Pediatric Dermatology

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Pediatric Dermatology

• Mary Tedesco-Schneck MSN, CPNP

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Objectives

• Discuss the basic physiology of skin
• Identify primary secondary lesions
• Understand the standards of care for some common
  pediatric dermatological conditions
• Discuss prevention strategies

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Physiology of Skin
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Epidermal appendages

• Hair/Hair Follicle Facilitates evaporative H2O
  warmth /protection
• Nails Protect distal phalanges
• Sebaceous glands Produces sebum (complex blend
  of lipids) stimulated by androgenic hormones
  decreases H2O loss largest glands are found in
  the face, scalp, upper back, and chest

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Epidermal appendages

• Eccrine glands Sweat glands help regulate body
  temperature through evaporative H2O loss remove
  urea, ammonia from the tissue contain IG.
• Apocrine glands Sweat glands extend deeper into
  the dermis than eccrine glands found in face,
  scalp, axillary, and anogenital regions.

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Definition

• Primary Lesions

• Secondary Lesions

• De novo
• Earliest lesions to appear

• Changes either from an external factor or the
  natural evolution of the lesion

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Primary Lesions

• Less than 1 cm

• Greater than 1 cm

• Macule
• Papule
• Vesicle
• Pustule
• Nodule

• Patch
• Tumor
• Bulla
• Abscess
• Plaque

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Table 1. Common Primary Lesions4 Modified from
Toronto Notes 2010
Profile lt1 cm gt1 cm
Flat Macule Patch
Elevated Papule Plaque Plaque
Palpable, deep Nodule Tumor Tumor
Fluid filled Vesicle Bulla Bulla
Retrieved from http//learnpediatrics.com/
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Macule Flat lt 1 cm
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Papule Raised lt 1 cm
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Vesicle Fluid filled lt 1 cm
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Pustule Purulent fluid lt 1 cm
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Nodule Raised solid lt 1 cm

• Distinct borders
• Neurofibroma
• Greatest mass is below the skin surface

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Patch Flat gt 1 cm

• Café au lait
• Tinea versicolor

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Plaque Raised gt 1 cm

• Solid raised flat-topped lesion.
• May show epidermal changes.

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Tumor Solid gt 1 cm

• Raised and solid
• Greatest masses below the skin surface.

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Bulla Fluid filled gt 1 cm
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Abscess Purulent d/c gt 1 cm

• Circumscribed, elevated lesion

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Secondary Lesions

• Crusts
• Erosions
• Scale
• Atrophy
• Excoriations
• Fissures
• Ulcers

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Crusts

• Dried exudate composed of serum, blood, or pus

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Erosion vs. Excoriation

• Erosion loss of the surface of the epithelial
  i.e. un-roofing of a vesicle or bulla
• Excoriation an erosion with loss of the
  epidermis in an angular configuration related to
  picking

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• Erosion

• Excoriation

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Fissures

• Linear breaks in the skin often down to the
  dermis often result from excessive xerosis

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Ulcers

• Full thickness loss of epidermis extending into
  the dermis (e.g. aphthous ulcer)

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Scale (ichthyosis)

• Desiccated plates of keratin (fibrous structural
  protein of the epidermis) results from
• Increased shedding
• Proliferation

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Scar

• Fibrotic skin changes as a result of tissue injury

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Atrophy

• Epidermal wasting away of the epidermis (e.g.
  wrinkling, increased underlying vascular
  prominence)
• Dermal reflects loss of fat or subcutaneous
  tissue (e.g. see this with intra-lesional steroid
  injection)

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Morphology

• Mobile versus immobile
• Hard versus soft
• Fluctuant
• Sclerosed
• Compressible
• Diffuse verus well-demarcated

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Color of Lesion

• Red vasodilation or hyperemia
• Blanching vasodilation
• Non-blanching vascular damage with
  extravasations of blood in dermis (petechiae,
  purpura)
• White de-pigmentation or hypo-pigmentation
• Yellow lipid accumulation or bile
• Brown/Black/Blue/Grey related to ?melanin or
  blood/blood byproducts

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Configuration of the lesions

• Annular
• Nummular

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Distribution

• Generalized
• Grouped
• Linear

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Distribution

• Acral
• Extensor
• Flexor

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Distribution

• Symmetrical

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Blaschko lines vs Dermatome
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Additional Terminology

• Lichenification thickening of the epidermis
  with exaggerated skin markings caused by chronic
  scratching
• Xerosis dry
• Polymorphous More than one primary lesion

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Additional Terminology

• Umbilicated central depression
• Verrucous warty
• Pedunculated stalk
• Flat-topped

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Skin Color

• Melanin producing cells in the stratum basale
  epidermis
• Melanin absorbs and scatters solar radiation.

