19ce031-ppt abrahams pediatric dermatopic dermatitis (eczema) •chronic inflammatory skin disease...
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Pediatric DermatologyJennifer Abrahams, MD, FAAD, DTM&HCollaborators: Kate Oberlin, MD; Nayoung Lee MDSeptember 27th, 2019
Disclosures• Nothing to disclose
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Disclaimer*Pediatric dermatology is taught over 3 years of derm-specific residency training and there is an additional year of subspecialized fellowship!
*We won’t cover all of pediatric derm in an hour but I hope to give you some common highlights
A 9 month old infant presents with the following skin lesions. Which of the following is most likely true of this disease?
A.) Asthma generally precedes skin findingsB.) The majority of affected children will outgrow the skin diseaseC.) There is no way to avoid or decrease risk of progression of the diseaseD.) Genetic factors account for approx 1% of susceptibility to early onset of this disease
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A 9 month old infant presents with the following skin lesions. Which of the following is most likely true of this disease?
A.) Asthma generally precedes skin findingsB.) The majority of affected children will outgrow the skin diseaseC.) There is no way to avoid or decrease risk of progression of the diseaseD.) Genetic factors account for approx 1% of susceptibility to early onset of this disease
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Atopic Dermatitis (Eczema)•Chronic inflammatory skin disease that begins during infancy or early childhood
•Often associated with other “atopic” disorders
• Asthma
• Allergic rhinitis (seasonal allergies)
• Food allergies
•Characterized by intense itch and a chronic relapsing course
•Prevalence almost 30% in developed countries
Triad of atopy: atopic dermatitis, asthma, allergic rhinitis
AD has a predilection for infants and young children, asthma favors older children and allergic rhinitis predominates in adolescents/adults
Table courtesy of Bolognia, et al.
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Epidemiology:Three main stages based on age of onset
Early onset type:
– Begins in the first two years of life with 60% presenting prior to age 1
– Most common type
– Most go into remission by age 12
Late onset type
– AD that starts after puberty
Senile onset type:
– Unusual subset that begins after age 60
PathogenesisComplex genetic disease with both gene-gene and gene-environmental interactions
Parental history of AD is a stronger risk factor than asthma or allergic rhinitis
Two major sets of genes implicated in AD:
– Epidermal proteins
– Proteins with immunologic function
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Rundle CW, Bergman D, Goldenberg A, Jacob SE. Contact dermatitis considerations in atopic dermatitis. Clin Dermatol. 2017. Jul‐Aug;35(4):367‐374.
Morphology of Lesions
•Acute lesions: edematous, erythematous plaques with oozing & serous crusting•Subacute eczematous lesions: erythema, scaling and variable crusting•Chronic lesions: thickened plaques with lichenification, scale, prurigo nodules
•Perifollicular accentuation and papular eczema: common in individuals with darker skin
•Any stage can evolvegeneralized exfoliative erythroderma
Acute Subacute Chronic
courtesy of Fitzpatrick, et al.
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Distribution of lesionsChildhoodInfantile Adulthood
<2 years of age
Edematous papules on cheeks with oozing
Face & neck*, scalp, extensors, trunk
2‐12 years
Lesions become more lichenified, + xerosis
Antecubital and popliteal fossa (flexural)
>12 years
Lichenification
Flexors, hand dermatitis, eyelid involvement
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Associated clinical features
Table courtesy of Bolognia, et al.
Keratosis Pilaris•Discrete perifollicular papules with central keratotic core
•Seen in >40% of patients with AD
•Upper arms, thighs and lateral cheeks (children)
•Keratosis pilaris rubra: features numerous tiny, follicular papules superimposed on confluent erythema.
•Tx: exfoliation with pumice stone, urea, salicylic acid, alpha‐hydroxy acids, topical retinoids
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Dennie-Morgan folds & Allergic shiners
• Symmetric, prominent horizontal fold originating at the medial canthus
• Also see central facial pallor “headlight sign” [perioral, perinasal and periorbital pallor]
• Skin around the eyes appears gray to violet–brown
courtesy of Fitzpatrick, et al.
Palmar hyperlinearity
• Accentuation of the palmar creases
• Also seen in ichthyosis vulgaris
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Pityriasis alba
• Hypopigmented patches with minimal scale
• Etiology: Low grade eczematous dermatitis that disrupts the transfer of melanosomes to keratinocytes
courtesy of Bolognia, et al.
Common allergens in atopic patients?NickelCobaltThimerosalCAPB (detergent)Quaternium-15
– All formaldehyde releasing preservatives
Lanolin (Aquaphor)
Atopics are predisposed to sensitization of chemical allergies of topical medications and personal care productsRundle CW, Bergman D, Goldenberg A, Jacob SE. Contact dermatitis considerations in atopic dermatitis. Clin Dermatol. 2017. Jul‐Aug;35(4):367‐374.
