EO_018.08 Treat Paediatric Skin Conditions
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Transcript EO_018.08 Treat Paediatric Skin Conditions
PAEDIATRIC
DERMATOLOGY
OBJECTIVES
Common paediatric dermatologic
conditions
Dermatologic presentation of systemic
disease
Conditions which may require
urgent/emergent management
ASSESSMENT OF SKIN
PROBLEMS
History
DESCRIBE WHAT YOU SEE!
ASSESSMENT OF SKIN
PROBLEMS
History
Onset,
progression, change
blister,
bleed, drain
Distribution
Duration
Aggravating/relieving
Itch,
factors
pain, triggers
Treatment
Associated S & S e.g. fever
ASSESSMENT OF SKIN
PROBLEMS
Past Medical History
Asthma,
atopy
Illnesses
Allergies
Food,
drugs, seasonal, environmental
ASSESSMENT OF SKIN
PROBLEMS
Family History
Skin
disease
Systemic
Social
Others
affected at home, school or daycare
Crowding, poverty
5 ITCHES
1.
2.
3.
4.
5.
Dermatitis
Varicella
Urticaria
Scabies
Insect bites
DERMATITIS
Itching, redness, swelling, oozing, scabbing,
scaling, lichenification, +blisters
DERMATITIS
Atopic (eczema)
Diaper dermatitis
Seborrheic dermatitis (cradle cap)
ATOPIC DERMATITIS
(ECZEMA)
Site:
Infant
- face, scalp, extensor surfaces
Child - flexor surfaces
FH atopy (asthma, hayfever, anaphylaxis,
allergies)
Inheritance:
1 parent >60%
2 parents >80%
ATOPIC DERMATITIS
(ECZEMA)
ATOPIC DERMATITIS
(ECZEMA)
Complications:
Secondary
bacterial infections
Eczema herpeticum (herpes infecting the
lesions)
Prognosis:
50%
clear by age 13
MANAGEMENT OF
DERMATOLOGICAL
PROBLEMS
If it’s dry – wet it
If it’s wet – dry it
And if you don’t know what to do give
steroids!!
ATOPIC DERMATITIS
(ECZEMA)
Management
Bathing
Bath
oil (e.g. Aveeno, Keri)
Pat dry
Ointments when wet
ATOPIC DERMATITIS
(ECZEMA)
Management
Topical
corticosteroids
Vaseline
Antihistamines
Warn about course!
TOPICAL STEROIDS
Weak = 1% hydrocortisone
Moderate = 0.05% betamethasone
3 times a day and reduce…
BEST ANTI-ITCH
Hydroxyzine 0.5 mg/kg QID
(max
400 mg/day)
DESCRIBE WHAT YOU SEE!
DIAPER DERMATITIS
DIAPER DERMATITIS
Contact iirritation
DIAPER DERMATITIS
Management
Keep
area dry – expose to air
Protect
DESCRIBE WHAT YOU SEE!
CANDIDIASIS
CANDIDIASIS
Folds
Management:
Nystatin
– 4 times a day/every diaper change
Consider oral too
Nystatin
7-10
days
– 1 mL PO 4-6 times a day after food
DESCRIBE WHAT YOU SEE!
SCALP SEBORRHEIC
DERMATITIS (CRADLE CAP)
SEBORRHEIC DERMATITIS
(CRADLE CAP)
Occurs in any baby
Sebaceous glands pump out greasy
substance that keeps the old skin cells
attached as it dries
Greasy
Yellow
SEBORRHEIC DERMATITIS
(CRADLE CAP)
Onset most commonly in first 3 months
gone by 8 to 12 months
Teens often have a similar scalp condition
= dandruff!!
