Dermatitis: Smf/bagian I.k Kulit & Kelamin Fk Uns/rsud Dr.moewardi Surakarta

DERMATITIS

SMF/Bagian I.K Kulit & Kelamin FK UNS/RSUD Dr.Moewardi Surakarta

DERMATITIS • Definisi

Inflamasi pd kompartemen dermo epidermal, sbg reaksi dari rangsang/injuri eksogen atau endogen.

Inflamasi ini biasanya berdasarkan reaksi alergi/respons imun.

Dermatitis Endogen

Dermatitis Eksogen

Dermatitis Atopik

Dermatitis Kontak Iritan

Dermatitis Seboroik

Dermatitis Kontak Alergi

Dermatitis Numularis

Dermatitis Fotosensitif

Pomfoliks

Dermatophytid

Liken simpleks kronis Dermatitis Asteatotik Dermatitis Gravitational Juvenile plantar dermatitis

DERMATITIS ATOPIK

DEFINISI adalah keadaan peradangan kulit kronis dan residif, disertai gatal yang umumnya sering terjadi selama masa bayi dan anak-anak, sering berhubungan dengan peningkatan kadar IgE dalam serum dan riwayat atopi pada keluarga atau penderita (dermatitis atopi, rhinitis alergika, asma bronkhiale, dan konjungtivitis alergika)(Sularsito.S.A & Djuanda, 2005)

STIGMATA ATOPI Kata “atopi” pertama kali diperkenalkan oleh Coca (1923) Yaitu istilah yang dipakai untuk sekelompok individu yang mempunyai riwayat kepekaan dalam keluarganya, misalnya : • • • •

Asma bronkial Rhinitis alergik Konjungtivitis alergik Dermatitis atopik

ETIOLOGI • Interaksi berbagai faktor : genetik , imunologik , farmakologik , lingkungan, sawar kulit.

• 80 % penderita DA memiliki kadar IgE dan eosinofil yang meningkat. • Terdapat defisiensi imunologik, karena fungsi sel – T menurun

PEMICU • • • •

Kulit yang kering Infeksi  kebanyakan oleh S.aureus Perbedaan iklim Alergi oleh inhalan (debu,serbuk bunga) , makanan tertentu, kimiawi (lotion, sabun, detergen) dan autoalergen. • Pakaian terlalu tebal , misal wool • Stress

Gambaran Klinis • Umumnya kulit kering , pucat/kusam , kadar lipid epidermis kurang. • Pruritus >>, hilang timbul terutama malam hari  “eczema is the itch that rashes” • Krn garukan  kelainan polimorfi

Fase Infantil

Fase Anak

Fase Dewasa

Usia 3-10 thn Fossa Cubiti-Poplitea Lesi kering

Usia 2 bln - 2 thn Muka, leher>>, Lutut, madidans

Tipe Infantil

Tipe Anak

Dermatitis Atopik

Tipe Remaja-Dewasa Usia 13-30 thn Fossa Cubiti- Poplitea Frontal periorbita

KRITERIA DIAGNOSTIK (Hanifin & Rajka) • Anamnesis • Gambaran klinis sesuai umur • 3 kriteria mayor + minor (menurut Hanifin-Rajka) MAYOR : • Pruritus • Dermatitis di muka / ekstensor pd bayi-anak • Dermatitis pd fleksura pd remajadewasa • Dermatitis kronis residif • Riwayat atopi penderita keluarga

MINOR: •Xerosis •Infeksi kulit (khususnya oleh S.aureus dan virus herpes simpleks) •Dermatitis nonspesifik pada tangan atau kaki •lktiosis/hipediniar palmads/keratosis pilaris •Pitiriasis alba •Dermatitis di papila mamae •White dermographism dan delayed blanch response •Keilitis •Lipatan infra orbital Dennie-Morgan •Konjungtivitis berulang •Keratokonus •Katarak subkapsular anterior •Orbita menjadi gelap

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       

Muka pucat atau eritem Gatal bila berkeringat Intolerans terhadap wol atau pelarut lemak Aksentuasi perifolikular Hipersensitif terhadap makanan Perjalanan penyakit dipengaruhi oleh faktor lingkungan dan atau emosi Tes kulit alergi tipe dadakan positif Kadar IgE di dalam serum meningkat Awitan pada usia dini1.

