation, extensive skin thickening, bleeding, oozing, cracking and alteration of pigmentation. It names EASI for objective severity and the Children's Dermatology Life Quality Index (CDLQI) for quality-of-life impact, and it describes discoid (nummular) eczema as a variant of coin-shaped pruritic plaques developing in later childhood, more common in people with dark skin and in males, associated with increased persistence and treatment resistance and often requiring extended courses of potent steroids. Uncarried: the Hanifin and Rajka and UK Working Party criteria, the Dennie-Morgan folds and the other examination signs, and SCORAD.

4. Investigations and AU-specific cutoffs

Atopic eczema is a clinical diagnosis and routine investigations are not required in uncomplicated disease. Targeted investigations are indicated in specific circumstances.

Total serum IgE is often elevated but lacks specificity and does not alter initial management. Specific IgE or skin-prick testing for food allergens (milk, egg, peanut, wheat, soy) is appropriate in infants with moderate to severe eczema poorly responsive to optimised topical therapy, particularly if there is a temporal association with food triggers. Patch testing is reserved for adults with suspected allergic contact dermatitis complicating the picture, such as sensitisation to topical medicaments.

Skin swabs for bacterial culture (Staphylococcus aureus, group A streptococcus) are indicated when secondary infection is suspected: features include weeping, crusting, frank pustules, or sudden deterioration. In children with severe treatment-resistant disease, a short course of food elimination with supervised reintroduction under dietitian guidance may be considered, though broad elimination diets are generally discouraged given nutritional risk.

5. Management

Management follows a stepwise approach anchored to eTG Dermatology and the Australasian College of Dermatologists (ACDA) guidelines.

Baseline care for all patients involves twice-daily liberal application of a bland emollient to restore barrier function. Emollient choice should account for patient preference; cream or ointment vehicles are preferred over lotions in dry climates. Trigger avoidance (woollen or synthetic fabrics, fragranced products, extremes of temperature, known allergens) is advised. Soap substitutes should replace conventional soaps.

Mild flares are managed with a low-potency topical corticosteroid (TCS) such as hydrocortisone 1 percent on the face and intertriginous areas, and a moderate-potency agent such as betamethasone valerate 0.02 to 0.05 percent on the body. TCS should be applied once or twice daily to active lesions until clearance, then ceased. Prolonged use on the face, neck, and flexures risks skin atrophy and is avoided. Corrected 2026-09-22, and this was the worst error in the note, because the previous wording taught steroid phobia that the captured Australian guideline explicitly refutes. The captured RCH eczema CPG states that topical steroids "do not cause atrophy, hypopigmentation, hypertrichosis, osteoporosis, purpura or telangiectasia when used as per guidelines", and that rare complications such as striae, adrenal suppression and ophthalmological disease have been reported only with prolonged and excessive use of potent topical steroids. It further states that there is "no requirement to use steroids 'sparingly' or for regular breaks from steroids during treatment for eczema flares", and that "steroids should be applied generously", followed by moisturiser, once or twice daily until the skin is completely clear, and that they can be applied to broken and infected skin. The captured PCH eczema page is consistent: topical steroids are safe and effective when used as prescribed, ointments are preferred because they are more effective, more moisturising and less likely to sting, steroids should be applied liberally to all affected areas and not just to the worst areas until the skin feels normal, and medical review is suggested if the eczema is not clear after 2 weeks. The RCH page does still direct that mild to moderate facial eczema be treated with low-potency steroids to avoid chemical skin irritation, which is the one part of this note's facial caution that survives. It also gives the fingertip unit dosing table this note lacks, with per-body-area units by age band from 3 to 12 months up to over 10 years. Uncarried: the specific hydrocortisone 1 percent and betamethasone valerate 0.02 to 0.05 percent potency selections, which neither captured page names.

Topical calcineurin inhibitors (TCIs), tacrolimus 0.03 percent (children) or 0.1 percent (adults) and pimecrolimus 1 percent, are steroid-sparing alternatives for sensitive sites or where TCS use has been prolonged. They are particularly useful for facial and periocular disease. Corrected and partly carried, 2026-09-22: the captured PCH eczema page gives pimecrolimus 1% cream as approved for children aged 3 months and over with mild to moderate facial eczema, applied twice daily, and tacrolimus 0.03% ointment for children aged 2 years and over with moderate to severe facial eczema, applied once to twice daily as directed, and notes that the 0.03% ointment is not available commercially and must be compounded or dispensed by PCH Pharmacy. The RCH page describes pimecrolimus as a non-steroid second-line option for moderate eczema in sensitive areas such as the face, eyelids and groin. This note previously gave pimecrolimus as approved from age 2, which is 21 months later than the captured PCH figure, and the age has been corrected. The tacrolimus 0.1 percent adult strength is uncarried: no captured page names it, and the PCH page covers children only.

Proactive therapy, using low-dose TCS or TCI two to three times per week on previously affected skin, reduces flare frequency in patients with frequent relapse.

