Name That Rash: Pediatric Dermatology Cases · Name That Rash: Pediatric Dermatology Cases I have...

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© The Children's Mercy Hospital, 2016

Kimberly A. Horii, MDProfessor of Pediatrics

Children’s Mercy Hospitals & ClinicsDivision of DermatologyKansas City, Missouri

Name That Rash: Pediatric Dermatology Cases

Name That Rash: Pediatric Dermatology Cases

I have no financial relationships with the manufacturers of any commercial products and/or provider of commercial services discussed in this CME activity

I do intend to discuss off label use of a commercial product/device in my presentation for the treatment of SJS/TEN, alopecia areata, vitiligo, and tinea versicolor

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Practice ChangeAs a result of attending this lecture, I encourage you to

incorporate these changes in your practice

Change 1: Comfortably recognize several dermatoses commonly encountered in the pediatric outpatient setting

Change 2: Develop a brief differential diagnosis for several pediatric dermatoses

Change 3: Devise an initial treatment plan for several common dermatoses

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Name That Rash: Pediatric Dermatology Cases

Urticaria Blistering & Desquamating Rashes Contact Dermatitis Hair Loss Pigmentary Changes Scabies Atypical Hand Foot & Mouth

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Case 13 year old with a 3 day history of spreading erythematous papules and plaques with central clearing. The child also has mild URI symptoms and a recent low grade fever. 5

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Case 1

What is this skin condition?

A. Erythema multiformeB. Urticaria (Hives)C. Viral exanthemaD. Vasculitis

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Urticaria (Hives) Variants

– Transient/acute– Chronic Idiopathic (6 week cutoff)– Physical

10-25% of all people will develop urticaria at some point in their lives

Pathogenesis:– Histamine release from mast cells triggered by the presence of certain

antigens – Causes localized inflammation and “leaky” blood vessels 8

Transient/Acute Urticaria

Development of skin lesions typically follows– Infection– Ingestion of a medication or food– Rarely associated with collagen vascular

disorders or autoimmune disorders9

Transient/Acute Urticaria

Pruritic, erythematous, edematous papules and plaques (wheals) which blanch May have central paleness or clearing Lesions can vary in size from 2-3 mm to 30

cm Lesions typically migrate and are present in

one location for less than 24 hours10

Urticaria

• Differential diagnosis– Erythema multiforme– Dermatographism– Drug Eruption– Vasculitis– Mastocytosis

Work up Careful history Selected laboratory

evaluation dependent upon history

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Dermatographism (Physical Urticaria)

Urticaria versus Erythema Multiforme

Drug EruptionDrug Eruption

Vasculitis

Treatment Treatment

– Symptomatic control with oral antihistamines (H1 blockers) Hydroxyzine Diphenhydramine

– Non-sedating H1 antihistamines less effective if used alone– Oral steroids have not been proven to be necessary for

transient/acute urticaria– Attempt to identify underlying cause and treat or avoid

possible inciting agent 21

Case 312 year old male with a 2-3 day history of crusted papules in the

perioral region and new development of erythematous macules with dusky centers (targetoid) on the palms

Case 2

What is the eruption on the palms?A. Erythema multiformeB. UrticariaC. Secondary syphillisD. Vasculitis

Erythema Multiforme

Self limited cutaneous hypersensitivity syndrome

Characterized by fixed concentric erythematous rings with blistered or dark centers- “target” lesions Symmetrically distributed Palms & soles, arms & legs Can have oral lesions

May be precipitated by an underlying infection or medicine

Resolves over 1-3 weeks

Mucocutaneous Reaction Underlying etiologies: medications and infections (mycoplasma

pneumoniae) Toxic epidermal necrolysis (TEN) more severe variant of Stevens-

Johnson Syndrome (SJS) Clinical presentation Prodromal symptoms 1-14 days before abrupt cutaneous eruption Fever Malaise Headache Sore throat

Stevens-Johnson Syndrome (SJS)

Stevens-Johnson Syndrome (SJS)

Usually involvement of ≥ 2 mucous membranes (eyes, lips, genital mucosa)

