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Transcript of Name That Rash: Pediatric Dermatology Cases · Name That Rash: Pediatric Dermatology Cases I have...
© 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
2
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
3
Name That Rash: Pediatric Dermatology Cases
Urticaria Blistering & Desquamating Rashes Contact Dermatitis Hair Loss Pigmentary Changes Scabies Atypical Hand Foot & Mouth
4
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
6
Case 1
What is this skin condition?
A. Erythema multiformeB. Urticaria (Hives)C. Viral exanthemaD. Vasculitis
7
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
16
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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