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An 8yo girl has had abrupt worsening of her long-standing eczema. Which organism is most likely involved?
A.) StreptococcusB) Herpes Simplex VirusC.) VaricellaD.) Staphylococcus
An 8yo girl has had abrupt worsening of her long-standing eczema. Which organism is most likely involved?
A.) StreptococcusB) Herpes Simplex VirusC.) VaricellaD.) Staphylococcus
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Impetiginization •Staph!
•Staph!!
•Staph!!!
• Predisposed to skin infections due to their impaired skin barrier• Reduced amount of innate antimicrobial peptides:
• human β defensin• cathelicidins
• S. aureus colonizes the skin of the vast majority of patients with AD• Bacterial infections exacerbate AD by stimulating the inflammatory
cascade via S. aureus exotoxins that act as superantigens (exotoxin B IL4, IL5, IgE)
A 4 year old male with a history of atopic dermatitis presents with the following skin lesions. Which of the following therapies would be most essential for treatment?- Corticosteroids- Antiviral- Antibiotic- Emollients and observation
courtesy of Fitzpatrick, et al.
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A 4 year old male with a history of atopic dermatitis presents with the following skin lesions. Which of the following therapies would be most essential for treatment?- Corticosteroids- Antiviral- Antibiotic- Emollients and observation
courtesy of Fitzpatrick, et al.
Eczema herpeticum
•Rapid dissemination of HSV
•Numerous monomorphic, punched-out erosions with hemorrhagic crusting
•Watch for:
– Keratoconjunctiviti
– Meningoencephalitis
courtesy of Bolognia, et al.
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Molluscum contagiosum
•Poxvirus; typically self-limited in children
•Multiple pearly umbilicated papules•Intertriginous areas, face, genitals, buttocks
• propensity to contract molluscum contagiosum in AD and with a more widespread distribution
Molluscum dermatitis
Inflammation of MC lesions
May herald the development of a host immune response
Id reaction-like eruptions can occur manifesting with pruritic erythematous papules favoring elbows, knees + molluscumdermatitis
What is an id reaction?
• “Autosensitization reaction”• Disseminated secondary dermatitis, in response to a
primary localized dermatitis
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• Adjunctive therapies: bleach baths (1/4 cup bleach in tub), PO antihistamines, probiotics, sensitive skin care
Dupixent
courtesy of Bolognia, et al.
Targeted molecular therapy
•Dupilumab (Dupixent)
• Human monoclonal IgG4 Ab binds IL‐4Rα, thus blocks IL‐4 and IL‐13
– JAAD article (June 2016) demonstrates early and sustained improvements in sleep, mental health, and quality of life in adults with AD
– FDA granted Breakthrough Therapy designation for Dupixent for the treatment of moderate‐to‐severe (adolescents 12 to 17 years of age) and severe (children 6 months to 11 years of age) atopic dermatitis not well controlled on topical prescription medications.
– Dosing: 600 mg SQ once, then 300 mg SQ every other week
– AE’s: injection site reactions, conjunctivitis (10%), HSV (2‐4%)
– Need to fail topical corticosteroids and TCIs
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PreventionProlonged breastfeeding (>4-6 months)
Vitamin D3 supplementation– May help reduce Staph colonization through vitamin D‐stimulated in cathelicidin LL‐37 (innate antimicrobial peptide)
Use of emollients once daily within 3 weeks after birth may reduce the incidence of atopic dermatitis at 6 months by 50%!11Simpson EL, Chalmers JR, Hanifin JM, et al. Emollient enhancement of the skin barrier from birth offers effective atopic dermatitis prevention. J Allergy ClinImmunol. 2014;134(4):818‐823.
Other Eczematous Eruptions
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Infantile seborrheic dermatitis(Cradle Cap)
Self-limited
Common chronic dermatitis confined to skin regions with high sebum production
first 3 months of life, usually starts 1 week after birth
Mild greasy scale adherent to scalp (“cradle cap”) and in intertriginous areas
– Acutely inflamed, oozing, sharply demarcated, superimposed with Candida
May also appear psoriasisiform
Other Eczematous Eruptions
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DDx seborrheic dermatitis
Infant:– Atopic dermatitis
• Later onset, distribution, +pruritus
– Irritant diaper dermatitis
– Infantile psoriasis
– Langerhans cell histiocytosis
– Wiskott‐Aldrich syndrome
– Tinea capitis
TreatmentInfantile:
– Self‐limited
– Emollients, 2% ketoconazole cream, low potency corticosteroids, keratolytic shampoos
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Lumps and bumps…
A 12 yo boy presents with a bump on his elbow for 8 months that he picks at, but otherwise is asymptomatic. Which of the following is true of this lesion?
