U3 medicine - pediatric dermatology

biopsy methods

1. shave biopsy

-horizontal section of the skin if removed for diagnosis or treatment -used for aised lesions; benign tumors; or lesions that are suspicious for skin cancer

2. punch biopsy

-standard punch device is used ranging from 2-8mm in diameter

-used for inflammatory diseases, unknown rashes, cysts, alopecia Safolyma

3. excision

-lesion is completely removed with margins

-used for dysplastic/atypical nevus, superficial skin cancers, atypical pigmented lesions, cysts, lipomas

nevus sebaceous

area of no hair growth

congenital hamartoma composed of malformed sebaceous glands, apocrine glands and follicular units

represents a defect in the cutaneous embryologic development

M/C affects the head and neck, with scalp being the most common area

Initially presents as a solitary, well-circumscribed, oval or linear, hairless, pink/yellow/orange/tan plaque

can present as a large pedunculated lesion at birth

at puberty, lesions will thicken, become darker and more papular/verrucous, +/- friable or pruritic

nevus sebaceous

clinical diagnosis

complete surgical excision remains treatment of choice ➢

-due to warty proliferation, permanent alopecia and development of secondary tumors

-RBA for removing lesion during infancy vs. late childhood/early pubert

nevus simplex

aka salmon patch

most common vascular birthmark of infancy

etiology is unknown

30-40% of newborns

Ill defined, flat, dull pink or red, blanchable patch

common on posterior scalp, glabella, forehead, upper eyelids, nose, and upper lips

NS becomes darker with crying and physical exertion

>95% of lesions on the face have complete resolution within 2 years of life

occipital lesions can persist for longer time frames and sometimes no resolution

nevus simplex

or salmon patch

nevus flammeus (port wine stain)

congenital capillary malformation

presents as a deep pink to red-purple discoloration of the skin on the head/neck

unknown pathogenesis

presents at birth as a flat, well demarcated, pink to dark red, blanchable patch commonly on the face

usually unilateral

lesions darken progressively overtime and can also thicken

PWS in a high risk area such as face, midforehead, glabella, upper eyelids, dermatotal capillary malformation on the back etc) -> refer to pediatric dermatologist to rule out any syndrome associations

if no association with any syndromes - can be treated as a cosmetic concern -> early initiation of PDL treatment can lead to complete clearance in infancy

cafe au lait spots

light brown flat macules noted at birth

commonly children will have less than 3 isolated spots

light brown, evenly pigmented, round to oval, flat macules or patches

lesions persist and remain stable over lifetime

6 or more spots should prompt consideration for neurofibromatosis (refer to Pediatric Dermatology)

no treatment needed

reassurance

spitz nevus (epitheloid cell nevus)

melanocytic neoplasm that develops in children

formerly known as "benign juvenile melanoma"

present as pink or flesh colored, dome shaped papule or nodule; can appear to be dark brown to black purple

common on head/neck or lower extremities

lesions rapidly grow over 3-6 month period and then stabilize

management

-complete excision recommended for Spitz nevi with atypical features (size >1cm, ulceration, asymmetry)

infantile hemangioma

most common tumor of infancy; 5-10% of all infants

more common in female patients and in low birth weight newborns

IHs are not present at birth; they develop the first few weeks of life with a precursor lesion that can appear as a blueish bruise like patch, telangiectasia with a rim of pallor or a red flat stain

infantile hemangioma

radiology shows well defined mass with high flow vessels

3 clinical subtypes

1. superficial (upper dermis; bright red with a finely lobulated surface; strawberry hemangiomas; change to purple-red and gray during involution)

2. deep (lower dermis; warm, ill defined, light blue-purple, rubbery nodules or masses

3. mixed (Superficial and deep components; well defined red plaque overlying a poorly circumscribed bluish nodule

infantile hemangioma

complications

-ulcerations

-disfigurement

treatment

-monitor lesions

-topical timolol; superpotent CS for superficial lesions; intralesional CS for thicker lesions

-systemic therapy: Oral propanol, oral prednisone

>consider systemic tx if vision or airway threatened; potential for disfigurement of nose, lip or face; severe ulceration or high output cardiac failure

