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CBD DERMATITIS ATOPI

IDENTITAS
Nama : An. MKT
Usia / TTL : 1 tahun 2 bulan
Jenis kelamin : Lelaki
No. RM : 427-55-90
Alamat : Jakarta

MRS :29 Oktober 2018

Keluhan utama
• Ruam pada kulit disertai gatal-gatal sejak usia 2 bulan yang
memberat 1 minggu SMRS
RIWAYAT PENYAKIT SEKARANG

Usia 2 bulan : Usia 5 bulan :


• Terdapat keluhan gatal-gatal di • Pada usia 5 bulan ruam-ruam bertambah di sekitar
wajah, bentuk seperti ruam, pipi, ruam di lipat lengan juga bertambah.
terutama di dahi, sekitar mata, dan • Sejak lahir hingga usia 5 bulan pasien minum ASI
lipat lengan dan susu formula.
• Ruam hilang timbul, terutama • Tidak ada keluhan grok-grok atau bunyi mengi, tidak
muncul saat cuaca panas atau ada keluhan BAB cair atau disertai darah, tidak ada
gerah keluhan colic
• Karena keluhan yang semakin bertambah orang tua
• Tidak ada keluhan gatal apabila
membawa pasien ke DSA dan dikatakan alergi susu
udara dingin, gatal bila berkeringat
sapi sehingga susu diganti menjadi soya
• Keluhan gatal selalu timbul di • Menurut orang tua sejak diganti soya ruam di pipi
lokasi yang sama, tidak berpindah perbaikan namun masih ada keluhan ruam di sekitar
mata dan lipat lengan saat gerah
RIWAYAT PENYAKIT SEKARANG

• Sejak 2 minggu terakhir ruam bertambah banyak dan menyebar mulai dari wajah
hingga ke seluruh tubuh, menurut ibu ruam bertambah banyak ketika sabun
lactacyd diganti menjadi lactacyd mild.
• Ibu membawa pasien ke poli umum dan diberikan sebamed dan atopiclair serta
cetirizine namun gejala belum perbaikan sehingga dikonsulkan ke divisi Alergi
Immunologi.
• Di rumah tidak ada ada hewan peliharaan, tidak ada karpet bulu-bulu, rumah
dibersihkan 1x/minggu
Riwayat penyakit sebelumnya
 Alergi susu sapi (+)
 Pilek pagi hari (-)
 Bunyi ngik-ngik atau batuk di malam hari (-)
 Riwayat kelahiran:
 spontan, cukup bulan, tidak ada riwayat resusitasi aktif. Anak ke 1..
 Riwayat imunisasi:
 lengkap
 Riwayat tumbuh kembang:
 Pasien belum bisa mengangkat kepala, belum bisa duduk, belum bisa bicara
 Riwayat keluarga:
 Ibu pasien: Riwayat alergi dingin
 Ayah: tidak ada riwayat asma, rihintis alergi maupun dermatitis
 Riwayat nutrisi:
 Susu soya, bubur susu
PEMERIKSAAN FISIS

Keadaan umum
• Tampak sakit ringan
• Kesadaran compos mentis
• Gizi baik, perawakan normal

Tanda Vital
• GCS 15
• TTV stabil
Organ Deskripsi

Wajah Tidak dismorfik

Mata Konjungtiva tidak pucat, sklera tidak ikterik, edema tidak ada
Dennie morgan lines (-), allergic salute (-), allergic shiner (-), ruam pada pipi,
Wajah
tampak kering
THT Tonsil ukuran T1-T1, tidak hiperemis, geographic tongue (-)

Leher Tak teraba pembesaran KGB multipel

Dada Gerakan simetris saat statis dan dinamis

Jantung Bunyi jantung I/II normal, tidak ada bising jantung, tidak ada irama derap

