A registrar-level reference: the barrier/immune pathophysiology behind the disease, distribution & assessment by age, stepwise everyday and flare management, topical corticosteroid reasoning and dosing, infection recognition and treatment — in ED and on the ward.
Read first. Decision-support, not a substitute for senior/dermatology review. Confirm every drug and potency choice against CREDD / the current CHQ flowchart / local formulary before prescribing — LAM (List of Approved Medicines) restrictions vary by site. Doses here follow the CHQ statewide eczema guideline (CHQ-GDL-60034) cross-checked with RCH.
Eczema (atopic dermatitis, AD) is a chronic inflammatory, pruritic skin disease characterised by flare-ups and remissions on a background of impaired skin barrier function. Both pruritus and a rash must be present for the diagnosis.
Children with untreated moderate-to-severe eczema starting under 6 months of age have a significantly higher subsequent incidence of food allergy. This group should be prioritised for follow-up — early, effective skin treatment is thought to reduce allergen sensitisation through the skin barrier (see §2).
Eczema arises from a complex interplay of genetic skin-barrier defects, immune dysregulation and environmental triggers. Understanding the barrier defect explains why moisturiser is not cosmetic, and understanding the immune dysregulation explains why steroids work and why itch persists even on clear-looking skin.
Loss-of-function mutations in filaggrin (and related structural proteins) impair formation of the stratum corneum's "brick and mortar" barrier. The result is increased trans-epidermal water loss (dry, xerotic skin), reduced natural moisturising factor, and a barrier that is permeable to irritants, allergens and microbes it would normally exclude.
A leaky barrier allows environmental antigens to engage skin immune cells, driving a Th2-skewed inflammatory response (IL-4, IL-13, IL-31 among the key cytokines). This inflammation itself further impairs barrier proteins — a self-perpetuating cycle — and IL-31 in particular is a direct itch (pruritogen) mediator, which is why eczema itches even without an obvious rash.
Barrier disruption and inflammatory mediators (especially IL-31) cause itch → scratching mechanically damages the barrier further → more antigen/microbial penetration → more inflammation → more itch. Breaking this cycle (steroid to suppress inflammation, moisturiser to restore the barrier, short nails/mittens to limit mechanical damage) is the basis of all flare management.
The same barrier defect that lets allergens in lets pathogens in, and eczematous skin has reduced antimicrobial peptide production — so colonisation and infection with Staphylococcus aureus, Streptococcus pyogenes, and viruses (HSV, coxsackievirus, molluscum) are all more common than in normal skin. This is why treating the underlying eczema is part of treating the infection, not a separate problem.
Topical corticosteroids reduce the Th2-driven cytokine cascade directly — this is why early, adequate treatment shortens flares and reduces total steroid exposure over time compared with underdosing (the CHQ/RCH "treat early and adequately" principle). Under-treatment prolongs inflammation, prolongs barrier damage, and paradoxically increases cumulative steroid need.
Eczema is often the first step in a sequence — eczema → food allergy → allergic rhinitis → asthma — thought to be driven partly by allergen sensitisation through a defective skin barrier (epicutaneous sensitisation) rather than through the gut. This is the mechanistic rationale behind early, effective skin treatment and against reflexive dietary restriction (§11).
Over 12 years: erythematous papules/plaques with xerotic scale and crust on scalp, face, trunk, and extensor or flexural surfaces (varies by ethnicity); lichenified plaques common with chronic disease. Nose, groin and axillae are typically spared at all ages — involvement of these sites should prompt reconsideration of the diagnosis.
| Term | Description |
|---|---|
| Papules | Elevated, solid, palpable lesions ≤1 cm, solitary or multiple, no fluid content. |
| Lichenification | Palpably thickened skin with increased skin markings from chronic rubbing — a sign of long-standing, poorly controlled disease. |
| Discoid (nummular) eczema | Papules/papulovesicles coalescing into coin-shaped plaques; more common in dark skin and males; associated with treatment resistance — often needs bleach/antibacterial baths and potent steroids. |
| Post-inflammatory hypo/hyperpigmentation | Not a steroid side effect — a temporary pigmentary response to the inflammatory process itself. Not scarring; normalises over months once the area has been eczema-free. |
Conventional severity scoring can underestimate erythema in darker skin tones — consider up-grading the assessed severity by one grade when uncertain (e.g. mild → moderate).
