atopic dermatitis in children

2. -
 Definition
 Epidemiology
 PathogenesisPathogenesis
 Clinical ManifestationsClinical Manifestations
 DiagnosisDiagnosis
 Differential DiagnosisDifferential Diagnosis
 ComplicationsComplications
 Treatment
 Prognosis
 Prevention

3. ATOPIC DERMATITIS
 Introduction:
The word "dermat itis"
skin inflammation
Atopic" refers to diseases that are hereditary,
tend to run in families, and often occur together.
Atopic dermatitis (AD) is a pruritic disease of
unknown origin that usually starts in early
infancy (an adult-onset variant is recognized)

4. ATOPIC DERMATITIS
 Introduction:
characterized by:
pruritus
eczematous lesions
xerosis (dry skin)
lichenification (thickening of the skin
and an increase in skin markings).
Atopic dermatitis (AD), or eczema is the
most common chronic relapsing skin
disease seen in infancy and childhood.

5. EPIDEMIOLOGY
It affects 10-30% of children worldwide
frequently occurs in families with other atopic
diseases, such as asthma, allergic rhinitis, and
food allergy
AD may be more common among Caucasian
and Chinese persons, but it affects all races.
Sex: The male-to-female ratio is 1:1.4.
Begins in infancy with 50% occurring in 1st
year
of life & 30% diagnosed between 1 to 5 yr of age.

6. PATHOGENESISPATHOGENESIS
1. Genetic predisposition
2.
Defective skin barrier
3. Abn immune
response
Host
EnvironmentEnvironment
Allergens
Irritants
Infections
Pollutants
Stress
Weather change
AD

7. PATHOGENESISPATHOGENESIS
Family history of atopy Child risk of atopy
Biparental (same allergy)
Biparental or uniparental + sibling
(different allergy)
Uniparental or sibling
None
50-80%
40-50
20-40
5-15
Genetic Predisposition

8. PATHOGENESISPATHOGENESIS
Defective skin barrier
 defective barrier function in the stratum
corneum of Atopic dermatitis patients, leading to
excess transepidermal water loss
the entry of antigens that result in the
production of inflammatory cytokines
to impairment of innate immunity
 Mutations in the filaggrin gene, which encodes a
protein necessary for terminal differentiation of
epidermis, have been shown in up to 50% of
severe patients with AD.

9. PATHOGENESISPATHOGENESIS
Abnormal immune responseAbnormal immune response
 The immune hypothesis invokes an imbalance in
the T lymphocytes
Acute AD:
 TH 2 cells predominating cytokine
production of interleukins 4, 5, 12, and 13 and
granulocyte macrophage colony-stimulating
factor, causing:
an increase in IgE and lowered interferon
gamma levels.

10. PATHOGENESISPATHOGENESIS
Abnormal immune responseAbnormal immune response
chronic AD:
 the TH 1-type cells predominate. Other cell types are
also involved in the process, including eosinophils,
Langerhans cells, keratinocytes, and B cells.

11. EXACERBATING FACTORS
(TRIGGERS)
 Environmental Factors
Food
Cow’s milk, egg, peanuts, soy, wheat, fish
Aeroallergens
House dust mites
Irritants
wool, acrylic, soaps, detergents
Microbes
S. aureus toxins (superAg specific IgE)
Extreme of temperature & humidity, sweating,
stress

12. FLARE FACTORS IN
ATOPIC DERMATITIS

13. CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Intense pruritus, especially at
night, and cutaneous reactivity
are the cardinal features of AD
Scratching and excoriation cause increased skin
inflammation that contributes to the
development of more pronounced eczematous
skin lesions
Eczematous eruption leads to lichenified
dermatitis

14. CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
 Acute AD: intensely pruritic erythematous
papules and plaques with secondary excoriations;
Vesicles and serous crusting also seen

15. CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Erythematous, scaling papules & plaques
with excoriation
Sub-acute

16. CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
 Chronic AD: characterized by thickened,
hyperkeratotic plaques with lichenification as
well as prurigo nodularis (“picker’s nodules

17. CLINICAL PHASES
Three Stages of Atopic Dermatitis
Infantile Atopic Dermatitis
Childhood Atopic Dermatitis
Adolescent and Adult Stage Atopic
Dermatitis

