Pediatric Dermatology

RJ Lim & Jo Lomuljo

 PEDIATRIC DERMATOLOGY

Atopic Seborrheic Contact Hypopigmented

Dermatitis Dermatitis Dermatitis Lesions
 1. Atopic dermatitis
most common skin disease in children
The skin manifestation of atopy accompanied by
asthma and allergic rhinitis
Manifests with:
Defective skin barrier
Reduced innate immune response
Exaggerated responses to allergens & microbes

Genetics and environment both play roles in

devt
 Atopic dermatitis
ETIOLOGY:
GENES assoc. w/ skin barrier dysfunction &
inflammation
T HELPER CELLS (TH2 acute lesions; TH1-
chronic)
Langerhans, IgE, and eosinophils
ENVIRONMENTAL allergens, irritants, extremes
of temp, infection, sweat, lack of humidity
FAMILY history of atopy

Asthma develops in 50% of kids with Atopic

Dermatitis
Assoc w/ food allergies
Atopic dermatitis
Chronic, relapsing disease
characterized by pruritus,
xerosis and characteristic skin
findings.
Improves w/age and remits in
adulthood
Relapse of disease in adults can occur and
commonly manifests as face or hand
dermatitis.

Frequently, adults have generalized

dry skin
 Atopic dermatitis: Manifestation

LESION
Erythematous papules or
LOCATION
plaques w/ ill-defined borders &
Infantile: face, extensors, generalized
overlying scale or hyperkeratosis
Child: flexors (antecubital,popliteal),
wrists, ankles, hands and feet
Atopic dermatitis
 Atopic dermatitis: Differentials
DIFFERENTIAL DESCRIPTION LOCATION
Seborrheic Circumscribed, well- Scalp
Dermatitis defined borders Eyebrows
Scale is thicker, Perinasal region
greasy & yellowish Upper chest & back

Psoriasis Salmon color at the Localize in elbow, knees,

base w/ overlying lower back, scalp
hyperkeratosis that
is much thicker and
silver in color
Allergic contact Bizarre, linear, Limited to one area
dermatitis square, angulated corresponding to contact
w/allergen
 Atopic dermatitis
DIAGNOSIS
Based on clinical findings
Skin biopsy can overlap w/ other conditions
PBS eosinophilia and elevated IgE
Skin prick test or measurement of IgE levels detect sensitization to allergens
 Atopic dermatitis
TREATMENT
1. Frequent use of bland emollients to
restore the skin barrier
2. Avoidance of triggers of inflammation
3. Topical Anti-inflammatory meds on
affected area (most effective imm. after
bath)
Daily short bath with WARM not hot water
apply moisturizing cream to entire
body to trap moisture, apply topical
anti-inflame meds
 Atopic dermatitis
TOPICAL CORTICOSTEROIDS
Mainstay of tx, Class I-VII
Enhanced penetration
Natural occlusion (groin, axilla)
External occlusion (bandage, diaper)
Open skin (excoriations)
Heat and hydration

Class I-II avoided in children

Ointments are preferred, applied 2x daily
SE: skin atrophy, striae, acne, hypopigmentation

Other Treatment
Topical Calcineurin Inhibitors
Tacrolimus, Pimecrolimus
Sedating antihistamines
Diphenhydramine, Hydroxyzine
Systemic Corticosteroids
Ultraviolet light therapy
Systemic Cyclosporine
Prevention: Breastfeeding
Atopic dermatitis
2nd line
No skin atrophy, used for face & genital lesions
Adjunct used in flares, improve sleeplessness due to itching at night
When topical tx fails
Tapered, rebound flare common
For moderate to severe cases in older children
2-3x weekly until improvement is seen
Severe cases
Used for 1 year to gain control, tapered once controlled
at least 4 months prevents or delays the occurrence of
atopic dermatitis in early childhood.
 Atopic dermatitis
Increased tendency toward bacterial, viral and fungal skin infections
Most common: SECONDARY IMPETIGO (S. aureus)

ECZEMA HERPETICUM (HSV)

 2. Seborrheic dermatitis
Chronic, inflammatory disease
Different clinical manifestations at different ages
Pathology: abnormal inflammatory response to
commensal Malessezia species in sebum-rich
areas
 Seborrheic dermatitis
CRADLE CAP CLASSIC SD/DANDRUFF
Begins in first month 1st year of life Adolescence

