152 terms

Pediatric Dermatology

Risk factors, etiology, pathophysiology, clinical findings, assessment (diagnostics/imagine), DDx, prognosis, complications, prevention, management of the following: eczematous eruptions desquamation acneiform lesions dermatophyte infections insects/parasites viral diseases bacterial infections misc.

Terms in this set (...)

Hx of allergies, asthma (controversial?)
Urban, developed environments
Female > Male
Age < 5
Risk factors for atopic dermatitis
Two models:
1. Epidermis disfunction allows breakdown of epidermal barrier from outside-in
2. Inflammatory response by Langerhans cells and T-cells within the epidermis to antigens
Etiology of atopic dermatitis
Disfunction of epidermis
Loss of epidermis moisture
Entry of antigens into epidermis that stimulate immune inflammatory response
Pathophysiology of atopic dermatitis
< age 1 (65%), < age 5 (85%)
Dry skin
Secondary changes from scratching: scaling, exudate, crusts
Pustules = consider S. aureus infection

Infantile: Extensor surfaces, cheeks, scalp, spares diaper area
Childhood: Lichenified plaques, flexor surfaces
Adults: Lichenified plaques, flexor surfaces, hands/feet
Clinical findings of atopic dermatitis
Diagnostic and imaging studies for atopic dermatitis
contact allergic dermatitis
seborrheic dermatitis
drug reactions

Infants: psoriasis, scabies, Wiskott-Aldrich syndrome, hyperimmunoglobulin E syndrome, nutritional deficiency, acrodermatitis enteropathica, Netherton syndrome
DDx of atopic dermatitis
Younger = more severe
Widespread, +allergies/asthma, High IgE, FHx = more persistent
Complete remission in 20%
Good control, not complete remission possible
Prognosis of atopic dermatitis
Skin infection (impetigo or herpes)
S. aureus colonization = increased severity (stimulates inflammation/immune response)
Impetigo = honey-colored crusts, exudate
HSV = herpetiform vesicular lesions, may hemorrhage
Eczema vaccinatum
exposure to smallpox vaccine or vaccinated individual = vaccinial superinfection
Warts (HPV) and molluscum common
Complications of atopic dermatitis
Avoid allergens/irritants:
sopa, detergent, fragrance, chemicals, smoke, temp/humidity extremes, wool, synthetics, sweating, foods, dust, dander, pollen
Trim fingernails to prevent secondary lesions and infection
Prevention of atopic dermatitis
Principles: avoid irritants, restore normal function of epidermis, hydrate skin, alleviate symptoms

Skin Hydration:
Emolients - apply immediately after bathing
-Eucerin, Cetaphil, Nutraderm, Aquaphor, Vaseline/petroleum

Antihistamines - 1st gen more effective (but more sedating) than 2nd gen
-1st Gen: diphenhydramine, chlorpheniramine, promethazine, meclizine
-2nd Gen: cetirizine, fexofenadine, loratadine

1st line: Topical Corticosteroids (QD)
-mild: hydrocortisone 1%
-mod: fluocinolone 0.025% or triamcinolone 0.1%
Oral Corticosteroids - severe eczema
-prednisone burst
2nd line: Topical calcineurin inhibitors - for face, neck, skin folds (no thinning)
-tacrolimus, pimecrolimus BID

