Pediatric Dermatology Pearls - UTHSCSA

Forty-Eighth Annual Teaching Conference Pediatrics for the Practitioner -UT Health Science Center

San Antonio School of Medicine –June 10-12, 2011

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Pediatric Dermatology Pearls

Chad Hivnor, M.D.John C. Browning, M.D.

June 11, 2011

John C. Browning, M.D. has no relevant financial relationships with commercial interests to

disclose.

Camp Dermadillo

• Summer camp for children with chronic skin problems, Ages 8-16

• Located at Camp For All in Burton, Texas

• Part of the AAD’s Camp Discovery Program

• Other Camps: Little Pine & Big Trout (Minnesota), Horizon (Pennsylvania), Reflection (Washington), Liberty (Connecticut)

• August 7-12, 2011 -- Free for all campers

• www.campdiscovery.org





Objectives

• Identify common dermatologic conditions seen in children.

• Develop a treatment strategy for affected patients.

• Know when referral to a pediatric dermatologist is needed.

Conflicts of Interest

– Speaker for Galderma (Cetaphil Restoraderm)

– Consultant for ViroXis

Atopic Dermatitis





What is eczema?

• Chronic, relapsing dermatitis associated with dry skin and intense pruritus

• It results from a complex interplay of genetic, immune, infectious, and environmental factors

Eczema Subtypes

• Infantile eczema

• Childhood eczema

• Adulthood eczema

• Dyshidrotic eczema

• Nummular eczema

• Follicular eczema





• Acute

• Sub-acute

• Chronic

Intense pruritus is the hallmark of atopic dermatitis.

Pathophysiology

• Impaired skin barrier function

• Abnormal immune response

• Environmental and genetic factors (polygenic)





Barrier DefectLesional and Non-lesional Skin

• Increased trans epidermal water loss (TEWL)

• Reduced irritancy threshold

• Increased percutaneous absorption of substances

• Dry skin

Impaired Skin Barrier

• The epidermal differentiation complex (EDC) on chromosome 1q21 encodes filaggrin, loricrin, and other proteins involved in terminal differentiation in the epidermis

• Filaggrin has recently emerged as playing an important role in eczema and ichthyosis vulgaris AND asthma and allergic rhinitis

• Probably other genes involved as well (polygenic)

“Bricks and Mortar” Structure of the Stratum Corneum

Covalently

bound lipid

Cornified

cell envelope

Intracellular humectants

(NMFs)

Intracellular

lamellar lipids

Keratin macrofibrils

Corneodesmosome

Corneocyte

20

Layers

LipidsChol

Chol S

Ceramide

Harding CR. Dermatol Therapy. 2004;17:6-15.





Stratum Corneum Disruption in Atopic Dermatitis

J Allergy Clin Immunol., 2006 118:3-21.

Immunodysregulation

• Langerhans cells may be associated with a state of heightened antigen presentation activity for autoreactive T-cells

• Monocytes have increased expression of the high affinity IgE receptor

• T lymphocytes show increased levels of activation

Immunodysregulation

• Eosinophilia is often seen but is neither sensitive nor specific enough to be of diagnostic utility

• Relationship between elevated IgE levels to foods, pollens, and dust mites and the aggravation of atopic skin is controversial





• Nearly 80% of patients with eczema will develop allergic rhinitis or asthma later in childhood (atopic march)

• Many of these patients report improvement in their eczema as they are developing respiratory allergies

Infantile Eczema





Infantile Eczema





Dyshidrotic Eczema = Pompholyx





Nummular Eczema





Follicular Eczema

• Pruritic, perifollicular papules





Lichen Simplex Chronicus

Associated Findings

• Xerosis

• Keratosis pilaris

• Ichthyosis vulgaris

• Dennie-Morgan Lines

• Palmoplantar hyperlinearity

• Pityriasis alba

• Lichen simplex Chronicus





Associated Infections

• Over 90% of patients with severe, acute atopic dermatitis will grow S. Aureus from swab cultures taken from exudative skin

• MRSA more common than MSSA

• Viral diseases: flat warts, molluscum contagiosum, herpes simplex virus infection (eczema herpeticum)

Skin Infections in Atopic Dermatitis

• Cathelicidins and β-Defensins produced by keratinocytes

• Expressed by injury/inflammation

• High levels seen in psoriatic skin

• Negligible levels in atopic skin

• Lack of these peptides may provide explanation for unusually high number of skin infections in AD (bacterial, viral, and fungal)NEJM 2002;347:1151





Evaluation

• History

• Physical Exam

• Consider patch testing

• RAST and skin prick tests can be used to support the diagnosis of an atopic state but are seldom useful in counseling eczema patients regarding avoidance procedures





Curr Opin Allergy Clin Immunol. 2010 Jun;10(3):226-30.