-surgical excision

sebaceous gland hyperplasia

maternal androgens stimulate sebaceous glands

yellow to white/skin colored monomorphic tiny macules and elevated papules on the nose, cheeks, forehead, upper lips

tx: reassurance it will go away

milia

-tiny epidermal cysts that are common the face of newborns

-lesions consist of trapped keratin underneath the epidermis

-tiny pinpoint white or yellow superficial papules, commonly on the cheeks, nose, chin and forehead

-40-50% of newborns affected; self resolve within a month

-no treatment necessary in newborns

-if persists or in older children- can perform manual extraction using a comedone extractor or 11 blade

-topical retinoids = tretinoin

erythema toxicum neonatorum

common idiopathic, self limited eruption in healthy full term newborns

affects up to 50% of all full term babies; it is rare in premature infants

usually not present at birth, develops on the 3rd or 4th day of life; begins as ill defined pink macules or edematous papules that later develop into yellow to pale pink papules or pustules

common face, trunk and extremities - palms and soles typically not involved

self resolves without sequalae over several days

sucking blisters

blisters or erosions on the extremities in newborns due to vigorous sucking in utero

single, oval shaped, superficial vesicle or bullae or an erosion with a collarette of scale

usually on the dorsal hands or fingers; forearms and sometimes on the lips

usually self resolve within 2 weeks

vaseline ointment can be used for healing

miliaria

common vesicular eruption seen in first few weeks of life

results from keratin plugging of immature neonatal eccrine sweat ducts with trapping of sweat in the skin ●

the trapped sweat triggers a localized inflammatory response called miliaria rubra

triggers: excessive swaddling, heat, fever, occlusive dressings

miliaria rubra "prickly heat": grouped, small pink to red papules or vesicles with a surrounding rim of erythema

commonly seen on occluded areas of body- body folds; back

palms and soles never affected

miliaria

rule out infectious etiology

spontaneous resolution with cooling

avoid excessive heat, humidity and swaddling

avoid use of thick ointment in hot/humid climates

use loose fitting cotton clothing; cool baths and air conditioning during hot temp

mottling (cutis marmorata)

unique infant response to cold

physiologic response of the dermal capillaries to cooler temperatures

cool ambient temperatures causes vasodilation of capillaries

affects 50% of children

symmetric, blanchable, reticulated deep red to violaceous patches

commonly on the extremities; less often on the trunk

resolves with rewarming

usually completely resolves with no sequelae

clinical diagnosis; evidence of resolution with rewarming is confirmatory

neonatal acne

neonatal cephalic pustulosis

~25% of neonates are affected

fares are associated with an inflammatory response to Malassezia spp and increase rate of sebum secretion during neonatal period

flare ups present at 2-3 weeks of life

discrete erythematous papules/pustules on cheeks, forehead, chin, scalp, chest

self limited, asymptomatic, resolved spontaneously in weeks to months

neonatal acne treatment

self resolves within 3-6 months of age

gentle cleanser and moisturizer daily

if severe, Ketoconazole 2% cream or econazole 1% cream twice daily, +/- Hydrocortisone 1% cream

avoid oils, ointments/occlusives

infantile acne

commonly seen in boys between ages of 3-6 months

due to increased androgens (elevated levels of LH and testosterone) and sebum excretion

in infant boys, testes produce LH and testosterone to levels that can rise equal to those seen in puberty

infantile acne is typically similar to acne vulgaris seen in adolescents

mixture of acneiform papules, pustules, open/closed comedones, cysts

lesions can be on the cheeks, forehead, chin and back

management = topical retinoid (Tretinoin 0.025%) + topical antibiotics (Benzoyl Peroxide 2.5%/5% + clindamycin 1%)

in severe cases, oral antibiotics may be warranted (Erythromycin vs. Bactrim)

acne vulgaris

disorder of the pilosebaceous unit

begins in puberty; however, may present in 4th or 5th decade of life

pathogenesis

-increase in sebum production (by androgens) and retention of sebum

-keratin and sebum plugging of hair follicle (comedone formation)

-overgrowth of P. acnes (release of enzymes and stimulates release of pro-inflammatory cytokines)