Secondary infection:
S. aureus
-topical: mupirocin, retapamulin
-oral: cephalexin, dicloxacillin, augmentin
-oral/topical antifungal
Management of atopic dermatitis
Facial atopic dermatitis with secondary imeptigo
Lichenification due to chronic atopic dermatitis
Infantile atopic dermatitis
Infantile atopic dermatitis
Atopic dermatitis with papules
Atopic dermatitis
Atopic dermatitis
Atopic dermatitis with hemorrhagic, herpetiform HSV secondary infection
Atopic dermatitis with hemorrhagic, HSV secondary infection
Atopic dermatitis with secondary S. aureus infection (impetigo)
Contact irritant:
-repeated wet-dry cycles
-exposure to chemical/irritant
Contact allergic:
-exposure to allergen
Risk factors for contact dermatitis
Contact irritant: physical, chemical, mechanical irritation causes cytotoxic effect
-diapers, dry skin, soaps
Contact allergic: T cell mediated, allergic response
Etiology of contact dermatitis
Contact irritant: disfunction of epidermal moisture retention by surface cells results in inflammatory cascade
Contact allergic: allergen absorption through skin barrier provokes T cell mediated immune inflammatory response
Pathophysiology of contact dermatitis
Contact irritant:
-Hx: frequent soaping, water exposure, sweating
-PE: dry, cracked, chapped, scales, erythema, often on hands, feet, mouth (<- saliva)
Contact allergic:
-Hx: exposure to allergen
-PE: acute onset (1-2 weeks post-exposure 1st occurrence, within hours 2nd occurence), patterned/demarcated distribution, brightly erythematous, pruritic, vesicles and bullae +/- serous exudate
Clinical findings of contact dermatitis
Atopic dermatitis
Pompholyx (Vesiculobullous hand eczema)
Porphyria cutanea tarda
Diaper: psoriasis, seborrheic dermatitis, Langerhans cell histiocytosis
Differential diagnosis for contact dermatitis
Affects 10% of infants under 2
Self limited
Resolves in 2-3 weeks
Prognosis for contact dermatitis
Secondary lesions and infection (impetigo, herpetic infection, fungal (diaper - candida)
Complications of contact dermatitis
Contact irritant: remove irritating agents, limit excessive handwashing, moisturize, let skin air-dry
Contact allergic: avoid triggers, wash clothing
Prevention of contact dermatitis
Contact irritant: moisturize BID, topical steroid
Contact allergic: topical and/or oral steroids, antihistamines for itching
Management of contact dermatitis
Prolonged time spent in wet, soiled diapers
Plastic, non-breathable diaper liners
Risk Factors for diaper dermatitis
Dermatitis of diaper area, either caused/worsened by diaper or occurring regardless
Etiology of diaper dermatitis
Increased moisture, irritant/allergen/infectious exposure, friction
Pathophysiology of diaper dermatitis
Contact dermatitis: Erythema, papules, erosions on convex areas
Candida: involvement of skin folds, red beefy plaques, satellite papules, pustules, scales, Hx of antibiotic use, diarrhea, thrush
Seborrheic: erythema, greasy yellow scales in skin folds (inguinal folds)
Impetigo: honey-colored crusts
Group A strep: demarcated rash, perirectal fissures, blood-streaked stool, painful defecation, SHx of strep pharyngitis contacts
HSV: vesicles, papules, pustules
Psoriasis: erythematous papules and plaques, FHx
Scabies: widespread pruritis, papules, excoriations
Langerhans cell histiocytosis: papules, erosions, petechiae
Clinical findings of diaper dermatitis
Candida: can confirm with KOH prep
Diagnostic studies for diaper dermatitis
Caused by diaper:
-contact irritant dermatitis
-contact allergic dermatitis
-candidal dermatitis
-Jacquet's erosive dermatitis
-Granuloma gluteale infantum

Occurs independently of diaper:
-seborrheic dermatitis
-atopic dermatitis
-Langerhans histiocytosis
-nutritional deficiency
-child abuse
DDx for diaper dermatitis
Common: affects 10% of kids under 2
Should clear in 2-3 weeks
Prognosis for diaper dermatitis
Candidal infection
HSV infection
GAS infection (progression to sepsis)
Complications of diaper dermatitis
Frequent diaper changing
Periods of air exposure
Barrier creams
Prevention of diaper dermatitis
Irritant: barrier ointments (Desitin, Triple paste, A&D ointment, Balmex, Vaseline, zinc oxide, sucralfate), hydrocortisone
Seborrheic: topical low-potency corticosteroids
Impetigo/Group A strep: mupriocin, antibiotics
Candida: nystatin, clotrimazole, miconazole, ketoconazole
Management of diaper dermatitis
Contact allergic dermatitis
Contact allergic dermatitis
Contact allergic dermatitis (poison oak)
Contact irritant dermatitis
Contact irritant dermatitis
children < 5, female > male
Women age 16-45
Risk factors for perioral dermatitis
Common correlation = Topical corticosteroid use; initial relief with steroids but then worsens with continuation, and discontinuation causes POD,
Other proposed causes = fluoride toothpaste, facial lotions/cosmetics, Candida, hormonal fluctuations, OCPs
Etiology of perioral dermatitis
Atopy, skin barrier dysfunction suspected
Pathophysiology of perioral dermatitis
Clusters of erythematous papules, papulovesicles, papulopustules, +/- scaling
Symmetrical distribution
Sparing of vermillion border of the lip
Perinasal and periorbital involvement possible
Scarring unusual
Clinical findings of perioral dermatitis
Biopsy if diagnosis uncertain
Diagnostic studies for perioral dermatitis
acne vulgaris
seborrheic dermatitis
allergic contact dermatitis
irritant contact dermatitis
dermatophyte infection (tinea corporis, barbae)
DDx for perioral dermatitis
Often self-limited, benign
Resolves in months - years
Prognosis of perioral dermatitis
Secondary excoriations and infection
Complications of perioral dermatitis
Avoid prolonged use of steroids
Avoid irritants
Prevention of perioral dermatitis
Discontinue steroids (can transition to low-potency) or irritants

