UVEITIS

WINARTO
Sub depart. of E.E.D.
DEPT. of OPHTHALMOLOGY
FAC. of MEDICINE, DIPONEGORO UNIVERSITY /
DR KARIADI HOSPITAL

S EMARAN 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

Autoimmunediseaseoftheeye

Eyecanbeaffectedbymanyautoimmunediseases
primarilytargetingtheeye
targetotherpartsofthebodybutalsotheeye
Ocularsymptoms:
mildorseverevisualchanges
completelossofvision
devastatingsystemicandoculareffects

Noninfectiousuveitis:asight
threateningocularinflammation
TheProblems:
Noninfectiousuveitisisanimportant
causeofblindness
Complicationscancausepermanent
structuresdamage
Uveitisrarebutmorbid
Cannotbediagnosedquickly

Thebeliefsthat
Difficulttofindtheunderlyingcause
Uselessmakingabigefforttofindthe
cause
Toodangeroustoconsidersystemic
chemotherapy

Mata normal
Matanormal
Siliaposisinormal
Konjungtivatenang
Korneajernih
Reflekspupilnormal

posterior

UVEA
intermedia
anterior
lensa
cornea
conjungtiva
sclera

retina
choroid

uvea

UVEA :
1. IRIS
mspinchterpupilae: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

I.

KELAINAN KONGENITAL

1. Koloboma

2. Aniridia

UVEITIS
UVEITIS: adalahinflamasiuvea yang
mengancamketajamanpenglihatan.
Gejala:matamerah,nyeri,fotofobia,epifora,
kabur responinflamasiinjeksi silier,
eksudasi khemosis.
UVEITIS:
Uvetisinfeksi
Uveitisnoninfeksi=idiopatik

 Penyebabterbesardarikebutaanyang
dapatdiobatipadausia25 65.
Penyebabkeduakebutaansetelah
retinopatidiabetik.
Merupakangabungandariberbagai
macamkeadaaninflamasimata.

USA: 10 15%penyebabkebutaan
bilateral
22%penyebabkebutaanunilateral
UK:10%gangguantajampenglihatan
Prevalensidinegarabarat115/100.000.
Kurangdarimemerlukanobat
immunosupresi35%visustetap
kurang.

Uveitismemerlukanpengobatansteroid
jangkalama Efeksamping:
1.KadarGulanaik
2.Glukomasekunder
3.Katarak
4.Moonface
5.Hipertensi
6.Dll
Obatlain? efekterapidicapai,SEminimal

PATOGENESIS

ETIOLOGIUVEITIS
INFEKSI

AUTOIMMUNE
NSAID
Steroid
ImprovedDiagnostics
AssessSeverity
MonitorResponseofTreatment
UnderstandingImmunology
IdentificationRiskofVisualAcuity
TargetedTherapy

KEMAJUANPENGOBATAN

Imunologi:4tipereaksiGell&Coombs:
1.Reaksianafilaktoid
2.Reaksisitotoksik
3.Reaksiimunkompleks
4.Cellmediatedimmunity
Traumapadauveadapatsebabkanperusakandan
imunisasisensitizedcellatauantibodipadamata
yangtidaktrauma(oftalmiasimpatika)
Peny.tertentuberhubungandgnHLAB27
Mekanismeautoimunbanyakbhbdgnbentuk
inflamasinoninfeksidariretinadanuvea:pars
platinis,oftalmiasimpatika,endoftalmitis
anafilaktik,vaskulitisretina

Uvea anterior

APC,selefektor,responimunlokaltdkterbentuk
SelT,selMast:ada
SelB,eosinofil,pmn:tdkada

Imuneprivilege
=ACAID
(AnteriorChamberAssociated
ImmuneDeviation

Imunosupresisitokin&neuropeptide
Fungsi APCygunik
Inhibitorkomplemen

RobertE.ConeandRoshanPais.Hypothesis AnteriorChamberAssociated
ImmuneDeviation(Acaid):AnAcuteResponsetoOcularInsultProtectsfrom
Future ImmuneMediatedDamage?OphthalmologyandEyeDiseases2009:13340

