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ATOPIC DERMATITIS AND OTHER ECZEMAS  Inhalants

Lalaine R. Visitacion, MD o Dust mites


o Animal furs, dander
Scope o Pollens
I. ATOPIC DERMATITIS  Ingestants
 Etiology o Cow’s milk
 Epidemiology o Nuts; peanuts, …
 Three stages o Eggs
 Diagnostic Criteria
 Contactants
 Management
o Wool fibers
II. OTHER ECZEMAS
o Lipid solvents; soaps, detergents
 Ear eczema
 Breast Eczema o Chlorine in swimming pools
 Hand Eczema  Microbial agents
 Diaper Dermatitis o Staph aureus (superantigen)
 Xerotic Eczema o Candida
 Nummular Eczema  Climate
 Clinical Manifestations and Management o Extremes of temperature
o Dryness
ATOPIC DERMATITIS  Emotional stress
 Also known as atopic eczema, infatile eczema, flexural
eczema, disseminated neurodermatitis and prurigo
diathsique (Besnier)
 Coca: atopy means “out of place” or “strange”
 Together with asthma and allergic rhinitis forms part of
the ‘atopic triad’

Epidemiology
 Increasing prevalence – 2x to 10x in the last 3 decades
 10-20% of schoolchildren in US, northern and western
Europe, urban Africa, Japan, Australia, and other
industrialized countries and Asia
 Lower rates in Eastern Europe, Mediterranean, African
countries and Central Asia
 1-3% in adults
Diagnostic Criteria by Hanifin and Rajka
 Sex: female/male ratio of 1.3:1.0
A. MAJOR CRITERIA: Must
 Age: 85% occurs in the first year of life; 95% before age
have three of the following:
5 years
1. Pruritus
Etiology
2. Typical morphology and distribution
 A highly pruritic inflammatory skin disease that results
a. Flexural lichenification in adults
from complex interactions between genetic susceptibility
b. Facial and extensor involvement
genes resulting in:
3. Chronic and chronically relapsing dermatitis
o Defective skin barrier
4. Personal and family history of atopic disease
o Defects in the immune system (asthma, allergic rhinitis, atopic dermatitis)
o Heightened immunologic responses to allergy B. MINOR CRITERIA: Mus have three of the following:
and microbial antigens 1. Xerosis
2. Icthyosis/hyperlinear palms/keratosis pilaris
Reported Immunologic Features of Atopic Dermatitis 3. IgE reactivity (Immediate skin test reactivity, RAST
 Increased IgE production test positive)
 Specific IgE to multiple antigens 4. Elevated serum IgE
 Increased basophil spontaneous histamine release 5. Early age of onset
 Decrease CD8 suppressor/cytotoxic number and 6. Tendency for cutaneous infections (esp S. aureus and
function herpes simplex virus)
 Increased expression of CD 23 on mononuclear cells 7. Tendency to nonspecific hand/foot dermatitis
 Chronic macrophage activation with increased secretion 8. Nipple eczema
of GM-CSF, PGE2 and IL-10 ……
 Expansion of IL-4 and IL-5 secreting Th 2-like cells 17. Itch when sweating
 Decreased numbers of IFN-gamma-secreting Th 1-like 18. Intolerance to wool and lipid solvents
cells 19. Perifollicular accentuation
20. Food hypersensitivity
Pathophysiology 21. Course influenced by environmental and/or
 IL4/IL5/IL10 are all increased emotional factors
 Laboratory findings suggest an abnormality of T helper 2 22. White dermographism or delayed blanch to
(TH2) cells resulting in increased production of cholinergic agents
interleukin 4 (IL-4) and increased IgE. The excess IL-4
causes decreased interferon γ levels. Cells may react Criteria Modification for young Infants
with environmental anrigens to produce increased levels A. THREE MAJOR FEATURES:
of IgE 1. Family history of atopic dermatitis
 Serum histamine is increased 2. Typical facial or extensor dermatitis
 Stratum corneum abnormalities of lipid (particularly 3. Evidence of pruritus
ceramide production) B. THREE MINOR FEATURES:
 Abnormality of prostaglandin metabolism 1. Xerosis/Icthyosis/hyperlinear palms
2. Perifollicular accentuation