Paru Vesikular kanan = kiri, tidak ada mengi/ronki

Abdomen Datar, lemas, bising usus baik, tidak ada organomegali

Ekstremitas Akral hangat, perfusi perifer <2 detik, tidak sianosis


Pemeriksaan Fisis
Status lokalis
a/r pipi, lipat lengan kanan, dan kiri : Plak eritema multipel, dengan papul multipel,
kering, dengan skuama kasar di atasnya, tidak ada edema, tidak ada nyeri tekan
a/r dada, punggung : Plak eritema multipel
Diagnosis Kerja
 Dermatitis Atopi
Tatalaksana
 Atasi dermatitis atopi  Atopiclair® lotion (sehabis mandi)
 Elocon® cream 1x sehari
 Atasi gatal  Cetirizine 2x 2.5 mg
PEMBAHASAN
Definition
 Dermatitis atopik (DA) adalah peradangan  Atopic dermatitis (AD) is a chronic
kulit kronis residif disertai gatal yang disease of the skin based on skin
umumnya sering terjadi selama masa bayi barrier dysfunction, which leads
dan anak, sering berhubungan dengan together with environmental factors and
peningkatan kadar IgE dalam serum dan multiple changes of the immune system
riwayat atopi pada penderita atau to eczematous and itchy lesions at
keluarganya the flexural folds and other typical
distributions.

Akdis CA, et al, Allergy 2006 ;


Santosa H, Buku Ajar Alergi&Imunologi
(AAP, 2015)
Anak, 2007
Pathogenesis
 The pathogenesis of AD is complex and multifactorial.
 Skin barrier dysfunction, environmental factors, genetic pre- disposition,
and immune dysfunction all play a role in its development

 Some theories :
 T helper cell dysregulation, production of immunoglobulin E (IgE), and mast
cell hyper-activity leading to the development of pruritus, inflammation, and the
characteristic dermatitis.
 skin barrier dysfunction
Skin Barrier Dysfunction Theory
 The primary function of the skin barrier is to restrict water loss and to
prevent entry of irritants, allergens, and skin pathogens.

 Stratum corneum, is critical to the integrity of the skin barrier, with the
protein filaggrin being a key player in stratum corneum structure and
formation.
Skin Barrier Dysfunction Theory
 Several mechanisms :
 Inadequate filaggrin production  reduced ability of keratinocytes to
maintain hydration and to restrict epidermal water loss  xerosis  pruritus 
AD
 Inadequate skin barrier  allow for the entry of aeroallergens  in-
flammatory response  AD
 Altered skin barrier  change of local pH  overgrowth bacteria such as S.
aureus  trigger innate immune response  lead to inflammatory skin lesions
Immune mechanisms of staphylococcal superantigen action
(Leung, J Allergy Clin Immunol, 2000)
Allergies and AD
 The relationship between AD and food allergy is complex but likely
overemphasized.

 More than 90% of parents incorrectly believe that food allergy is the sole or
main cause of their child’s skin disease

 True food-induced AD is rare.


