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Common Pediatric Dermatology
Overview
Skin conditions are among the most frequent reasons for pediatric office visits. Many pediatric rashes are benign and self-limited but can cause significant parental anxiety. The key skills for managing these conditions include pattern recognition, understanding when to treat versus reassure, and identifying red flags for serious conditions. This chapter covers atopic dermatitis, viral exanthems, fungal infections, molluscum contagiosum, and contact dermatitis.
Atopic Dermatitis (Eczema)
Epidemiology and Pathophysiology
Atopic dermatitis is the most common chronic inflammatory skin condition in children, affecting 15-20% of the pediatric population. Onset occurs by age 1 in 60% of cases and by age 5 in 90%. It forms part of the "atopic triad" along with asthma and allergic rhinitis, a progression often described as the "atopic march." The pathophysiology involves two converging mechanisms: epidermal barrier dysfunction (frequently related to filaggrin gene mutations) and immune dysregulation with Th2 predominance. The impaired skin barrier leads to transepidermal water loss, allergen penetration, and microbial colonization.
Clinical Presentation
The distribution of atopic dermatitis varies with age. Infants typically present with erythematous, weeping, crusted patches on the cheeks, scalp, and extensor surfaces. Older children develop dry, lichenified, excoriated plaques in flexural areas including the antecubital and popliteal fossae, neck, and wrists. Adolescents and adults often have hand and eyelid involvement. The hallmark feature is intense pruritus, sometimes described as "the itch that rashes." The condition follows a chronic relapsing course with flares and remissions.
Management Stepladder
| Severity | Treatment | Examples | Notes |
|---|---|---|---|
| All patients (foundation) | Emollients + trigger avoidance | Soak and seal; fragrance-free ointments; cotton clothing | Cornerstone of all therapy |
| Mild | Low-potency TCS | Hydrocortisone 1-2.5% (face); Desonide 0.05% | Safe for face and intertriginous areas |
| Moderate | Medium-potency TCS + steroid-sparing agents | Triamcinolone 0.1% (body); Tacrolimus 0.03%; Pimecrolimus; Crisaborole (≥3 mo) | TCIs for face/folds; proactive maintenance 2×/week |
| Moderate-Severe | High-potency TCS + wet wraps | Fluocinonide 0.05% (limited periods, thick skin) | Wet wrap therapy for severe flares |
| Severe/Refractory | Biologics and systemic agents | Dupilumab (≥6 mo); JAK inhibitors; Phototherapy | Dupilumab is first-line biologic |
All patients require foundational skin care: daily lukewarm baths followed by immediate emollient application (the "soak and seal" technique), fragrance-free thick emollients (with ointments preferred over creams, which are preferred over lotions), trigger avoidance (harsh soaps, wool, overheating, known allergens), and cotton clothing next to skin.
For mild disease, low-potency topical corticosteroids (TCS) are appropriate: hydrocortisone 1-2.5% for face and intertriginous areas, or desonide 0.05% for mild-to-moderate areas. Moderate disease requires medium-potency TCS such as triamcinolone 0.1% for the body, with topical calcineurin inhibitors (TCIs) like tacrolimus 0.03% (ages 2-15) or pimecrolimus 1% (ages 2 and older) serving as steroid-sparing agents for the face and skin folds. Crisaborole, a PDE4 inhibitor, is FDA-approved for ages 3 months and older.
Moderate-to-severe disease may require higher-potency TCS (fluocinonide 0.05%) for limited periods on thick-skinned areas, proactive "maintenance" therapy (applying TCS or TCI twice weekly to flare-prone areas after clearance), and wet wrap therapy for severe flares.
Severe or refractory disease now has multiple biologic and systemic options. Dupilumab (anti-IL-4/IL-13) is FDA-approved for ages 6 months and older with moderate-to-severe atopic dermatitis. JAK inhibitors include abrocitinib and upadacitinib (oral) and ruxolitinib (topical, ages 12 and older). Traditional systemic immunosuppressants (cyclosporine, methotrexate, mycophenolate) remain available off-label, and phototherapy with narrowband UVB is useful for widespread disease.
Infection Management
Staphylococcus aureus colonizes more than 90% of atopic dermatitis patients and contributes to disease flares. Dilute bleach baths (1/4-1/2 cup household bleach per full bathtub, 2-3 times weekly) reduce bacterial colonization. Intranasal mupirocin can be used for decolonization in recurrent infections. Overtly infected (impetiginized) eczema requires oral antibiotics such as cephalexin or TMP-SMX. Eczema herpeticum, a widespread vesicular eruption from HSV superinfection, is a medical emergency requiring IV acyclovir.
