Dermatology




Types of Lesions



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Primary: Specific Changes Caused Directly by Disease Process




  • Macule: Nonpalpable, <1 cm
  • Patch: Nonpalpable, >1 cm
  • Papule: Solid, palpable, <1 cm
  • Nodule: Solid, palpable, 1–2 cm, dermal
  • Tumor: Solid, palpable, >2 cm
  • Plaque: Solid, palpable, >1 cm, width > thickness
  • Vesicle: Raised, clear, fluid filled, <1 cm
  • Bulla: Raised, clear, fluid filled, >1 cm
  • Pustule: Raised, pus filled
  • Wheal: Transient, palpable edema




Secondary: Nonspecific Changes Caused by Evolution of Primary Lesions




  • Scale: Accumulation of loosely adherent keratin
  • Crust: Accumulation of serum, cellular, bacterial, and squamous debris over damaged epidermis
  • Fissure: Superficial, often painful break in epidermis
  • Erosion: Loss of epidermis; heals without scarring
  • Ulcer: Loss of epidermis and part or all of dermis; heals with scarring
  • Excoriation: Linear erosion
  • Lichenification: Accentuated skin markings caused by thickening of epidermis; usually caused by scratching or rubbing
  • Scar: Fibrous tissue replacing normal architecture of dermis
  • Atrophy: Epidermal (thinning of epidermis) or dermal (decrease in the amount of collagen or causing depression of skin)




Characterization of Skin Lesions



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Description


Distribution


Duration


Exposure


Signs and Symptoms



  • Primary vs. secondary changes
  • Color
  • Consistency and texture
  • Mobility
  • Configuration
  • Shape
  • Well vs. ill-defined
  • Arrangement
  • Discrete
  • Localized
  • Grouped
  • Disseminated


  • Symmetry
  • Dermatomal
  • Photodistribution
  • Mucous membrane involvement
  • Contact areas
  • Flexor vs extensor surfaces
  • Koebner phenomenon: areas of previous trauma


  • How long?
  • Since birth?
  • Recurrent?


  • Sick contacts
  • Recent travel
  • Medications
  • Personal care products
  • Environmental exposures
  • Occupational exposures
  • Recreational exposures
  • Seasonal variation
  • Family history


  • Local
  • Pruritus
  • Pain and tenderness
  • Paresthesias
  • Bleeding
  • Systemic
  • Fever or chills
  • Malaise or fatigue
  • Arthritis or arthralgias




Atopic Dermatitis and Eczema



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  • Risk factors: Family history, other atopic diseases (asthma, allergic rhinitis), food hypersensitivity, environmental allergens
  • Clinical manifestations: Pruritic, erythematous, scaly papules and plaques → edema, serous discharge, crusting → lichenification, hyperpigmentation, fissuring → superinfection (primarily with Staphylococcus aureus; also with HSV)




Distribution




  • Infantile: Cheeks, forehead, trunk, extensor surfaces
  • Childhood: Wrist, ankle, antecubital and popliteal fossae
  • Adolescent and adult: Flexor surfaces, face, neck, hands, feet




Eczema Complications



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Type


Clinical Features


Treatment or Prevention


S. aureus superinfection


Honey-crusted erosions, pustules, weeping, acute increase in erythema



  • Topical or oral antibiotic
  • Obtain culture

Eczema herpeticum (HSV superinfection)



  • Source of contact often adult caretaker with “cold sore”


  • First-degree lesions: Crops of vesicles on inflamed base at sites of eczema
  • Late: “punched-out” erosions
  • Common associated symptoms: Fever, malaise, irritability, intense itching, eczema flare
  • Severe: Widespread viral dissemination with multiorgan involvement


  • Stop TCS or TCI
  • Acyclovir or valacyclovir
  • Treat for secondary bacterial infection if indicated
  • Treat known contacts
  • Eye exam for periorbital involvement
  • Obtain culture &/or DFA

