NUR-507 D4

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Dermatologic Disorders

Chapter 37

Anatomy and Physiology

Epidermis – thin outer layer

Five layers of stratified squamous epithelium

Keratinocytes comprise most epidermal cells

Melanin produced in basal layer

Dermis – thick middle layer

Regulates heat loss

Provides host defenses

Aids in nutrition/regulatory functions

Subcutaneous layer

Primarily adipose tissue

Contains arteries/arterioles for thermoregulation

Anatomy and Physiology

Skin appendages – hair, nails, sweat and sebaceous glands

Terminal hair – scalp, axillae, pubis

Vellus hair – on remainder of body

Nails – keratin – grow continually

Three types of sweat glands

Eccrine – entire body; maintain fluids/lytes/temperature

Ceruminous – external ear canal

Apocrine – axillary, genital, periumbilical – body odor

Sebaceous glands – secrete sebum/prevent excessive evaporation, minimize heat loss, lubricate skin

Pathophysiology and Defense Mechanisms

Disruption of skin/subcutaneous tissue

Bacterial, fungal, viral infections

Allergic and inflammatory reactions

Infestations

Vascular reactions

Papulosquamous and bullous eruptions

Congenital lesions

Hair and nail disorders

Pathophysiology and Defense Mechanisms

Three cutaneous reactions to trauma, infection, inflammation

Pigment lability – postinflammatory hypo- or hyperpigmentation; may be temporary or permanent

Follicular response – prominent papule and follicle formation

Mesenchymal response – scarring, keloids

Special Considerations in Children with Dark Skin

Preventive care

Immunize for varicella to prevent scarring

Use insect repellants

Treat pruritic/inflammatory conditions early

Reduce causes of traction alopecia

Use moisturizing agents/eliminate soaps if dry skin

Use oral antipruritics for dry, itchy skin

Caution about use of topical medications

Avoid trauma/procedures that induce keloids

Special Considerations in Children with Dark Skin

Cutaneous reaction patterns

Pigment lability common

Keloids/hypertrophic scars frequent

Lichenification, vesicular/bullous reactions occur

Normal variations and common problems

Color/texture may vary from one part of body to another

Pigmentation of mucosa/nails correlates with cutaneous pigmentation

Increased melanin in thicker-skinned areas

Line of differentiation between hyperpigmented dorsal/extensor surfaces and less-pigmented ventral surfaces

Mongolian spots/café au lait spots

Special Considerations in Children with Dark Skin

Normal variations and common problems (Cont.)

Normal exfoliation produces gray scales

Color alterations difficult to assess

Erythema may appear as purple tinge

Tightly curled hair tangles when dry/mats when wet

Atopic dermatitis with pityriasis alba and postinflammatory hypopigmentation

Special Considerations in Children with Dark Skin

Cultural/ethnic practices with skin sequelae

Hair pomade – acne

Bleaching creams – discoloration, erythematous nodules

Chemical/thermal hair straighteners – alopecia

Tightly braided hair – traction folliculitis

Henna – orange discoloration of skin

Decorative practices – scars

Coining/cupping – ecchymoses

Assessment of the Skin and Subcutaneous Tissue

History

Onset, duration

Original appearance of lesions/treatments

Associated symptoms

Exposures, medications, allergies

Physical examination

Examination of entire body

Good light/Wood’s lamp

Location, type, color, pattern, distribution

Diagnostic studies

Scrapings of skin for microscopic examination

Microbial cultures

Biopsies/patch testing

Management strategies

Hydration and Lubrication

Bathing – lukewarm water long enough for skin to become moistened; pat skin dry

Environmental considerations – humidity; greater than 90% can macerate skin. Water consumption helps hydrate skin

Skin care agents

Soaps, oils, colloids – non-allergic, mild best

Moisturizers and lubricants – retain water in skin

Hydration and Lubrication

Wet dressings

Moisturize skin, decrease itching, remove crusts

Should be moderately wet/lukewarm water

Apply 10-20 minutes 2-4×/day

Saline, Burow solution used

Apply creams/ointments after wet dressings

Occlusive dressings

Decrease water evaporation

Enhance hydration and absorption of medications

Other considerations

Avoid irritants – wool, sweat, saliva

Milk, eggs, wheat, tomatoes, citrus, chocolate, fish, nuts most common food allergens

Sunscreens and Sunblocks

Protect skin from UV light

Daily application of sunscreen with SPF of 30

Chemical-containing sunscreens applied 30 minutes before exposure to allow binding to stratum corneum

Reapply after swimming, perspiring, washing

Never a substitute for sun protection

Medications

General considerations

Usually topical medications

Restore hydration, alleviate symptoms, reduce inflammation, protect skin, reduce scale/debris, clean, eradicate organisms

Must consider preparation – stabilizers, preservatives, perfumes

Acute inflammation – wet dressings, powders, suspension lotions, alcohol- or water-based lotions, aerosols

Chronic inflammation – creams, oil-based lotions/gels, ointments

Patient’s tolerance for/willingness to use

Dry or humid environment

Medications

Antibacterial agents

Soap, antibacterial soap, topical antiseptics

Avoid neomycin – contact sensitization

Oral antibiotics for more severe infections

Culture/sensitivity if MRSA suspected

Antifungal agents

Many topical antifungal agents are OTC

Oral agents – hair, nail, refractory skin infections

Use oral agents with caution in children

Medications

Antiviral agents

Topical antivirals – cutaneous herpes

Oral antivirals – shorten course; treat recurrent

Wart therapy agents – destroy keratinocytes

Anti-acne agents

Topical keratolytics – relieve follicular obstruction

First-line – benzoyl peroxide/retinoic acid

Combine with other agents for moderate to severe

Topical antibiotics

Systemic antibiotics

Medications

Anti-inflammatory agents

Topical glucocorticoids (Table 37-1)