Mucosal lesions may precede cutaneous eruption by 1-2 days– Mouth: hemorrhagic crusts, painful erosions– Genital mucosa: painful erosions, dysuria– Purulent conjunctivitis: ophthalmologic emergency

– May lead to permanent visual impairment

Stevens-Johnson Syndrome (SJS)

Cutaneous lesions Erythematous macules with dusky centers Vesicles and bullae with epidermal detachment

High Risk Medications for SJS

“Old drugs” with high risk: Sulfonamides Aromatic anticonvulsants (phenytoin, carbamazepine,

phenobarbital) Penicillins Allopurinol Oxicam-NSAIDs

Newer meds with increased risk: Nevirapine Lamotrigine Zonisamide

Treatment of SJS

Prompt discontinuation of offending medication Optimal supportive care (Burn unit or ICU for TEN)

Fluid & electrolyte balance Temperature control Prevention/treatment of infections Rule out concurrent organ involvement (renal, hepatic, hematologic) Respiratory & nutritional support Adequate analgesia

Wound care Isolation/sterile handling

Emergent Ophthalmologic consultation Controversial (non-FDA approved) treatment with steroids or IVIG

Case 3

2 year old male with a 2 day history of low grade fever, fussiness, & spreading erythema with superficial desquamation, mainly in the creases. Mucous membranes are not involved & vitals are stable.

What is this eruption?

A. Stevens-Johnson syndrome

B. Staph scalded skin syndrome

C. Pemphigus vulgaris

D. Toxic shock syndrome

Staphylococcal Scalded Skin Syndrome (SSSS)

Affects mainly neonates and children <5 years– In newborns known as Ritter’s disease

Caused by systemic circulation of staphylococcal exfoliative exotoxin– Leads to superficial separation of stratum corneum (upper

skin layer)

Often prodrome of pharyngitis followed by fever & generalized painful erythema (sunburn like)

Staph Scalded Skin Syndrome

Erythema begins on face & spreads to rest of body– Rapid superficial desquamation in areas of erythema (not as

deep at SJS)– Crusting on the face, neck, axilla & groin (flexures)– Does not involve the oral mucosa

May have associated problems with thermoregulation and fluid & electrolyte balance

Staph Scalded Skin Syndrome

Bacteria is usually not cultured in areas of desquamation as it is toxin mediated Usually requires systemic anti-staphyloccocal

antibiotics to eradicate underlying infection– Wound/skin care with bland emollients– Supportive care

Case 44 year old boy with a 3 week history of a worsening

symmetric pruritic eruption on the bilateral dorsal feet. He has no prior history of rashes.

What is the most likely diagnosis?A. Atopic DermatitisB. Contact DermatitisC. Tinea pedisD. Keratoderma

Contact Dermatitis

Distribution of lesions provide clues to diagnosis Linear Asymmetric Specific shape

Common Contact Allergens Metal

Nickel or cobalt

Preservatives Formaldehyde releasing

products Shampoo, lotion, cosmetics, baby

wipes

Topical medications Neomycin Bacitracin

Dyes Paraphenylenediamine

Hair dye

Henna tattoos

Lanolin Fragrances Plant resins

Contact Dermatitis

Erythematous papules, vesicles, or plaques

May have weeping and crust

Usually extremely pruritic

Contact Dermatitis

Treatment– Avoid allergen– Moisturize– Mid potency topical steroids– Topical soaks with aluminum acetate for oozing lesions– Oral antihistamines– Severe cases may require oral steroids

May require slow taper

Case 57 year old female with a 2-3 month history of enlarging

bald spots on the scalp. She denies any itching.