Long-term TCS use



  • Skin atrophy, ecchymoses, striae, telangiectasias, poor wound healing, perioral dermatitis or steroid rosacea, hypothalamus–pituitary axis suppression with systemic absorption


  • Limit use for flares only (usually <1- 2-wk intervals)
  • Use lower potency TCS for face, underarms, and groin
  • If indicated, evaluate for adrenal suppression and treat appropriately

Postinflammatory pigment changes



  • Hypo- or hyperpigmented macules or patches in areas of previous involvement
  • Fades over months to years

Sun protection and continued treatment of flares of dermatitis


TCS, topical corticosteroid; TCI, topical calcineurin inhibitor





Treatment




  • Maintenance: Short, lukewarm baths or showers under 10 minutes with mild soap; frequent moisturization with thick, bland emollients (cream or ointment)
  • Mild flare: Class 6 to 7 TCS or TCI BID (approved for ≥2 yo; use for ≤2 weeks at a time; good for face); ointment preferred
  • Moderate flare: Midpotency TCS for body BID (eg, triamcinolone 0.1%); ointment preferred; class 6 to 7 TCS or TCI BID for face; oral antihistamines PRN for pruritus
  • Severe flare: Midpotency TCS followed by warm, wet wraps BID for at least 15 min; ointment preferred; then application of emollient; oral antihistamines PRN for pruritus and antibiotics for superinfection




Contact Dermatitis



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Type


Description


Causes


Course


Treatment


Irritant



  • Acute: Erythema, scaling, edema, vesicles, pustules, erosions
  • Chronic: Lichenification, fissures

Results from contact with a substance that chemically or physically damages skin



  • Urine or feces → diaper rash
  • Lip licking or thumb sucking
  • Detergents or solvents
  • Topical medications
  • Battery acid


  • May occur after single contact with a strong irritant or after repeated contact with milder irritants
  • Rash minutes to hours after exposure


  • Avoidance of irritants
  • Emollients, barrier creams
  • May consider TCS if no improvement (controversial)

Allergic (type IV cell- mediated immune reaction)



  • Acute: Erythematous, scaly, vesicular, crusted, weeping
  • Chronic: Lichenification, fissuring, excoriations


  • Poison ivy, oak, sumac
  • Nickel (jewelry, metal clasps, glasses)
  • Rubber (shoes, clothing)
  • Paraphenylenediamine (hair dyes, leather, black-dyed henna)
  • Topical antibiotics (eg, neomycin, bacitracin)
  • Emollients
  • TCS


  • 1° exposure → rechallenged by allergen → dermatitis
  • Rhus (poison ivy, oak, sumac): patchy or linear vesicles or bullae on exposed surfaces 2–7 days after exposure, lasting 3–4wk


  • May use patch testing to confirm diagnosis
  • Avoidance of allergen (may take >6 wk for complete clearing of rash)
  • Topical or systemic corticosteroids

Data from Dermatol Ther 2004;17:334.





Other Eczematous or Papulosquamous Eruptions



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Disease


Description


Course


Treatment


Other


Seborrheic dermatitis (infantile form)



  • “Cradle cap”: Greasy scales on scalp
  • Disseminated: Bilateral, well-demarcated, symmetric pink patches and plaques with scaling in diaper area, retroauricular areas, neck, trunk, and proximal extremities, prominent in skin creases/folds


  • Usually begins 1wk after birth
  • May persist for months


  • Bathing
  • Frequent moisturization
  • Ketoconazole 2% cream if extensive or persistent
  • Short course of low-potency TCS if inflamed


  • Linked with sebum overproduction and Malassezia spp. infection

Keratosis pilaris*



  • Skin-colored follicular hyperkeratotic or erythematous papules on the upper arms, thighs, cheeks


  • May become more pronounced at puberty (some may improve at puberty)
  • Often improves with age
  • Improvement in summer; worsening in winter