Exacerbating Factors (Triggers) 3. Postauricular fissures
4. Chronic scalp scaling  Locations: antecubital and popliteal fossa, flexor
wrists, eyelids, face and around the neck
Three Stages of Atopic Dermatitis  Pruritus: constant feature
 Infantile atopic dermatitis – 2 months to 2 years  Lesions: les acute – less exudative, drier, more
of age popular, often lichenified scaly infiltrated plaques
 Childhood atopic dermatitis – 2 to 10 years old  Vicious cycle established: itch  scratch  itch
 Adolescent and adult atopic dermatitis - >10 y/o  Results to lichenification, secondary bacterial
infection
1. Infantile Atopic Dermatitis  Other factors:
 60% of atopics >2 mos to 2 years of age o Wool irritation: winter
 Begins as itchy erythema of the cheeks  o Feather sensitivity – onset at age 2
minute intraepidermal vesicle  rupture  moist o Sensitivity to cat & dog dander
crusted areas extend to other parts of the body:
scalp, neck, forehead, wrists and extensor of 3. Adolescent and adult atopic dermatitis
extremities  Forms:
 Areas spared: buttocks and diaper area o Localized eryhthematous, scaly, popular
or vesicular plaques
o Lichenified pruritic plaques
Sites of predilection Adolescent: classic antecubital and popliteal
fossae, front and sides of the neck, forehead, area
about the eyes
 Infiltrated, erythematous facial skin with scalines
in an adolescent with atopic dermatitis. Note
lateral thinning of eyebrows and intra-ocular
(Dennie-Morgan) fold
Adults: less characteristic distribution –generalized
but more severe in the flexures
 Universally lichenified
 Paroxysmal pruritus
 Typical lesions: dry scaly papules coaslescing
into lichenified scaly plaques
 Maybe become exudative, crusted or infected
 Dry skin
 Moist lesions – most common type  Flares in adults: triggered by
 Significant exudates and secondary effects from o Acute emotional upsets: stress, anxiety
scratching: crusts, pustules and infiltrated areas  and depression decreased the threshold
lichenified for itch
 Lesions may become generalize with erythroderma and o Exercise due to inability to sweat
desquamation  Hand dermatitis
o 20-80% of pxs
Course o Hands and wrists
 Symptoms disappear before or towrd the end of second o Palmar and dorsal surfaces
year – able to eat food which previously cause flares
o Clinically indistinguishable from contact
without exacerbation – appear to outgrow sensitivity
dermatitis
 Worsening observed after immunizations and viral
o Triggered by increased exposure to
infections
 Summer: partial or complete remission – relate to the soaps and water
therapeutic effects of UVB in atopics
 Winter: relapse – aggravation of wool and low humidity
of forced air in winter Associated Features and Complications of Atopic
Dermatitis
Role of Food (also applicable to children) 1. CUTANEOUS STIGMATA:
 60% of patients had at least 1 positive food challenge a. Dennie Morgan sign – a linear
 85% of challenges are associated with cutaneous transverse fold just below the edge of
symptoms the lower eyelids
 Majority of positive tests: egg, peanut, milk, wheat, fish, b. Xerosis – skin dryness
soy and chicken  Represents low-grade
 Positive challenges correlate with rise in plasma dermatitis
histamine  Transepidermal water loss is
 Withholding the implicated food: clinical improvement decreased
and decrease in histamine  Water barrier is diminishes
 45% lost food sensitivity over a 1-2 year period  Decreased threshold to
 A negative skin prick test: reliable indicator of absence of irritancy
food sensitivity c. Icthyosis – fish-like scales
 Food allergy may play a role in a selected population of d. Pityriasis alba – a form of subclinical
young atopic patients dermatitis
 Withholding cow’s milk: conflicting results  Poorly, marginated slightly scaly
 Withholdingcow’s milk and eggs during pregnancy and patches on the cheeks, upper
