10.1 Atopic Dermatitis, Contact Dermatitis & Inflammatory Skin Disease
Key Takeaways
- Infantile atopic dermatitis maps to itchy cheeks and extensors with xerosis and often a spared diaper area; older children map to flexures
- AAD/AAP care is daily emollients, trigger avoidance, and low-to-mid potency topical corticosteroids for flares: hydrocortisone on the face, medium potency on the body, wet wraps for a bad flare
- Oral antihistamines do not treat atopic dermatitis inflammation and are not a substitute for topical anti-inflammatory therapy
- Eczema herpeticum is HSV on eczematous skin — punched-out monomorphic vesicles plus fever — and is an emergency for prompt systemic acyclovir
- Do not put high-potency steroid on the face or diaper area, and do not use oral systemic corticosteroids for routine eczema
Dermatology is clinical category #2 by exam volume on the PNCB CPNP-PC outline. Domain II wants a pattern diagnosis: itch, age-specific distribution, and xerosis versus a geometric contact rash, greasy seborrheic scale, or drop-like plaques after strep. Domain III wants a primary-care plan that starts with emollients and the right-potency topical corticosteroid — and that recognizes eczema herpeticum as an emergency. You are not running a pediatric dermatology clinic. You are deciding what this rash is, what the family can apply tonight, and when the child cannot wait until Monday.
Clinic opening. A 7-month-old is always scratching. Both cheeks are erythematous and rough. Extensor arms and legs are dry and excoriated. The diaper area is clear. Grandmother wants the strong cortisone from her own tube and a daily antihistamine to treat the eczema. If you smear a super-potent steroid on the face, promise that cetirizine will calm inflammation, or miss punched-out vesicles at the next flare, you missed this section.
Atopic dermatitis: itch plus a map
Atopic dermatitis (AD, eczema) is a chronic, relapsing, pruritic inflammatory dermatitis on a xerotic (dry) barrier. The itch is required. If it does not itch, reopen the differential. Personal or family atopy (asthma, allergic rhinitis, food allergy) supports the diagnosis but is not mandatory at the first visit. Primary-care diagnosis is clinical. You do not need an IgE panel to name AD. Food-allergy testing belongs to children with immediate-reaction histories or with moderate-severe AD that remains refractory after skin care is actually optimized — not a reflex RAST on every dry-cheeked infant.
Distribution is age-mapped. Get the map wrong and you will call seborrheic dermatitis, psoriasis, or candidal diaper disease by the wrong name.
| Age | Typical AD map | What is usually spared |
|---|---|---|
| Infants | Cheeks, scalp, trunk, and extensor extremities | Diaper area (occlusion is relatively protective); often the nose |
| Older children and adolescents | Flexures: antecubital and popliteal fossae, neck, wrists, ankles | Palms and soles unless palmoplantar involvement is truly present |
Chronic AD shows lichenification, excoriations, and post-inflammatory pigment change. Families may read hypopigmentation as scars, dirt, or tinea versicolor. Pityriasis alba — faintly scaly, hypopigmented patches on the cheeks of a school-age child — is a related dry-skin finding, not a fungus, and it is treated with emollients and sun protection, not an azole cream by default.
AAD/AAP management: barrier first, steroid for the flare
American Academy of Dermatology (AAD) guidelines and American Academy of Pediatrics (AAP) clinical reports use the same stack:
- Emollients — frequent, fragrance-free, ointment-preferring moisturizers. Apply at least twice daily and immediately after a short, lukewarm bath (soak and seal). This is daily disease-modifying care, not optional lotion when the child remembers.
- Trigger avoidance that is specific: overheating, harsh soaps, wool, known irritants, and documented allergens. You do not prescribe a sterile household or a six-food elimination diet for uncomplicated AD.
- Topical corticosteroids (TCS) for active flares, stepped by site and skin thickness.
| Site | Typical primary-care potency | Example the exam expects you to name |
|---|---|---|
| Face, eyelids, folds, diaper/groin | Low | Hydrocortisone 1% or 2.5% |
| Body and extremities (non-fold) | Low-to-medium | Hydrocortisone 2.5% or triamcinolone 0.1% (medium) for thicker plaques |
| Thick lichenified plaques on limbs | Medium, short course | Triamcinolone 0.1%; do not jump to clobetasol in primary care without a reason |
Use the lowest effective potency for the shortest flare that actually clears itch and erythema, then return to emollients. Ointments are generally more potent and more occlusive than creams at the same molecule. Finger-tip units beat a dab. Counsel steroid phobia with facts: appropriate TCS on intact eczematous skin for a defined course is not the same as chronic super-potent use on the face. Chronic TCS on the face is how periorificial dermatitis is born.
Wet wraps (a damp layer plus a dry layer over emollient with or without TCS) are AAD-endorsed for moderate-severe flares when the family can be taught the method. They are not a reason to start oral prednisone. Topical calcineurin inhibitors (tacrolimus, pimecrolimus) and other steroid-sparing nonsteroid topicals are options for face and folds or for children who need maintenance beyond TCS. On this exam, know they exist, that burning on application is common, and that they are not first-line for an untreated, unmoisturized infant. Systemic biologics and oral JAK inhibitors are referral territory.