 The most common cutaneous manifestations of food allergy are often
IgE-mediated and consist of acute urticaria, angioedema, contact
reactions, or in some cases, an increase in AD symptoms.
Allergies and AD
 AD that is worsened by exposure to a food allergen, these
reactions are not IgE-mediated but rather delayed- type
hypersensitivity reactions and usually develop 2 to 6 hours after
the exposure to the food.
 The prevalence of food allergy in all children in the first 5 years of
life is approximately 5%.
 In children with AD, however, the prevalence of food allergy is
approximately 30% to 40%, and up to 80% will have high food-
specific IgE concentrations, even in the absence of a true food
allergy.
 Patients who have food allergy often have earlier- onset and more
Clinical
 Usually begin at 6 months old,
Features
 60% manifest in the 1st year of life,
rarely before 8 weeks 90% in 5th year
 Types  > 75% become asthma, 90%
 Infantile: The predilection are become allergic rhinitis
on face (cheek), extensor. Itch is
the most prominent manifestation  Triggers:
 Irritant: soap, detergent, desinfectan
 Childhood: flexural folds,  Contact allergen/ aeroallergen: dust, pollen
popliteal folds, hands, legs  Microorganisms: candida, dermatophyt,
and periorbital, chronic staphilococcus aureus
xerosis kutis  Viral infection
 Adult: chronic dermatitis,
lichenification, skuamation
 Pruritus is a hallmark of AD, which
Clinical features (Hanifin & Rajka, 1980)
Major Minor
 Itching/pruritus  Early age of onset
Typical dermatitis with a chronic or
relapsing  Dry skin/xerosis
 Keratosis pilaris
 history
Patient or family members with atopy  Ichthyosis vulgaris
Typical distribution and age-specific
patterns  Lip dermatitis
 Hand eczema
 Lichenification
 Elevated IgE level
 Itching on sweating
 Recurrent infections
Hanifin & Rajka, 2001
Hanifin & Rajka, 2001
Treatment
 Treatment principles
 (1) maintenance skin care, designed to repair and maintain a healthy skin
barrier
 (2) topical antiinflammatory medications, to suppress the inflam- matory
response
 (3) itch control
 (4) managing infectious triggers, recognition and treatment of infection- related
flares.
Maintenance of skin care
 Maintenance skin care is the foundation of AD management; its
goal is to repair and maintain a functional skin barrier
 The key facets of maintenance care :
 maintaining skin hydration
 avoiding irritants and triggers.
 The optimal frequency of bathing for children with AD has not
been well studied and remains controversial.
 The specific frequency of bathing should be titrated to the
individual patient and his or her response to bathing.
Maintenance of skin care
 Second and extremely important component of maintaining skin
hydration is lubrication of the skin, commonly referred to as
moisturization.
 Frequent moisturization advantages :
 Alleviates the discomfort associated with xerosis
 helps to repair the skin barrier
 reduces the quantity and potency of pharmacologic interventions.
 Frequent reapplication of lotions is needed to maintain skin
hydration.
 In general, ointments tend to have the greatest moisturizing effect,
followed by creams, and then lotions.
Maintenance of skin care
 Triggers may be unavoidable, but minimizing exposure to them can be
helpful.

 Common triggers may include


 aeroallergens or environmental allergens
 infections (particularly viral illnesses)
 harsh soaps and detergents
 Fragrances
 rough or non- breathable clothing fabrics
 Sweat
 excess saliva
 psychosocial stress.
Topical anti-inflammatory medication
 The eczematous dermatitis seen in AD is the manifestation of an
inflammatory immune response in the skin

 Treatment is focused on suppressing the inflammatory response


 When used inappropriately, there are potential risks of cutaneous atrophy,
striae, telangiectasia, and systemic ab- sorption with resulting adrenal sup-
pression.
Topical anti-inflammatory medication
 For acute flares and moderate to severe cases, wet wrap therapy (wet
dressings) can be used in conjunction with topical steroids to quickly
control the dermatitis.

 Wet dressings advantages :


 increase penetration of topical steroids into the skin
 decrease itch
 serve as an effective deterrent to scratching.
 The technique is straightforward:
 after a soaking bath, topical steroid is applied to affected areas followed by
application of moisturizer to the rest of the skin
 moist gauze or cotton clothing that has been dampened with warm water is
then applied
 the wet layer is covered with dry cotton clothing
 The dressings can be left in place for 3 to 8 hours before being changed.
 Wet dressings can be used continuously for 24 to 72 hours or overnight for
up to 1 week at a time.
Kesimpulan Tatalaksana
Non-farmakologis Farmakologis
 Jangan memakai sabun yang bersifat  Kortikosteroid lokal potensi ringan sampai
basa. sedang,
 Mencegah kekeringan kulit dengan  Antihistamin diberikan untuk menghilangkan
menjaga hidrasi dan pelembab. rasa gatal.

 Identifikasi pencetus dan hindari  Antibiotik oral bila terdapat infeksi sekunder.
pencetusnya
 Leukotrien inhibitor
 Wet dressings  untuk meningkatkan
penetrasi dari steroid topical, mengurangi  Calcineurin inhibitor topikal dapat diberikan
rasa gatal, mengurangi kecenderungan untuk daerah kulit tipis atau lipatan kulit
untuk menggaruk.  Kortikosteroid sistemik; hanya pada kasus yang
berat, diberikan jangka pendek dan harus
diperhatikan efek sampingnya.
Thank you