High potency

Moderate potency

Low potency

Nonfluorinated are less potent/fewer side effects

Key to use – be familiar with a few low-, medium-, and high-potency steroids/use consistently

Potency: ointments > creams > lotions

Rare use of high-potency recommended

Only low-potency on face, buttocks, groin, axillae

Medications

Anti-pruritic agents

Antihistamines for sedation/to relieve itching

Avoid topical antihistamines – contact sensitization

Topical calcineurin inhibitors

Immunosuppressive, nonsteroidal

Expensive; do not use in children <2 years

Scabicides/pediculicides

Toxic to mites/lice

Hair and scalp preparations

Infection, psoriasis, dandruff, dermatitis

Bacterial infections of the skin and subcutaneous tissue

Impetigo

Contagious bacterial infection of superficial layers of skin

Nonbullous – honey-colored crusts (70%)

Bullous – Figure 27-4

Group A streptococcus, S. aureus, or MRSA

Spread through autoinoculation via hands, towels, clothing, nasal discharge, droplets

Impetigo

Clinical findings – history

Pruritus; spread of lesion to surrounding skin

Weakness, fever, diarrhea with bullous impetigo

Clinical findings – physical examination

Nonbullous – 1-2 mm erythematous papules or pustules, progress to vesicles or bullae which rupture – honey-colored crusts

Bullous – large, flaccid, thin-wall, superficial, annular or oval blisters/bullae – rupture

Lesions common on face, hands, neck, extremities, perineum

Regional lymphadenopathy

Impetigo

Clinical findings – diagnostic studies

Gram stain/culture if needed

Differential diagnosis – herpes, varicella, nummular eczema, contact dermatitis, tinea, kerion, scabies

Management

Topical antibiotics if superficial, nonbullous, localized

Oral antibiotics for multiple lesions, spread of infection to family members

Bullous impetigo in infant – parenteral beta-lactamase-resistant antistaphylococcal penicillin

Obtain culture if no response in 7 days

Educate about hygiene

Exclude from day care until treated for 24 hours

Impetigo

Complications

Cellulitis

Lymphangitis

Staphylococcal scalded skin syndrome

Patient and family education

Thorough cleansing of breaks in skin

Pigment changes may last weeks to months

No school/day care until 24 hours of treatment

Cellulitis

Localized bacterial infection of dermis, subcutaneous layers

May be periorbital, perivaginal, perianal, buccal, or involving joint/extremity

S. pneumoniae, S. aureus most common

Clinical findings – history

Previous skin disruption at site

Fever, pain, malaise, irritability, anorexia, chills

Recent sore throat/URI

Anal pruritus, stool retention, constipation

Cellulitis

Clinical findings – physical examination

Erythematous, indurated, tender, swollen, warm areas of skin

Blue to purple tinge associated with H. influenzae

Regional lymphadenopathy

Well-demarcated perianal erythema

Erysipelas – superficial variant – tender, bright red, sharp margins; “orange peel” look

Clinical findings – diagnostic studies

Most treated empirically

CBC/blood culture for ill-appearing child

Culture if pus present

Cellulitis

Differential diagnosis – pressure erythema, giant urticaria, herpetic whitlow

Management

Hospitalization if febrile infant; toxic child

Antibiotic therapy depending on organism

Complications

Necrotizing fasciitis, TSS

Patient and family education

Thorough cleansing of breaks in skin

Keep bites, scrapes, rashes clean/bandaged

Frequent handwashing

Folliculitis and Furuncle

Folliculitis – superficial bacterial inflammation of hair follicle

Furuncle – deeper infection of base of follicle and deep dermis (boil)

Clinical findings – history

Pruritus – folliculitis; tenderness – furuncle

Hot-tub exposure

Irritating surface agent

Occasional fever, malaise, lymphadenopathy

Folliculitis and Furuncle

Clinical findings – physical examination

Discrete, erythematous 1-2 mm papules or pustules on inflamed base near follicle

Face, scalp, extremities, buttocks, back

Nodules with furuncles

Pruritus papules, pustules, deep red/purple nodules in areas under swimsuit

Clinical findings – diagnostic studies

Gram stain culture if needed

Differential diagnosis – candida, tinea, acne, chemical folliculitis

Folliculitis and Furuncle

Management

Warm compresses after bathing

Topical keratolytics

Topical antibiotics

Oral antibiotics

Review of hygiene/avoid shaving

Complications – deep abscess formation

Patient and family education – hygiene

Fungal infections of the skin

Candidiasis

Yeast infection/thrush

Skin or mucous membranes

Normal flora/overgrowth can occur

Infants, obese children, adolescents

Secondary infection with diaper rash or when antibiotics/steroids used

Clinical findings – history

Antibiotic/steroid use

Occurrence of rash in moist, warm area

Candidiasis

Clinical findings – physical examination

Mouth – friable, adherent white plaques on erythematous base (thrush); cracked lips (cheilitis); fissured corners of mouth (angular cheilitis)