18. CLINICAL PHASES
Infantile Phase ( 0-2 years)
 60% of case AD present in the first year of
life, after 2 months of age
 Xerosis occurs early and often involves the
whole body
 Begin as itchy erythema of the cheeks
 Most cases the symptoms will disappear
toward the end of the second year

19. CLINICAL PHASES
Oozing, crusted,
erythematous, scaly
plaques on the scalp and
face, sparing the diaper
area
When baby begins to crawl,
the extensor extremities
become more involved
Infantile Phase

20. CLINICAL PHASES
Infantile Phase
 May become desquamate leading to
erythroderma.
 The role of food allergy in infantile and
childhood atopic dermatitis has been
clarified
 Egg, peanut, milk, wheat, fish, soy, and
chicken may exacerbate infantile AD

21. The skin is often dry, scaly and red with
small scratch marks made by sharp
baby nails.

22. Involvement of the cheeks is characteristic of the infantile pattern of AD.

23. CLINICAL PHASES
Childhood Phase ( 2-12 years )
 Characterized by less acute lesions
 Distribution: antecubital and popliteal
fossae, flexor wrist, eyelids, and face.
 Persistent rubbing and scratching leads to
lichenified plaques and excoriations
 Severe atopic dermatitis involving more
than 50% of body surface area is
associated with growth retardation

24. Childhood Phase
erythematous crusted patches located in the
antecubital fossae

25. CHILDHOOD ATOPIC DERMATITIS
marked lichenification and postinflammatory hyperpigmentation

26. ADOLESCENCE/ ADULT ATOPIC
DERMATITIS
 Age > 12 years old
 Flexural lichenified eczema with facial
involvement in periorbital regions , Upper
trunk, shoulders, scalp affected
 chronic remissions and exacerbations
 70% develop hand dermatitis some times
in their lives

27. ADOLESCENCE/ ADULT ATOPIC
DERMATITIS

28. ADOLESCENCE/ ADULT ATOPIC
DERMATITIS

29. DIAGNOSISDIAGNOSIS
Hannifin & Rajka diagnosis of AD in 1980
 MAJOR FEATURES
1.pruritus
2.typical morhology and distribution
Facial and extensor eczema in
infants and children
Flexural eczema in adolescent
3.chronicity
4. Personal or family family history of atopy

30. DIAGNOSISDIAGNOSIS
 ASSOCIATED FEATURES
Keratosis Pilaris –
perifollicular hyperkeratosis on
extensor arms, thighs and
cheeks
Ichthyosis Vulgaris – This
common genetic d/o is seen in 50% of
AD patients

31.  Dennie-Morgan Lines - symmetric, prominent fold
(single or double) just beneath the margin of the lower
eyelid
 Periorbital darkening or “allergic shiners” -
asymptomatic, symmetric, blue-gray discolorations of the
periorbital skin with accentuation of the lower orbit
(seen in up to 60% of atopic patients)

32. DIAGNOSISDIAGNOSIS
 Associated features
Ant. Subcap. Cataract
Xerosis

33. • Pityriasis Alba - patches of
hypopigmentation with fine
scale, most common on the
face, most noticeable in darkly
pigmented children.
•Chelitis - dry, crusty,
chapped lips or fissuring of the
commissures aggravated by
licking.

34. ASSOCIATED FEATURES
Keratoconus
Hertophe’s sign:
thinning or loss of the outer third of the eyebrows
Conical deformity of the cornea

35.  Periorbital milia
Discrete, 1- to 2-mm
dome-shaped white or
yellowish
papulonodules
Occur individually or in
clusters
Due to rubbing

36. • Lichen Simplex Chronicus - due to chronic rubbing
• Prurigo Nodularis – “picker’s nodules” Intensely
and paroxysmally pruritic. Mostly on extremities.

37. ASSOCIATED FEATURES
Palmar hyperlinearity
Dermographism
Nipple eczema

38. ASSOCIATED FEATURES
Immediate skin test reactivity
Elevated serum IgE
Early age of onset
Tendency toward cutaneous infections
Nonspecific hands & feet dermatitis
Facial pallor/ erythema
Course influenced by environmental factors
DIAGNOSISDIAGNOSIS