-inflammatory response

-hyperandrogenism

acne vulgaris

classification = comedonal- open or closed , inflammatory- papules or pustules , nodulocystic- nodules and/or cysts

distribution = face, neck, upper trunk, upper arms (sebaceous glands are abundant)

comedones are hallmark of acne; tiny, flesh colored, white or black non inflamed lesions

mild tenderness, pain, itching

inflammatory papules, pustules, cysts, scarring, post inflammatory hyperpigmentation

complications

-scarring, pigmentation changes, poor quality of life, depression, anxiety

acne treatment

avoid any use of oils, fragranced products to the face

gentle cleanser and moisturizer (oil free)

avoid any OTC products, TIKTOK prescribed treatments

avoid picking lesions- leads to scarring

diet: decrease intake of sugar/fatty foods

prescriptions can take about 2-3 months to be effective- STAY COMPLIANT, do NOT SWITCH medications unless necessary due to side effects

topical retinoids

-tretinoin, adapalene, tazarotene, trifarotene

-effective for comedonal acne; scarring; anti-inflammatory properties- preventing formation of inflammatory papulopustular lesions

-generally, will start with Tretinoin 0.025% and increase in % over time

-main side effect: dryness/flaking of skin/irritation

-have pt start using it 2-3 nights per week, pea sized amt applied at bedtime mix with moisturizer, increase to nightly as tolerated over 4-6 weeks

topical benzoyl peroxide

-antibacterial and comedolytic properties

-start with 2.5% and increase in %

-can consider combination formulations with topical antibiotics (clindamycin or erythromycin)

-side effects: erythema, scaling, irritation, xerosis, skin tightening, burning

mild acne treatment

topical antibiotic + topical benzoyl peroxide+ topical retinoid

topical antibiotics

-clindamycin phosphate topical 1%: solution, gel, lotion and pledget

-clindamycin/BP combination

-topical dapsone

-erythromycin 2% -

-erythromycin/BP combination

-topical minocycline

-topical azelaic acid

topical retinoids - same as comedonal

moderate acne treatment

mild Acne treatment + addition of oral medication

antibiotics = tetracyclines, doxycycline, minocycline

alternative antibiotics

-TMP-SMZ

-Cephalexin

-Azithromycin

-Spironolactone

severe acne treatment

acutane = Isotretinoin

vitamin A analogy

monotherapy - pt discontinues topical and oral treatments

patients need to be off doxy for at least 2 weeks prior to starting

contraindicated in pregnancy

warts

caused by HPV

transmitted by skin to skin contact

virus infects epidermal keratinocytes which stimulates cell proliferation

virus found in moist, warm environments

presents as papillomatous, corrugated, hyperkeratotic growth that is confined to the epidermis

warts

4 variants

1. common warts

-on hands, fingers

-exophytic growth that disrupts fingernails

2. plantar warts

-on feet

-endophytic growth, grows inward

3. flat warts

-common on face, legs, hands

4. filiform warts

-common on face, nose, mouth, eyelids

-tan, slender, finger like projections

wart treatment

duct tape occlusion

SA preparations (compound w duofilm)

cryotherapy

topical

-Imiquimod

-topical retinoids

-topical chemotherapy Efudex

wart treatment

in office

1. cryotherapy with LN2 using a cotton swab or cryogun

-5-10 sec freeze times; repeated free-thaw cycles; repeat every 2-3 weeks

-cons: painful, blisters, hypopigmentation, scarring, multiple visits

2. cantharone- "beetle juice"

-applied directly onto the wart; left on for 4-8 hours

-generally will form a blister 1-2 days after tx

-cons: blisters, scarring, painful

3. surgical excision- dependent on site and age of child

4. laser ablation using CO2 laser

molluscum contagiosum

superficial viral injection common in toddlers and school aged children

member of the Poxvirus family

spread by skin-to-skin contact; wet towels gyms, school equipment, pools

presents with dome shaped, waxy, pearly papules with a central white core or umbilication

can present anywhere on the body; but very commonly on the axillae, groin, buttocks, posterior thighs, popliteal fossa

molluscum dermatitis- eczematous flare around the MC lesions

molluscum contagiosum treatment

in office

1. cantharidin therapy

2. cryotherapy-

3. curettage

prescription therapy

-Imiquimod cream

-tretinoin cream

-potassium hydroxide

impetigo

superficial bacterial skin injection that can occur in all age groups; common in infants and children

most common cause by S. Aureus or S. pyogenes (Group A beta-hemolytic Streptococcus GABHS)

often starts at the site of a minor skin injury such as bug bite, eczema, abrasion etc u

non-bullous vs. bullous

non bullous impetigo

most common in children

pink macule or papule followed by a transient vesicle/pustule which evolves into a yellow honey colored crusted plaque

common on the face- around the nose and mouth; can occur on exposed body areas

bullous impetigo

more common in the neonatal period

small vesicles that can enlarge into 1-2cm superficial flaccid transparent bullae; can easily rupture and leave a collarette of scale

bullous form can be associated with weakness, fever, and diarrhea

impetigo

confirm w culture

treatmen

-topical Mupirocin 2% ointment (Bactroban)

