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U V E I T I S

WINARTO

Sub depart. of E.E.D.DEPT. of OPHTHALMOLOGY

FAC. of MEDICINE, DIPONEGORO UNIVERSITY /

DR KARIADI HOSPITAL

S E M A R A N G

Competence of general practitioners:

1. Able to diagnose of anterior uveitis which need

prompt treatment by ophthalmologist ASAP

2. Able to differentiate anterior uveitis from acute

angle closure glaucoma give initial tretment

3. Able to diagnose of vitreus opacity which needs

prompt treatment by ophthalmologist

4. Able to recognized an emergency cases of uveitis

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Autoimmunediseaseoftheeye

Eyecanbeaffectedbymanyautoimmunediseases

primarilytargeting theeye

targetotherpartsofthebodybutalsotheeye

Ocularsymptoms :

mildorseverevisualchanges

completelossofvision

devastatingsystemicandoculareffects

TheProblems:

Noninfectiousuveitisisanimportant

causeofblindness

Complicationscancausepermanent

structuresdamage

Uveitisrarebutmorbid

Cannotbediagnosedquickly

Noninfectiousuveitis:asight

threateningocularinflammation

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Thebeliefsthat

Difficulttofindtheunderlyingcause

Uselessmakingabigefforttofindthe

cause

Toodangeroustoconsidersystemic

chemotherapy

Mata normal

Matanormal

Siliaposisinormal

Konjungtivatenang Korneajernih

Reflekspupilnormal

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U V E A

anterior

intermedia

posterior

conjungtiva

sclera

choroid

retinauvea

cornea

lensa

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UVEA :

1. IRISmspinchterpupilae:tepi,parasimpatis

m.dilatatorpupilae:radier,simpatis

2.CORPUSSILIARIS,epitheliriskebelakang:

luar (pigmented) RPE

dalam(nonpigmented) humoraquos

terdiridari3macamotot:m.radialisint,m.

longitudinalisekstdanm.oblique kontraksi

lensacembung

3.KHOROID

fungsi:suplainutrisi

vask:asiliarislongusdanbrevis

saraf:nsiliarisanteriorlongusdanbrevis

DIAGNOSIS:

1. Riwayat penyakit

2. Pemeriksaan mata

3. Pemeriksaan tambahan:

a. Fluorescein angiography

b. OCT

c. B-scan

d. Pemeriksaan Lab.

Yeh S, Faia LJ, Nussenblatt RB. Semin Immunipathol; 2008;30:145-164

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I. KELAINAN KONGENITAL

1. Koloboma

2. Aniridia

UVEITIS

UVEITIS: adalahinflamasiuvea yang

mengancamketajamanpenglihatan.

Gejala:matamerah,nyeri,fotofobia,epifora,

kabur responinflamasi injeksi silier,

eksudasi khemosis.

UVEITIS:

Uvetisinfeksi

Uveitisnoninfeksi=idiopatik

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Penyebabterbesardarikebutaanyang

dapatdiobatipadausia25 65.

Penyebabkeduakebutaansetelah

retinopatidiabetik.

Merupakangabungandariberbagai

macamkeadaaninflamasimata.

Prevalensidinegarabarat115/100.000.

Kurangdarimemerlukanobat

immunosupresi 35%visustetap

kurang.

USA: 10 15%penyebabkebutaan

bilateral

22%penyebabkebutaanunilateral

UK:10%gangguantajampenglihatan

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Uveitismemerlukanpengobatansteroidjangkalama Efeksamping:

1.KadarGulanaik

2.Glukomasekunder

3.Katarak

4.Moonface

5.Hipertensi

6.Dll

Obatlain? efekterapidicapai,SEminimal

PATOGENESIS

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ETIOLOGIUVEITIS

INFEKSI AUTOIMMUNE

Steroid

ImprovedDiagnostics

AssessSeverity

MonitorResponseofTreatment

UnderstandingImmunology

IdentificationRiskofVisualAcuity

TargetedTherapy

KEMAJUANPENGOBATAN

NSAID

Imunologi:4tipereaksiGell&Coombs:1.Reaksianafilaktoid

2.Reaksisitotoksik

3.Reaksiimunkompleks

4.Cellmediatedimmunity

Traumapadauveadapatsebabkanperusakandan

imunisasisensitizedcellatauantibodipadamatayangtidaktrauma(oftalmiasimpatika)