39. DIFFERENTIAL DIAGNOSESDIFFERENTIAL DIAGNOSES
Atopic dermatitis Eczematous D/O of Infancy Systemic D/O with
eczematous dermatitis
Scabies Atopic dermatitis Wiskott-Aldrich syndrome
Seborrheic dermatitis Seborrheic dermatitis Selective IgA deficiency
Allergic contact
dermatitis
Scabies X-linked
agammaglobulinemia
Mycosis Fungoides Psoriasis Ataxia-telangiectasia
Nummular eczema Allergic contact dermatitis Chronic granulomatous
disease
Dermatophytosis Irritant contact dermatitis Biotin deficiency
HIV-associated disease Ichthyosis vulgaris Cystic Fibrosis
Familial keratosis pilaris Tinea corporis Netherton syndrome
Dermatitis herpetiformis Nummular eczema Langerhans cell
histiocytosis

40. DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS
Seborrheic dermatitis
Scabies Contact dermatitis
Localized to areas of exposure & not
associated w/ xerosis

41. COMPLICATIONSCOMPLICATIONS
Infections (BacterialInfections (Bacterial
Staphylococcus aureusStaphylococcus aureus
 Seen in >90% of ADSeen in >90% of AD
skin lesionsskin lesions
Moist oozing red scaly plaques & pustules with honey colored
crust formation, folliculitis, impetigo & pyoderma.

42. COMPLICATIONSCOMPLICATIONS
Infections (Viral)
Herpes simplex (Eczema herpeticum
Painful cluster of vesicles on erythematous base
that ulcerate & then form crust

43. COMPLICATIONSCOMPLICATIONS
Molluscum contagiosum
Smooth dome shape papule (2-6 mm) with central
umbilication
Infections (Viral)

44. Eczema Vaccinatum
• Serious complication
that occurs in atopics
receiving the smallpox
vaccine.
• Vaccinia lesions
spread to skin that is
currently or recently
affected by AD.
• Tx: Vaccine Immune
Globulin (VIG)

45. COMPLICATIONSCOMPLICATIONS
Infections (Fungal)
Malassezia furfur
 Usually in head and neck dermatitis
Trichophyton rubrum
Exfoliative dermatitis: may develop in
patients with extensive skin involvement

46. COMPLICATIONSCOMPLICATIONS
Exfoliative dermatitis
associated with
,
caused by:
superinfection (e.g., with toxin-producing S. aureus or HSV
infection
inappropriate therapy
In some cases, the withdrawal of systemic glucocorticoids
used to control severe AD precipitates exfoliative
erythroderma
generalized redness, scaling, crusting,
systemic toxicity, lymphadenopathy, and
fever

47. COMPLICATIONSCOMPLICATIONS
 Ocular
Cataracts may be a primary manifestation of
AD or from extensive use of systemic and
topical glucocorticoids, particularly around the
eyes
Atopic keratoconjunctivitis
usually bilateral
itching, burning, tearing, and
copious mucoid discharge

48. COMPLICATIONSCOMPLICATIONS
 Ocular
Vernal conjunctivitis
typically occurs in younger
patients
is associated with papillary
hypertrophy of the upper eyelid
conjunctiva
Keratoconus i
conical deformity of the cornea

49. TREATMENT
The treatment of AD requires a
systematic, multifaceted approach that
incorporates:
healing theskin and keeping it healthy
identification and elimination of flarefactors
treating symptomswhen they do occur

50. TREATMENT
Cutaneous Hydration
 Lukewarm soaking baths for 15-20 min
 followed by the application of an occlusive
emollient
 Hydrophilic ointments of varying degrees of
viscosity can be used according to the patient's
preference
 Occlusive ointments are sometimes not well
tolerated
 Dressings may also serve as effective barriers
against persistent scratching

51. TREATMENT
Topical Corticosteroids
 There are 7 classes of topical glucocorticoids
 Potency classified from group I (most potent) to
VII (least potent)
 First introduced in the 1950s and are currently
the mainstay of prescription therapy for atopic
dermatitis
 Safe and effective when used as recommended
 Weakest steroid that will keep the eczema under
control should be used
 Potent steroids should be used in short pulses,
generally 2-3 weeks

52. TREATMENT
FACTORS TO CONSIDER WHEN CHOOSING A
TOPICAL STEROID
 Age of patient
 Site to be treated
 Total area of body to be treated
 Severity of disease
 Duration of treatment