What is this skin condition?A. Tinea capitisB. Telogen effluviumC. Alopecia areataD. Trichotillomania

Alopecia Areata Acquired non-scarring alopecia (bald spots) Cause is unknown, but autoimmune basis is

hypothesized Males=females 20% of all cases occur in children Family history of alopecia areata is common Commonly seen in families with autoimmune diseases

– Vitiligo, thyroid disease, rheumatoid arthritis, diabetes

Alopecia Areata Hair loss in circumscribed areas

– May have several patchy oval or round areas

Frontal, parietal areas commonly affected No underlying skin changes (no scale,

erythema, or pustules) Usually asymptomatic

Alopecia Areata Prognosis:

– Spontaneous remission is common with limited patchy hair loss if <1 year duration

– 1/3 will have future episodes– ~10% will have chronic course– Worse prognosis if more diffuse involvement upon initial presentation

Support Group and Information– National Alopecia Areata Foundation

www.naaf.org

Alopecia Areata Treatment Treatment options: (not FDA approved)

– Active nonintervention – Supportive psychotherapy– Wigs/hair bands

Locks of Love www.locksoflove.org

– Topical steroids– Intralesional steroids– Contact sensitization

Alopecia Areata

Differential diagnosis includes– Tinea capitis– Telogen effluvium– Trichotillomania– Traction alopecia

Tinea Capitis

Trichophyton tonsurans is the most common dermatophyte to cause tinea capitis in the United States

Humans are the main reservoir– More common in African Americans – Most common in 3-7 year olds

“Classic clinical triad”– Scalp scaling, alopecia, & cervical adenopathy

Clinical Features Seborrheic type:

– Diffuse scaling/dandruff, may have subtle hair loss “Black dot” type:

– Patches of hair loss with broken hairs at follicular orifice Inflammatory type:

– Pustules, abscesses, or kerions Higher risk of scarring

Tinea Capitis Treatment

Requires systemic treatment Griseofulvin

– Gold standard– Good safety profile– Due to resistance, dosing may need to be higher than recommended on

package insert for 6-8 weeks– Absorption dependent on dietary fat intake

Terbinafine– Possible option with shorter treatment duration

Telogen Effluvium Acquired hair thinning (can be diffuse) Rapid conversion of scalp hairs

Growing phase Resting phase (>25%) Normally: 85-90% is growing (anagen)

10-15% is resting (telogen) Acute stressful events act as trigger No areas of focal alopecia, scale, or erythema May develop several months after a high fever, illness,

surgery, traumatic or stressful event

Telogen Effluvium Diagnosis:

– History of preceding event– Clinical exam– Consider obtaining CBC, iron studies, thyroid

studies Treatment:

– Reassurance & time

Trichotillomania

Self induced hair loss resulting from pulling/rubbing/twisting

Patient often denies pulling hair Preadolescence is most

common age of onset Hairs of varying lengths often in

an unusual pattern Scalp>eyelash>eyebrow

Trichotillomania

Treatment– Psychiatric referral– Cognitive behavioral therapy by an

experienced therapist– MedicationsAntidepressants

Case 5

14 year old presents with 3-4 month history of spreading hypopigmented patches with fine scale on the neck, back and chest with minimal associated pruritus.

What is this skin condition?A. VitiligoB. Tinea versicolorC. PsoriasisD. Seborrheic dermatitis

Tinea Versicolor Superficial skin infection with the yeast Malassezia sp

– Usually affects adolescents or adults

Infection may cause temporary melanocyte damage Oval hypopigmented or hyperpigmented macules with fine,

powdery scale Lesions commonly located on the upper chest, neck, and

shoulders Usually asymptomatic Recurrence is common

Tinea Versicolor

Differential diagnosis: Seborrheic dermatitis Tinea corporis Vitiligo Pityriasis alba Secondary syphillis

Work up KOH Classic short curved

hyphae and circular spores “spaghetti & meatballs”

Tinea Versicolor

Treatment (no FDA approved treatments)– 2% Ketoconazole or 2.5% selenium sulfide shampoo applied for 10-15

minutes (as a lotion) daily for 1-2 wks Reapplication at least monthly to prevent recurrence

– Topical antifungal cream twice daily for 1-2 weeks Econazole (Spectazole®)

Ketoconazole (Nizoral®)

– Severe diffuse cases may require oral antifungal therapy Ketoconazole or Fluconazole

– Repigmentation or lightening may take several months

Vitiligo

Acquired depigmenting disorder 50% of individuals with vitiligo developed the

disorder before age 20 Possible autoimmune etiology Can run in families with autoimmune disorders Vitiligo can be localized or generalized