Peny.tertentuberhubungandgnHLAB27

Mekanismeautoimunbanyakbhbdgnbentuk

inflamasinoninfeksidariretinadanuvea:pars

platinis,oftalmiasimpatika,endoftalmitis

anafilaktik,vaskulitisretina

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APC,selefektor,responimunlokaltdkterbentuk

SelT,selMast:ada

SelB,eosinofil,pmn:tdkada

Imuneprivilege

=ACAID(AnteriorChamberAssociated

ImmuneDeviation

Imunosupresisitokin&neuropeptide

Fungsi APCygunik

Inhibitorkomplemen

Uvea anterior

RobertE.ConeandRoshanPais.Hypothesis AnteriorChamberAssociated

ImmuneDeviation(Acaid):AnAcuteResponsetoOcularInsultProtectsfrom

Future ImmuneMediatedDamage?OphthalmologyandEyeDiseases2009:13340

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Hypothetical model for events in the anterior chamber following

the intracameral injection of antigen. The trauma of injection

induces damage associated molecular pattern (DAMP) molecules

that induce the production of MCP1 and TNFa. TNFa is also

induced and/or maintained by TGFb in aqueous humor. TNFa

increases the production of MCP1. MCP1 attracts circulating

F4/80+ cells that enter the anterior chamber and obtain

antigen from resident iris/ciliary body F4/80+,CD11c+ cells. The

infiltrated monocytes are influenced by TGFb and exit the

anterior chamber via Schlemms canal. These cells recirculate to

the thymus and spleen where they participate in the induction of

regulatory thymocytes and splenic T cells.

RobertE.ConeandRoshanPais.Hypothesis AnteriorChamberAssociated

ImmuneDeviation(Acaid):AnAcuteResponsetoOcularInsultProtectsfrom

Future ImmuneMediatedDamage?OphthalmologyandEyeDiseases2009:13340

Checkpointsindiseasepathogenesiscanserveastargetsforimmunotherapy.

CaspiRR.Mechanisms UnderlyingAutoimmuneUveitis.DrugDisvoveryToday:Disease

Mechanisms.2006;XXX(XX):17

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Keadaanawalpenyebabuveitispadamanusia

tidakjelas, proseskebutaandapatdisebabkan

terjadinyakerusakanjaringanakibatproses

inflamasi.

Uveamerupakanbagianygbanyak

mengandungpembuluhdarah,mensuplai

darah

dan

sel

imun.

Sehingga

uvea

merepresentasikankeadaanperadanganintra

okuler.

Peranoxidativestress

Yadav UCS, Kalariya NM and Ramana KV. Emerging Role of Antioxidants in the Protection of

Uveitis Complications. Current Medicinal Chemistry, 2011, 18, 931-942

Oxidativestressmempunyaiperansebagai

penyebabperadanganpadauveitisinfektif

maupunnoninfektif.

Pengurangankerusakanjaringandanfungsidenganpemberianantioxidandapat

memperbaikikomplikasivisual.



Peranoxidative stress

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Effekantioxidanmencegahkomplikasipadauveitis



CyclosporineA

Steroid, cyclosporine

II. UVEITIS

Pembagian :

1. Uveitis anterior

2. Uveitis intermedia3. Uveitis posterior

4. Panuveitis

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Bagian apakah yang terlibat inflammasipada Uveitis ?

1. Kornea

2. Iris

3. Conjungtiva

4. Uvea anterior

5. Sclera

6. Uvea posterior

Bagian apakah yang terlibat inflammasi

pada Uveitis ?

1. Kornea

2. Iris

3. Conjungtiva

4. Uvea anterior

5. Sclera

6. Uvea posterior

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II. U V E I T I S

International Uveitis Study Group (anatomical) :

1. Anterior Uveitis

2. Intermediate Uveitis

3. Posterior Uveitis

4. Pan Uveitis

UVEITIS adalah inflamasi uvea.Gejala : mata merah, nyeri, foto fobia, epifora,

kabur respon inflamasi cilier injeksi, eksudasi

khemosis.

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2004: Standardization of Uveitis

Nomenclature (SUN) menambah kriteriaonset, duration dancourse of the disease.

Manfred Zierhut,1 Christoph Deuter1 and Philip I Murray. Classification of

Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:77-

78

1987: International Uveitis Study Group(IUSG)

Type Primary Site of

Inflammation

Includes

Anterior uveitis Anterior chamber Iritis

Iridocyclitis

Intermediate uveitis Vitreous Pars planitis

Posterior uveitis Retina or choroid Focal, multifocal or

diffuse choroiditisChorioretinitis

Retinochoroiditis

Retinitis

Neuroretinitis

Panuveitis Anterior chamber,

vitreous and retina or

choroid

Table 1: SUN Working Group Classification of Uveitis



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Category Description Comme nt

Onset Sudden

Insidious

Duration Limited

Persistent

< 3 months duration

> 3 months duration

Course Acute

Recurrent

Chronic

Episode characterised by sudden onset

and limited duration.