Normal skin, no active eczema. No QoL impact.
Dry skin, infrequent itch ± small areas of redness. Little impact on activities/sleep.
Dry skin, frequent itch, redness ± excoriation/localised thickening. Frequently disturbed sleep.
Widespread dryness, incessant itch, redness ± excoriation, extensive thickening, bleeding, oozing, cracking. Nightly sleep loss.
Formal tools: SCORAD (mild <25, moderate 25–50, severe >50) or EASI (mild <7, moderate 7.1–21, severe >21.1) for objective severity/response tracking; CDLQI or POEM for quality-of-life impact.
| Condition | Distinguishing feature |
|---|---|
| Seborrhoeic dermatitis (infantile) | Greasy scale, scalp/face/nappy area; generally not itchy. |
| Tinea | Annular, well-demarcated, active edge; dermatophyte on scraping. |
| Scabies | Burrows, papules/pustules to palms/soles/web spaces; affects multiple family members. |
| Periorificial dermatitis | Small papules around mouth/nose/eyes; worsened by moderate/potent steroid. |
| Psoriasis | Well-defined, salmon-pink, silvery-scaly plaques on extensors and scalp. |
| Miliaria | Heat-related, fine papulovesicles, resolves with cooling. |
| Nutritional deficiency (e.g. zinc) | Peri-orificial/acral distribution; consider with poor growth/diet history. |
Superimposed infections are the most common complication of eczema. Systemic features (fever, malaise) point to a more significant infection needing more than topical measures.
Investigate only if infection is suspected. Send bacterial M/C/S and HSV PCR (± VZV PCR if varicella suspected). For a suspected viral blistering process: de-roof the blister and firmly swab the base with a dry swab (no transport medium) for best PCR yield.
Everyday skin care is required even when skin looks clear — the barrier defect persists between flares, and consistent care is what reduces flare frequency.
Moisturiser directly compensates for the filaggrin/barrier defect — restoring lipid content and reducing trans-epidermal water loss breaks the entry point for irritants and allergens and interrupts the itch–scratch cycle. This is why it continues lifelong, in remission as well as in flares, and why several small daily applications outperform one large one.
Early, liberal TCS use is recommended — it limits total corticosteroid exposure over time compared with under-treatment. There is no requirement to use TCS "sparingly" or to take routine breaks during a flare — apply once (or twice) daily until the skin is completely clear, then stop and return to moisturiser-only maintenance. Underuse of TCS is the most common cause of treatment failure.
A fingertip unit = the amount expressed from a standard nozzle, distal skin crease to fingertip of an adult index finger (≈0.5 g), and covers an area equivalent to two adult hand-prints of skin.
| Age | Face & neck | Arm & hand | Leg & foot | Trunk (front) | Back & buttocks |
|---|---|---|---|---|---|
| 3–12 months | 1 | 1 | 1½ | 1 | 1½ |
| 1–3 years | 1½ | 1½ | 2 | 2 | 3 |
| 3–6 years | 1½ | 2 | 3 | 3 | 3½ |
| 6–10 years | 2 | 2½ | 4½ | 3½ | 5 |
| >10 years | 2½ | 4 | 8 | 8 | 7 |
FTUs given are per single application, per side (double arm/leg figures for both limbs). 1 FTU ≈ 0.5 g — use this to calculate how many tubes to prescribe for the expected treatment course.
| Class | Example agents | Typical use |
|---|---|---|
| I — mild | Hydrocortisone acetate 1% | Mild face / neck / genital inflammation |
| II — moderate | Triamcinolone 0.02%; methylprednisolone aceponate 0.1% | Mild–moderate body/scalp; moderate–severe face; excoriated skin (also minimises infection risk) |
| III — potent | Betamethasone dipropionate 0.05%; mometasone furoate 0.1% | Moderate–severe body & scalp inflammation |
| IV — very potent | Betamethasone dipropionate 0.05% (optimised vehicle); clobetasol propionate 0.05% | Severe inflammation — dermatologist only |
Class III (potent) and Class IV (very potent) TCS should not be used in children ≤12 months without specialist guidance — greater surface-area-to-weight ratio increases systemic absorption risk in infants.