Intertriginous areas – bright erythema in flexural folds of neck, axillae, groin

Diaper area – moist, beefy-red macules/papules with satellite lesions

Vulvovaginal area – thick, cheesy, yellow discharge; erythema, edema; itching

Nail plates – transverse ridging; loss of cuticle

Candidiasis

Clinical findings – diagnostic studies

KOH-treated scrapings if treatment failure

Differential diagnosis – erythema toxicum, miliaria, staphylococcal pustulosis, neonatal herpes simplex, congenital syphilis

Management

Thrush

Oral nystatin or gentian violet

Apply to nipples if breastfeeding

Oral fluconazole if resistant to treatment

Candidiasis

Management

Skin infection

Topical antifungals

Hydrocortisone if severe inflammation

Keep area dry and cool/minimize irritation

Discontinue oral antibiotics/steroids if possible

Complications – chronic mucocutaneous candidiasis; paronychia with thumb sucking

Patient and family education – good handwashing

Tinea Corporis

Ringworm – superficial fungal skin infection

Dermatophytes

Transmission by direct contact with humans, fomites, animals

Clinical findings – history

Contact with infection

Clinical findings – physical examination

Annular, oval, circinate lesions with red, scaly borders

Lesions spread peripherally; clear centrally

Often prominent over hair follicles

Multiple secondary lesions may merge

Tinea Corporis

Clinical findings – diagnostic studies

KOH-treated scrapings – hyphae/spores

Fungal culture

Wood’s lamp does not fluoresce most tinea

Differential diagnosis – pityriasis herald patch, nummular eczema, psoriasis, seborrhea, contact dermatitis, tinea versicolor, granuloma annulare, Lyme disease

Tinea Corporis

Management

Topical antifungals

Griseofulvin – tinea faciei, extensive infection, immunosuppression, coexisting tinea capitis

Identify/treat contacts

Exclude from day care/school until 24 hours of treatment

Complications – is response to fungus

Patient and family education – treat or eliminate source of infection; keep skin dry

Tinea Cruris

Jock itch – superficial fungal infection on groin, upper thighs, intertriginous folds

More common in adolescent males

Clinical findings – history

Hot, humid weather; tight clothing; sports or vigorous activity

Often associated with tinea pedis

Clinical findings – physical examination

Erythematous/slightly brown, sharply marginated plaques; raised border of scaling, pustules, vesicles; may have central clearing

Usually bilateral/symmetric

Inner thighs – genitalia usually spared

Tinea Cruris

Clinical findings – diagnostic studies

KOH-treated scraping – hyphae/spores

Fungal culture

Differential diagnosis – psoriasis, candidiasis, contact dermatitis, intertrigo

Management

Same as for tinea corporis

Duration of topical treatment 4-6 weeks

Tinea Pedis

Athlete’s foot – superficial fungal infection

Three clinical forms:

Vesicles/erosions on instep

Occasional fissure between toes with surrounding scale and erythema

Rare diffuse scaling on weight-bearing surface with exaggerated scaling in creases

Clinical findings – history

Sweaty feet/nylon socks or non-breathable shoes

Exposure in family/at school

Itching, intense burning

Microtrauma to feet

Contact with damp areas – pools, showers, locker room

Tinea Pedis

Clinical findings – physical examination

Red, scaly, cracked rash on soles, interdigital spaces, instep

White, peeling lesions progressing to erythematous, vesicular, macerated, fissured, scaly lesions

Dorsum of foot clear

Differential diagnosis – contact dermatitis, dyshidrotic eczema

Tinea Pedis

Management

Keep feet dry; use absorbent antifungal powder

Rinse feet with water/vinegar

Wet compresses for acute, vesicular lesions

Complications – secondary bacterial infections

Tinea Versicolor

Superficial fungal infection; predominantly on the trunk

Caused by yeast-like organism: Malassezia furfur

Clinical findings – history – warm, humid weather

Clinical findings – physical examination

Multiple annular, scaling macules/patches

Hypopigmented in dark-skinned

Hyperpigmented in light-skinned

Guttate or raindrop pattern

Tinea Versicolor

Diagnostic studies – KOH scraping

Differential diagnosis – pityriasis alba, PR, vitiligo, seborrhea

Management

Selenium sulfide lotion or shampoo

Oral antifungal if resistant

Patient and family education

Sun exposure makes lesions appear hypopigmented

Repigmentation takes several months

Absence of flaking indicates effective treatment

Viral infections of the skin

Herpes Simplex

Contagious infections – mild to life threatening/subclinical to severe

Direct contact with secretions/mucocutaneous lesions

Incubation days to weeks

HSV type 1 – oral mucosa, pharynx, lips

HSV type 2 – neonatal infection/vulvovaginitis or genital infection

Both types can be found in all locations

Herpetic whitlow – finger/thumb – swollen, painful

Herpes Simplex

Clinical findings – history

Primary herpes – fever, malaise, sort throat, decreased fluid intake

Primary genital HSV – painful vesicles

Recurrent – painful prodrome of burning, tingling, paresthesia, itching

Clinical findings – physical examination

HSV-1

Gingivostomatitis

Herpes labialis

Herpetic whitlow

Herpes Simplex

Clinical findings – physical examination

HSV-2

Grouped vesicopustules/ulceration

Vaginal mucosa, labia, perineum, cervix in females; penile shaft and perineum in males