Repeated episodes separated by periods

of inactivity without treatment >3months duration.

Persistent uveitis with relapse in 50

* Field Size is a 1 x 1 mm slit beam.



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Table 4: SUN Working Group Grading Scheme for Anterior

Chamber Flare

Grade Description

0 None

1+ Faint

2+ Moderate (iris and lens details clear)

3+ Marked (iris and lens details hazy)

4+ Intense (fibrin or plastic aqueous)



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Table 5: SUN Working Group Activity of Uveitis Terminology

Term Definition

Inactive Grade 0 cells*

Worsening

activity

Two step increase in level of inflammation

(e.g. anterior chamber cells, vitreuas haze)

or increase from grade 3+ to 4+

Improved activity Two step decrease in level of inflammation(e.g. anterior chamber cells, vitreuas haze)

or decrease to grade 0

Remission Inactive disease for 3 months after

discontinuing all treatment for eye disease

PENTING UNTUK EVALUASI PENGOBATAN

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Ocular Manifestations of Autoimmune DiseaseDisease Ocularmanifestations

Rheumatoid

arthritis (25%)

Juvenile R.A

Sjgren's syndrome

Ankylosing

spondylitis

Uveitis

Reiter'ssyndrome Recurrentconjunctivitis,uveitis,keratitis,

arthritis(knee, sacroiliac),urethritis

Enteropathic

arthritis

Uveitis,episcleritis,peripheralulcerativekeratitis

Psoriaticarthritis Uveitis,conjunctivitis,keratitis

Sarcoidosis Uveitis,conjunctival nodules,cranialnerve

Disease Ocularmanifestations

Systemiclupus

erythematosus

Keratoconjunctivitis sicca,conjunctivitis, uveitis,episcleritis,

scleritis,keratitis,retinalhemorrhages,retinalvasculitis,

proliferativeretinopathy,opticneuritis,ischemicoptic

neuropathy,hemianopia,amaurosis,internuclear

ophthalmoplegia, pupillary abnormalities,oculomotor

abnormalities, visualhallucinations

Multiplesclerosis Afferent:opticneuritis,retrobulbar neuritis,visualfielddefects

Efferent:internuclear ophthalmoplegia,

dysmetria,

nystagmus,cranialnervepalsies

Giantcellarteritis Amaurosis fugax,diplopia,visionloss

Proptosis/exophthalmos,lidlagandretraction,keratitis,

decreasedvisualacuity,reducedvisualfields,relative

afferentpupillary defect,lossofcolorvision

Myastheniagravis Diplopia,eyelidptosis

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Disease Ocular Manifestations

Wegener'sgranulomatosis Proptosis/exophthalmos,orbitalcellulitis,

uveitis,corneal

ulcers,

optic

neuropathy

Uveitis ,hypopion

Antiphospholipid

syndromeVasoocclusiveretinopathy,ischemic

opticneuropathy

Polyarteritis nodosa Episcleritis,scleritis,opticneuropathy

Takayasu's arteritis Vasoocclusiveretinopathy,ischemic

opticneuropathy,

cataracts

Dermatomyositis Eyelid/conjunctival edema,uveitis

retinopathy

Ankylosing spondylitis

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ANTERIOR UVEITIS

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Iris dan pupil normal

Gambaran kripte iris jelas

Pupil bulat konsentris

Apakah yang menyebabkan glaukoma

sekunder pada Uveitis ?

1. Synekhia anterior

2. Produksi humor aquos berlebihan

3. Synekhia posterior

4. Iris bombans

5. Occlusio pupillae

6. Seclusio pupillae

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Apakah yang menyebabkan glaukomasekunder pada Uveitis ?