Food allergy and atopic eczema. Worth A, Sheikh A.

PURPOSE OF REVIEW: To review recent developments on the inter-

relationship between food allergy and atopic eczema, with a particular focus

on understanding the role of filaggrin gene defects. RECENT FINDINGS:

Filaggrin gene defects have recently been identified as a major risk factor for

the development of atopic eczema. These skin barrier defects increase the

risk of early onset, severe and persistent forms of atopic eczema. They also

increase the risk of allergic sensitization, and asthma and allergic rhinitis in

those with co-existent eczema. These skin barrier defects are also likely to

increase the risk of food allergy. SUMMARY: Atopic dermatitis and food

allergy are frequently herald conditions for other manifestations of 'the

allergic march'. They commonly co-exist, particularly in those with early

onset, severe and persistent atopic eczema. Filaggrin gene defects

substantially increase the risk of atopic eczema. The increased skin

permeability may increase the risk of sensitization to food and other

allergens, thus pointing to the possible role of cutaneous allergen avoidance

in early life to prevent the onset of atopic eczema and food allergy. Emerging

evidence also indicates that oral exposure to potentially allergenic foods may

be important for inducing immunological tolerance.

Eczema causes food allergy, not vice versa.

Differential diagnosis

• Contact Dermatitis

• Psoriasis

• Wiskott-Aldrich syndrome

• Hyperimmunoglobulin E syndrome

• Langerhans Cell Histiocytosis

• Cutaneous T-cell lymphoma (mycosis fungoides)

• Scabies

Treatment

• Use mild, non-alkali soaps or cleansers such as Cetaphil cleanser or Dove

• Avoid irritants to skin

• Short, warm baths

• Application of emollients immediately after bathing and several times a day





Emmolients

• Lotions, Creams, Ointment (water/oil ratio)

• Ointments are the most effective but are often not tolerated due to excessive greasiness

• CeraVe (with ceramides) or Cetaphil cream / Restoraderm, Aquaphor (petrolatum + lanolin)

• Vaseline (most cost-effective), good to use in patients with suspected contact allergy

Why Moisturize?

• Epidermal barrier dysfunction is central to the pathogenesis of atopic dermatitis (AD)

• Improving skin barrier will improve xerosis, decrease TEWL, lessen the severity of AD

• Used as primary and preventive therapy

• In the “bricks and mortar” model, ceramides and other lipids are the mortar

Ceramide Moisturizers

• CeraVe® 16oz = $15.79

• Restoraderm® 10oz = $14.99

• Mimyx® 140g = $119.76

• Atopiclair® 100g = $121.45

• Epiceram® 50g = $79

• Triceram 3.4oz = $32





Topical Steroids

• Low potency

– Hydrocortisone acetate 1% ointment or cream (OTC)

– Hydrocortisone acetate 2.5% ointment or cream (Rx), can be prescribed in a 1 pound jar

– Desonide, aclovate (cream, ointment, lotion, foam)

• Ointments are more effective than creams

Topical Steroids

• Medium potency

– Triamcinolone 0.1% cream or ointment, can be dispensed in a 1 pound jar

– Hydrocortisone butyrate (Locoid®)

– Mometasone (Elocon®)

– Fluticasone (Cutivate®)

– Desoximetasone (Topicort®)

Topical Steroids

• High Potency

– Clobetasol

– Betamethasone

– Fluocinonide





Topical Steroids

Wet Wraps

• Apply topical steroid

• Cover with warm wet towels or warm wet pajamas

• Cover with dry towels or dry pajamas

• After 20 minutes, remove towels and cover skin with Vaseline

Wet Wraps





Topical Steroids – Side Effects

• Striae

• Systemic absorption

– HPA axis suppression

– Cataracts

– Infection

• Tachyphylaxis

• Only use low-potency topical steroids on the face, under arms, and groin

• Try to limit steroid use to no more than 2-weeks at a time without a 1-week break in order to avoid tachyphylaxis and other side effects

• AVOID SYSTEMIC STEROIDS

Topical Calcineurin Inhibitors

• Tacrolimus (Protopic®) 0.03% & 0.1% ointment

– 0.03% approved for children >2 years

– 0.1% approved for adults

• Pimecolimus (Elidel®) 1% cream

– Approved for children > 2 years of age and adults

• Both drugs FDA-approved as 2nd line therapies for atopic dermatitis





Infection

• S. Aureus functions as a superantigen, aggravating the atopic dermatitis

• Superinfected patients are often erythrodermic

• Treat superinfection with appropriate antibiotics (clindamycin, TMP-SMX, doxycycline)

Infection – Prevention

• Intranasal mupirocin twice daily for 1-week out of every month

• Bleach baths: ¼ to ½ cup Clorox® to a full tub of water for a 15-minutes bath once a week, rinse with clean water