– Generalized vitiligo is usually symmetric

Vitiligo Treatment No FDA approved treatments Photoprotection! Topical corticosteroids Topical calcineurin inhibitors Vitamin D derivatives (calcipotriene) Phototherapy-narrow band UVB Excimer laser Cosmetic camouflage

Pityriasis alba

Pityriasis alba

Localized hypopigmented disorder in children– Common on the face

Usually seen in patients with darker complexions Associated with dry skin and atopic dermatitis Exacerbated by sun exposure

– More noticeable in summer Treatment

– Emollients and photoprotection

Case 6

6 month old infant with a 2 month history of a worsening pruritic eruption consisting of multiple small papules, some with scale or crust, on the trunk, arms, legs, hands, feet, & scalp.

Case 6

What is first line therapy for this rash?

A. Topical steroidsB. Topical permethrinC. Oral antibioticsD. Oral steroids

Scabies Infestation with mite (Sarcoptes scabiei) Severe pruritus Erythematous papules, pustules, nodules, crusted

papules, possible burrows & excoriations Involves trunk, hands, feet, web spaces, axilla &

genitalia– Infants can have scalp and face involvement

Spread by close skin contact

Scabies Treatment

Topical treatment:– Older than 8 weeks of age: 5% Permethrin cream applied

to entire body surface left for 8-12 hours then washed off– Recommend reapplication in 1 week– Treat all family members and close contacts– Wash bedding and clothing in hot water followed by drying

in dryer Seal other items in a plastic bag for 72 hours

Differential Diagnosis

Dyshidrotic eczema Atopic dermatitis Contact dermatitis Papular urticaria Acropustulosis of infancy

Papular Urticaria

Papular Urticaria Also known as “insect bite-induced

hypersensitivity” Chronic or recurrent eruption of itchy papules Lesions often clustered in exposed areas of the

body-face, neck, arms, legs, but spares palms & soles– May have excoriations, hyperpigmentation, and

scarring

Papular Urticaria Usually only one family member is affected Lesions may increase in spring & summer Treatment

– Protective clothing & insect repellent when outdoors– Topical steroids– Antihistamines– Emollients

Case 7

3 year old presents with 2-3 day history of low grade fever, fussiness, and decreased po intake. Small erosions are noted on her posterior pharynx. She also has multiple crusted papules and erosions on her face, arms, legs, and buttocks

Case 7

What is this rash?

1. Hand Foot & Mouth2. Impetigo3. Diffuse Herpes Simplex Virus infection4. Varicella (chicken pox)

Typical Hand, Foot, & Mouth (HFM) Common viral illness caused by enteroviruses

– Serotype coxsackievirus A16 or enterovirus 71

Summer & fall Children <5 years of age

– Spread by contact with saliva, respiratory secretions, fluid in vesicles, and feces

Typically asymptomatic Mild febrile illness Sores in mouth, vesicles on palms & soles Nail dystrophy may follow initial infection

Atypical Hand, Foot, & Mouth Outbreak initially in 2011-2012

– 74% cases were PCR positive for Coxsackievirus A16

Clinical manifestations– Fever

– More severe rash on hands or feet or in mouth

– “Severe” rash on arms, legs, face, buttocks, and trunk Vesicles, large bullae, and erosions

May have accentuation in areas of atopic dermatitis

Confused with varicella, eczema herpeticum, & bullous impetigo

Hospitalization was more common than with typical HFM

– Nail shedding after initial infection

Name That Rash: Pediatric Dermatology Cases

Urticaria Blistering & Desquamating Rashes Contact Dermatitis Hair Loss Pigmentary Changes Scabies Atypical Hand Foot & Mouth

126

Practice ChangeAs a result of attending this lecture, I encourage you to

incorporate these changes in your practice

Change 1: Comfortably recognize several dermatoses commonly encountered in the pediatric outpatient setting

Change 2: Develop a brief differential diagnosis for several pediatric dermatoses

Change 3: Devise an initial treatment plan for several common dermatoses

127

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