1. Synekhia anterior

2. Produksi humor aquos berlebihan

3. Synekhia posterior

4. Iris bombans

5. Occlusio pupillae

6. Seclusio pupillae

UVEITIS ANTERIORProduction

VasodilatationMiosis

= IRIDOSIKLITIS

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Keratic

presipitathipopion

UVEITIS ANTERIOR

UVEITIS ANTERIOR

Synechia posterior

Iris bombans

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UVEITIS ANTERIOR

Oclusio pupillae

UVEITIS ANTERIOR

Seclusio pupillae =syn. post. perifer totalis

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Production >>>

Viscosity >>>

Cells >>>

Resistance >>

Secondary glaucoma mechanism

Hypopion

Post. synechiae,occlusio pupillae,seclusio pupillae

Tanda:

Bag.depan :keraticprecipitat(KP)

*akut putih/abuabu,bulat

*kronik krenasi,hitam

Granulomatous:besarkekuningan,muttonfat

TIO:rendah,bisatinggibilaTMtertutupkotoran

inflamasi,siliarinjeksi,katarakkomplikata,band

keratopati

Bag.Intermedia :

selinflamasidivitreous

Bag.2/3posterior :

infiltratinflamasichoroid/retina kekeruhanCV,

oedem/atrofichoroid,retina

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DIAGNOSIS

DIAGNOSIS:

1. Riwayat penyakit

2. Pemeriksaan mata

3. Pemeriksaan tambahan:

a. Fluorescein angiography

b. OCT

c. B-scan

d. Pemeriksaan Lab.


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Mata merah

Injeksi konjungtiva

Injeksi konjungtiva

Pembuluh darah

melebar ke perifer

Terdapat pada

konjungtivitis

Mata merah

Injeksi perikornea

Injeksi perikorneal

Pembuluh darah

kecil di sekitar

limbus berwarna

ungu, terdapat pada

Uveitis

Keratitis

Glaukoma

Endoftalmitis

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Iris dan pupil pada iridosiklitis

Gambaran kripte iris tidak jelas,

warna : muddy appearance Pupil kecil (miosis)

UVEITIS ANTERIOR

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ACUTE IRIDOCYCLIITS MUTTON FAT K.P.

FINE KERATIC PRECIPITATES

MUTTON FAT K.P. : pada

granulomatous iridocyclitis

FINE K.P.:

pada non

granulomatous

iridocyclitis

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Opticalcoherence

tomography (OCT).

(A)Normaleye. (B)uveitis

SeldiCOAdan

vitreus

PEM. SLIT LAMP dan OCT

ENDOPHTHALMITIS

DIAGNOSIS BANDING

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INTERMEDIATE UVEITIS

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Intermediate Uveitis

Boke subtype classification :

1. Diffuse inflammatory type :

dust-like opacities

Snowball-like precipitate

No massive snowbank-like exudates

2. Exudative type :

extensive exudations overs the ora and

pars plana

3. Vasoproliferative type :

vascular sheating, occlusion and

neovascularisation

Figure 1. Vitreous condensation (arrow) overlying

the pars plana with extension to the pars plicata

(white arrowhead). Sclera (asterisk). Anterior

chamber angle (black arrowhead).

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Figure 3. Vitreous condensation overlying the pars plana

and peripheral retina with thin filaments extending into the

vitreous (arrow). Anterior part of the pars plana

(arrowhead). Sclera (asterisk).

Figure 2. Vitreous condensation with smooth

surface (arrow) overlying the pars plana and

peripheral retina in a phakic patient after pars plana

vitrectomy. Anterior part of the pars plana

(arrowhead).

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Figure 4. Delicate epiretinal condensations of the vitreous (arrow).

Figure 5. Vitreous condensation with tractional force on the

peripheral retina (arrow) and towards the pars plana (arrowhead).

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Figure 6. Vitreous condensation with tractional force on the pars

plana/peripheral retina (arrow). Pars plicata (arrowhead).

POSTERIOR UVEITIS

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VITRECTOMY

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PANUVEITIS

PAN UVEITIS

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BECHET

Peradangan kronis berulang dengan

penyebab tidak diketahui, terdiri dari

peradangan mata, lesi oral dan genital,

kelainan kulit (erithema nodusum).Mengenai sendi, SSP dan gastrointestinal.

Terdapat vaskulitis retina buta.

Foste CS, Vitale AT. Diagnosis and Treatment of Uveitis.WB Saunders Co.2002.

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VOGT-KOYANAGI-HARADA

SYNDROMEPenyakit multiorgan meliputi mata,

telinga, saraf dan kulit. Lebih banyak

mengenai:

- orang berwarna dari pada kulit

putih.- usia dekade kedua keenam.

Minimum ada 3 dari 4 gejala:

1. Iridosiklitis bilateral kronis.

2. Uveitis posterior

3. Tanda saraf: tinitus, kaku leher, pusing,

masalah saraf pusat, LCS pleositosis.Foste CS, Vitale AT. Diagnosis and Treatment of Uveitis.WB Saunders Co.2002.