A.) pinpoint black dots are common findings in this lesionB.) Once the lesion resolves, he is immune from future lesionsC.) The lesion is secondary to a pox virusD.) He is not contagious after a course of antibiotics
courtesy of Habif, et al.
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A 12 yo boy presents with a bump on his elbow for 8 months that he picks at, but otherwise is asymptomatic. Which of the following is true of this lesion?
A.) pinpoint black dots are common findings in this lesionB.) Once the lesion resolves, he is immune from future lesionsC.) The lesion is secondary to a pox virusD.) He is not contagious after a course of antibiotics
courtesy of Habif, et al.
Verruca Vulgaris (Warts)
courtesy of Habif, et al.
• >100 strains HPV• Low risk: 11/16 (warts); High risk 16/18• Most common warts spontaneously
resolve (but may take years)• Risk of spread with manipulation• Treatment based on destruction:
• Cryotherapy/Curette/Excision
• Salicylic acid
• Cantharone
• Imiquimod
• Injections/other Immunotherapy
• 9-valent HPV vaccine may help decrease prevalence
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This 17yo M has noted dramatic worsening of his acne over the past year with a new medication. All of the following medications can cause an acneiform eruption except:
A.) PhenytoinB.) SteroidsC.) LithiumD.) MethotrexateE.) Isoniazid
This 17yo M has noted dramatic worsening of his acne over the past year with a new medication. All of the following medications can cause an acneiform eruption except:
A.) PhenytoinB.) SteroidsC.) LithiumD.) MethotrexateE.) Isoniazid
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Acne Vulgaris• Disorder of the pilosebaceous unit- many factors
Types
Comedonal• ice-pick scars• Topical retinoids +/- abx/antibacterial
Papulopustular• Topical AM Abx, PM retinoid +/- oral abx• Alternatives: OCPs, anti-androgens in women
Nodulocystic• Topicals +oral abx• Oral Isotretinoin• Alternatives: OCPs,
anti-androgens, ILK
courtesy of Bolognia, et al.
courtesy of Bolognia, et al.
Pro tip: Benzoyl peroxide has a synergistic effect with antibiotic treatments and decreases risk of resistance!
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Tips for topical retinoid education• Dryness/irritation is expected with topical retinoids • Increase adherence by starting low strength and good education!
• Pea‐sized amount on fingertip
• Dab around face then rub in thin layer
• Can put moisturizer on top at night and also moisturize in AM
• Start q3‐4 nights and gradually increase over weeks as tolerated
• If too dry/irritated, decrease frequency but encourage to keep going!
• Can flare first month (may want to have adjuvant treatment to help)
• Can also note it can help pigmentation issues & even help fine wrinkles
Pediatric Vascular Lesions
Vascular TumorsVascular MalformationsCapillary (PWS, salmon patch)Venous LymphaticArterialArteriovenousMixed
Errors in development
Infantile HemangiomaTufted angiomaKaposiformhemangioendothelioma (KHE)Pyogenic granulomaHemangiopericytoma
Cellular proliferation
“oma”
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132. Which of the following is the greatest risk factor for the development of hemangioma of infancy?
A. First bornB. JaundiceC. Premature birthD. PostmatureE. Small for gestational age
132. Which of the following is the greatest risk factor for the development of hemangioma of infancy?
A. First bornB. JaundiceC. Premature birthD. PostmatureE. Small for gestational age
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Risk Factors for HOI
HOI is more common in premature infants– 10% incidence within normal infants– 12% incidence in premature infants– Increased prevalence correlated with both decreasing gestational
age and birth weight• Premature infants < 1500 gm = 15% HOI• Premature infants < 1000 gm = 22% HOI
HOI is more common in female infants for unclear reasons (ratio of 3:1)
Low birth weight most significant risk factor• 40% for every 500 gram in birth weight
20% incidence of HOI in infants exposed to chorionic villus samplingPediatr Dermatol. 1986 Sep;3(4):331‐2.