• Swimming in chlorinated pools (rinse with clean water and immediately apply emollient)

Cases





Case 1

• Daily bath in warm water – Bleach baths twice a week

• Avoid harsh soaps

• Moisturize after bath

• Triamcinolone ointment 0.1% Mon-Fri

• Hydroxyzine if needed for sleeping





Case 2

• Mild soap

• Moisturize regularly

• Phototherapy / natural sunlight

• Medium + topical steroid, cream usually preferred over ointment for older kids

• Consider cyclosporine





Case 3

• Consider 3 week taper of prednisolone

• May consider cyclosporine if flares after prednisolone

• Triamcinolone ointment 0.1% M-F

• Mild soaps, regular moisturization





Case 4

• Clindamycin PO x 10 days

• Mild soap, regular moisturization

• Hydrocortisone 2.5% ointment or desonide 0.05% ointment qHS Mon-Fri (avoid eyelids)

• Consider Elidel or Protopic 0.03% for eyelids if needed BID

Fungal Infections





Cutaneous Fungal Infections

• Dermatophytes

• Yeasts

• Deep Fungal

Dermatophytes

• Superficial fungal infection that invades the stratum corneum (dead layer) of the skin

• 3 Genera:

– Epidermophyton

– Trichophyton

– Microsporum





Clinical Presentations

• Tinea corporis

• Tinea cruris

• Tinea barbae

• Tinea capitis

• Tinea pedis

• Tinea unguium (onychmycosis)

Tinea Capitis

• Can be caused by any dermatophyte except E. floccosum and T. concentricum

• Most common:

– Worldwide: M. Canis

– USA: T. tonsurans

• Involvement of scalp skin and hair

Tinea Capitis

• Endothrix

– Black dot tinea

• Ectothrix

• Non-inflammatory

• Inflammatory

– Boggy, kerion





Diagnosis

• Clinical exam

– History, age of child

– Presence of lymphadenopathy

• KOH scraping

• Fungal culture





Differential Diagnosis

• Seborrheic dermatitis

• Psoriasis

• Alopecia areata

• Trichotillomania

• Folliculitis decalvans

Alopecia Areata

Seborrheic Dermatitis





Trichotillomania

Folliculitis Decalvans

Tinea Capitis: Treatment

• Griseofulvin microsize 125mg/5ml: 20-25mg/kg/day given once daily with dinner

• Terbinafine 250mg PO daily x 6-week

– 10-20kg: 62.5mg/day x 6 weeks

– 20-40kg: 125mg/day x 6 weeks

– >40kg: 250mg/day x 6 weeks

• TOPICALS ARE NOT EFFECTIVE





Tinea Corporis

• Dermatophytosis of glabrous skin except palms, soles, and groin

• Transmitted directly from infected humans or animals, via fomites, or via autoinoculation (feet)

• Risk groups: athletes engaging in contact sports, contact with animals





Tinea Corporis: Diagnosis

• History

• Physical exam

• KOH exam

• Fungal culture

• Skin biopsy

Differential Diagnosis

• Nummular eczema

• Granuloma annulare

• Pityriasis rosea

• Pityriasis lichenoides chronica

• Secondary syphilis





Pitfalls

• Majocchi’s granuloma

• Tinea incognito

• Tinea facei

• Not treating onychomycosis

• Using a weak antifungal

• Using topical steroids

Treatment

• Topical

– Allylamines (fungicidal)

• Naftifine, terbinafine

– Azoles (fungistatic)

• Clotrimazole, ketoconazole, oxiconazole

• Systemic

– Griseofulvin, terbinafine, itraconazole, fluconazole





Tinea Cruris

• Erythematous papulovesicles with a scaly raised and well-marginated border

• Characterized by pruritus, can be painful due to maceration and secondary infection

• Differential Dx: psoriasis, candidiasis, seborrheic dermatitis, erythrasma

• Treatment: same as for tinea corporis





Tinea Mannum and Pedis

• “One hand, two feet” disease

• Subtypes:

– Chronic intertriginous

– Chronic hyperkeratotic

– Vesicullobullos

– Acute ulcerative (mixed toe web infection)

• Treatment: same as for tinea corporis

• Minimize moisture, antifungal powders





Onychomycosis

• Fungal infection of the nails (feet > hands)

– Distal subungual

– Proximal subungual

– White superficial

– candidal

• Diagnosis: clinical, culture, nail clipping for PAS

• Treatment: terbinafine 250mg PO daily x 3-months, itraconazole, concomitant use of antifungal foot powder





Yeasts

• Tinea versicolor

• Seborreic dermatitis

• Candidiasis

Tinea Versicolor

• Caused by Malessezia furfur (normal flora in sebum rich areas)

• Normally exists as a yeast on the skin

• Converts to mycelial form under appropriate conditions (heat, humidity, immunosuppresion)

• Characterized by scaly hypo- or hyperpigmented macules on the upper chest, back, and proximal extremities





Tinea Versicolor

• Diagnosis: history, clinical exam, KOH exam (spaghetti and meatballs)

• Treatment:

– Selenium sulfide shampoo, ketoconazole 2% shampoo

– Ketoconazole 400mg PO x 1, repeat in 1-week

• Prognosis: chronic, recurring condition

Seborrheic Dermatitis

• Colonization with Malessezia furfur

• Abnormal immune response

• Release of free fatty acids

• Seen in infants, adolescents, and adults

• In children, think about tinea capitis!