Topical pimecrolimus*, erythromycin, metronidazole
Oral Tetracycline (adults), erythromycin (<9 yo)
Management of perioral dermatitis
Risk factors for seborrheic dermatitis
Etiology of seborrheic dermatitis
Pathophysiology of seborrheic dermatitis
Infants: Nonpruritic, cradle cap, intertriginous areas, umbilicus
Adolescents: scalp (dandruff), eyebrows, eyelashes, nasolabial folds, external auditory canals, posterior auricular folds
Clinical findings for seborrheic dermatitis
Atopic dermatitis (spares diaper area)
Diaper dermatitis (spares folds)
Psoriasis (silvery plaques, well demarcated)
Pityriasis (tinea) amiantacea
Langerhans cell histiocytosis
Tinea capitis
Pityriasis rosea
Secondary syphillis
DDx for seborrheic dermatitis
Often disappears around 1 year of age
Not a cause of hair loss
Prognosis for seborrheic dermatitis
Hypopigmentation after resolution
Secondary infection
Complications of seborrheic dermatitis
Frequent shampooing at early signs
Prevention of seborrheic dermatitis
Emolient (petroleum, veg/mineral/baby oil) overnight, brush in AM
Frequently shampoo
-zinc pyrithione (Head & Shoulders)
-selenium sulfide (Selsun Blue)
-salicylic acid (T-Sal)
Extensive cases: hydrocortisone QD x7d or ketoconazole cream/shampoo (Nizoral)
Management of seborrheic dermatitis
IL-2 transcription inhibition by T-helper cells (immunosuppressant)
Action of tacrolimus, pimecrolimus, cyclosporine (calcineurin inhibitors)
Infantile seborrheic dermatitis
Infantile seborrheic dermatitis
Periocular dermatitis
Perioral dermatitis, periocular distribution
Perioral dermatitis
Perioral dermatitis
Spring season
female > male
all ages; average age = 25-47
infection (HIV, viral)
genetics (HLA subtypes, slow acetylators)
physical factors (UV/radiation)
Risk factors for Stevens-Johnson syndrome/toxic epidermal necrolysis
(most to least common): Medication use*, infection, vaccination, systemic disease, chemicals, herbals, food
-adults: allopurinol, sulfonamides>>penicillins>cephalosporins, carbamazepine, dilantin, lamotrigine, phenobarbital, NSAIDs, piroxicam
-peds: sulfonamides, phenobarbital, carbamazepine, lamotrigine, valproic acid, acetaminophen/paracetamol, azithromycin + ibuprofen, Mycoplasma pneumonia, herpes virus
Etiology of Stevens-Johnson syndrome/toxic epidermal necrolysis
Incompletely understood
Immunologic process (cytotoxic T cells, NK cells) in skin
Slow acetylators --> high active drug metabolites
Pathophysiology of Stevens-Johnson syndrome/toxic epidermal necrolysis
Hx: drug exposure 1-3 weeks prior
Sx: fever, influenza symptoms, 2+ sites of mucocutaneous erosions/crusting (oral, conjunctiva, pulmonary, urogenital), skin tenderness, photophobia, conjunctival itching/burning, widespread erythroderma or erythematous macules with purpuric centers, facial edema, palpable purpura, skin necrosis, blisters, tongue swelling
SJS: more commonly favors the trunk
Iris lesions: 2 concentric color zones
Clinical findings of Stevens-Johnson syndrome/toxic epidermal necrolysis
CBC: anemia, neutropenia, lymphopenia
AST/ALT elevation
Skin biopsy
Skin, blood, wound cultures
Diagnostic studies for Stevens-Johnson syndrome/toxic epidermal necrolysis
Erythema multiforme minor
Erythroderma/drug eruption
Acute generalized exanthematous pustulosis
Phototoxic eruption
Toxic shock syndrome
Staphylococcal scaled skin syndrome (kids)
Paraneoplastic pemphigus
DDx for Stevens-Johnson syndrome/toxic epidermal necrolysis
Dependent on age, extent of skin detachment
Younger fair better than older
Resolution typically occurs in 2-4 weeks
Prognosis of Stevens-Johnson syndrome/toxic epidermal necrolysis
Infection, sepsis
Ocular scarring
Urinary retention
Tracheobronchitis, pulmonary edema, pneumonia, bronchiolitis obliterans
Complications of Stevens-Johnson syndrome/toxic epidermal necrolysis
Remove triggers
Supportive care: critical care, wound care (often in burn unit), fluid management, parenteral nutrition, ocular care, temperature management, pain control, infection control
Therapy: glucocorticoids, IV gammaglobulins
Management of Stevens-Johnson syndrome/toxic epidermal necrolysis