53. TOPICAL STEROIDS
• Group I
• Temovate Cream/Ointment
• Ultravate Cream/Ointment
• Psorcon Cream/Ointment
• Diprolene Ointment
•
• Group II
• Diprolene Cream
• Halog Cream/Ointment
• Lidex Cream/Ointment
• Topicort Cream/Ointment
•
• Group III
• Aristocort Cream/Ointment
• Cutivate Ointment
• Elocon Ointment
• Kenalog Cream/Ointment
• Topicort Cream
• Valisone Ointment
• Group IV
• Elocon Cream
• Synalar Cream/Ointment
• Westcort Ointment
•
• Group V
• Aristocort Cream
• Cutivate Cream
• Dermatop Cream
• Kenalog Cream
• Locoid Cream/Ointment
•
• Group VI
• Aclovate Cream/Ointment
• DesOwen Cream/Ointment
• Synalar Cream
• Hytone Cream

54. TREATMENT
• Local side effects of TCS
hyperpigmentation Telangiectasia Acne

55. TREATMENT
Skin atrophyStriae
Local side effects of TCS

56. TREATMENT
Adverse effects of TCS
 Suppression of hypothalamic-pituitary-adrenal
axis
 Iatrogenic Cushing’s syndrome
 Growth retardation in infants and children
These effects are usually associated with the large
body surface area use of potent TCS.

57. TREATMENT
Topical Calcineurin Inhibitors
Pimecrolimus cream 1% (Elidel)
is indicated for mild to moderate AD.
Tacrolimus ointment 0.1% and 0.03% (Protopic)
is indicated for moderate to severe AD.
Both are approved for short-term or
intermittent long-term treatment of AD in
patients ≥2 yr whose disease is
unresponsive to or who are intolerant of
other conventional therapies .

58. TREATMENT
Topical Calcineurin Inhibitors
 may be better than topical corticosteroids in the
treatment of patients whose AD is
poorly responsive to topical steroids
patients with steroid phobia,
and of patients with face and neck
dermatitis, in which ineffective, low-potency
topical corticosteroids are usually used because of
fears of steroid-induced skin atrophy.

59. TREATMENT
Tar Preparations
are useful in reducing the potency of topical
glucocorticoids required in long-term
maintenance therapy of AD.
Tar shampoos can be particularly beneficial for
scalp dermatitis.
Adverse effects associated with tar preparations
include skin irritation, folliculitis, and
photosensitivity.
Antihistamines
Systemic Corticosteroids

60. TREATMENT
Cyclosporine
is a potent immunosuppressive drug that
acts primarily on T cells by suppressing
cytokine gene transcription.
(5 mg/kg/day) for short-term and long-term
(1 yr) use has been beneficial for children
with severe, refractory AD.
Possible adverse effects include renal
impairment and hypertension.

61. TREATMENT
Phototherapy
 Natural sunlight is often beneficial to patients with
AD
 as long as sunburn and excessive sweating are
avoided.
 Many phototherapy modalities are effective for AD,
including ultraviolet A-1, ultraviolet B …)
 Phototherapy is generally reserved for patients in
whom standard treatments fail.
 Short-term adverse effects with phototherapy include
erythema, skin pain, pruritus, and pigmentation.
 Long-term adverse effects include predisposition to
cutaneous malignancies.

62. TREATMENT
Unproven Therapies
Other therapies that may be considered in
patients with refractory AD are as follows.
 Interferon-γ
 Omalizumab
 Allergen Immunotherapy
 Probiotics
 Chinese Herbal Medications
 Antimetabolites

63. PROGNOSIS
 Spontaneous resolution of AD has been reported
to occur after age 5 yr in 40-60% of patients
affected during infancy.
 Earlier studies suggested that approximately
84% of children outgrow their AD by adolescence;
 later studies reported that AD resolves in
approximately 20% of children monitored from
infancy until adolescence and becomes less
severe in 65%.
 Of those adolescents treated for mild dermatitis,
>50% may experience a relapse of disease as
adults, which frequently manifests as hand
dermatitis, especially if daily activities require
repeated hand wetting.

64. PROGNOSIS
Predictive factors of a poor
prognosis:
 widespread AD in childhood
 concomitant AR & asthma
 family history of AD in parents/sibling
 early age of onset
 being an only child
 very high serum IgE levels
 filaggrin gene null mutations

65. PREVENTION
 Breast-feeding or a feeding with a hypoallergenic
hydrolyzed formula may be beneficial.
 If an infant with AD is diagnosed with food
allergy, the breast = feeding mother will need to
eliminate the implicated food allergen from her
diet.
 Identification and elimination of triggering
factors is the mainstay for prevention of flares as
well as for the long-term treatment of AD.

66. Flawless Skin