| What is atopic dermatitis? | Chronic, relapsing pruritic inflammation of the skin, affects more children than adults (adults have specific morphology and distribution), associated w/increased IgE and hx of allergies.
One of the most common skin disorders (20% of children, 1-3% of adults)
Primary symptom (pruritis), periods of remission and exacerbation. |
| What are associated findings w/atopic dermatitis? | Asthma, allergic rhinitis, xerosis, (itching and dry skin), chronic relapsing course, morpholgy and age-specific patterns. |
| How is clinical presentation of atopic dermatitis? | Variation of eczema between individuals, most people get acute flares w/inflamed weepy patches.
Between flares skin may be normal or chronic eczema w/dry thickened itchy skin.
We see Lichenification and Xerosis cutis |
| How is rash distribution in atopic dermatitis? | Infants (Face, behind ears, extensors of limbs, widely distributed eczema, dry scaly red skin w/small scratch marks due to baby nail , 1st place is cheek)
Children (2-3 yrs) (trunk, flexors of limbs, may affect genitals, eyelids, earlobes, neck and scalp, can get recurrent itchy blisters on palm fingers or feet (Pompholyx/vesicular hand))
Adults (ankles, flexors of knees and elbows, neck and gluteal fold, diffuse, more dry and lichen than children, recurrent staph infection may occur, may cause ICD in hands (blistered)) |
| How is perioral dermatitis? | Inflammatory rash involving skin around the mouth, may spread to nose, eyes -->periorificial dermatitis.
Causes (topical steroids, bacterial/fungal infections, drooling, fluorinated toothpaste, OCP, sunscreen, rosacea. |
| How do we assess severity of atopic dermatitis? | Thickness of lesion, body surface area involved, pruritis, and QoL impact.
QoL (child [impair sleep, embaressment, limited lifestyle], Parents [impair sleep, tiredness, angry on drs, auxilliary caregiver for siblings]) |
| What are some comorbidities associated w/atopic dermatitis? | in children and teens (Increased risk of ADHD, autism, anxiety, depression, poor attention span (pruritis)) |
| How is clinical manifestation of atopic dermatitis? | Lesions benign erythematous papules, form erythematous plaques that may display weeping, crusting or scale.
Various distribution w/age, xerosis at all stages
Pt w/inadequately controlled atopic dermatitis we see 90% dry skin for 5-7 days a week, 50% bleeding/ cracking/ flaking 3-7 days a week, can be associated w/ skin infections
Dx gold std (Hanfin and Rajka (3 out of 4: pruritis, typical morphology and distribution according to age, chronic dermatitis, personal/family hx of atopic disease (50-80% of children will have asthma or allergic rhinitis)) |
| How is pathogenesis of atopic dermatitis? | Multifactorial (genetics, skin barrier dysfunction, impaired immune response and environment)
may be filaggrin deficiency, T helper produces cytokines (IL4/ IL13 by Th2) that initiate positive feedback loop, reduce KC differentiation and increase epidermal hyperplasia by reducing expression of epidermal structural proteins and may cause itchy lesions
Hyperplasia causes lichenification, decreased structural proteins cause pruritis and allergen entry. |
| How is SA superinfection in Atopic dermatitis? | 73-100% of pt w/AD have Staph colonization, helps cause skin exacerbation and increase atopic eczema severity |
| How is family predisposition of atopic dermatitis? | 1 parent has it ->60% risk child has it, 2 parents have it ->80% |
| What are complications of AD? | Secondary infections (Staph, HSV1, Tinea) Psychosocial (sleep disorder, decreased QoL)
Extension/generalization, impetigo, Kaposi-Juluisberg, Contact eczema, psycho-emotional impact
Viral infection usually appears unilateral (HSV)
May be hand blistering, HS to insect bites, |
| What is tx of atopic dermaitis? | Goal is to prevent exacerbation, education, stop itching, prevent scratch damage and space recurrence.
Recommendation non-pharmaco (hydration, identify aggrevating allergens, symptomatic tx)
Short-term and long-term tx manage it (manage flare and control symptoms between flares)
Gentle skin care (tepid bathes w/out scrubbing, specific cleansers instead of soap, pat dry, emollients moisturizers, avoid triggers/irritants, breast feeding during infancy. |
| What are the pharmacologic tx of atopic dermatitis? | Moisturizers (ointments best since less preservatives, no sting or burn)
Topical corticosteroids (in acute flares, ointments preferred, face low potency, body and extremities medium potency, side effects include acne, atrophy, striae, telangiectasis)
Cleaning (warm water, no perfume, bath oil, cut nails, emolient after bath, no lotions, cotton gloves at night)
Immunomodulators (tacrolimus/ pimecrolimus, supress T lymphocytes interest in long term, children 2-17, reduces relapses)
Antibacterial (tx co-existing infections systemic Abx (oral not topical)
Antihistamines (never topical always oral, for itching and sleep, short term) |
| What is duplimab and crisaborole? | Duplimab indicated for 6 years and older, human monoclonal Ab, tx of moderate to severe AD not controlled by topical therapies or contraindicated tx FDA approved.
Crisaborole Phosphodiesterase inhibitor ointment tx mild-moderate AD children > 3 months of age. |