DIAGNOSA BANDING • • • • • •

Dermatitis seboroik Dermatitis kontak alergi Dermatitis kontak iritan Dermatitis numularis Psoriasis Dermatofitosis

Dermatitis kontak alergi

dermatitis atopik

Psoriasis Dermatitis atopik

Dermatitis numularis

Dermatitis seboroik

dermatofitosis

PEMERIKSAAN LABORATORIUM • • • • • •

Darah : p↑ IgE serum, eosinofilia. White demographisme Percobaan asetilkolin Tes alergi pd kulit Kultur bakteri : koloni S.aureus di hidung dan lesi kulit PA kulit : berbagai tingkat akantosis, spongiosis, infiltrasi dermis oleh limfosit, monosit,sel mast, dan eosinofil.

40-60 % Sembuh spontan Pada usia > 5 thn

30-50%

20 %

Tipe infantil Bersama Asma Bronkial

DA meghilang saat Remaja

65 % DA gejala ↓ saat Remaja

PROGNOSA

84 % Kadang2 berlangsung hingga Masa Remaja

Kronik residif Remisi pada masa anak dapat kambuh saat remaja – dewasa Dapat komplikasi dengan infeksi S.aureus dan HSV

PENANGANAN UMUM • No rubbing, no scratching ! • Cari faktor pemicu dan sebisa mungkin dihindari • Warning : infeksi sekunder oleh S.aureus dan herpes simplex  segera ke dokter.

Hindari Kontak Iritan

Moist urizer

Gunting kuku Penanganan umum

Sabun Lunak pH <<

Sarung tangan Kompres dingin

MEDIKAMENTOSA • Pengobatan Topikal 1. Hidrasi Kulit diberikan pelembab misalnya krim hidofilik urea 10%, asam laktat 5%, emolien 2. Kortikosteroid Topikal 3. Imunomodulator topikal  Takrolimus (untuk anak usia 2-15 tahun  0,03%; dewasa  0,03%, 0,1%)  Pimekrolimus 4. Preparat Ter (Likuor Karbonis Detergen 5%10% atau crude coal tar 1%-5%) 5. Antihistamin

• Pengobatan Sistemik 1. Kortikosteroid (Sistemik : Prednison (30-60 mg/hari) 2. Antihistamin  Sistemik  generasi I dan II  Generasi I  difenhydramin Hcl, klorfeniramin maleat, hidroxyzine  Generasi II  loratadin 1. Antiinfeksi 2. Interferon 3. Imunomodulator • siklosporin 2mg-5mg/kg/hari setelah gejala hilang tap off

PENGOBATAN SESUAI LESI Penatalaksanaan

Dermatitis Atopik AKUT

Kompres Dingin Krim Steroid Balut Basah Antibiotika Antiviral

KRONIS

AntiPruritus Salap Tar LCD Krim Steroid poten Balut Oklusif Injeksi KIL

DERMATITIS NUMULARIS

DEFINISI DAN INSIDENSI DEFINISI • = discoid eczema • Khas: lesi seperti uang logam/lonjong, batas tegas INSIDENSI • Anak-anak << • >> pada usia 55-65 tahun • >

FAKTOR PENCETUS • Penyebab pasti ?? • Diduga: • infeksi stafilokokus  mekanisme hipersensitivitas • Dermatitis atopik pada anak-anak • Bahan, sabun, air, stres emosional, alkohol, obat– obat topikal & sistemik