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Melanogenesis The process by which melanocytes
produced melanin.

• Light-skinned people lower levels of
  melanogenesis.
• Melanogenesis stimulated by exposure to UV-B
  radiation.
• Melanin produced by melanogenesis is dark and
  absorbs and blocks UV-B radiation from going
  deeper into the skin layers.
• Other factors stimulate melanogenesis such as
  hormones, medications.

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Evolution of Skin Type

• We have different skin colors related to how
  close we are to the equator because dark skin is
  protective of UV light.

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Type I
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Type II
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Type III
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Type IV
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Type V
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Type VI
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Common Dermatological Disorders

• Atopic Dermatitis
• Psoriasis
• Acne
• Hemangioma
• Nevi

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Atopic Dermatitis
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Characteristics

• Transepidermal H2O loss (skin barrier
  dysfunction)
• Intense itchy
• Cutaneous inflammation

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Precedes other atopic diseases

• ATOPIC MARCH
• Asthma
• Food allergies
• Allergic rhinitis

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Consequences

• Decreased quality of life
• Delayed social development
• Poor sleep
• Secondary infection

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Treatment

• Emollient therapy
• Treatment of exacerbations with
• Mid-potency topical steroid ointments (body)
• Low-potency topical steroid ointments (face,
  folds, diaper area)
• Topical calcineurin inhibitors
• Pimecrolimus
• Tacrolimus
• Wet wraps
• Anti-histamines
• Infection Bleach baths

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Gelmetti, C. et al (2012). Quality of life of
parents living with a child suffering from atopic
dermatitis before and after a three-month
treatment with an emollient. Pediatric
Dermatology, 29(6), 714-718.

• Shea butter (aka Karite Butter) yellowwhite to
  ivory-colored high content of nonsaponifiable
  fatty acids.
• absorbed rapidly into skin
• No greasy feeling
• May have some anti-inflammatory properties
• Excellent vehicle for dermatologic preparations

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Psoriasis Chronic inflammatory multisystem
disorder

• Lesions papulosquamous
• Location scalp, elbows, knees, genital area
• Appendages pitting the nails

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Treatment

• Corticosteroids
• Vitamin D analogue
• Tazorotene
• Coal tar
• Salicylic acid

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Topical corticosteroids

• Action anti-inflammatory, anti-proliferative,
  immunosuppressive, and vasoconstrictor
• Choice consider potency and vehicle based on
  disease severity
• Adverse effects
• Local skin atrophy, telangiectasia, striae,
  acne, folliculitis, and purpura
• Systemic Cushings syndrome and HPA suppression

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Vitamin D analogues

• Action binds to vitamin D receptors and inhibits
  care to keratinocyte proliferation and
  differentiation
• Adverse effects
• Local burning, pruritus, edema, peeling,
  dryness, and erythema
• Systemic hypercalcemia and parathyroid hormone
  suppression (extremely rare)

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Tazorotene

• Action normalizes abnormal keratinocyte
  differentiation and decreases hyper-proliferation
  by decreasing expression of inflammatory markers.
• Adverse effects
• Local irritation, photo sensitizing

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Tacrolimus Pimecrolimus

• Action blocks synthesis of inflammatory
  cytokines
• Adverse effects
• Local burning and itching
• Systemic potential risk of developing
  malignancies

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Coal tar

• Action suppressive DNA synthesis of
  keratinocytes
• Adverse effects
• Local irritant dermatitis, folliculitis and
  photosensitivity

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Salicylic acid

• Action reduces scaling by diminishing
  keratinocyte-two-keratinocyte binding and
  reducing pH of the stratum corneum
• Adverse effects
• Local drying
• Systemic gt 20 of TBSA systemic toxicity

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Acne

• Androgenic stimulation ?sebum production
• Hyperproliferation shedding of keratinocytes
  obstruction of pilosebaceous unit
• Proliferation of Propionibacterium acnes
• Inflammation sebum seeps into the dermis
  proinflammatory mediators secreted by P. acnes