HSV infection
Drug use
Risk factors for erythema multiforme minor/major
Most common: Herpes Simplex
Others: Mycoplasma pneumoniae (*esp kids), infections (90%), meds, malignancy, immunizations, sarcoidosis, autoimmune disease, menstruation
Etiology of erythema multiforme minor/major
Cellular immune response to offending target in skin tissues
Pathophysiology of erythema multiforme minor/major
Recent herpes outbreak (common) or atypical pneumonia (or other causative exposure Hx)
EM minor: more commonly favors the extensor surfaces, palms, soles (no mucus membranes)
EM major: above and 2+ mucus membranes involved
Mucosal erythema multiforme: only mucus membranes affected
Target lesions: 3 concentric color zones
Clinical findings of erythema multiforme minor/major
Culture if blistering/infection or differential diagnosis warrants it
Mycoplasma suspected: throat swab PCR, or serum IgM or IgG 2-fold increase
Diagnostic studies for erythema multiforme minor/major
Drug eruptions
Rowell Syndrome (Lupus)
Sweet syndrome
DDx of erythema multiforme minor/major
Lasts 2-6 weeks
May reoccur
Prognosis of erythema multiforme minor/major
Secondary infection
Complications of erythema multiforme minor/major
If blistering: see patient daily, treat as 2nd degree burn
Corticosteroids ok if started before blistering occurs
If HSV infection: acyclovir prophylactically
Management of erythema multiforme minor/major
(Least to most severe body surface area involvement):
1. erythema multiforme minor: 1-3 cm lesions on extensor surfaces, palms, soles, trunk
2. erythema multiforme major: all of above + mucosal involvement
2. Stevens-Johnson syndrome: <10% BSA loss
3. SJS/TEN overlap: 10-30% BSA loss
4. toxic epidermal necrolysis: >30% BSA loss
Describe the differences between erythema multiforme major and minor, Stevens-Johnson syndrome, and toxic epidermal necrolysis
Calculate burn percentages for adults and children
Erythema multiforme minor
Erythema multiforme major
Stevens Johnson Syndrome
Toxic epidermal necrolysis (TEN)
Diet - effect unknown. Possible link to increased IGF-1 in response to dairy and carbohydrates that increases androgen secretion and stimulates acne formation.
Family history of acne = greater risk
Risk factors for acne vulgaris
Proliferation of keratinocytes, P. acnes and inflammatory response
Etiology of acne vulgaris
Increased proliferation of keratinocytes at the follicle opening plug the pore, trapping sebum (oil) within. P. acnes proliferates and inflammatory response occurs.
Pathophysiology of acne vulgaris
noninflammatory: comedones - closed/open (whiteheads/blackheads) must be present to be acne
inflammatory: papules, pustules, nodules
women - flare up before menses
Clinical findings of acne vulgaris
If hyperadrogenism suspected: DHEAS, testosterone (free and total), LH and FSH
Diagnostic studies for acne vulgaris
perioral dermatitis
tuberous sclerosis
facial angiofibromas
flat warts
DDx of acne vulgaris
May persist into adulthood
Women more likely affected past age 30
Prognosis of acne vulgaris
Scarring: ice pick, rolling, boxcar, hypertrophic
Psychologic consequences
Complications of acne vulgaris
Prevention of acne vulgaris
Wash 2x/day
Use gentle cleansers - w/ or w/o benzoyl peroxide or salicyclic acid
Cleansing principles for acne vulgaris
Sulfur/sodium sulfacetamide/resorcinol (antimicrobial, keratolytic)
Salicyclic acid (keratolytic, comedolytic)
Benzoyl peroxide (antimicrobial)
Azelaic acid (antimicrobial, comedolytic)
Topical abx: erythromycin, clindamycin +/- benzoyl peroxide (less likely to develop bacterial resistance), dapsone (antimicrobial)
Retinoids (comedolytic, anti-inflammatory): tretinoin, adapalene, tazarotene
Glucocorticoid injections for nodules: triamcinolone
Phototherapy, laser therapy
Topical treatments options for acne vulgaris
dapsone (Aczone) + benzoyl peroxide
Which two topical products for acne tx can turn the skin orange if used together?
Oral Antibiotics:
tetracyclines, minocycline, doxycycline
macrolides: erythromycin, azithromycin
Bactrim (TMP-SMZ)