GAMBARAN KLINIS • Stadium akut: • Papula & vesikel bersatu  lesi khas: uang logam berwarna merah dan diskret • Lesi mengalami penyembuhan di tengah • Eksudasi, edema, dan krusta

• Stadium lanjut: skuama dan likenifikasi. • Predileksi: • tungkai, lengan termasuk punggung tangan dan tubuh • >> anggota gerak bawah

PENATALAKSANAAN • Kulit harus dalam keadaan hidrasi: • Pelembab • Hindari pemakaian bahan wol

• Pengobatan: • Topikal: • Kortikosteroid • Takrolimus • Pimekrolimus

• Sistemik: • Antibiotik: bila ditemukan infeksi sekunder • Antihistamin

PROGNOSIS • Cenderung bertahan beberapa waktu  sembuh • Rekuren

Also known as “Dyshidrotic eczema” A form of eczema of the palm and soles, oedema fluid accumulated prominent vesicular eruption or bullae: The palms  Cheiropompholyx The soles  Podopompholyx

>> young adults (<40 y) on both sexes Aetiolgy : obscure, no exogenous cause is found

Clinical picture Intensely itch No erythema but a sensation of heat and prickling may precede attacks Deep-seated vesicle confluent large bullae 2 -3 weeks : subsides spontaneously & resolution with desquamation dryness, cracking & scaling 80% the palms & lateral aspect of finger 12% involvement of instep & sole

Acute phase : hand or feet soaked in sol burrowi (aluminium acetat 10%) or sol rivanoli 1/2000 : 3-4 X daily, large bullae aspirated Systemic and or topical antibiotics When eruption << : soak stop

zinc cream or

topical corticosteroids (subacute & chronic) Oral corticosteroid

Also known as “Circumscribe neurodermatitis” A cutaneous response to reapeted rubbing or scrubbing >> adults with family history of atopic disorders (as localized form of AD) Women more common than men Well-defined hyperpigmented lichenified lesion Intensely itch  Itch-scratchinflammation cycle Emotional factors is important

The common site of LSC: • • • • • •

The nape Lower legs Scalp Upper thighs Vulva, scrotum,pubis Extensor fore arms

Potent topical corticosteroids under occclusion & short period

Triamcinolone : intra dermal injection Sedatian & anti pruritic

Scratching habit must be stopped Antipruritic

Also known as : Xerosis Eczema craquele, Winter itch Ecz. Associated with & possibly caused by in skin surface lipid Particularly on leg, arms & hand predominantly in elderly during winter months and clearing in the summer Clinically :

Fine dry scaling and cracking “Crazy paving” skin appearance Cracks & fissures may be red & inflammed

Greasy emollients preparation Bath oil & an emollient cleanser daily Mild topical corticosteroids, in urea base or non-steroid cream (R/atopiclaire)

Also known as : Stasis dermatitis,Hypostatic eczema Varicose eczema

Due to venous stasis resulting from varicose vein, secondary to venous hypertension & deep vein thrombosis Clinical features : Inner aspect of lower legs Dry skin, pruritic, edema,

Erythematous & purpuric with accumulation of thick greasy scale Thinning of skin & shiny Hyperpigmented following healing

Elasticated support stocking or compression bandage Leg fully elevated for at least several hours each day Bland, non-sensitising astringent White soft paraffin

Mild potency topical corticosteroid Systemic corticosteroid rarely indicated

Juvenile Plantar Dermatosis  Occurs primarily in children with an atopic diathesis  Prepubertal children have thinner stratum corneum of the plantar skin  Worsens during the winter  Humid environment in shoes leads to swelling and maceration of the stratum corneum, which is then less resistant to friction.

Juvenile Plantar Dermatosis Plantar foot may be tender, red, dry, shiny; may have cracks and fissures

Juvenile Plantar Dermatosis  Observed more often since impermeable materials like plastic and rubber have been used for sports shoes

 Consider allergic contact dermatitis, tinea pedis in DDx  Tx: Change shoes. Apply emollients, keratolytics.