  • No definitive treatment
  • May try emollients, lactic acid or glycolic acid creams, urea cream, salicylic acid, short course of TCS for inflamed areas


  • Can be associated with ichthyosis vulgaris, atopic dermatitis

Pityriasis alba



  • Small, ill-defined, symmetric, hypopigmented patches with fine scales, often on cheeks; may be seen on upper extremities


  • May become more obvious in summer on tanned skin
  • May last for months to years
  • Resolves spontaneously

Emollients, low-potency TCS, sunscreen


Pityriasis rosea



  • “Herald” patch: Initial 1- to 10-cm salmon-colored oval patch or plaque with collarette of fine scale, usually on trunk
  • Within days: “Christmas tree” distribution of oval, hyperpigmented, smaller, thin plaques or papules similar to a herald patch on trunk
  • Face, palms, soles usually spared
  • May see oral erosions
  • Inverse pityriasis rosea: Variant involving axillae and inguinal areas; more common in younger children and darker-skinned patients


  • Most common in adolescents and young adults
  • More common in spring


  • Reassurance
  • TCS ± PO antihistamine PRN for pruritus
  • Possible benefit of 14-day course of erythromycin† (controversial)
  • UVB light treatment for severe cases


  • May have mild prodrome: Fever, HA, malaise
  • May be pruritic
  • Lasts 6–8 wk; sometimes months
  • May be mimicked by syphilis (check RPR if indicated)
  • Possible association with HHV-6, HHV-7

Psoriasis



  • Well-demarcated erythematous papules and plaques with thick, silvery scales; often on elbows, knees, scalp, trunk, but can occur anywhere
  • Diaper area in infants
  • Scalp scaling, papules & plaques
  • Nail dystrophy pitting, other


  • Guttate type: Drop-like lesions on trunk, often after streptococcal infections, URI
  • Localized pustular type: Discrete pustules, scaly plaques on palms or soles
  • Generalized pustular type: Erythema with sheets of small pustules, migratory annular erythematous plaques on tongue, possible after corticosteroid withdrawal, fever, arthralgias
  • Koebner phenomenon


  • Topical corticosteroids, calcipotriene, coal tars, phototherapy, methotrexate, cyclosporine, acitretin, TNF-α inhibitors, mycophenolate mofetil
  • Never use systemic steroids because of psoriasis flares when stopped


  • Inverse psoriasis: Variant involving flexural areas

*Cutis 2008;82(3):177.


J Am Acad Dermatol 2000;42:241.


Pediatr Dermatol 2001;18(3):188.





Acne



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Type


Description


Pathogenesis


Treatment


Course


Mild comedonal


Open comedones (blackheads) or closed comedones (whiteheads)


Accumulation of keratinous debris in pilosebaceous unit → occlusion of follicles → sebum accumulation


Topical retinoid ± BPO


Continue treatment for at least 2–3 mo


Moderate to severe comedonal


Same but more extensive


Mild inflammatory


Scattered small papules or pustules


Proliferation of Propionibacterium acnes → inflammation


Topical retinoid ± topical antibiotic ± BPO



  • Until no new lesions, then taper off antibiotics
  • Usually 2–4 mo

Moderate inflammatory


Generalized papules or pustules on face or trunk


Topical retinoid ± oral antibiotic ± BPO


Nodulocystic


Large, deep inflammatory nodules, cysts


Isotretinoin



  • 4–6+ mo
  • Total dose: 120–150 mg/kg

Data from Pediatr 2006;118(3):1188. BPO, benzoyl peroxide.