Glucocorticoids (anti-inflammatory)
leuprolide (GnRH agonist)
spironolactone (aldosterone antagonist)
isotretinoin (oral retinoid)
Systemic treatment options for acne vulgaris
vitamin B2, B6, B12
Drugs than can cause acne
"Hot tub" folliculitis: P. aeruginosa
HIV infection - "eosinophilic folliculitis"s
Shaving - "pseudofolliculitis/sycosis barbae"
Risk factors for folliculitis
Most common: S. aureus
Others: gram negative bacteria - Escherichia, klebsiella, enterobacter, proteus
fungus (pityrosporum folliculitis)
Etiology of folliculitis
Infection of hair follicle results in pustule formation in the epidermis
Pathophysiology of folliculitis
Papule or pustules surrounded by a red, erythematous border with a hair in the center
Clinical findings of folliculitis
Culture if fungal or herpetic cause suspected, or KOH prep
Diagnostic studies for folliculitis
Grover's disease
keratosis pilaris
acne vulgaris (comedones present)
DDx of folliculitis
Good: often self-resolving or resolves with I&D/treatment
Prognosis of folliculitis
Chronic folliculitis
Complications of folliculitis
Good hygiene - keep skin clean and dry, clean clothes, loose and breathable materials
Avoid chemical irritants
If due to shaving, stop if possible
Diabetics: glucose control
Prevention of folliculitis
"Hot tub" folliculitis due to P. aeruginosa: fluoroquinolone (cipro)
Superficial folliculitis: topical mupirocin or fusidic acid
Deep/severe folliculitis: oral cephalosporin, penicillin, macrolide, fluoroquinolone
Pityrosporum folliculitis: oral antifungals, topical azoles, selenium, zinc
Herpetic folliculitis: acyclovir, valacyclovir, famciclovir
Management of folliculitis
Maternal androgenic hormones
Etiology of acne neonatorum
Stimulation of sebaceous glands causes blockage with keratin
Pathophysiology of acne neonatorum
Average onset: 3 weeks old
Inflammatory lesions (no comedones) on face and scalp
Clinical findings of acne neonatorum
Diagnostic studies for acne neonatorum
infantile acne (3-6 months old)
erythema toxicum neonatorum
neonatal pustular melanosis
DDx for acne neonatorum
Typically resolves within four months on its own
Prognosis of acne neonatorum
None: no scarring
Complications of acne neonatorum
Cleanse with mild soap and water
Avoid heavy lotions
Prevention of acne neonatorum
Clean with mild soap and water
ketoconazole or hydrocortisone may speed healing
Management of acne neonatorum
milia: noninflammatory blockage of hair follicles
miliaria: noninflammatory blockage of sweat glands
acne neonatorum: inflammatory epidermal lesions, no comedones present
infantile acne: comedones and inflammatory papules, pustules, nodules
infantile acropustulosis: itchy vesiculopustular lesions on the hands, feet, limbs
Differentiate milia, miliaria, acne neonatorum, infantile acne, and infantile acropustulosis
Contact exposure - humans, animals
Risk factors for tinea corporis/pedis
Fungal infection by dermatophytes (Trichophyton, Microsporum, Epidermophyton)
Etiology of tinea corporis/pedis
Fungal infection of the skin results in annular erythematous lesions with central clearing and peripheral scaling
Pathophysiology of tinea corporis/pedis
Circular erythematous lesion with central clearing and peripheral scaling
found on any part of face or body
Clinical findings of tinea corporis/pedis
KOH prep of scrapings
Culture if needed
Skin biopsy if negative KOH and culture
Diagnostic studies for tinea corporis/pedis
Granuloma annulare
erythema annulare centrifugum
cutaneous larva migrans
nummular eczema
DDx for tinea corporis/pedis
With treatment clears within 1 month
Prognosis of tinea corporis/pedis
If treated with steroids: can cause increased growth and inflammation + hyperpigmentation of skin
Complications of tinea corporis/pedis
Avoid contact
Wash skin thoroughly
Treat affected pets
Keep feet dry and clean, use powder
Prevention of tinea corporis/pedis
Topical antifungals:
clotrimazole (Lotrimin), ketoconazole (Nizoral), miconazole (monistat-derm), terbafine (Lamisil), butenafine (Lotrimin ultra), tolnaftate (Tinactin)
*fastest results
**(topical nystatin is ineffective against dermatophytes)
Oral antifungals:
terbatine, fluconazole, itraconazole*, griseofulvin