Regional lymphadenopathy

Diagnostic studies

Tzanck smear

Viral cultures

ELISA serology

PCR tests

Herpes Simplex

Management

Burow solution compresses

Acyclovir to help shorten course

Topical acyclovir for initial genital HSV

Antibiotics for secondary infection

Oral anesthetics for comfort

Viscous lidocaine

Diphenhydramine/magnesium hydroxide 1:1 rinse

Newborn, immunosuppressed child, lesions in eye – consult

Exclude from day care if child cannot control secretions

Complications – eczema herpeticum, erythema multiforme, Stevens-Johnson syndrome

Herpes Zoster

Recurrent varicella infection – shingles

Reactivation of latent varicella zoster from sensory root ganglia

Rare in childhood

Clinical findings – history – burning, stinging pain, hyperesthesia, tingling

Clinical findings – physical examination

2-3 clustered groups of macules/papules progressing to vesicles

Develop over 3-5 days; last 7-10 days

Commonly follow dermatomes; do not cross midline

Herpes Zoster

Clinical findings – diagnostic studies

Clinical diagnosis

Tzanck smear or viral culture if needed

Differential diagnosis – local cutaneous HSV, impetigo

Management

Burow solution/warm, soothing baths

Antihistamines/analgesics for comfort

Moisturizing ointment

Antiviral medications not recommended unless immunosuppressed

Refer if eyes, forehead, nose involved for ophthalmologic exam

Herpes Zoster

Complications

Rare except in immunocompromised children

Occasionally is initial finding in AIDS

Patient and family education

New vesicles appear up to 1 week

Contagious for varicella until all lesions crusted

Molluscum Contagiosum

Benign viral skin infection

Disappears in weeks to months; not easily treated

Spread by direct contact, fomites, autoinoculation

Clinical findings – history

Itching at site

Possible exposure to molluscum

Clinical findings – physical examination

Small, firm, pink-flesh-colored papules

Become umbilicated with cheesy core/surrounding dermatitis

Single papule to numerous, clustered papules

Can be severe in children with eczema, HIV

Molluscum Contagiosum

Clinical findings – differential diagnosis – warts, cysts, blisters, folliculitis, condyloma cuminatum

Management

Lesions resolve over time

Therapy for comfort, to reduce itching, minimize autoinoculation, cosmetic reasons

Mechanical removal of central core

Irritants (surgical tape) may cause resolution

Topical medications may be beneficial

Cimetidine orally if treatment fails

Report genitally grouped lesions

Evaluate for HIV if hundreds of lesions

Molluscum Contagiosum

Complications

Molluscum dermatitis

Patient and family education

Patients are contagious but no need to exclude from day care or school

Scarring unusual

Warts

Human papillomavirus lesions

Trauma promotes inoculation

Most warts on hands, fingers, elbows, plantar surfaces of feet

Transmission from fomites/skin-to-skin; auto-inoculation frequent; incubation may be years

Clinical findings – history – exposure

Warts

Clinical findings – physical examination

Verruca vulgaris – common warts – elevated, flesh-colored papules

Plantar warts – weight-bearing surfaces; grow inward

Flat warts – face, neck, extremities

Condylomata acuminata – genital mucosa

Differential diagnoses – calluses, corns, foreign bodies, moles, comedones

Warts

Management

Watchful waiting

No treatment necessary if asymptomatic

Avoid harm/scarring if treating

Complications

Scarring from removal

Patient and family education

Multiple/prolonged treatments may be necessary

Infestations of the skin

Pediculosis

Lice – can affect scalp, body, pubic area

Infestation = nits or lice

6-10 eggs/day – nits incubate for 1 week, then hatch and begin laying eggs in 2 weeks

Direct or indirect contact

Head lice not health hazard – do not spread disease

Pediculosis corporis uncommon in childhood – can spread disease

Pubic lice – scalp, eyebrows, eyelashes, pubic area

Pediculosis

Clinical findings – history

Infestation

Dandruff-like substance in hair

Itching of scalp/crawling sensation

Clinical findings – physical examination

Lice can be visualized; nits are small white oval cases attached to hair shaft

Common sites – back of head, nape of neck, behind ears

Body lice – excoriated macules/papules; belt line, collar, underwear areas/regional lymphadenopathy

Pediculosis

Diagnostic studies – tests for other STIs if pubic lice found

Differential diagnosis – scabies, dermatitis herpetiformis, necrotic excoriation

Management

Correct diagnosis imperative

Treat when live lice/viable nits present

Treatment failure common due to resistance

Pediculosis

Management (Cont.)