lactation: conflicting results arms and trunk in young
 Restrictive measures may be considered only when the children
risk for atopy in a child is high or where infantile AD is e. Keratosis pilaris – horny follicular lesions
severe of the outer aspects of the upper arms
and legs
2. Childhood Atopic Dermatitis  Associated with dry skin
 Refractory to treatment
f. Hertoghe’s sign – thinning of the lateral  Humidifiers in rooms are helpful
eyebrows  AVOID emotional stress
g. Keratosis punctata palmaris et plantaris – chiefly
in black atopic patients Specific Therapeutic Strategy
h. “Dirty neck” – reticulated pigmentation of the Step I – Induction of remission
neck Step II – Stabilization and maintenance
i. Ear eczema Step III – Rescue of flares
j. Nipple eczema
k. Cheilitis Topical Therapy –Mainstay of therapy
l. Exaggerated palmar creases  Wet compresses for oozing lesions:
o Aluminum acetate 5% (Burow’s solution)
2. VASCULAR STIGMATA 20-30 minutes, 4-6 times daily
a. “Headlight sign” – perinasal or periorbital pallor  Topical corticosteroids (problems!)
b. White dermographism  Hydrating agents for dry skin:
 Blanching of the skin at the site of stroking o 10% urea in hydrophilic cream
with a blunt instrument o Eucerin cream
 Caused by local accumulation of edema  Tar preparations
which obscures color of underlying vessels  Macrolide immunomodulators:
o Tacrolimus 0.3% ointment
3. OPHTHALMOLOGIC ABNORMALITIES o Ascomycin macrolactam derivatives
a. Cataract – 10% of patients – anterior or (Pimecrolimus 1%)
posterior subcapsular  General principles on the use of topical steroids
b. Keratoconus – 1% in Atopic eczema:
c. Atopic keratoconjunctivitis o Provide symptomatic relief and safe in
4. SUSCEPTIBILITY TO INFECTIONS
the short term
a. Staphylococcus aureus
o Regular review of steroid use in terms of
b. Eczema herpeticum –herpes simplex 1 infection
potency and quantity
 Usually in young children
o Few days to 1 week in acute eczema
 Transmitted from a parent or a sibling with
cold sore or fever blister o Up to 4-6 weeks for induction of
 May have recurrences remission in chronic eczemas
c. Fungal infection: Tinea faciale o Constant education of parent/caregiver
d. Molluscum contagiosum on appropriate use
e. Verruca vulgaris o Potency should match the disease
severity and the affected site
Differential Diagnosis of Atopic Dermatitis - Weaker steroids: infants, face,
 Contact dermatitis (allergic and irritant) flexures
 Seborrheic dermatitis - Stronger steroids: palms and
 Scabies soles
 Psoriasis
 Ichthyosis vulgaris Systemic Therapy
 Keratosis pilaris  Antihistamines
 Dermatophytosis o Sedating; hydroxyzine, doxepin
 Antistaphylococcal antibiotics
Investigations o Penicillins, cephalosporins, erythromycin
 Skin prick test  Systemic corticosteroids
 Total IgE (RIST) o Side effects!
 Specific IgE (RAST) o Only for acute flare-ups
 Eosinophilia; blood, lesions  Phototherapy: PUVA, UVB
 Th2 cytokine profile; IL-4, IL-5, IL-13  Cyclosporine
 Reduced Th1 response ; interferon-g, DTH to contact o Side effects!
allergens o Expensive
 Interferon-g: Th1 promoter
Management of Atopic Dermatitis  Papaverine: PDE inhibitor
General Management in Infancy and Childhood  Evening Primrose oil: g-linolenic acid, PG
 To prevent precipitation of attack, AVOIDANCE of modulator
external irritation:
o Excessive bathing, vigorous rubbing or chafing
o Heavy, tight or soiled clothing
o Insufficient cleanliness in the diaper region
o Irritating, secretions
o Medicated baby oils
 PROTECTION of affected parts from Scratching
 EMOLLIENT SOAPS
 ANTIHISTAMINES with accompanying sedative effects
– esp at night to reduce pruritus Approach to a patient with atopic dermatitis
 DIETARY RESTRICTIONS – in cases where specific Patient presents with history of pruritic dermatitis
food allergies are implicated – elimination diet