Burow's dressings: aluminum acetate wet dressing, 20 min TID

Athletes: treat with oral agent. Restrict sports participation for 10-15 days.
Management of tinea corporis/pedis
Risk factors for tinea versicolor
Yeast (Malassezia)
Etiology of tinea versicolor
Yeast infection of the skin by normal skin flora that changes into a pathogenic form
Pathophysiology of tinea versicolor
Macule: white, red, pink, brown
Non-scaling to the naked eye - fine scaling seen when scraped
Does not tan
Most common site: upper trunk in adults, face in kids
Rare: itching
Clinical findings of tinea versicolor
KOH prep
Wood's lamp - yellow-green fluorescence
Culture is not useful
Diagnostic tests for tinea versicolor
seborrheic dermatitis
pityriasis rosea
pityriasis alba
secondary syphillis
mycosis fungoides
DDx for tinea versicolor
Good: scaling will clear in several weeks, but it may take several months for normal pigmentation to return
Prognosis of tinea versicolor
Persistent hyper or hypopigmentation
Resistance to therapy
Complications of tinea versicolor
Topical or oral preventative therapy during warm months
Prevention of tinea versicolor
Topical antifungals:
clotrimazole (Lotrimin), ketoconazole (Nizoral), miconazole (monistat-derm), terbafine (Lamisil), butenafine (Lotrimin ultra), tolnaftate (Tinactin)
Selenium sulfide
Oral antifungals: itraconazole, fluconazole
**oral terbinafine or griseofulvin is not effective
Management of tinea versicolor
Exercise to the point of sweating, and do not shower for 8-12 hours: drug delivery occurs through sweat
Patient education directions for ketoconazole
hair casts (keratin sheaths)
white or black piedra (fungus)
DDx for lice (pediculoses)
permethrin (Nix)
malathion (Ovide)
benzyl alcohol
lindane - neurotoxicity risk, 2nd line tx; use only one application
wet combing

wash linens and clothing in hot water, dry on high heat
store unwashable items in sealed plastic bags for 2 weeks
Management of lice (pediculoses)
seborrheic dermatitis
atopic dermatitis
Langerhans cell histiocytosis
acropustulosis of infancy
DDx for scabies
permethrin (Nix)
oral ivermectin
antihistamines - loratidine (Claritin), cetirizine (Zyrtec)

Noncrusted scabies - bag used items for 3+ days, wash clothing/linens in hot water, dry on high heat

Crusted scabies - isolation, wash clothing/linens in hot water, dry on high heat, vacuum/clean
Management of scabies