Pediculicides are first-line treatments

Permethrin – first choice

Then remove nits – use special comb

Then cleanse environment

Launder sheets, towels, clothing, headgear

Store items that cannot be washed/dry-cleaned in plastic bag for 2 weeks

Vacuum play areas

Soak brushes, combs, hair accessories in pediculicide

Pediculosis

Complications

Secondary bacterial infection

Patient and family education

Daily to weekly checks for lice

Educate about course, that lice not a social disease, need to avoid excessive/unnecessary treatment

Discourage “no nit” policies in schools

Scabies

Sarcoptes scabiei – a mite; burrows into epidermis – causes intense itching

Highly contagious – close contact, sharing clothing/linen

Female mite lays up to 3 eggs/day; hatch in 3-4 days – life span of 15 days

Clinical findings – history

Itching; worse at night; progressively intense

Fitful sleep, crankiness

Scabies

Clinical findings – physical examination

S-shaped burrows; webs of fingers; sides of hands; folds of wrists, armpits

Vesiculopustular lesions in infants/young children

Secondary lesions – itchy papules, red-brown nodules

Clinical findings – diagnostic studies

Microscopic exam of scrapings; do not use KOH

Burrow ink test to stain burrow

Scabies

Differential diagnosis – papular urticaria, dermatitis, insect bites, folliculitis

Management

Pharmacological treatment – scabicide in thin layer to entire body; reapply in 7 days

Permethrin – apply from neck down; rinse off in 8-14 hours

Simultaneous treatment of close contacts

Wash linens, clothing; vacuum house

Store non-washable items in sealed plastic bags

Complications – secondary bacterial infection

Patient and family education – rash/itching persist up to 3 weeks

Allergic and inflammatory reactions of the skin

Acne Vulgaris

Inflammatory disorder – excess sebum, keratinous debris, bacteria accumulate

Produce inflamed or noninflamed microcomedones

May cause permanent scarring/decreased self-esteem

Four mechanisms

Sebaceous follicles plugged with keratinous material

Colonies of anaerobic bacteria grow

Sebum/androgen production expand follicle

Inflammation, pustules form

Acne Vulgaris

Clinical findings – history

Family history

Pubertal development/menstrual history

Facial/hair products used

Oral/topical medications

Treatments/results

Sports, jobs

Other medical conditions

Acne Vulgaris

Clinical findings – physical examination

Noninflammatory lesions

Microcomedone – follicular plug; localized on face and trunk

Open comedone (blackhead) – papule; blockage at mouth of follicle; face, upper back, shoulders, chest

Closed comedone (whitehead) – semisoft; precursor to inflammatory acne

Inflammatory lesions

Secondary to rupture of noninflamed lesions

Papules, pustules, excoriation, crusting, nodules, cysts, scars, sinus tracts

Acne Vulgaris

Differential diagnosis – cosmetic/drug-induced acne, rosacea, flat wart, folliculitis

Management

Reduce excess sebum production

Counteract desquamation of epithelial cells

Decrease proliferation of bacteria

Prevent/decrease scarring

Choice of treatment depends on extent, severity, duration of disease, type of lesions

Table 37-7, Box 37-7

Acne Vulgaris

Education

Wash face twice daily with mild soap

Only use noncomedogenic products

Identify aggravating substances/factors

Medications

Topical keratolytic/comedolytic agents – minimize follicular obstruction

Topical retinoids – tretinoin, adapalene, tazarotene

Antibacterial/keratolytics – benzoyl peroxide (BPO), azelaic acid

Acne Vulgaris

Medications (Cont.)

Topical antibiotics – control inflammatory process

Topical clindamycin, erythromycin, sulfacetamide

Topical erythromycin or clindamycin with BPO

Oral antibiotics – to decrease bacteria; use for shortest time possible

Tetracycline

Erythromycin

Minocycline

Doxycycline

Acne Vulgaris

Medications (Cont.)

Oral retinoids – severe, recalcitrant acne; contraindicated in pregnancy; required evaluation by dermatologist, iPledge

Hormonal/other therapies – in females to oppose effects of androgens on sebaceous glands

Noncomedogenic moisturizers – for dryness common with treatment

Complications

Treatment failure – may be from lack of motivation or education

Decreased self-esteem/poor body image

Contact Dermatitis

Acute or chronic inflammation from hypersensitive reaction to substance

Dry skin dermatitis – low humidity, excess soap

Nickel dermatitis – jewelry, belts, snaps

Lip-licker dermatitis – frequent lip licking

Phytophotodermatitis – sun exposure after contact with plants/juices

Plant oleoresins – poison ivy, oak, sumac

Juveline plantar dermatosis – mimics tinea pedis

Latex dermatitis – contact with latex

Contact Dermatitis

Saliva, urine, feces; baby wipes, bubble bath, adhesives can cause – diaper dermatitis

Allergens can cause contact dermatitis

Sensitization to allergen with subsequent type IV delayed hypersensitivity response

Shoes, nickel, wool/rough clothing, topical medications, soaps, preservatives, poison ivy

Contact Dermatitis

Clinical findings – history

Contact with new/unusual substances

Repeated exposure to any substance

Diarrhea/infrequent changing of diapers

Rash localized to specific area

Clinical findings – physical examination

Area of involvement/shape of rash

Severity depends on length of exposure

Chafed, shiny, mild to severe erythema, peeling, fissures, red patches – due to irritant

Erythema, vesicles, weeping in acute stage

Hyperpigmentation/lichenification in chronic conditions

Id reaction – secondary, “sympathy” rash

Contact Dermatitis

Differential diagnosis – atopic dermatitis, impetigo, herpes, psoriasis, seborrhea

Management

Burow solution

Emollients to restore moisture

Topical corticosteroids

Do not use flavored lip creams for lip-licking dermatitis

Oral antihistamines

Refer to dermatologist/allergist if worsening

Diaper Dermatitis

Most frequent contact dermatitis

Improper hygiene/cleansing

Chemical irritation – prolonged contact with irritants – urine, feces, products

Mechanical irritation from diapers

Occlusion of skin from diapers/plastic pants

Aggravation of other skin conditions by wearing diapers

Diaper Dermatitis

Clinical findings – history

Type of diapers used; recent changes

Frequency of wet diapers/stools

Frequency of diaper changes/methods of cleaning

Any new baby care products

Medications

Recent use of antibiotics

Clinical findings – physical examination

Chemical causes – shiny, peeling, erythematous rash

Mechanical causes – erythematous, macerated or dry

Hygiene causes – any finding; poor general hygiene

Diaper Dermatitis

Differential diagnosis – contact dermatitis, infection, atopic dermatitis, psoriasis, seborrhea, scabies

Management

Prevention best!

