Paeds Vivas · allergy-and-immunology
Atopic dermatitis and the atopic march — viva
Branching clinical structured oral on the assessment, barrier-and-Th2 pathophysiology and stepwise management of an infant with atopic dermatitis and the atopic march.
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Target exams
Opening (2 minutes)
The candidate should recognise the classic picture of infantile atopic dermatitis in a child with a strong atopic family history, apply the UK Working Party diagnostic criteria, and commit to excluding alternative diagnoses. The intensely itchy rash on the cheeks, scalp and extensor surfaces, the nocturnal scratching and sleep disturbance, the sparing of the nappy area, and the bilateral parental atopy together make atopic dermatitis the leading diagnosis. [1]
Branch 1 — classification and pathophysiology
Examiner: "How would you confirm this diagnosis and what is the underlying mechanism?" The expected answer applies the UK Working Party criteria: an itchy skin condition plus at least three of five supporting features — flexural or extensor dermatitis in the relevant age group, onset before two years, a personal or family history of atopy, generally dry skin, and visible eczema on examination. This child meets all five, and the sparing of the nappy area is a distinctive supportive clue. [1]
The mechanism rests on barrier failure and Th2 inflammation. Loss-of-function variants in filaggrin reduce natural moisturising factor and ceramides, raise transepidermal water loss, and admit antigens and Staphylococcus aureus. Antigens breaching the barrier ignite a Th2 response with interleukin-4, interleukin-13 and interleukin-31 that drives IgE class-switching, recruits eosinophils, and — through interleukin-31 — directly stimulates itch, completing the itch-scratch cycle that sustains chronicity. A strong candidate names filaggrin and interleukin-31 and links them to the atopic march. [3]
Branch 2 — assessment and differential diagnosis
Examiner: "What will you look for on examination and what else could this be?" Expected findings include the erythematous, weepy, crusted, excoriated plaques on cheeks, scalp and extensors with sparing of the nappy area, generally dry skin, and the atopic stigmata; a full examination also checks for signs of secondary infection (honey-coloured crusting, weeping) and documents body-surface-area involvement for severity scoring. [1]
The candidate should articulate the key differentials and the features that separate them. Seborrhoeic dermatitis produces greasy yellow scales and involves the nappy area, which atopic dermatitis spares; scabies causes intense nocturnal itch but shows burrows in the finger-webs and axillae and is contagious; immunodeficiency syndromes — severe combined immunodeficiency, Wiskott-Aldrich, hyper-IgE and IPEX — present with severe early-onset eczema accompanied by failure to thrive, recurrent infection or chronic diarrhoea and must be considered when eczema is severe, early and atypical. [1]
Branch 3 — management and escalation
Examiner: "What is your stepwise management plan and how would you counsel about topical corticosteroid safety?" The plan follows the stepwise ladder: a generous fragrance-free emollient at least twice daily, a soap-free wash, trigger avoidance and a written action plan as the foundation; a low-potency topical corticosteroid such as hydrocortisone 1% for the face and a moderate-potency agent such as triamcinolone for the extensor limbs for a defined course; and, if response is inadequate, a topical calcineurin inhibitor such as pimecrolimus for the face. [6]
On safety, the candidate should state that topical corticosteroids are safe when potency is matched to site and used in defined courses with fingertip-unit dosing, that the fear of skin thinning (steroid phobia) is the commonest cause of under-treatment, and that the American Academy of Dermatology guidelines affirm this approach. If the disease is severe or refractory, escalation includes wet-wrap therapy, bleach baths for recurrent infection, and systemic therapy with dupilumab under specialist supervision. The candidate should name eczema herpeticum as the cutaneous emergency requiring systemic aciclovir. [6]
Closing (1 minute)
Summarise the plan: confirm the diagnosis clinically against the UK criteria, start an emollient foundation with potency-matched topical corticosteroids for active eczema, give a written action plan, reassure about corticosteroid safety to address steroid phobia, grade severity with SCORAD or POEM, counsel about the atopic march, and review in two to four weeks with escalation to a calcineurin inhibitor or dermatology referral if control is inadequate. [1]
References
- [1]Williams HC Clinical practice. Atopic dermatitis. N Engl J Med, 2005.PMID 15930422
- [3]Palmer CN, Irvine AD, Terron-Kwiatkowski A Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet, 2006.PMID 16550169
- [6]Sidbury R, Alikhan A, Bercovitch L Executive summary: American Academy of Dermatology guidelines of care for the management of atopic dermatitis in adults with topical therapies. J Am Acad Dermatol, 2023.PMID 36623556