Moderate to severe disease uncontrolled on topical therapy warrants dermatology referral. Second-line options include phototherapy with narrowband UVB, and oral immunosuppressants including ciclosporin (most rapidly effective), methotrexate, or azathioprine. Wet dressings over TCS can provide short-term control in acute severe flares and are used in paediatric inpatient settings. Added 2026-09-22, carried by the captured pages: the RCH CPG gives the wet dressing schedule this note lacked, applied with every flare 1 to 4 times daily for at least 3 days, with more frequent dressings or longer treatment required in severe eczema, and notes they may be used in eczematous skin infections in addition to antimicrobial treatment; it also records that bleach baths can be used daily with every flare to reduce bacterial skin load, that the face and head should be wet but not submerged, and that the child should not be rinsed after bathing. Bathing itself should be daily where water quality and access allow, with baths and showers kept luke-warm under 31 degrees Celsius, and soap and shampoo should not be used in favour of soap-free cleansers; moisturiser is applied on top of other topical medicines such as steroids, at least twice a day. The captured PCH page adds that proactive topical treatment is usually prescribed twice a week for three months, and longer if the child has recurrent skin infections. Both captured pages list the common reasons treatment fails, foremost among them inadequate caregiver education and inadequate application of moisturisers, topical steroids or wet dressings, together with delayed use of flare treatment, ongoing trigger exposure and untreated skin infection including MRSA. Uncarried: the phototherapy, ciclosporin, methotrexate and azathioprine content, the "most rapidly effective" ranking of ciclosporin, and the dupilumab paragraph below.

Dupilumab, a monoclonal antibody targeting IL-4Ralpha, is the first biologic approved in Australia for moderate to severe atopic dermatitis in adults and children aged six years and over. It is administered as a subcutaneous injection every two weeks after a loading dose.

6. Pharmacology and AU PBS notes

Topical corticosteroids are the mainstay of flare treatment and are listed on the PBS for atopic eczema.

Dupilumab (Dupixent, Sanofi) is PBS listed under Section 100 Highly Specialised Drugs for patients aged 12 years and over with severe atopic dermatitis (EASI greater than or equal to 23 or SCORAD greater than or equal to 50) who have failed an adequate trial of at least two conventional systemic immunosuppressants or have a contraindication to them. Continuation requires at least 50 percent improvement in EASI or SCORAD at 16 weeks. For children aged 6 to 11 years, dupilumab is TGA approved but PBS listing criteria differ and should be verified at the time of prescribing. The streamlined authority code is 11355 (adult, initial) and 11356 (adult, continuing) as of mid-2026; confirm current codes via the PBS online formulary.

Tacrolimus 0.1 percent ointment (Protopic, Leo Pharma) is TGA approved for adults with moderate to severe atopic eczema. Tacrolimus 0.03 percent is approved for children aged 2 to 15 years. Pimecrolimus 1 percent cream (Elidel, Sun Pharma) is approved for mild to moderate disease aged 2 years and over.

Oral ciclosporin for atopic eczema is prescribed off-PBS but is available via private prescription or compassionate access; doses are typically 2.5 to 5 mg per kg per day with monitoring of renal function and blood pressure.

Oral antihistamines do not reduce itch in atopic eczema (which is predominantly IL-31 mediated rather than histamine mediated) and are not routinely recommended. Sedating antihistamines may be used short-term for sleep disruption only. Corrected 2026-09-22: the captured RCH CPG states that non-sedating antihistamines do not improve eczema itch, but may be considered if there is concomitant urticaria or allergic rhinitis. That exception was missing from this note and has been added. The captured page does not endorse sedating antihistamines for sleep disruption, so that sentence is uncarried. The same page states that allergy testing is usually not required, that restrictive diets are usually not helpful, and that parents should seek advice from a dermatologist or general paediatrician before eliminating foods from the diet, which is a firmer position against testing and elimination than this note's section 4 takes. It also carries the mupirocin regimen this note lacks: mupirocin 2% ointment or cream to crusted areas twice daily for 5 days, and it identifies Staphylococcus aureus, with MRSA in high-risk groups or where first-line antibiotics fail, and Streptococcus pyogenes as the common bacterial causes, alongside herpes simplex, coxsackievirus, molluscum contagiosum and varicella zoster as viral causes that often coexist. Uncarried: the IL-31 mechanism, and the sedating antihistamine advice.

7. Complications and monitoring

Secondary bacterial infection with Staphylococcus aureus is the most common complication. Eczema herpeticum (Kaposi varicelliform eruption), caused by disseminated herpes simplex virus infection across eczematous skin, is a dermatological emergency requiring systemic aciclovir. Recognition depends on identifying clustered punched-out erosions and haemorrhagic crusting, often with fever.

Ocular complications include keratoconus, anterior subcapsular cataracts (associated with prolonged periocular TCS use), and recurrent conjunctivitis. Ophthalmology review is warranted in patients with persistent periocular disease.

Growth faltering may occur in children with severe disease due to chronic inflammation, sleep deprivation, and systemic corticosteroid use. Height and weight should be monitored at each visit in paediatric patients.

Psychosocial burden is substantial. Quality of life impairment from pruritus, sleep disturbance, and social stigma is comparable to that of other chronic paediatric illnesses. Screening for anxiety and depression is appropriate in adolescents and adults with moderate to severe disease.

Patients on dupilumab should be monitored for conjunctivitis (a recognised side effect occurring in up to 10 percent), injection site reactions, and rare arthralgia. Dupilumab does not require routine blood test monitoring. Patients on ciclosporin require baseline and three-monthly monitoring of serum creatinine, electrolytes, blood pressure, and full blood count. Patients on methotrexate require monitoring of liver function tests and full blood count at initiation and then three-monthly.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.