<image>Clinical photograph series showing atopic dermatitis distribution patterns by age: infant with erythematous weepy patches on cheeks and extensor surfaces, school-age child with lichenified flexural eczema in antecubital and popliteal fossae, and the eczema management stepladder from emollients through biologics</image>
Viral Exanthems
Measles (Rubeola)
Measles presents with a prodrome of cough, coryza, conjunctivitis, and high fever (the "3 Cs" plus fever). Koplik spots, which are pathognomonic blue-white papules on the buccal mucosa, appear before the rash. The rash itself is erythematous and maculopapular, starting on the face and spreading cephalocaudally over 3-4 days. Complications include pneumonia, encephalitis, and subacute sclerosing panencephalitis years later. Cases must be reported to public health immediately with airborne precautions instituted.
Varicella (Chickenpox)
Varicella produces a pruritic vesicular rash in "crops" at different stages simultaneously, classically described as "dew drops on a rose petal." The distribution is centripetal (trunk greater than extremities). Complications include bacterial superinfection, cerebellar ataxia, pneumonia, and hepatitis. The condition is rare with varicella vaccination, and breakthrough varicella is milder with fewer than 50 lesions.
Hand-Foot-Mouth Disease
This condition is caused by Coxsackievirus A16 (classic) or Enterovirus A71 (more severe). It presents with oral vesicles and ulcers on the buccal mucosa and tongue along with vesicles on the palms, soles, and buttocks. The illness is self-limited over 7-10 days with supportive care. Atypical hand-foot-mouth disease caused by Coxsackie A6 features more widespread, larger vesicles that may involve the trunk and extremities, and can cause onychomadesis (nail shedding) weeks later.
Roseola (Exanthem Subitum)
Caused by HHV-6 (most commonly) or HHV-7, roseola presents with high fever (39-40.5 degrees Celsius) for 3-5 days in a well-appearing child. A maculopapular "rose-colored" rash appears as the fever breaks, primarily on the trunk with spreading to the extremities. It is non-pruritic and resolves in 1-2 days. Febrile seizures are common due to the rapid temperature rise. Most children are affected by age 2.
Erythema Infectiosum (Fifth Disease)
Caused by Parvovirus B19, this illness features "slapped cheek" erythema followed by a lace-like (reticular) rash on the trunk and extremities. The rash may wax and wane for weeks, triggered by sunlight, heat, or bathing. The child is no longer infectious once the rash appears. Important concerns include aplastic crisis in children with sickle cell disease and hydrops fetalis if pregnant contacts become infected.
Scarlet Fever
Scarlet fever results from Group A Streptococcus pharyngitis with erythrogenic exotoxin production. The rash has a characteristic sandpaper texture, often starting on the neck and trunk. Pastia lines (linear petechiae in skin folds), circumoral pallor, and strawberry tongue are associated findings. Treatment is penicillin or amoxicillin, with desquamation occurring during convalescence.
Fungal Infections
Tinea Corporis (Ringworm)
Tinea corporis is a dermatophyte infection presenting as an annular, erythematous, scaly plaque with central clearing and a raised border. Diagnosis is clinical, confirmed by KOH preparation of skin scrapings showing septate hyphae. Treatment consists of topical antifungals (clotrimazole, terbinafine) for 2-4 weeks, with oral terbinafine or griseofulvin for extensive disease.
Tinea Capitis
Tinea capitis is most common in prepubertal children, especially African American children. Trichophyton tonsurans is the predominant organism in the US; it is an endothrix infection that does not fluoresce under Wood lamp. Presentations include patchy alopecia with scale, "black dot" alopecia, and kerion (a boggy, inflammatory mass). Systemic antifungal therapy is mandatory because topical therapy does not penetrate the hair follicle. Griseofulvin at 20-25 mg/kg/day (microsize) for 6-8 weeks (taken with fatty food to improve absorption) or terbinafine at weight-based dosing for a shorter course are the primary options. Selenium sulfide or ketoconazole shampoo serves as an adjunct to reduce spore shedding. Kerions are treated with systemic antifungals plus a short course of oral corticosteroids to reduce scarring, though this remains controversial.
Tinea Pedis
Tinea pedis is less common in prepubescent children and presents with interdigital maceration, plantar scaling, and vesicles. Topical antifungals for 2-4 weeks are usually sufficient.