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ANKYLOSING

SPONDYLITISUveitis monokuler, berulang, dpt

binokuler.

Nyeri mendadak, fotopobia & kabur yang

ringan atau tanpa gejala.Reaksi inflamasi hebat hipopion.

Uvetis anterior tidak berhubungan dengan

beratnya spondylitis.

Uveitis anterior merupakan manifestasi

terbanyak, bisa konjungtivitis, skleritis.Foste CS, Vitale AT. Diagnosis and Treatment of Uveitis.WB Saunders Co.2002.

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PENGOBATAN

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MEMBINGUNGKAN

1. Mungkin merupakan manifestasi pertama

dari penyakit sistemik.

2. Merupakan gambaran penyakit yang

saling kait mengait.

Kosultasi ke internist dan pem lab seringkali

tidak mendapatkan penyebab.

Diagnosis awal hanya 17%, 85 % diagnosisdapat ditegakkan setelah diikuti bbrp lama,

berdasar pem klinik dan lab yang berulang.

Foster CS, Vitale AT. Diagnosis and Treatment of Uveitis.WB Saunders Co.2002.

FRUSTASI

1. Pada evaluasi seringkali tidak

mendapatkan apa-apa.

2. Idiopatik didapatkan pada 35% kasus.

3. Tidak adaclue untuk diagnostik walauanamnesis & diperiksa berulang (mata dan

sistemik) dan pem lab dokter menyerah.

Hal ini merupakan hal yang tragis karena

tanpa strategi diagnostik akan

menyebabkan kerugian besar.

Foster CS, Vitale AT. Diagnosis and Treatment of Uveitis.WB Saunders Co.2002.

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Pastikan adanya keadaan Inflamasi non

Infektif pada mata Risiko Buta.

Tegakkan Diagnosis Uveitis,

Tentukan: akut, intermiten, kronis

Rencana Pengobatan


Daz-Llopis M, Gallego-Pinazo R, Garca-Delpech S et al. General Principles for the Treatment of Non-

Infectious Uveitis.Inflammation & Allergy - Drug Targets, 2009, 8, 260-265

UVEITIS NON INFEKSI

AKUT

INTERMITEN

KRONIS

Pengobatan lebih agresif, fokus

pada efek jangka pendek untuk

mengontrol peradangan.

Pengobatan perlu perspektiflebih luas. Rencana pengobatan

lebih moderat, untuk jangka

panjang, pakai dosis terkecil

mengontrol peradangan dengan

efek samping minimal.Daz-Llopis M, Gallego-Pinazo R, Garca-Delpech S et al. General Principles for the Treatment of Non-

Infectious Uveitis.Inflammation & Allergy - Drug Targets, 2009, 8, 260-265

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Pengobatan terdiri atas:

1. Sikloplegi

2. Steroid:

a. Topikal

b. Sistemik

c. Periokuler

3. NSAID

4. Immunomodulatory:

a. Antimetabolite

b. Transcription factor

c. Alkylating agent.

5. Biologic:

a. TNF- inhibitor

b. Daclizumab

IMMUNOMODULATORYTHERAPY

(IMT)

1. Antimetabolites:

a. Azathioprine

b. Methotrexate

c. Mycophenolate

mofetil2. Alkylatingagents:

a. Cyclophosphamide

b. Chlorambucil

3. Tcellinhibitor:

a. Cyclosporine

b. Tacrolimus

4. Cytokines:IFN

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CYCLOSPORINE

11aminoacidpeptidemembentukkompleks

dengancyclophilin,berikatankecalcineurin

hambattranslokasinukleussitosolyang

mengaktifkanTcells.

memotongprosestranskripsiTcell

danproduksisitokin(IL2&TNF).

inhibisiselektifpadaselT.

efeknyakecilpadaselB.

Metabolisme

Lipophilic.

Konsentrasipuncak:1 8jam.

MetabolismedihatilewatensimsytochromeP450,diekskresidiempedu.

Interaksiobat:eritromicin,azole,

kontrasepsi,androgens,

methylprednisolone,calciumchannel

antagonists meningkatkankonsentrasi.

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Effek samping

Palingsering:toksikpadaginjal

Padadosistinggi10mg/kg/duntuk

transplantasiorgan.

Padadosisrendahkurangtoksik(25

mg/kg/dunutkpenyakitautoimun).

Toxisitasdapatkembali(reversible)bilaobatdihentikan.