Frequent diaper changes

Use greasy lubricant if skin is dry

Protective barrier ointment

Use thick, absorbent diapers

Diaper Dermatitis

Management (Cont.)

Expose area to air

Burow solution if weepy

Zinc oxide to decrease friction/moisture

Hydrocortisone cream

Increased fluids to dilute urine

Add topical antifungal cream if no response

Complications – secondary infection; refer to dermatologist if severe erosions, bullae, large papules/nodules, purpura

Seborrheic Dermatitis

Chronic inflammatory dermatitis

Cradle cap in infants; dandruff in adolescents

Overproduction of sebum and perhaps a saprophytic yeast

Clinical findings

History – age of onset

Physical examination – erythematous, flaky crusts of yellow, greasy scales on scalp, face, diaper area; mild flakes with dandruff; not pruritic

Differential diagnosis – atopic dermatitis, candida

Seborrheic Dermatitis

Management

Antifungal agents – azoles, selenium sulfide

Anti-inflammatory agents – topical steroids, calcineurin inhibitors

Keratolytic agents – salicylic acid, urea

In young children/infants:

Apply mineral oil to scalp before shampooing

Remove scales with brush/toothbrush

Facial dermatitis – ketoconazole topical preparation

Scalp dermatitis – medicated shampoos/steroids

Complications – secondary infections

Drug Eruptions

Variety of skin reactions to drugs; most common:

Morbilliform

Urticarial

May be immunologic or nonimmunologic

Most common drugs: NSAIDs, penicillins, cephalosporins, suflonamide antibiotics, anticonvulsants, oral fluconazole/ketoconazole

Drug Eruptions

History

Medications in past 3 weeks

Degree of itching

Possible systemic symptoms

Physical examination

Usually symmetric, macular erythematous rash; becomes papular/confluent

Begins on trunk; spreads to extremities

Diagnostic studies – any needed for differential diagnosis

Drug Eruptions

Differential diagnosis – viral exanthem, toxic erythema

Management

Discontinue drug

Antihistamines if itching

Systemic steroids not usually indicated

Refer if no improvement

Complications – body heat/water loss; progression may lead to toxic epidermal necrolysis or SJS

Patient and family education – may worsen before improving; risk with further exposure; wear medical alert if life-threatening allergy

Vascular reactions of the skin

Urticaria and Angioedema

Hypersensitivity reactions; usually type I – IgE-mediated

Urticaria – superficial dermis

Angioedema – deeper dermis/subcutaneous

Antigen-antibody responses – histamine release – other mediators – vasodilation and increased vascular permeability

Urticaria and Angioedema

Possible causes

Reactions to foods, stings, bites, parasites, pollen

Skin contact with chemicals, latex, caterpillars

Bacterial, viral, fungal infections

Cholinergic response to heat, cold, sun, water

Drugs

Genetic origin

Inflammatory systemic disease

Immunologic

Idiopathic

Urticaria and Angioedema

Clinical findings – history

Family/previous history

Atopy

Itching/scratching

Ingestion of foods/drugs; injections of agents

Infections

Inhalation of dander, pollen, dust, smoke, aerosols

Bites

Cold, heat, exercise, sun, water, pressure, vibration

Clinical findings – physical examination

Urticarial rash

Location of lesions may indicate causative agent

Angioedema – may involve upper airway – life-threatening

Urticaria and Angioedema

Diagnostic studies – refer to allergist if possible anaphylaxis for testing

Differential diagnosis – contact dermatitis, atopy, erythema multiforme

Management

Identify/remove offending substance

Oral antihistamines

Topical antipruritics

Aqueous epinephrine

Prednisone

Urticaria and Angioedema

Complications

Anaphylactic symptoms

Serum sickness

Patient and family education

Causes, course, treatment

Avoid allergen; wear medical alert bracelet

Refer for hyposensitization if life-threatening symptoms

Epinephrine kit

Erythema Multiforme, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis

EM a distinct disorder that does not progress to SJS or TEN

EM usually benign, acute, self-limited

SJS, TEN – syndrome; exist in a continuum

EM usually follows infection; is recurrent

Erythema Multiforme, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis

Clinical findings – history

EM – recent/current infections; exposure to UV light/trauma to area; low-grade fever, malaise

SJS/TEN – medications; SJS may be caused by virus; fever, sore throat; arthralgia with SJS

Erythema Multiforme, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis

Clinical findings – physical examination

Lesions vary within episode, from one patient to another

Dusky, red macules evolve into target lesions with multiple concentric rings

Fixed, symmetric, on face, extensor surfaces of arms and legs, dorsum of hands and feet, palms and soles