Infantile Hemangioma
MC vascular tumor of childhood
5%-10% of infants, especially Caucasians
Most common on head & neck
Most arise in first several weeks
Characteristic rapid growth period of proliferation during first year followed by involution over years
Early Proliferation (rapid ↑ in size) most growth in first 5 months• 80% reach final size, mean age of 3 months
Late Proliferation (slower growth rate) ends 9-12 monthsPlateauInvolution
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Clinical FeaturesSuperficial hemangiomas: superficial dermis
– Bright red with a lobulated surface, non-compressible– Focal plaque or segmental lesion
Deep hemangiomas: deep dermis/subcutis– Warm, ill-defined blue-purple mass – +/- telangiectasia– +/- significant blood supplythrill felt or bruit auscultated
Mixed: both superficial and deep components
What is the MC subtype? Superficial=50‐60%
Natural HistoryInvolution: May begin as early as the first year of life
Rule of 10’s:– 30% by age 3, 50% by age 5, 70% by age 7, 90% by age 9
What are the signs of involution?– Color change from bright red to gray-purple– Flattening, dividing into smaller islands– Develops fatty consistency– size with crying and activity
Some involute completely, while others leave fibrofatty, atrophy, scarring or telangiectatic residual=cosmetic significance
courtesy of Bolognia, et al.
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Complications
Ulceration
10% of lesions, most common complication
Why? Rapid expansion may outgrow blood supply, usually during proliferative phase
Lip and diaper region, skin folds, large size
Whitish discoloration in infants <3 monthsimpendingulceration
Painful, ↑ risk of infection, ↑ scarring, bleeding risk
ComplicationsDisfigurement & Functional ImpairmentLarge IH’s can distort tissue
Vulnerable locations– Periocularastigmatism (compressing the globe),
amblyopia, strabismus– Nasal tip: distort cartilage– Columella: destroy cartilage– Lip: painful ulceration, scarring– Ear: ulceration, conductive hearing loss– Breast: affect underlying breast budasymmetry– Anogenital: ulceration, infection
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Risky signsPHACES syndrome:Large segmental facial lesion a/w extracutaneous anomaliesWork-up:
– MRI/MRA H&N, echo, ophthalmologic exam, neuro exam, thyroid tests
“Beard” distribution: risk of airway involvement ENT eval!
Hemangiomatosis (>5 hemangiomas) eval internal involvement
LUMBAR syndrome:Midlinerisk for spinal dysraphism
– >2.5 cm, risk is ~35% (ie tethering of spinal cord)
TreatmentActive Non-intervention; Close observation with photography
Intralesional Steroidslocalized lesions
TopicalCorticosteroid for superficial lesionsβ-blockers 2-4x daily
Laser, excision, embolization (high risk threatening high output CHF)
SystemicCorticosteroid:
– VEGF production, 2-4 mg/kg/day prednisone
Propranolol 20mg/5mL or Hemangeol 4.28mg/mL– IH endothelial cells express β2 adrenergic R’svasoconstriction, apoptosis
Vincristine– Interferes with microtubule formation, need venous access
Interferon α (2a and 2b) for life threatening IH:– SQ; Most worrisome side effect: spastic diplegia [20% of patients]
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Vascular Malformations
Vascular MalformationsDevelopmental error
Categorized based on vessel type:– Slow flow:
• Capillary (CM) macular, ie port-wine stain (PWS)• Venous (VM); compressible, fills with dependency, a/w
thrombi, phleboliths• Lymphatic (LM), micro- and macrocystic lesions
– Fast flow: Arterial and AVM
Combined vascular malformations:
No gender predilection
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Questions!What specialist should you consult?
Questions!What specialist should you consult?
–ENTrisk of airway involvement
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Anyone recall this rash?
Anyone recall this rash?“dewdrops on a rose petal”
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Varicella (Chickenpox)
ReferencesBolognia, Jean., Jorizzo, Joseph L.Schaffer, Julie V., eds. Dermatology. [Philadelphia]: Elsevier Saunders, 2012. Print.Ezekowitz, R. Alan B., John B. Mulliken, and Judah Folkman. "Interferon alfa-2a therapy for life-threatening hemangiomas of infancy." New England Journal of Medicine 326.22 (1992): 1456-1463.Habif, Thomas P. Clinical Dermatology: A Color Guide To Diagnosis And Therapy. St. Louis : Mosby, 1990. Print.Kang, Sewon. Fitzpatrick's dermatology. [New York] : McGraw-Hill Education. 2019. Print.Mancini AJ, Krowchuk DP. Pediatric Dermatology. 2019 Feb 8.Paller AS, Mancini AJ. Hurwitz clinical pediatric dermatology: a textbook of skin disorders of childhood and adolescence. Elsevier Health Sciences; 2015 Oct 20.Rundle CW, Bergman D, Goldenberg A, Jacob SE. Contact dermatitis considerations in atopic dermatitis. ClinDermatol. 2017. Jul-Aug;35(4):367-374.Simpson EL, Chalmers JR, Hanifin JM, et al. Emollient enhancement of the skin barrier from birth offers effective atopic dermatitis prevention. J Allergy Clin Immunol. 2014;134(4):818-823.
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Thank you for your attention!
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