SEBORRHEIC DERMATITIS
(CRADLE CAP)
Management:
Oil
to soften/loosen scales
Soft brush or dry terry cloth to brush away
Consider mild topical steroid, if red/inflamed
Rarer now because cleaner
SCABIES
Management:
Permethrin 5% dermal cream – single
application
Neck
down for 12 hours adults
Include head and scalp in prepubertal
Hot
launder clothes from last 3 days or
Seal for 48 hours
Safety under 3 months not established
Hydroxyzine
IVERMECTIN
HEAD LICE
Nix (shampoo) cream rinse
Nits = dead
School after treatment
http://www.cps.ca/ENGLISH/statements/I
D/id08-06.htm
BIRTH MARKS
Mongolian
Spots
Café-au-lait spots
-
Transient macular stains (Salmon patches)
Port wine stains
MONGOLIAN SPOTS
Blue/grey macula
Appear at or shortly after birth
Base of spine, buttocks and back
Not associated with any conditions or
illnesses
Gradually disappear
MONGOLIAN SPOTS
CAFÉ-AU-LAIT SPOTS
CAFÉ-AU-LAIT SPOTS
Well-circumscribed, homogenously
pigmented, light brown macules
1.5 - 15 cm in diameter
Frequently present at birth, are almost
always present by 1 year of age
May increase in number during early
childhood
CAFÉ-AU-LAIT SPOTS
Approximately 2% of all newborn infants
Up to 25% of the normal adults
More common in darker-pigmented races
≥6 with diameter > 0.5 cm before
puberty, and 1.5 cm after puberty
suggests neurofibromatosis
SALMON PATCH
SALMON PATCH
Transient, macular
Present in up to 70% of newborns
Eyelids, nape of neck, glabella
Most fade by 1 year of age
Those in nape of neck persist in 25% of
adults
PORT WINE STAIN
PORT-WINE STAIN
Malformation of superficial capillaries of
skin
Pinkish/red macules
Well defined edges in infancy
Facial most common
PORT-WINE STAIN
Present at birth
Permanent
Variable size
Do not proliferate but enlarge as child
grows
Lesions darken to purple and may develop
a pebbly or slightly thickened surface with
time
MANAGEMENT
Most are uncomplicated
Laser therapy may help fade the lesion,
best done in infancy
Around eye innervated by branch 1 of
trigeminal nerve – need ophthalmology
assessment /neuroimaging
VASCULAR MALFORMATIONS
Hemangiomas
Capillary (strawberry)
Cavernous
HEMANGIOMAS
CAPILLARY (STRAWBERRY)
HEMANGIOMAS
Begin as flat, pale white spots & later
become larger & elevated, bright red, non
compressible
mm - several cm
Usually solitary
Females 3:1
55% present at birth, rest develop later
CAVERNOUS HEMANGIOMAS
CAVERNOUS HEMANGIOMAS
HEMANGIOMAS
CAPILLARY (CAVERNOUS)
Lie deeper in in skin with a slightly bluish
discoloration
Growth until 1 year of life
Involute over 3-10 years
COMPLICATIONS
Peri-orbital
risk
to vision ( amblyopia)
Ear
decreased
delay
auditory conduction, speech
Multiple cutaneous/large facial may be
associated with visceral hemagiomas
Subglottic
hoarseness,
Cosmetic
stridor, respiratory failure
CASE
5 week old with croup
6 day history of cough-initially harsh,loose
now high pitched seal-like cough
no distress, O2 sat 99%, HR 130, RR 30
erythema of left anterior tongue, left
posterior palate with ? thrush
…reassessment...
1 hour post epi
moderate-severe respiratory distress
classic “croupy” cough, RR40
severe intercostal indrawing, abd
breathing, tracheal tug
improved with 2nd dose epi
“let’s bring her in…”
admission
NPO/IV/epi/steroids/ O2
unable to discontinue steroids
breast feeding well limited to 10 mins
no better by day 10
SIDE EFFECTS STEROIDS
Cushingoid
hypernatremia/hypertension/wt gain
hyperglycemia
adrenal suppression/immunity
bone density
cataracts
MANAGEMENT
Natural history of haemangiomata
Oral systemic steroids were the mainstay
of Rx if complications arise
Propranolol 2 mg/kg/day
INFECTIONS
Fungal
Bacterial
TINEA CAPITIS
TINEA CAPITIS
Non-scarring alopecia with scales
Round, scaly patches of alopecia, +/broken hairs
+ Boggy, elevated, discharging
May be secondarily infected +/scarring
TINEA CAPITIS
Etiology: Fungal
Investigations:
Wood’s
light: green fluorescence only for
microsporum infections
Culture of scales/hair shaft
Microscopic exam of KOH preparation
showing hyphae
TINEA CAPITIS
Management:
Terbinafine
(Lamisil) for 1 month
10-20 kg 62.5 mg daily
20-40 kg 125 mg daily
TINEA CORPORIS
(RINGWORM)
TINEA CORPORIS
(RINGWORM)
Etiology: fungal
Pruritic (not severe), scaly, round/oval
plaque(s) with erythematous margin(s)
and central clearing
Peripheral enlargement of lesions
Mostly trunk, limbs, face
Contact with infected animals/pets
TINEA CORPORIS
(RINGWORM)
Management
Clotrimazole
(Canesten) cream
BACTERIAL INFECTIONS
Impetigo
Staphylococcal scalded skin syndrome
(SSSS)
Cellulitis
Furuncle/boil
IMPETIGO
IMPETIGO
Purulent, vesicular lesion golden
yellow crust
Pre-school & young adults
Crowded conditions, poor hygiene,
minor trauma
DDx: infected eczema, HSV, varicella
Organisms: Staph. Aureus, GAS, both
Potential complication: poststreptococcal glomerulonephritis
IMPETIGO
Organisms: Staph. aureus, GAS, both
Potential complication: poststreptococcal glomerulonephritis
TREATMENT
Topical
e.g.