Disain:Randomised,doublemasked,

placebocontrolledclinicaltrial.Evaluasi:

minggu1,2,dan4dantiapbulansampai1

tahun.

Pasien:uveitisposterioridiopatik,

panuveitis/intermediateuveitis,kurang

responterhadapsteroid.

Tujuan:menilaiefektifitas,keamanandantolerabilitascyclosporine.

de Vries. J, Baarsma GS, Zaal, et al. Cyclosporine in the treatment of severe chronic

idiopathic uveitis.BritishJournal ofOphthalmology, 1990,74,344-349

1

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Daz-Llopis M, Gallego-Pinazo R, Garca-Delpech S and Salom-Alonso D. General Principles for the

Treatment of Non-Infectious Uveitis.Inflammation & Allergy - Drug Targets, 2009, 8, 260-265



Probabilitytreatmentsuccespada27pasienidiopathic uveitis berat.

prednisonedancyclosporine prednisonedanplacebo.

p>005. Wilcoxon'sranksumtest,twosided.

Bulan1

12

TREATMENTSUCCES

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Meanvisualacuitydanmean inflammatoryactivitypada27pasien

idiopathic uveitis berat. prednisonedancyclosporine

prednisonedanplacebo. p>005. Wilcoxon'sranksumtest,twosided.

VA dan Inflamasi

Pasienuveitisposteriorkronis:

Pasienrefrakterdengansteroid.

Rekurensaatdosisprednisolone

diturunkan

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Visus, kadar kreatinin dan

inflamasiMathews D, Mathews J, Jones NP. Low-dose cyclosporine treatment for sight-threatening uveitis:

Efficacy, toxicity, and tolerance.Indian J Ophthalmol: 2010;58:55-58.

Lee SH, Chung H, Yu HG. Clinical Outcomes of Cyclosporine Treatment forNoninfectious Uveitis .

Korean J Ophthalmol2012;26(1):21-25

SeoulNationalUnversity:uveitisnoninfeksi

2001 2010.

Siklosporin( 5mg/kb/hari)diberikanbila

steroidgagal,SEsteroid,imunosupresilain

gagal.

Siklosporin+steroid:161pasien

Siklopsorin+imunosupresi:46pasien

Aktifitas:inactive,slightlyactive,active

4

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Lee SH, Chung H, Yu HG. Clinical Outcomes of Cyclosporine Treatment forNoninfectious Uveitis .

Korean J Ophthalmol2012;26(1):21-25

Waktu Klinis terkontrol setelah

pengobatan

Slightly active

Inactive

SIMPULAN

Uveitis Non Infeksi merupakan peradangan

kronis uvea, rekurent, dapat menyebabkan

kebutaan.

Uveitis seringkali membingungkan karena

dapat merupakan penyakit mata, bersama

penyakit sistemik lain atau menifestasi mata

berbagai penyakit sistemik.

Sering menyebabkan frustasi karena

penyebab tidak ditemukan sehingga rencana

pengobatan terarah menjadi sukar.

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SIMPULAN

Kortikosteroid masih merupakan obat

andalan utama tetapi efek sampingnya sangat

merugikan pasien.

Perlu kombinasi obat lain untuk mengurangi

dosis kortikosteroid tetapi perbaikan klinis

dapat dicapai, dengansteroid-sparing

immunomodulary therapy (IMT).

Salah satu IMT adalah Siklosporin.

Kombinasi Siklosporin dengan kortikosteroid

atau imunosupresi lain merupakan pilihan

yang efektif pada pengobatan uveitis non

infeksi, karena mengurangi SE kortikosteroiddan toxisitas imunosupresi.

Pada penggunaan siklosporin perlu

monitoring efek toksik.

SIMPULAN

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Siklosporin mempunyai nilai terbatas

sebagai obat lini kedua pada uveitis

dengan JIA.

Efektifitasnya lebih baik bila digunakan

sebagai kombinasi dengan steroid pada

kasus yang resisten dengan

imunosupresi lain.