General Management in Adults


Patient presents with history of pruritic dermatitis
 AVOID extremes of cold and heat
 AVOID overbathing (+) (-)
 USE of non-irritating emollient soaps
 AVOID dryness of skin: use EMOLLIENTS
Evaluate for
other conditions
o Removal of scales and cerumen by
lavage
o Instillation of antibiotic-corticoid
preparations

Eyelid dermatitis
 Causes:
o Nail polish – one eye involvement
(upper eyelid)
General skin care measures o Atopic dermatitis – one or both eyes;
 Education
 Appropriate skin hydration and use of emollients/skin barrier upper and lower eyelid involvement
repair measures o Allergens like mascara, eye shadow,
 Avoidance of irritants eyelash cement, eyeliner, or rubber
 Identification and avoidance of proven allergens
 Anti-inflammatory therapy steroids, (topical calcineurin tipped instruments use to apply
inhibitors) cosmetics – lids of both eyes
 Antipruritic interventions (sedating antihistamines, behavioral o Hair dye, rinse, tint, lacquer and hair
modification) spray contact dermatitis – eyelids and
 Identification and treatment of complicating bacterial, viral, or
fungal infections other sites
(+) (-) o Volatile gases: insect sprays, lemon
peel oil, benzalkonium chloride,
Titration of topical therapy, using preservatives of rinsing solution for
emollients/barrier repair measures
topical steroids or topical calcineurin
contact lenses, plastics in spectacle
inhibitors as needed intermittently frames
 Many cases are caused by substances
transferred by hands to the eyelids
 Re-assess diagnosis of
AD Breast Eczema (Nipple Eczema)
 Consider role of  Sites affected: nipples, areolae, skin or the folds
unrecognized infectious agents,
beneath
allergens, etc
 Eczema of the nipples: moist type with oozing
 Consider poor
and crusting
(+)  Nursing mothers: painful fissuring
Successful outcome?  If persistent for >3 months, unilateral = biopsy is
mandatory to rule out Paget’s disease of the
(-) breast
 Differential diagnosis: circumscribed
 Consultation with AD
specialist
neurodermatitis, atopic dermatitis and contact
 Consider skin biopsy dermatitis
 Consider hospitalization  Treatment: topical/IL steroids
 Consider cyclosporine A,
Hand Eczema
ultraviolet therapy etc
 Diagnosis: complete history, careful examination
of the rest of the body surface and patch testing
 Usually have 2 causes: atopic diathesis +
contact dermatitis
 A major occupational problem
 A major cause of emotional and financial stress
ECZEMA  In health care workers: increases risk for
 From the Greek word eksein: to “boil down” or to infection by blood-borne pathogens
“effervesce”  Frequently the initial or only adult manifestation
 Baer described eczema as: a pruritic papulovesicular of atopic dermatitis
process which in its acute phase is associated with  Types:
erythema and edema and which in its chronic phase, 1. Irritant Hand Dermatitis
while retaining some of its papulovesicular nature, is o Seen in homemakers, bartenders, food
dominated by thickening, lichenification and scaling service workers and health workers –
 Recognized as a descriptive term and not a diagnosis results from or aggravated by excessive
 Unifies a group of disorders into a morphologic category and prolonged exposure to soaps or
that is clinically characteristic detergents and water (defatting action
 Pruritus is the most common and prominent symptom and maceration)
 The itch threshold is lowered by stress o Also in occupation with exposure to
chemicals, solvents, acids or alkali:
Ear Eczema or Otitis Externa custodians and metal workers
 Helix, postauricular fold, and external auditory canal o The impaired barrier ICD induced may
 External ear canal – frequent affected site enhance development of allergic
 Traumatization by rubbing, wiping, scratching and reactions
picking – induces edema and infection with inflammation o Eruptions starts as dryness and redness
 Frequent causes: Atopic dermatitis and seborrheic
of the fingers
dermatitis
o Tips of the fingers: dry scales with
 Contact dermatitis from neomycin, benzocaine and
peeling
preservatives may result from topical remedies
o Backs of the hands: chapping
 Causes of infection: Staph, Strep, Pseudomonas
 Earlobe dermatitis: nickel allergy in pierced ears o Palms: hardening with fissures
 Treatment: 2. Vesiculobullous Hand Eczema (Pompholyx,
o Removal of causative agents Dishydrosis)
o Pompholyx or cheiropompholyx area offers no antimicrobial benefit to the infant
- an uncommon disorder and adds a risk of aspiration