2% mupirocin or fucidin tid
Systemic 7-10 days
e.g.
cephalexin 50 mg/kg divided tid/qid
BULLOUS IMPETIGO
Scattered, thin-walled bullae containing
yellow/turbid fluid
Staph. aureus
Complications:
Generalized
skin peeling
Staphylococcal Scalded Skin Syndrome
STAPHYLOCOCCAL
SCALDED SKIN SYNDROME
(SSSS)
STAPHYLOCOCCAL
SCALDED SKIN SYNDROME
(SSSS)
CELLULITIS
CELLULITIS
Erythematous, flat, poorly-demarcated
lesions, not uniformly raised
Tender
Warm
Group A Strep, Staph. aureus
Differential diagnosis:
necrotizing
fasciitis
CELLULITIS
TREATMENT
Cephalexin
q6h PO
Second
Cefazolin
severe
50 – 100 mg/kg/d divided
line = cloxacillin or clindamycin
IV +/- clindamycin for
FURUNCLES (BOILS)
Red, hot, tender, inflammatory nodules
Tense for 2-4 days, then fluctuant
Yellowish point ruptures with discharge
of pus
Commonly around hair follicles at areas
of friction & sweat
nose,
neck, face, axillae, buttocks
MANAGEMENT
Incision and Drainage
Relieves
pressure & pain
Hot packs
Antibiotic PO:
e.g.
cloxacillin
Consider:
Culture
blood/pus
SYSTEMIC ILLNESS
Erythema multiforme
Bullous erythema multiforme
Toxic epidermal necrolysis (Stevens
Johnson)
Henoch Schonlein purpura
Kawasaki disease
ERYTHEMA MULTIFORME
Target lesions (3 rings)
HERPES SIMPLEX VIRUS
Fixed (not transient e.g. giant urticaria)
No
pain
No pruritus
No scale/crust
May include palms/soles
May include mucosa
ERYTHEMA MULTIFORME
Management:
Herpes isolation
Oral acyclovir
Topical steroids
BULLOUS ERYTHEMA
MULTIFORME
Atypical targets
Central
vesicle
Vesicles without targets
Discrete lesions
Erosions & crusts
Mucous membranes involved
MYCOPLASMA
BULLOUS ERYTHEMA
MULTIFORME
Management:
Admit
Mycoplasma isolation
Antibiotics for mycoplasma
Ophthalmology, dermatology/wound oral
care
Systemic steroids often needed
STEVENS JOHNSON
SYNDROME
TOXIC EPIDERMAL NECROLYSIS
(STEVENS JOHNSON)
Vesicles & bullae
May begin as dusky papule
Rapid progression
Develops confluence
Mucous membrane involvement
Systemic involvement
DRUG CAUSE USUALLY
Antiepileptics
Sulphurs
Penicillins
TOXIC EPIDERMAL NECROLYSIS
(STEVENS JOHNSON)
Management:
Life threatening ICU/burns unit
Supportive treatment
History for all infections/medicines
IVIG (0.75-1 g/kg/d x 3 days)
Cyclosporin
Steroids are controversial
COURSE
<
5% mortality overall
Regrowth of epidermis by 3 weeks
COMPLICATIONS
•corneal scarring/blindness,
•phimosis, vaginal synechiae (stenosis)
• renal tubular necrosis
•renal failure
•esophageal strictures
•respiratory failure
•scarring/cosmetic deformity
HENOCH-SCHONLEIN PURPURA
“Anaphylactoid purpura”
Autioimmune vasculitis
Skin – petichiae, palpable, purpura
Joints – arthralgia/arthritis
Renal – hematuria, ↑BP,
(glomerulonephritis)
GI – pain secondary to edema,
intussusception
KAWASAKI DISEASE
>80% less than age 4
Seen in all races
Asian>Black>White
Most common cause of acquired heart
disease in children
Typical vs atypical
DIAGNOSTIC CRITERIA
FEVER > 38.5C > 5 days PLUS 4 of:
1.
EYES
Bilateral non-purulent conjunctivitis
2.
‘CENTRAL’
Oral mucosal changes – fissured red lips, strawberry
tongue
3.
NECK
Asymmetric cervical lymphadenopathy >1.5 cm
4.
PERIPHERAL
Desquamation (edema, erythema)
5.
RASH
Polymorphic
Illness not explained by other (e.g. Strep/measles)
ASSOCIATED FEATURES
Irritability ***
Arthritis
Aseptic meningitis
Hydrops of the gallbladder
Hepatic dysfunction
Diarrhea
Pneumonitis
Uveitis
COMPLICATIONS
Coronary artery ectasia/dilatation
20%
if untreated
2% treated
Myocarditis/pericarditis
Arrhythmias
TREATMENT
IVIG infusion
High dose then low dose aspirin
Supportive
SUMMARY
Assessment of skin problems
Itchy (2/5)
Birth Marks
Vascular malformations
Infections
Systemic illnesses
REFERENCES
E.O. 021.08, 021:09 and 021:11
Nelson’s Essentials of Pediatrics
Color Atlas/Synopsis of Clinical
Dermatology
Class Handout
Canadian Paediatric Society Policy
Statements
http://www.aboutkidshealth.ca