Pimecrolimus / tacrolimus inhibit calcineurin, blocking T-cell activation and cytokine transcription — anti-inflammatory without the cutaneous atrophy risk of TCS. Useful as a second-line, steroid-sparing agent for sensitive areas (face, eyelids, groin) or where prolonged topical steroid would otherwise be needed.
Topical antibiotics (e.g. mupirocin) are not recommended for infected eczema — less effective than oral therapy for this indication and contribute to antimicrobial resistance.
| Agent | Dose | Notes |
|---|---|---|
| Valaciclovir (oral) | 20 mg/kg every 8 h (max 1 g) for 7 days | Preferred route — good oral bioavailability. Requires ID approval per CHQ. |
| Aciclovir (IV) | 10 mg/kg every 8 h (max 500 mg) for 7 days | If systemically unwell / unable to tolerate oral. Most effective within 72 h of first lesion. Requires ID approval. |
There is a theoretical risk that TCS over HSV vesicles worsens the infection — but in practice, controlling the underlying eczema with TCS is usually more effective at limiting HSV spread. Start antivirals first; do not withhold eczema treatment indefinitely.
HSV reaching the ophthalmic branch of the trigeminal nerve risks corneal involvement (dendritic ulcers, keratitis) and, if systemic, can be fatal — periorbital or near-eye lesions need urgent ophthalmology input (locally or via CATCH).
Antihistamines — eczema itch is not primarily histamine-mediated (it's IL-31/cytokine-driven), so antihistamines don't meaningfully reduce eczema itch; reserve for coexisting allergic rhinitis/urticaria. Restrictive diets are not recommended empirically (§11).
A small proportion of children have disease that remains uncontrolled despite optimal everyday care, adequate TCS/TCI use and infection treatment. This group needs dermatology (± allergy/immunology) referral — these therapies are specialist-initiated, not started from the ward or ED.
Both guidelines share the same core philosophy — early, adequate TCS use; everyday skin care regardless of flare status; treat infection alongside, not instead of, the eczema. The practical differences are in how potency/duration is specified and the depth of the FTU table.
| Element | QLD / CHQ | RCH Melbourne |
|---|---|---|
| TCS philosophy | Early, liberal, daily until clear — limits total dose over time | Same — "apply generously," no sparing/breaks required |
| TCS frequency | Once daily standard; twice daily often used for inpatients with severe flares | Once–twice daily until clear (hydrocortisone specified twice daily) |
| Face/sensitive-site duration limit | Not specified as a fixed course length — potency-graded by severity | Explicit short-course caps: 3–5 days face/neck, 7–14 days groin for moderate-potency agents |
| Potency classification | 4-class system (I mild → IV very potent) with named LAM-listed brands | Descriptive mild/moderate/potent/very-potent, mapped to named agents by body site |
| FTU dosing table | Defines the FTU concept; does not tabulate by age/site | Full FTU table by age (3 mo–>10 yr) × 5 body regions — used in this reference (§8) |
| Bathing adjuncts | Detailed — Condy's crystals & bleach-bath recipes with exact concentrations | Bleach baths recommended; concentration per RCH factsheet |
| Eczema herpeticum antivirals | Valaciclovir 20 mg/kg q8h oral or aciclovir 10 mg/kg q8h IV, both ×7 days | Prompt antiviral initiation; IV for severe infection — consistent approach |
| TCI | Not detailed in the ED guideline | Pimecrolimus 1%, second-line, sensitive sites, course-length capped |
Where the two differ on a specific number (e.g. course length), defer to your local site's guideline and current dermatology advice — both are reasonable, evidence-aligned practice.
The commonest reasons eczema treatment "fails" are inadequate education, under-application of moisturiser/TCS, ongoing trigger exposure, delayed flare treatment, and unrecognised infection — not treatment resistance. A written, individualised action plan (ASCIA template) closes this gap.
Moderate–severe eczema not responding to treatment · widespread erythema with thermoregulation dysfunction · disseminated eczema herpeticum · severely infected eczema · significant parental distress · moderate–severe QoL impact · consider allergy/immunology referral if food allergy is suspected with signs/concern of allergic reaction.
First point of call for advice and referral.
QCH paediatric/dermatology advice (24 h) — required even when using the dermatology image-transfer portal.
Local/regional paediatric videoconference support (24 h).
Urgent review for periorbital/near-eye suspected eczema herpeticum — locally or via CATCH.