-empiric therapy with dicloxacillin or cephalexin (20-40 mg/kg/day)

if culture + MRSA: oral clindamycin (10-25mg/kg/day q6-8 hours) or trimethoprimsulfamethoxazole (8-10mg/kg/day q12 hours) -MRSA carriers: treat with mupirocin ointment to nares BID x 5 days, monthly for 3 months and then repeat culture

folliculitis

infection of the hair follicle

most often caused by staphylococcus

perifollicular pink papules and pustules

in children- common on scalp, thighs, back and buttocks

in adolescents- common on back and chest

irritant/occlusive folliculitis in areas of friction or occlusion

bacterial culture can be performed

management = antibacterial soap, topical antibiotics such as mupirocin ointment

-clindamycin 1% solution, gel or lotion

-Hibiclens wash

- +/- oral antibiotics (cephalexin or beta-lactamase resistant penicillin)

cellulitis

H. influenzae can be a cause of cellulitis

most commonly caused by S. aureus or Streptococcus pyogenes

infection of the deep dermis and sometimes subcutaneous fat

often seen secondary to skin injuries (abrasions, cuts, bug bites etc), eczema flares, impetigo

skin redness, warmth, +/- pain, swelling, lymphadenopathy

systemic symptoms of fever, malaise, chills

management: oral antibiotics, IV antibiotics

aphthous stomatitis

"canker sores"

shallow erosions of the mucous membranes

immune mechanism; psychological stress or local trauma

present as small, shallow, well demarcated, punch out erosions

grey or yellow center with ring of erythema

lesions are painful; tend to heal over 7-14 days

treatment: topical application of viscous lidocaine, super potent topical corticosteroid can be applied directly onto the lesions

staphylococcus scalded skin syndrome (SSSS)

secondary to S. aureus; exotoxin released by the bacteria leads to acantholysis of the upper epidermis

more commonly seen in infants and children

prodrome of malaise, fever, irritability, sore throat, tenderness of skin

clinical presentation:

-tender erythema on the face and in intertriginous areas that generalizes to the rest of the body over the next 1-2 days; appears almost like a "burn"

-skin appears "wrinkled" due to split in upper epidermis

-scale-crust develop around the eyes and mouth

-formation of fluid filled blisters in areas of friction

-no mucous membrane involvement (rules out TEN)

SSSS management

derm emergency, hospitalization w IV antibiotics

diaper dermatitis

most common type: irritant diaper dermatitis

triggers: urine, feces, moisture, occlusion, friction, topical ointments, wipes

cause→ overhydration of skin due to occlusion

can have a secondary infection by Candida Albicans

clinical presentation

-erythematous, shiny, moist patches on the convex surfaces of buttocks, vulva, perineal area, proximal thighs, lower abdomen

-spared inguinal folds

-untreated, can lead to ulceration/erosions

diaper dermatitis

management

-avoid wipes when skin barrier is compromised

-wash area with gentle cleanser- cetaphil, aveeno, eucerin

-mild flare = Hydrocortisone 2.5% cream/ointment twice daily x 1-2 weeks + Aquaphor/Vaseline/Cicaplast/A&D ointment

OR hydrocortsione valerate 0.02% or desonide 0.05% can be considered for strongr options

if not resolving with topical steroid + moisturizer → consider C. albicans

-triple Paste AF

-vusion ointment (miconazole nitrate, zinc oxide, and white petrolatum)

-nystatin cream

-ketoconazole 2% cream

diaper dermatitis

prevention

keep skin dry/clearn

change diapers promptly

minimize friction- M/C cause

gentle cleansers such as Cetaphil, Vanicream, Eucerin or Aveeno

apply skin protectant at each diaper change- Desitin, Aquaphor, Vaseline

diaper free time periods

candida diaper dermatitis

yeast induced diaper dermatitis

bright, "beefy" red, well demarcated scaly patches, with satellite papulopustules

inguinal fold is affected (unlike diaper dermatitis)