Antihistamines do not treat inflammation
This is a high-yield AAD statement. Oral antihistamines do not treat the inflammatory pathway of atopic dermatitis. They are not eczema medicine. A daily non-sedating antihistamine will not replace TCS. A sedating antihistamine at bedtime is sometimes used when sleep is wrecked by itch — that is a sleep adjunct, not anti-inflammatory therapy. Do not tell a family that cetirizine will heal the rash. Do not stack two antihistamines and call that a flare plan.
Infection: Staph versus HSV emergency
Broken eczematous skin colonizes Staphylococcus aureus. Honey-crust, weeping, sudden worsening of a known patch, or failure of an appropriate TCS flare plan should make you treat secondary bacterial infection (see 10.2) rather than only escalating steroid potency.
Eczema herpeticum (Kaposi varicelliform eruption) is HSV superimposed on AD. It is an emergency. Look for a sudden crop of painful, punched-out, monomorphic vesicles or erosions, often with fever, malaise, and lymphadenopathy. The face and eyelids can be involved. This is not worse eczema. Start systemic acyclovir promptly and arrange same-day specialty or hospital evaluation. Do not wait for a Monday viral culture. Do not cover the face with leftover clobetasol and send the child home.
Clinic vignette. A 2-year-old with AD flared overnight. Temperature 38.8°C. Cheeks and arms are peppered with 2–3 mm punched-out pits. Caregiver started leftover clobetasol from an adult relative. Stop the super-potent steroid on the face, treat as eczema herpeticum, and do not call it a routine winter flare.
Contact dermatitis versus atopic dermatitis
Irritant contact dermatitis is barrier injury: drool, lip-licking, irritant diaper dermatitis, over-washed hands. Allergic contact dermatitis is type IV delayed hypersensitivity: nickel, poison ivy/urushiol, fragrances, neomycin, and preservatives such as methylisothiazolinone in wipes. Clues: geometric or sharp borders, a new product, under a waistband or earring, or a linear plant streak. AD is symmetric, flexural or infantile-cheek, and chronically xerotic. Acute contact disease is treated by removing the exposure, bland emollients, and a time-limited TCS. Patch testing is referral when the trigger is occult and the rash is chronic.
Clinic vignette. A 9-year-old has a sharply bordered rectangular plaque exactly under a new belt buckle. Flexures are clear and the skin is not globally xerotic. That is nickel contact dermatitis, not a new flexural AD phenotype. Remove the buckle, treat the plaque, and do not start wet wraps for the whole body.
Seborrheic dermatitis (cradle cap)
Infantile seborrheic dermatitis is greasy yellow scale on the scalp, eyebrows, and sometimes the diaper area and skin folds in a well, non-itchy or minimally itchy infant. It is not AD. Management: mineral oil or emollient to loosen scale, gentle shampoo, soft-brush removal. Persistent scale: ketoconazole 2% shampoo or cream, or a low-potency TCS for a short course. Do not pick until it bleeds. Do not use adult high-potency scalp solutions on a 6-week-old.
Seborrheic dermatitis in the diaper area involves folds. AD usually spares the diaper. Candida (10.2) adds satellite pustules on a beefy-red base.
Psoriasis red flags — including guttate after strep
Pediatric psoriasis is well-demarcated erythematous plaques with silvery scale, often on extensors, scalp, and the umbilicus, with possible nail pitting. Guttate psoriasis is an eruption of drop-like papules after streptococcal pharyngitis (sometimes perianal strep). If the history fits, test and treat strep. Refer extensive, facial, genital, nail-destructive, or arthritis-associated disease. Do not call guttate psoriasis a viral exanthem and skip the strep thought.
Pitfalls the exam writes on purpose
- High-potency TCS on the face, eyelids, or diaper/occluded skin — atrophy, telangiectasia, striae, periorificial dermatitis, and HPA-axis risk in infants.
- Oral systemic corticosteroids for routine AD — AAD recommends against this for typical disease because of rebound and systemic harm. Rescue belongs in specialty or hospital-level severe disease, not a Friday prednisone pack for winter itch.
- Treating inflammation with antihistamines only.
- Missing eczema herpeticum.
- Calling cradle cap atopic dermatitis and starting medium-potency steroid on the scalp of a happy newborn.
- Ignoring guttate morphology after a sore throat.
Clinic close. Infant cheeks and extensors plus xerosis: AD, emollients, hydrocortisone on the face, medium TCS on thick body plaques if needed, wet wraps for a bad flare, no oral steroid, no super-potent face cream. Geometric rash under a belt buckle: contact, remove nickel. Greasy scalp in a smiling 8-week-old: seborrheic, not strong cortisone. Punched-out feverish vesicles: HSV until proven otherwise.
A 4-month-old has pruritic, erythematous, scaly patches on both cheeks and the extensor surfaces of the arms and legs. The diaper area is spared. The skin is xerotic. Which diagnosis and distribution pairing is most consistent with infantile atopic dermatitis?
A 3-year-old with known atopic dermatitis has nightly itch. The caregiver asks for a daily oral antihistamine to treat the eczema. Using AAD/AAP-aligned primary-care management, what should the CPNP-PC counsel?
A 6-year-old with poorly controlled atopic dermatitis arrives febrile with a sudden crop of painful, punched-out, monomorphic vesicles and erosions on eczematous skin. What is the priority?