Oral mucosa commonly involved

Erythema Multiforme, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis

Clinical findings – physical examination

SJS

Erythematous macules on head and neck; spread to trunk and extremities

Blister formation within hours; often hemorrhagic

Mucosal involvement of eyes, nose, mouth

TEN

Rapidly coalescing target lesions; widespread bullae

Full-thickness epidermal peeling in 24 hours

Conjunctivae, urethra, rectum, oral/nasal mucosa, larynx may or may not be involved

Erythema Multiforme, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis

Management

Care for EM supportive, self-limited

Mild analgesics, cool compresses, oral antihistamines

Topical intraoral anesthetics; debridement with hydrogen peroxide

Wound care

IV fluids if dehydration

Systemic antihistamines, analgesics, antimicrobials

SJS/TEN – potentially life-threatening

Hospitalize to PICU, burn unit for IV fluids, IVIG

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Papulosquamous eruptions of the skin

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Pityriasis Rosea

Common, mild, self-limiting

Clinical findings – history

Prodrome of mild symptoms

Clinical findings – physical examination

Herald patch – 2-5 cm ovoid lesion

Symmetric, small macular/papular, pale pink lesions

Christmas tree pattern, itching

Differential diagnosis – psoriasis, nummular eczema, scabies, tinea

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Pityriasis Rosea

Management

Calamine lotions; Aveeno, antihistamines, emollients

Minimal sun exposure

Oral erythromycin may hasten resolution of rash

Patient and family education

Benign, self-limited, noncontagious

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Psoriasis

Chronic papulosquamous skin disorder

Spontaneous remissions/exacerbations

Thick silvery scales, varied distribution

Immune-mediated disorder

Guttate – after streptococcal infection

Clinical findings – history

Family history

Streptococcal infections

Trauma before onset

Itching is variable

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Psoriasis

Clinical findings – physical examination

Scalp, elbows, knees, buttocks most common

Plaque – discrete, symmetric, well-marginated rash becoming papular with silver scales

Guttate – teardrop – widespread, symmetric, round or oval lesions on trunk/proximal extremities

Psoriasis vulgaris – well-circumscribed, erythematous plaques; thick silvery-white scales on elbows, knees, scalp, hairline

Koebner phenomenon – lesions occur in areas of injury

Auspitz sign – bleeding when scale removed

Napkin or diaper area – eczematous appearance

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Psoriasis

Diagnostic studies – ASO if guttate pattern; KOH-treated scrapings to rule out fungus; VDRL to rule out secondary syphilis

Differential diagnosis – seborrhea, candida, dermatitis, atopy

Management

Sun exposure in moderate amounts

Emollient creams

Topical steroids

Tar or keratolytic shampoos

Mineral oil to soften plaques

Referral to dermatologist

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Psoriasis

Complications

Candida infection

Erythrodermic/pustular psoriasis

Exfoliative erythroderma

Psoriatic arthritis

Patient and family education

Chronic with remissions/exacerbations

Guttate psoriasis often resolves with antibiotics

Lifestyle changes to prevent recurrence

Improves in summer/with pregnancy

National Psoriasis Foundation referral

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Lichen Striatus

Peculiar to childhood

Unilateral shiny papules along embryonic lines

Cutaneous defect from embryologic mutation

Spontaneously disappear with occasional short relapses

History – spontaneous appearance

Physical examination – linear, shiny, hypopigmented with adherent scale on one extremity

Differential diagnosis – lichen planus, lichen nitidus, psoriasis

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Lichen Striatus

Management

Resolve without treatment in 1-2 years

Lubricants/topical steroids to reduce scale and inflammation

Patient and family education

Benign, self-limited

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Keratosis Pilaris

Extensor aspects of extremities, buttocks, cheeks

“Chicken skin” appearance – small bumps

Common in children with atopic disorders

History – spontaneous appearance

Physical examination – rough dry skin; small papules, occasional diffuse eruption

Diagnostic studies – clinical diagnosis

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Keratosis Pilaris

Management

Lubricants/emollients to moisturize

Topical keratolytics

Antibiotics if folliculitis occurs

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Congenital lesions of the skin

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Vascular and Pigmented Nevi

Nevi common in children

Vascular nevi – malformations/hemangiomas

Pigmented nevi – mongolian spots, café au lait spots, atypical nevi

Vascular nevi – structural abnormality or overgrowth of blood vessels

Pigmented nevi – overgrowth of pigment cells

Atypical nevi – precursors for malignant melanoma

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Vascular and Pigmented Nevi

History

Age first noted; at birth

Progression of lesion

Familial tendencies

Physical examination

Vascular malformations present at birth; grow with child

Hemangiomas emerge by 2-3 weeks, proliferate, may ulcerate; eventually involute; may have residual changes

Pigmented nevi – present at birth or acquired

Atypical nevi – irregular, poorly defined borders; variable pigmentation

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Vascular and Pigmented Nevi

Management

Salmon patches – fade with time; no treatment

Port-wine stains – permanent defect; may need referral for possible laser treatment

Hemangiomas – reassurance about nature/course; refer if lesions on eyes, lips, oral cavity

Mongolian spots – document fade with time

Blue nevus – may develop melanoma

Café au lait – refer to rule out neurofibromatosis

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Acanthosis Nigricans

May be hereditary

Endocrine disorders – insulin resistance, hypothyroidism

Obesity

Drug administration – OCPs

Malignancy

Clinical findings

Symmetric, brown thickening of skin

Becomes velvety, leather, warty, or papillomatous

Axillae, neck, groin, belt line, dorsal surfaces of fingers, mouth, areola of breast, around umbilicus