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Global Assessment Scale

•  0 Normal, clear skin with no evidence of
  acne vulgaris
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• 1 Skin is almost clear rare
  non-inflammatory lesions present, with rare
  non-inflamed
• papules (papules must be resolving and
  may be hyperpigmented, though not pink-
• red)
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• 2 Some non-inflammatory lesions are present,
  with few inflammatory lesions
• (papules/pustules only no nodulo-cystic
  lesions)
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• 3 Non-inflammatory lesions predominate, with
  multiple inflammatory lesions
• evident several to many comedones and
  papules/pustules, and there may or may
• not be one small nodulo-cystic lesion
•  
• 4 Inflammatory lesions are more apparent
  many comedones and papules/pustules,
• there may or may not be a few
  nodulo-cystic lesions
•  
• 5 Highly inflammatory lesions predominate
  variable number of comedones, many
• papules/pustules nodulo-cystic lesions

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References

• Lehmann HP et al. Acne therapy a methodologic
  review. J Am Acad of Dermatol 200247231-240.
• Burke BM, Cunliffe WJ. The assessement of acne
  vulgaris-the Leeds technique. Br J Dematol 1984
  11183-92.
• OBrien SC, Lewis JB, Cunliffe WJ. The Leeds
  revised acne grading system. J Dermatol Treat
  1998 9215-220.
• Pochi PE et al. Report of the consensus
  conference on acne classification. J Am Acad of
  Dermatol 1991495-500.

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Treatment

• Antimicrobial (oral versus topical)
• Benzyl peroxide or salicylic acid
• Topical Retinoids
• OCP
• Cystic Acne
• isotretinoin

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Hemangioma

• Most common pediatric vascular tumors 5 of
  infants in the United States
• Increase incidence
• Prematurity
• Twins
• Family history

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Hemangioma

• Proliferation out of proportion to growth of
  the infant up to 9 months of age
• Involution
• 30 by 3 years
• 50 at 5 years
• 70 at 7 years
• 90 by 10-12 years

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Treatment if

• Permanent disfigurement
• Ulceration
• Bleeding
• Visual compromise
• Airway obstruction

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Treatment for hemangioma

• Collaborative
• Dermatologist for on-going treatment
• Cardiologist initial evaluation prn
• PCP on-going monitoring

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Topical timolol

• Monitor heart rate, blood pressure, and
  cardiopulmonary assessment
• 1 to 2 drops twice a day

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Propranolol

• Mechanism of action is unclear but hypothesized
• Vasoconstriction
• Decreased renin production
• Inhibition of angiogenesis
• Stimulation of apoptosis
• Monitoring is necessary for
• Bradycardia and hypotension
• Hypoglycemia
• Bronchospasm
• Hyperkalemia

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Contraindications to propranolol

• Cardiogenic shock
• Sinus bradycardia
• Hypotension
• gtfirst degree heart block
• Heart failure
• Bronchial asthma
• Hypersensitivity to propranolol

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Pretreatment exam diagnostic studies

• EKG
• Newborns less than a month old less than 70 bpm
• Infants less than 80 bpm
• Children less than 70 bpm
• Family history of congenital heart conditions
  arrhythmias or maternal history of connective
  tissue disease
• History of arrhythmia during physical exam
• Physical exam with emphasis on
• Heart rate
• Blood pressure
• Cardiac and pulmonary assessment

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During treatment

• HR BP baseline
• HR BP 1-2 hours after a dose increase and after
  target dose is achieved
• To prevent hypoglycemia
• Administer during daytime hours with the feeding
  shortly after administration
• Ensure child is fed regularly
• Discontinued during inter-current illness
  especially with restricted oral intake to prevent
  hypoglycemia

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References

• Drolet, B.A. et al (2013). Initiation and use of
  propranolol for infantile hemangioma Report of a
  conference. Pediatrics, 131(1), 128-140.
• Chen, T.S. et al (2013). Infantile hemangiomas
  an update on pathogenesis and therapy.
  Pediatrics, 131(1) 99-108

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Nevi

• Congenital versus Acquired
• Annual skin exam
• Dermoscopy by dermatologist
• Prevention
• Sunscreen or block 30 SPF for UVA UVB
• No tanning beds
• LD 272

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