SIMPULAN

III. OFTALMIA SIMPATIKA

panuveitis granulomatosa bilateral, setelah trauma

satu mata ( exiting eye) yang diikuti periode laten

kemudian terjadi uveitis pada mata sebelahnya

(sympathizing eye)

# 4 12 mgg setelah trauma, sangat jarang

# klinis :exiting eye panuveitis berat

sympathizing eye keluhan visus turun, fotofobia,

merah ringan tanda panuveitis

# etiologi : tidak diketahui

teori : - hipersensitifitas Retinal S-Ag

- autoimun

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# diagnostik : anamnesis

- riwayat trauma

- riwayat operasi intraokuler

# terapi :

- steroid lokal, sistemik dan periokuler efektif

- sikloplegik : kurangi keluhan

- anti metabolit bila steroid tdk responsif / tdk

ada perbaikan :* enukleasi exiting eye

IV. ENDOLFTALMITIS

peradangan intraokuler yg mengenai ruang corpus

vitreum dan COA

# bentuk yg sering : endoftalmitis infeksi, yg jarang :

endofalmitis steril, berhub dgn sisa lensa atau

bahan toksik yg masuk ke mata ketika trauma atau

operasi intraokuler# gejala & tanda : visus turun, hipopion, dan vitritis

nyeri, hiperemia konjungtiva, khemosis, edema

palpebra dan kornea

# profilaksi :

- sterilisasi sac conj pre op

- disinfeksi daerah operasi povidone iodine

- inj AB sub konj.

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#diagnosa:klinis+lab aspirasihumoraquosusdan

vitreusuntukkulturdansensitivitytest

#terapi:

vitrektomi

ABintravitreal

kalauhebat,proginfaust eviscerasi

#prognosis:

tergantungsaatdatang,jenisendoftalmitis

HIVANDEYE

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V.IMPACTOFHIVINFECTIONONTHEEYE

OccurinadvancedHIV,CD4+

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Hairy leucoplakia Oral candida

KONAS 03

Miliary tuberculosisCryptococcus

neoformans Cerebral toxoplasmosis

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HIV VIRUS

HIV TRANSMISSION

Dendritic cellsunderlying skinshelter andamplify virus

Spread of virus tolymphatic organ,bone marrow,circulation

Virus attachedto mucosalreceptors

Microscopicview ofproces

Membraneor skin

portal of

entry

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Life cycle of HIV

HIV infection in vivo

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Stages in HIV infection

Antibody (-) Antibody (+)

Periode of infectiousness (virus present)

2 weeks

I II III IV

Infection

2 months 2- 15 years Months - years

Incubation period Symptoms occur

Association between virological, immunological, and

clinical events and time course of HIV infection

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Herpes zoster

ophthalmicus

Periocular Molluscum

contagiosum

KONAS 03

Squamous cell carcinoma of the conjunctiva:

associated with HIV infection.

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Multiple Kaposis

sarcoma on the bulbar

conjungtiva

Conjungtival

microvasculopathy

Varicella-zozter keratitis in the absence

dermatitis

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1 32

1. Microvasculopathy

2. CMV retinitis

3. HIV related retinitis

Retinal microvasculopthy with cotton-wool spots

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Active CMV retinitis with full-thickness

retinal whitening with hemorrhage

Intravitreal ganciclovir device in the

vitreal cavity. The device is firmly sutured

to the incision and is immobile.

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Peripheral zone III inactive CMV retinitis in the left eye

Active varicella-zoster virus retinitis

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Toxoplasmic retinochoroiditis

MultiplePneumocystis carinii choroidtits

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Papilledema due to cryptococcal meningitis

(A) Right and

(B) left colour

fundus

photographs

showing

bilateral optic

disc pallor

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VI. UVEA TRAUMA

direct / countercoup

Vossious pigment ring

Traumatic iritis, miosis, mydriasis,

iridodialisis, angle recession, hifema,

trauma choroid, choroiditis, efusi uvea

(ciliochoroidal)

VII. DEGENERATION and ATROPHY of UVEA

Aging

Sclerosis

Gyrate atrophy

Angioid streaks

Myopic choroidal atrophy

Secondary atrophy and dystrophy

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Gyrate atrophy

Angioid streak atrophy

VIII. UVEAL NEOPLASM

Hyperplasty epithelial

Naevus

Melanoma maligna

Neurilemmoma, neurofibroma,

hemangioma

Secondary tumor : Ca mammae, Ca pulmo

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THANK YOU

PREVENTION OF

ENDOPHTHALMITIS

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Infective endophthalmitis :

- infection of posterior segment

- rare complications.

- devastating, frequently results

in visual loss.

- even major advances inasepsis, surgical technique

and antibiotic therapy.