Thick greasy and waxy, yellow-white scaling fine, white, dry scaling of the scalp with minor
and crusting of the scalp itching.
usually prominent on the vertex of the scalp Typically localized to the scalp
may extend to the face and posterior auricular
folds
diaper and intertriginous area
usually asymptomatic (vs. infantile atopic Pruritus may be minimal or severe.
dermatitis, which is pruritic)
 Seborrheic dermatitis
DIAGNOSIS
Laboratory studies and imaging are not
necessary.
Fungal cultures and KOH studies to help
differentiate from tinea capitis
TREATMENT
cradle cap: oil (such as mineral oil or
olive oil) may be gently massaged into
the scalp and left on for a few minutes
Daily shampooing with ketoconazole,
zinc pyrithione, selenium sulfide, or
salicylic acid shampoos
with inflamed lesions: low-potency
steroids two times daily.
 Seborrheic dermatitis
Cradle cap is self-limited and resolves during the first year of life.
Seborrheic dermatitis does not cause permanent hair loss.
 3. Contact dermatitis
Inflammation in the top layers of the skin, caused by direct contact with a substance

IRRITANT CONTACT DERMATITIS ALLERGIC CONTACT DERMATITIS

observed after the skin surface is exposed to cell-mediated immune reaction: antigens,
an irritating chemical or substance readily penetrate the epidermis and are bound
by Langerhans cells, presented to T
lymphocytes, and an immune cascade follows.
 3. Contact dermatitis
LESION - ill-defined, scaly, pink or red
patches and plaques
LOCATION - localized to skin surfaces
that are exposed to the irritant
 DIAPER DERMATITIS ALLERGIC CONTACT DERMATITIS

caused by irritation from urine and feces, Acute lesions: bright pink, pruritic patches,
typically affecting the perianal region and the often in linear or sharply marginated bizarre
buttocks while sparing the protected groin configurations. Within the patches are
folds and other occluded areas clear vesicles and bullae
 3. Contact dermatitis
DIAGNOSIS: via clinical presentation and
history of exposure
Patch testing may be used to determine
the allergen causing the reaction in
difficult cases.
TREATMENT:
Topical corticosteroids
Oral antihistamines may be required to
control itching.
candidal diaper dermatitis: topical
nystatin or topical azole antifungals
 4. Vitiligo
Depigmentation disorder
Complex interaction of environmental,
genetic, and immunologic factors
 4. Vitiligo: Possible
POSSIBLE Etiologies
ETIOLOGIES

Familial, polygenic, multifactorial inheritance

May also occur sporadically

Neurochemical factors
segmental, dermatomal presentations

Toxic melanin synthesis intermediate and/or hydrogen peroxide and other oxygen
radicals.
Auto-immune destruction of melanocytes
antibody to a surface antigen on pigmented melanocytes via specific CD8+ T-cells
 Types of Vitiligo
TYPES OF VITILIGO
 Diagnosis
DIAGNOSIS
May be clinical (depigmented patches with family history of Vitiligo and other
depigmentation skin disorders)
Definitive Diagnosis is made with skin biopsy
 Treatment
TREATMENT

Topical Corticosteroids
Topical Calcineurin Inhibitors
(Tacrolimus, pimecrolimus)
UV Light Therapy (UVB 311)
 ASSOCIATED ILLNESSES/SYNDROMES

May be associated with any number of auto-immune conditions

Vogt-Koyonagi-Harada Syndrome
Dysacussia, meningoencephalitis, uveitis

Alezzandrini Syndrome
Tapetorerinal degeneration and deafness
 5. Pityriasis alba
5. PITYRIASIS ALBA
Round/oval hypopigmented
patch
Poorly defined
May be erythematous and
mildly scaly
Unknown cause
May be exacerbated by
dryness
Viewed as a form of mild
eczema

Source: Medscape
 TREATMENT AND PROGNOSIS

Lubricant or emolient may be used (ie. Petroleum Jelly)

Low-potency steroid or calcineurin inhibitor for excessive pruritus
The lesions wax and wane but eventually disappear, and normal pigmentation often
takes months to return
 5. Tinea versicolor (Pityriasis versicolor)
Hypopigmented, scaling
macules
Caused by invasive, hyphal
form of Malassezia Furfur
Spaghetti and meatballs
appearance on KOH

Source: Medical-labs.net
 DIAGNOSIS AND TREATMENT

Microscopy of skin scrapings (using KOH)

Woods Lamp
Primary therapy is daily application of 2.5% selenium sulfide
for one week
May also use topical or oral azoles
 PROGNOSIS
Despite successful treatment, repigmentation might not occur for several months.
Relapses are common and can require repeat or alternative therapies.
Source: Noble Vitiligo Clinic Source: Nelsons 20th Edition

Source: Nelsons 20th Edition

 6. Pityriasis rosea
Classic Herald Patch followed
by Christmas Tree pattern of
skin lesions
Centrifugal or cephalocaudal
spread of lesions

Etiology: HHV 7
Acute, self-limiting

Source: St. Lukes Health System

 PROGNOSIS
Erythema subsides,
desquamation is
completed, and
eruption fades (4-6
weeks)
Post-inflammatory
hyperpigmentation
may persist in dark-
skinned individuals
and may take months
to resolve
 REFERENCES

Nelson Essentials of Pediatrics 7th edition

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