• Skin damage after inflammatory reaction due to contact with irritant (usually chem.) • 90% of industrial dermatitis • Commonly cause by weaker irritant : reapeted & cumulative • Stronger irritant  acute toxic contact dermatitis • In infant & elderly incontinent patients  napkin dermatitis • In adults  both palmar, dorsum of the hands and face exposed to occupational irritant

Weak (‘relative’) irritants Bleaches

Soaps

Cleanser

Solvents

Cutting Oils

Weak acids

Detergents

Weak alkalis

Enzymes, e.g in body secretions and biological washing powders

• Identified irritant factors and reduced • Barrier cream containing dimethicone • Liberal use of emollients • Mild topical cortocosteroids • Topical anticandidal for 2nd Candida albicans infection in napkin dermatitis

• A delayed-type hypersensitivity reaction of the skin following topical exposure to antigen • Sensitization may be after a short periode of contact or many years of regular exposure • The clinical patterns : erythema and edema follows the site of contact • >> flexures, the eyelids & hands • << The young & very old  because of  CMI

• Patch testing  the cornerstone of diagnosis • Appropriated antigens produce positive reaction after 48-96 hours of application (under occlusion) • Not performed during a periode of severe acute eczema  “Angry Back” syndrome

Substance (Common source) Antibiotics, e.g. penicillins, neomycin, sulphonamides Antihistamines, e.g. diphenhydramine, promethazine Antiseptics, e.g. thimerosal, hexachlorophene Balsam of Peru (polishes and cosmetics) Chromate (cement, leather, mathces) Cobalt (cement) Colophony (sticking plaster) Dyes, e.g. p-phenylenediamine (hair colourings, clothing, shoes) Lanolin (ointments, cosmetics) Local anaesthetics, e.g. benzocain (pain- and pruritus- relieving cream)

Nickel (jewelers, zips, fastenings) Plants, e.g. Rhus (poison ivy, poison oak), primula, chrysanthemums Preservatives, e.g. p-hydroxybenzoic acids (ointments, creams) Rubber preservative chemical (gloves, shoes, elastic, tyres)

• Avoid precipitating antigens • Cool bathing & compresses in very acute cases • Bland emollients of low sensitizing potential • Topical corticosteroids or non-steroid corticosteroid (atopiclaire) • Oral corticosteroids

• Certain substrats (drug or chemical) transformed into sensitizer after exposed to UV • Following topical or systemic administration of certain photosensitizing agents • Clinical features similar with ACD • Generally affecting sites exposed to sunlight

Substance (Photosensitizing agents) Aftershave lotion, perfumes & cosmetics (musk ambrette, 6methylcoumarin, psoralens) Animal foodstuffs (quinoxaline-n-dioxide) Coal tar Cutting oils Drugsa , e.g. antiarrhythmics, antibacterials, antifungals, antidepressant, antidiabetics, diuretics, NSAIDS, tranquilizers Dyes Furocoumarins, e.g. 8-methoxypsoralen Sunscreens, e.g. p-aminobenzoic acid (PABA), PABA esters, benzophenones, dibenzolymethanes, cinnamates a

Includes drugs applied topically or administered systemically

Abbreviation : NSAIDS = Non-Steroidal Anti-Inflammatory Drugs

Avoidance of exposure to sunlight Removal of the precipitating photosensitizer

High-protection, non-irritating sun screen Topical corticosteroids

Oral corticosteroids

Synonyms :

Autosensitisation or ‘id’ dermatitis • A secondary eczematous reaction, as a reaction to a dermatophyte infection elsewhere in the skin, in hypersensitive individual Clinical Feature: • Characterized by the sudden symmetrical eruption of tiny vesicles on distant site, e.g the sides of fingers or feet

The aim of treatment is to identify and treat the precipitating cause

Secondary lesions are treated as for pompholyx