• Treatment: ketoconazole 2% shampoo, hydrocortisone 2.5% cream or lotion





Psoriasis





Candidiasis

• Candida albicans

• Intertrigo

• Diaper dermatitis

• Erosio interdigitalis blastomycetica

• Balanitis

• Perianal infection

• Chronic paronychia

• Thrush





Deep Fungal

• Chromomycosis

• Histoplasmosis

• Blastomycosis

• Coccidioidomycosis

• Cryptococcosis

• Mucormycosis





Hemangiomas





Infantile Hemangioma

• Not present at birth

• Risk factors: female, preterm, h/o amniocentesis

• Appears as a red macule within first few weeks of life

• Rapid proliferation during first 4-6 months of life

• Slow involution after 1 year of age

• GLUT1 positive

Copyright restrictions may apply.

Metry, D. W. et al. Arch Dermatol 2000;136:905-914.

Annular, hypopigmented patch with central telangiectasias characteristic of an early hemangioma





Ulcerated Hemangioma





Pilomatrixoma

Spitz Nevus





Pyogenic Granuloma

Hashimoto-Pritzker

Photo Courtesy of Dr. Meena Julapalli

Congenital, Self-regressing Tufted AngiomaJohn Browning; Ilona Frieden; Eulalia Baselga; Annette Wagner; Denise Metry

Arch Dermatol. 2006;142:749-751.





Multifocal tufted angiomas in 2 infants.Maronn M, Chamlin S, Metry D.

Arch Dermatol. 2009 Jul;145(7):847-8.

Kaposiform Hemangioendothelioma

PNET/Ewing’s Sarcoma





PNET/Ewing’s Sarcoma

Malignant Rhabdoid Sarcoma

RICH





NICHNoninvoluting congenital hemangioma: a rare cutaneous vascular anomaly.

Enjolras O, Mulliken JB, Boon LM, Wassef M, Kozakewich HP, Burrows PE.Plast Reconstr Surg. 2001 Jun;107(7):1647-54.





Hemangiomas: When to Worry

• Near the eyes

• Nasal tip

• Lip – crossing over the vermillion border

• Segmental hemangioma on the face

• Midline on back

• Beard area

• Perineum

• Anywhere prone to ulceration (e.g. axilla, back, diaper area)

Infantile Hemangioma: Treatment

• Active Non-Intervention

• Topical Steroids

• Intralesional steroids

• Imiquimod

• Surgery

• Laser (when flat)

• Prednisolone 3mg/kg/day

• Propranolol 2mg/kg/day

• Timolol 0.5% Soln

Propranolol x 3-months





6-weeks

Propranolol x 1-month







Courtesy of Dr. Moise Levy

Timolol Solution 0.5%





Propranolol

• Possible mechanism of action:

– Vasoconstriction

– Inhibition of angiogenesis

– Induction of apoptosis

• Dexamethasone: found to inhibit VEGF in hemangioma stem cells (N Engl J Med. 2010 Mar 18;362(11):1005-13.)

British Journal of Dermatology

Vol. 163, 2 Pages: 269-274

Other Common Skin Conditions





Warts: Subtypes

• Verruca vulgaris: common wart

• Verruca palmares et plantaris: hand & foot warts

• Verrucae plana: flat warts

• Condyloma acuminata: genital warts





Molluscum Contagiosum

• Caused by infection with the pox virus

• Very common

• Often mistaken for warts

• Infection occurs by direct contact or indirect contact (swimming pools)

• Genital molluscum: think STD





Molluscum: Treatment

• Most molluscum will self-resolve within an average of 2 years

• Destructive therapy may also be used

– Liquid nitrogen

– Cantharadin (topical blistering agent)

– Curettage

• Topical therapy

– Imiquimod, tretinoin





Pityriasis Alba

• Hypopigmented macules, most commonly on the face

• Due to decreased pigmentation within dry patches of skin

• Treatment: Moisturization, sunscreen

Vitiligo

• Depigmentation of skin

– Likely autoimmune

– Can be seen with type 1 DM, thyroid disease

• Segmental

• Diffuse

• Treatment: topical steroids or topical calcineurin inhibitors, phototherapy





The End

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Pediatric Dermatology Pearls - UTHSCSA

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