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Acanthosis Nigricans

Differential diagnosis – terra firme-form dermatosis, which can be removed with rubbing alcohol

Management

Determine/treat underlying causes

Topical retinoic acid for thicker lesions

Patient and family education

Teach about underlying cause

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Vitiligo and Hypopigmentation Disorders

Lack of skin pigment – white/light-colored areas

Congenital or acquired; diffuse or localized

History

Family history

Onset of depigmentation

Systemic or skin diseases

Recent trauma to skin

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Vitiligo and Hypopigmentation Disorders

Physical examination

Vitiligo – flat, milk-white macules/papules; symmetric or asymmetric; few to multiple

Hypopigmentation – macules, patches; linear or patterned

Diagnostic studies – skin biopsy, CBC, endocrine function

Differential diagnosis – pityriasis rosea, pityriasis alba, tinea versicolor, albinism

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Vitiligo and Hypopigmentation Disorders

Management

Vitiligo – sunscreens, cover-up agents; mild to moderate steroids; referral if indicated

Hypopigmentation – reassure that repigmentation will occur

Complications

Other immune disorders with their complications

At risk for severe sunburn

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Hair and nail disorders

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Tinea Capitis

Ringworm of scalp

History – hair loss, itching, contact with infected person or pet

Physical examination

Scaling, erythema, crusting

Bald patches

Occipital or posterior cervical adenopathy

Diagnostic studies – KOH-treated scraping; Wood’s light fluoresces yellow-green; fungal culture of plucked hair is most reliable

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Tinea Capitis

Differential diagnosis – traumatic alopecia, alopecia areata, seborrhea, atopic dermatitis, impetigo

Management

Topical antifungals ineffective

Griseofulvin for 6-8 weeks

Shampoo with selenium sulfide

Clinical monitoring if change in status

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Tinea Capitis

Complications – id reaction to fungus

Patient and family education

Sites and modes of transmission

Side effects of medication

Hair regrowth is slow

Launder sheets, clothes in hot water/hot dryer

Grooming practices may predispose

High rate of asymptomatic carriers

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Traumatic Alopecia

Incomplete hair loss; hair of varying lengths

Chemical exposure, thermal damage, traction

African-American females from cornrows, ponytails, braids

Trichotillomania – repeated hair pulling or twisting

History

Hair styling methods

Habits – nail biting, hair pulling

Recent change or stress

Medications

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Traumatic Alopecia

Physical examination

Possible erythema/pustules

Thinning/breaking of hair

Circumscribed hair loss

Differential diagnosis – tinea capitis, alopecia areata, child abuse

Management

Traction alopecia – avoid hairstyle/device; mild shampoos; antibiotics if pustules present

Trichotillomania – teach parents/apply oil to hair at night; behavior modification may be needed

Complications – trichobezoars

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Alopecia Areata

Asymptomatic, complete hair loss

Cause unknown; may be autoimmune

History – other family members

Physical examination – hair loss without erythema or scaling; nail ridge/pitting; possible atopic dermatitis or vitiligo

Diagnostic studies – rule out tinea; skin biopsy, thyroid screening

Differential diagnosis – tinea capitis, traumatic alopecia

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Alopecia Areata

Management

Open discussion/support

Refer to dermatologist for extensive involvement

Refer to National Alopecia Areata Foundation

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Onychomycosis

Fungal infection of nails

Destroys nail integrity; separates nail plate from nailbed

History – thickened, discolored nail

Physical examination

Opaque white/silvery nail becomes thick/yellow

Toenails more commonly involved with tinea

Fingernails more common with candida

Seldom symmetric

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Onychomycosis

Diagnostic studies – KOH preparations

Differential diagnosis – psoriasis

Management

Often requires oral medication

Cure is difficult

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Paronychia

Acute/chronic infection around a nail

History – tenderness/drainage

Physical examination – erythema, tenderness, purulent exudate, broken/absent cuticle

Diagnostic studies – culture of exudate

Differential diagnosis – herpetic whitlow

Management

Oral antibiotics

Loosen cuticle from nail

Frequent warm soaks

Care and trimming of nails

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Tattoos and Body Piercing

Most done in unregulated, unlicensed tattoo parlors

History – when and where was this done

Physical examination – signs of infections, erythema, crusting, scabs

Management

Tattoos – basic wound care

Piercings – clean twice daily; observe for infection

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Discussion Questions

What factors do you need to consider when prescribing topical preparations for skin disorders?

You diagnose a 3-year-old to have eczema; the mother has a history of eczema and continues to suffer skin lesions as an adult. Describe your management of this child. What techniques will you use in counseling families about skin care for children with eczema?

There is an outbreak of lice in the community. What role can you play in helping to solve the problem?

A 13-year-old male comes for a well-child visit. He is doing well in school and is a star basketball player. Mom is very concerned about his acne and spends 5 minutes of the visit telling you how she had severe acne growing up. She does not want her son to get severe acne. On examination, there are several small whiteheads on his forehead and a few blackheads on his nose. There are no pustules, nodules, or cysts. How severe is his acne? What would be your treatment? What else do you need to discuss with this family?

A 5-year-old with impetigo was placed on Keflex 2 days ago. The family reports compliance with the medication, but the impetigo is spreading. What is the likely pathogen? How would you manage care for this child?

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