- severe sudden outbreaks with long disease free  C = Cleansing and anti-candidal treatment.
periods Gentle cleansing with plain water, mineral oil, or
- primary lesions: macroscopic, deep-seated unscented gentle cleanser is recommended.
vesicles on the sides of the fingers, palms and Avoidance of friction or rubbing is important. A
soles – coalescence lead to bulla formation topical anti-candidal agent should be added for
- eruption: symmetrical and pruritic any signs of candidiasis. Oral nystatin is
- patch testing: to rule out allergic contact indicated if oral thrush is present.
dermatitis  D = Diapers. Diapers should be changed as
o Chronic vesiculobullous hand frequently and as soon after soiling as possible,
eczema especially if cloth diapers are used.
- common and difficult to manage  E = Education of parents and caregivers
- Sex: Female: Male – 3:1
- Vesicular eruption of the palms and soles Xerotic Eczema (Winter itch, eczema craquele,
characterized by eczematous, weeping patches asteatotic eczema)
containing intraepidermal vesicles and by  Dehydrated skin showing redness, dry scaling
burning or itching and fine crackling that may resemble crackled
- Bilateral and roughly symmetrical porcelain or the fissures in the soil in the bed of
- Cyclic with exacerbations and relapses and may a dried lake or pond
persist for long periods  Favored sites; anterior shins, extensor arms and
3. Hyperkeratotic Dermatitis of the Palms flank
o Male: Female ratio – 2:1  Factors; elderly, wintertime, excessive bathing
o Age: older adults >45  Management: Moisturizers, topical steroid
o Hyperkeratotic, fissure prone infiltrated lesions of the ointments for inflamed areas
middle or proximal palm
Nummular Eczema (Nummular Neurodermatitis)
o Volar surfaces of the fingers may also be involved
 Sites: lower legs, dorsa of the hands, extensors
o Plantar lesions: 10% of patients
of the arms
o Atopic dermatitis and allergic contactants are not  Age: middle aged men – 60’s to 70’s
found  Lesions: discrete, coin-shaped, erythematous,
o Occasionally will develop to psoriasis edematous, vesicular and crusted patches 5-50
mm dm
Treatment of Hand Eczema  Manifests Koebner phenomenon
 Wearing white cotton gloves under vinyl gloves  Symptom: severe pruritus – paroxysmal,
 Moisturizing: critical component of management compulsive quality and nocturnal timing
 Soaking in drying solution for acute vesicular disease:  Emotional stress maybe present
potassium permanganate solution 1:5000, Burow’s
solution Management of Nummular Eczema
 Superpotent and potent topical steroids are the initial  Topical steroids in the mid- to high-potency
therapy – enhanced by occlusion range are the mainstay of treatment
 Use of systemic steroids – dramatic improvement but not  The calcineurin inhibitors, tacrolimus and
safe for long term use pimecrolimus, and tar preparations are also
 Phototherapy – UVA or PUVA – have some success effective
 Emollients can be added adjunctively if there is
Diaper (Napkin) Dermatitis accompanying xerosis
 A common cutaneous disorders – 7% to 35% on infants  Oral antihistamines are useful if pruritus is
in diapers severe
 Highest prevalence: between 6 and 12 months of age  Oral antibiotics are indicated when secondary
 Also seen in elderly incontinent patients and children infection is present
and adults with urinary and fecal incontinence  For widespread involvement, phototherapy with
 Erythematous and papulovesicular dermatitis distributed broad or narrow band ultraviolet B may be
over the lower abdomen, genitals, thighs and the convex benificial
surfaces of the buttocks
 Folds remain unaffected – not in direct contact with -END-
diaper
 Factors: moist skin is more easily abraded by friction of
the diaper
o Wet skin is more permeable to irritants such as
ammonia
o Skin wetness allows the growth of bacteria 
increase local pH  increase the activity of fecal
lipases and proteases (major irritants in feces)
 Candida albicans is a frequent secondary invader

ABCs in the Treatment of Diaper Dermatitis


 A = Air. The diaper should be left open as much as
possible when the infants sleeps to allow drying of the
skin
 B = Barrier ointments. Zinc oxide pastes, petrolatum,
and other bland, unmedicated barrier preparations are
mainstays of therapy. A continuous layer of barrier paste
or ointment should be maintained, reapplying with every
diaper change, if necessary. Baby powder on the diaper

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