KOH prep: pseudohyphae and budding yeast

treatment

-miconazole 2% cream BID for 2-3 weeks

-nystatin cream or ketoconazole cream BID for 2-3 weeks

contact dermatitis

inflammatory, eczematous eruption 2ndary to contact with an external agent

irritant vs. allergic contact dermatitis

-ICD: eczematous eruption by direct irritation of the skin with an external agent

-ACD: requires prior sensitization; no reaction on the first exposure

irritant contact dermatitis

inflammatory cutaneous eruption that is not caused by an allergen, but from direct toxic effects of a single or repeated application of a chemical/physical insult to the skin

examples

-underarm shaving, deodorants, antiperspirants, shampoos

eruption is typically confined to the area(s) of exposure

allergic contact dermatitis

delayed type IV hypersensitivity reaction

when skin comes in contact with an allergen to which it has been previously sensitized

ACD is not dose dependent

ACD may spread beyond the site of the original contact site

In the US, poison ivy and poison oak are the principal causes of ACD

ACD/ICD management

gentle moisturizers and cleansers

-eucerin moisturizer, Aveeno lotion, Aveeno Oatmeal Bath

oral antihistamines

-children's zyrtec

-identification of agent causing the dermatitis and strict avoidance

-topical corticosteroid creams mild-high potency: will depend on location of flare

local measures

-acute weeping dermatitis: gentle cleansing/drying compresses; can use Domeboro solution; Calamine lotion

-subacute or chronic dermatitis- mild to high potency topical steroid creams/ointment

systemic therapy

-PO antihistamines as needed daytime and nighttime

-Oral corticosteroids solution

atopic dermatitis

chronic, relapsing skin condition

Type I immunoglobulin E mediated hypersensitivity reaction (release of histamines)

onset in childhood is most common; tendency to recur in adulthood

personal or family history of atopy (asthma, allergic rhinitis, atopic derm) ○ AD is commonly the first manifestation of the atopic triad

symptoms can begin in infancy ( after 2 months; onset is usually before 5 years of age in 90% of patients

distribution

-infants: face, scalp, extensor surfaces

-childhood: flexural surfaces (>18 months)

atopic dermatitis

caused by...

intrinsic defect in the epidermal barrier

-mutation in the filaggrin (FLG) gene

-decrease in epidermal lipid content

-increased transepidermal water loss

alterations in the innate and adaptive immunity

environmental triggers

atopic dermatitis

presents with severe itching

ill defined, scaly, red plaques and patches

dry and lichenified skin hyperpigmentation

acute flares: weeping lesions due to superficial skin infection

keratosis pilaris- "chicken skin" red bumps on the back of arms and medial thighs

atopic dermatitis treatment

keep showers short, non fragance soaps, pat dry body instead of rubbing

apply moisturizing right after shower

bleach baths if chronic atopic dermatitis

moisturizers = eucerin, aveeno, aquaphor, vaseline

atopic dermatitis treatment

topical

-topical corticosteroid + antihistamine

face/intertriginous areas: hydrocortisone, desonide

trunk/extremities: triamcinolone 0.1%, mometasone, clobetasol, halobetasol

atopic dermatitis treatment

oral corticosteroids

antihistamines/antipruritic: hydroxyzine, diphenhydramine, doxepin

Dupilumab (Dupixent) targeted immunomodulator (IM)

seborrheic dermatitis

cause by Malassezia yeast species

increased sebaceous gland activity

acute or chronic papulosquamous dermatitis

yellow-ish brown, greasy plaques to scalp

aka "cradle cap"

scalp is almost always affected

if face is involved, presents as pink-orange greasy patches +/- scales

if body is involved, pink to salmon colored, shiny patches with greasy scales; usually on the folds

typically as erythematous scaly patches to the scalp

aka "dandruff" ○ scalp, central face,

can be seen in patients with HIV, parkinson's disease

seborrheic dermatitis

typically self resolves

can use mild topical in extensive case

use mineral oil or baby oil to scalp to remove scales

Scalp - ketoconazole 2% shampoo, Zinc pyrithione or selenium shampoos, Tar shampoo/ SA shampoo, Clobetasol solution or mometasone solution

facial/intertriginous areas - mild topical corticosteroid ( hydrocortisone or desonide + ketoconazole 2% cream)

eyelid - undiluted baby shampoo or eyelid cleanser

scabies

infestation by Sarcoptes scabiei var. hominis, a mite that lives within the stratum corneum of skin

transmission is skin to skin contact

incubation period can be up to 6 weeks

symptomatic cases: pruritis is severe, often worse at night and precipitated by a hot shower

initial lesions appear as tiny pinpoint vesicles and erythematous papules, which then evolve into burrows

linear burrows that is pinkish white and slightly scaly

burrows often found on the hands, flexor wrists, in the finger webs in adults and on palms and soles in infants

infants tend to have more widespread involvement, including face, scalp, palms and soles

diagnosis: clinical diagnosis can be confirmed with mineral oil exam of skin scrapping

scabies treatment

permethrin 5% (elmite or Acticin)