Acne Treatment



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Treatment Type


Mechanism


Dose


Side Effects


Monitoring


BPO


Bactericidal


2.5%, 5%, and 10% gel, liquid, cream


Dryness, irritation, desquamation, may bleach clothing


Topical retinoid (tretinoin, adapalene, tazarotene)


Normalizes keratinocyte desquamation, anti-inflammatory


Use highest concentration tolerated, pea-sized amount every evening


Dryness, desquamation, irritation, photosensitivity


Topical antibiotics


Eliminate P. acnes from follicles


Erythromycin 2% solution, clindamycin 1% solution


Rarely pseudomembranous colitis with clindamycin


Systemic antibiotics


Reduce resident skin bacteria, inhibit neutrophil chemotaxis, alter macrophage and cytokine production



  • Doxycycline 50–200 mg/d
  • Minocycline 50–200 mg/d
  • Tetracycline 250–1500 mg/d
  • Trimethoprim/Sulfamethoxazole


  • Candidiasis, photosensitivity, GI upset, pseudotumor cerebri
  • Minocycline: Drug-induced lupus, blue-gray hyperpigmentation, drug hypersensitivity

Use Tetracycline, Doxycycline, Minocycline only in patients >8 yo


Isotretinoin


Reduce sebum secretion → decreased P. acnes proliferation, inhibits comedogenesis, anti-inflammatory properties


Total treatment course of 120–150 mg/kg over 4-6+ mo


Teratogenicity, cheilitis, dryness, peeling, photosensitivity, pruritus, hypertriglyceridemia, possible association with depression or suicide,* hepatoxicity, bone marrow suppression, pseudotumor cerebri, IBD



  • Registration with IPLEDGE and two forms of birth control (one may be abstinence)
  • Check monthly: pregnancy test, CBC, liver enzymes, lipid profile

Hormonal


Blocks androgen production → reduces sebum production



  • FDA approved: Estrostep, Ortho Tri-cyclen, Yaz
  • Spironolactone 50–100 mg BID


  • OCPs: Nausea, abnormal menses, weight gain, breast tenderness, thrombophlebitis, pulmonary embolism, hypertension
  • Spironolactone (dose related): Hyperkalemia, abnormal menses, breast tenderness, HA, fatigue


  • Especially useful for those who have premenstrual flares or in PCOS patients
  • Consultation with gynecologist or endocrinologist

* Int J Dermatol 2006;45(7):789.


Am J Gastroenterol 2006;101(7):1569.





Vascular Birthmarks



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Type


Description


Course


Treatment


Other


Hemangioma



  • Circumscribed, bright red masses; blue if deeper
  • More common in girls, preterm or LBW infants, infants from multiple gestations


  • Usually appear within days to few weeks of age
  • Growth phase: First 6–9 mo
  • Slow involution: 50% resolve by 5 yr, 70% by 7yr, 90% by 9 yr


  • Observation for most
  • Vaseline and topical antibiotics for minor ulceration or bleeding
  • Treatment decision based on size, location, functional problems
  • Prednisone, intralesional corticosteroids, vincristine, IFN-α propanolol (isolated reports)*


  • Kasabach-Merritt syndrome: Tufted angioma, kaposiform hemangioendothelioma, platelet sequestration → thrombocytopenia with risk of severe hemorrhage
  • PHACES: Posterior fossa malformation, segmental hemangioma, arterial anomalies, cardiac anomalies, eye anomalies, sternal cleft or supraumbilical raphe
  • Lumbosacral: May be associated with tethered spinal cord or GU abnormalities

Capillary malformation (port wine stain, nevus flammeus)



  • Pink to purple, sharply demarcated patches


  • Present at birth
  • Darken with age
  • Some expand at puberty, with illness or trauma
  • Regression is not expected


  • Observation, symptomatic care, laser, surgery


  • Sturge-Weber syndrome: Port wine stain in V1 distribution, ipsilateral meningeal and cortical vascular malformations, seizures, mental retardation, glaucoma
  • Klippel-Trenaunay syndrome: Ipsilateral hypertrophy of limb or body part (caused by bone and soft tissue hypertrophy) in association with varicose veins, capillary malformation, ± arteriovenous fistulas (Parkes-Weber)

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Jan 9, 2019 | Posted by in PEDIATRICS | Comments Off on Dermatology

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