Candidal Diaper Dermatitis
Candidal diaper dermatitis presents with beefy red erythema and satellite papules or pustules in the diaper area, with notable involvement of the inguinal folds. This fold involvement and the satellite lesions distinguish it from irritant contact dermatitis. Treatment consists of topical nystatin or clotrimazole with each diaper change, barrier cream (zinc oxide) applied over the antifungal, and oral fluconazole for refractory cases or concurrent oral thrush.
<image>Side-by-side comparison of common pediatric fungal infections showing tinea corporis (annular plaque with central clearing), tinea capitis with "black dot" alopecia and a kerion, and candidal diaper dermatitis with satellite papules, each with KOH preparation findings where applicable</image>
Molluscum Contagiosum
Molluscum contagiosum is a poxvirus infection presenting as firm, dome-shaped, umbilicated papules measuring 2-5 mm. It is common in children ages 1-10 and spreads by direct contact and autoinoculation. The condition is self-limited, resolving in 6-12 months and sometimes up to 2-4 years. The "BOTE sign" (beginning of the end) refers to inflammation developing around lesions, signaling immune recognition and impending resolution. Treatment with observation is reasonable for most cases. Options for extensive, cosmetically bothersome, or spreading disease include cantharidin (applied in office), cryotherapy, curettage, or topical retinoids/imiquimod (off-label, limited evidence). Children with atopic dermatitis tend to have more extensive and persistent disease.
Contact Dermatitis
Irritant contact dermatitis is the most common form, resulting from direct chemical or physical damage to the skin by substances such as saliva, urine, or detergents. Diaper dermatitis typically shows convex surface erythema sparing the folds (in contrast to candidal dermatitis which involves folds). Lip licker's dermatitis presents with perioral erythema and scaling.
Allergic contact dermatitis is a type IV delayed hypersensitivity reaction requiring prior sensitization. Common allergens include nickel (jewelry, belt buckles), poison ivy/oak/sumac (urushiol), fragrances, preservatives, and neomycin. Poison ivy produces a linear vesicular dermatitis treated with high-potency TCS or oral corticosteroids if extensive. Patch testing is indicated for recurrent or unexplained dermatitis.
When to Refer for Biopsy
Referral for biopsy should be considered for atypical lesions not responding to treatment, rapidly growing or ulcerating lesions, suspected malignancy (rare in children but includes melanoma precursors from congenital melanocytic nevi, dermatofibrosarcoma, and pilomatricoma), persistent solitary lesions lasting more than 4-6 weeks not consistent with common diagnoses, and suspected mastocytosis (urticaria pigmentosa with positive Darier sign).
Clinical Pearls
The fundamental principle of dermatologic therapy is "if it's dry, wet it; if it's wet, dry it." Tinea capitis requires systemic antifungal therapy without exception because topical creams alone will not work. The entire skin surface should always be examined because parents often focus on one area while missing more concerning findings. The "sandpaper" texture of scarlet fever rash is often more palpable than visible. Eczema herpeticum is a dermatologic emergency; punched-out erosions and clustered vesicles superimposed on eczematous skin demand immediate IV acyclovir. Mongolian spots and pigmented lesions should be documented carefully to avoid confusion with non-accidental trauma.
Key Controversy: Topical Calcineurin Inhibitors
The FDA issued a black box warning in 2006 based on a theoretical cancer risk (lymphoma and skin cancer observed in animal models at high systemic exposure). However, more than 15 years of post-marketing surveillance and large cohort studies have shown no increased cancer risk in humans. TCIs remain valuable steroid-sparing agents for sensitive areas (face, eyelids, groin). Proactive maintenance therapy (twice-weekly TCI application to flare-prone areas) reduces flare frequency and total steroid exposure. Many experts and dermatology societies advocate for removal of the black box warning. Families should be counseled that the warning exists but the risk is theoretical and not supported by clinical evidence.
References
- Eichenfield LF, et al. Guidelines of Care for the Management of Atopic Dermatitis. J Am Acad Dermatol. 2014;71(1):116-132.
- Sidbury R, et al. Guidelines of Care for Atopic Dermatitis (AAD 2023 Update). J Am Acad Dermatol. 2023.
- Chen X, et al. Tinea Capitis in Children: A Systematic Review. Pediatr Dermatol. 2020;37(3):423-432.
- Paller AS, et al. Dupilumab in Children Aged 6 Months to 5 Years with Atopic Dermatitis. Lancet. 2022;400:908-919.
- Leung DYM, et al. Atopic Dermatitis. Lancet. 2003;361(9352):151-160.
- American Academy of Dermatology. Clinical Guidelines and Position Statements. aad.org.