-two overnight applications of a topical, 1 week apart

-cream applied head to toe (include palms, soles, face, scalp for infants); left on for 8-12 hours and washed off in the morning

-all household member should be treated

wash all bed linen and clothing in hot water and dried in high heat after treatment

can store clothing in a bag for 10 days

pruritus and skin lesions can persist for 2-4 weeks even after successful treatment

adjunctive treatment includes topical corticosteroid creams such as clobetasol and systemic antihistamines

pediculosis

P. Humanus capitis vs. P. Humanis corporis

head lice is spread human to human- common in schoolchildren

body lice is often found in situations of poor personal hygiene

itching is the main symptom

no primary skin lesions; secondary skin lesions noted from scratching

nits are firmly stuck onto scalp hairs and can be visualized with side lighting

white nits can be seen on darker hair

hair can be plucked and examined for nits using low power

pediculosis treatment

nits are removed manually with a fine tooth metal comb

all clothing, bedding, hats, towels etc should be washed in hot water

topical therapy

-Permethrin 1% or 5% cream (tigh rates of resistance_

-Spinosad 0.9% cream rinse (Natroba)-

induced muscle spasms and paralysis in lice

vaseline/mayonnaise or Cetaphil cleanser

oral ivermectin

alopecia areata

autoimmune form of hairloss

one or more focal patches of complete non-scarring alopecia

sudden onset of well-circumscribed, localized patches of smooth hairloss

can have multiple patches coalescing into areas

most commonly on the scalp; however can affect eyebrows, eyelashes, beard, arms, legs

no associated redness or scaling

peripheral hairs are short and thin; appear as exclamation point hairs under dermoscopy

clinical variants: alopecia totalis; alopecia universalis

nails will show pitting in a grid like pattern in 10-20% of patients

alopecia areata treatment

topicals

-superpotent topical corticosteroids such as clobetasol 0.05%

- tacrolimus/ pimecrolimus (Elidel)

intralesional treatment -intralesional Kenalog- triamcinolone injections

systemic therapies

-prednisone PO

-JAK inhibitors

tinea capitis

very contagious; spread by person to person contact

presents as inflamed, scaly, alopecic patches (can mimic seb derm), "gray patch"- round, scaly plaques of alopecia, "black dot alopecia" short broken hairs within the alopecia patches

kerion- boggy, pustular, indurated, tumor like mass; inflammatory hypersensitivity rxn to the fungus

secondary bacterial infections- staphylococcus aureus; sometimes gram-negative organisms

non-tender regional adenopathy

KOH prep or fungal culture is confirmatory

management

-PO griseofulvin

-terbinafine, itroconazole or fluconazole in cases of griseofulvin failure

-topical therapy is ineffective for tinea capitis

hand foot and mouth disease

enteroviral exanthem

typically occurs in 1-4 year olds

most commonly cause by by coxsackie A16 but can be caused by other enteroviruses

virus is spread via from fecal-oral route

incubation period is 4 to 6 days

outbreaks are common in the summer or early fall

1 to 2 day prodrome of fever, malaise and abdominal pain may be seen

illness most commonly begins as a sore throat/mouth, refusal to eat due to oral lesions

hand foot and mouth

exanthem presents as 1 to 5 mm vesicles or shallow erosions with a rim of erythema

appears commonly on the tongue, buccal mucosa, lips, palate, gums, palms and sole

xanthem follows the development of oral lesions and presents as round/angulated, grayish white tense vesicles

diaper area in infants is common area of involvement

lymphadenopathy

virus can be cluttered or detected with PCR from throat washings or stool

treatment

-fever and pain treated with Tylenol or Ibuprofen

-encourage ample liquid intake to prevent dehydration

-ice pops and cool liquids help throat pain

-usually lasts less than a week in most cases