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ETIOLOGIC AGENT

Own bacterial flora :

eye lid margin, conjungtiva, pre ocular

tear film

microbiology

phage typingDNA finger print

TO TREAT

TO PREVENT

OR

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AGENT HOST

ENVIRONMENT

Innate immunity

Adaptive immunity

Normal microflora

Pathogenicity

Virulence

Infective dose

HOST AGENT RELATIONSHIP

Immunocom

promise

HOST AGENT RELATIONSHIP

ENDOPHTHALMITIS or NO

Operating theatre

S. epidermidisS. aureus

St. pneumoniaE coli

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TO PREVENT

PRE OPERATIF DURANTE OPERATIF POST OPERATIF

Primary line defence mechanism

Intact

Recovery ?

Damage

Risk of infection :

NONE HIGH HIGH ?

C L E A N O P E R A T I O N

Intact ?

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PROPHYLACTIC ANTIBIOTICS

1 2 3

PRE OPERATIF

PERI OPERATIF

POST OPERATIF

4

1. Risk factor :

a. local : bacterial flora.

infecton : dermatitis, blepharitis,

conjungtivitis, dacryocystitis, prosthesis.

b. systemic : DM, malignancies.

2. No infection and Good host immunity

I. Reduce number of bacteria :

1. Antibiotics : quinolone ( levofloxacin )

Day before surgery, morning and at operation room

2. Desinfection:povidine iodine 5 % better than 1 %.

II. Avoid contamination : cilia drap

PRE OPERATIF

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Personnel : standard infection control measuresOperation time, operation condition : capsule

rupture, excessive manipulation, etc

DURANTE OPERATIF

1. Sterility

2. Minimal trauma

3. Avoid multiple op.

4. IOL ( silicone are at risk )

5. Avoid post capsule rupture

Postop. care

Wound leak

1. Hygiene

2. Medication :

antibiotics

POST OPERATIF

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1. No infection

2. Good host

immunity

I. Reduce number of

bacteria :

1. Antibiotics

2. DesinfectionII. Avoid contami

nation : cilia,

Replace old ED bottle

1. Sterility

2. Minimal

trauma3. Multiple op.

4. IOL

Postop. Care

Wound leak

1. Hygiene

2. Medication

1. Personnel

2. Operation

condion

PERI OPERATIF ANTIBIOTIC PROPHYLACTIC

TO TREAT

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1. Clinical diagnosis

2. Microbiologic examination :

Anterior chamber aspirate

Vitreus tap

BA, CH.A, SDA, BHI, Thyogl. broth

aerobic anaerobic & Sens. Test.

Culture positive endophthalmitis

or

Sterile endophthalmitis

ANTIBIOTIC

DIRECTLY INJECT

INTO THE VITREUS

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a. Subconjungtival injection :

controversial.

b. Intra cameral / infusate : decreased

contamination, controversial.

c. Intra vitreal : EVS recomended

d. Systemic antibiotics : bad penetration

MIC within the eye variables

1. ANTIBIOTIC

The uses : controversial.

Animal models : concomitant use of

dexamethasone beneficial and no SE.

Despite the conflicting results,

dexamethasone frequently used in

severe cases

2. ANTI INFLAMMATORY DRUGS

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VA light perception :

core vitrectomy + intra vitreal AB

VA better than light perception :

biopsy vitrectomy + intra vitreal AB

Intra vitreal AB post vitrectomy (Gan 2001):

Vancomycin 0.2 mg in 0.1 ml PBS

Gentamicin 0.05 mg in 0.1 ml PBS

Second inj. 3-4 days AB levels within the

vitreus adequate over a week

3. VITRECTOMY

SUMMARY

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2. Ocular surface :

Important role of :

aseptic procedures : desinfection, sterility,

draped lashes.antiseptics : povidine iodine 5 %

topical antibiotics :

quinolone ciprofloxacin, ofloxacin,

levofloxacin, maxifloxacin, gatifloxacin.

1. Pre-operative preparation :

a. No external eye infection

b. No lacrimal obstruction

c. Prosthesis : be carefully

d. Previous eye drops change with fresh bottle.

PREVENTION

4. High Endophthalmitis Risk :

a. Wound leak.

b. Wide corneo-scleral incision.

c. Negative pressure during A/I.

d. Posterior capsule rupture.

e. Phaco-burn.

3. Intraocular antibiotics :

a. subconjungtival injection : controversial.

b. intra cameral / infusate : controversial.

c. intra vitreal

d. Post operative care.

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1. Established diagnosis :

Clinical and microbiological

2. Antibiotics :

a. intra vitreal, second injection.

b. concomitant systemic ? quinolone3. Vitectomy : depend on presenting VA

4. Anti inflammatory controversial.

TREATMENT = MANAGEMENT

2. UVEITIS

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