10

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.MechanismsUnderlyingAutoimmuneUveitis.DrugDisvoveryToday:Disease
Mechanisms.2006;XXX(XX):17

11

Peranoxidativestress
Keadaanawalpenyebabuveitispadamanusia
tidakjelas, proseskebutaandapatdisebabkan
terjadinyakerusakanjaringanakibatproses
inflamasi.
Uveamerupakanbagianygbanyak
mengandungpembuluhdarah,mensuplai
darahdanselimun.Sehinggauvea
merepresentasikankeadaanperadanganintra
okuler.
Yadav UCS, Kalariya NM and Ramana KV. Emerging Role of Antioxidants in the Protection of
Uveitis Complications. Current Medicinal Chemistry, 2011, 18, 931-942

Peran oxidative stress

Oxidativestress mempunyaiperansebagai
penyebabperadanganpadauveitisinfektif
maupunnoninfektif.
Pengurangankerusakanjaringandanfungsi
denganpemberianantioxidandapat
memperbaikikomplikasivisual.

Yadav UCS, Kalariya NM and Ramana KV. Emerging Role of Antioxidants in the Protection of
Uveitis Complications. Current Medicinal Chemistry, 2011, 18, 931-942

12

CyclosporineA

Steroid, cyclosporine

Effekantioxidanmencegahkomplikasipadauveitis
Yadav UCS, Kalariya NM and Ramana KV. Emerging Role of Antioxidants in the Protection of
Uveitis Complications. Current Medicinal Chemistry, 2011, 18, 931-942

II. UVEITIS
Pembagian :
1. Uveitis anterior
2. Uveitis intermedia
3. Uveitis posterior
4. Panuveitis

13

Bagian apakah yang terlibat inflammasi

pada 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

14

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.

15

1987: International Uveitis Study Group

(IUSG)

2004: Standardization of Uveitis

Nomenclature (SUN) menambah kriteria
onset, duration dan course of the disease.
Manfred Zierhut,1 Christoph Deuter1 and Philip I Murray. Classification of
Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:7778

Table 1: SUN Working Group Classification of Uveitis

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 choroiditis
Chorioretinitis
Retinochoroiditis
Retinitis
Neuroretinitis

Panuveitis

Anterior chamber,
vitreous and retina or
choroid
Manfred Zierhut,1 Christoph Deuter1 and Philip I Murray. Classification of
Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:7778

16

Table 2: SUN Working Group descriptors of Uveitis

Category

Description

Onset

Sudden
Insidious
Limited
Persistent

Duration

Course

Acute
Recurrent

Chronic

Comme nt

< 3 months duration

> 3 months duration
Episode characterised by sudden onset
and limited duration.
Repeated episodes separated by periods
of inactivity without treatment >3
months duration.
Persistent uveitis with relapse in <3
months after discontinuing treatment

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

Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:7778

Table 3: SUN Working Group Grading Scheme for Anterior

Chamber Cells

Grade

Cells in Field*

<1

0.5+

15

1+

6 15

2+

16 25

3+

26 50

4+

> 50

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

Manfred Zierhut,1 Christoph Deuter1 and Philip I Murray. Classification of
Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:7778

17

Table 4: SUN Working Group Grading Scheme for Anterior

Chamber Flare

Grade

Description

None

1+

Faint

2+

Moderate (iris and lens details clear)

3+

Marked (iris and lens details hazy)

4+

Intense (fibrin or plastic aqueous)

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

Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:7778

Table 5: SUN Working Group Activity of Uveitis Terminology

Term
Inactive
Worsening
activity

Definition
Grade 0 cells*
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

Manfred Zierhut,1 Christoph Deuter1 and Philip I Murray. Classification of
Uveitis Current Guidelines. EUROPEAN OPHTHALMIC REVIEW. 2007:7778

18

Disease
Rheumatoid
arthritis(25%)

Ocularmanifestations

Ocular Manifestations of Autoimmune Disease

JuvenileR.A
Sjgren's syndrome
Ankylosing
spondylitis
Reiter'ssyndrome

Enteropathic
arthritis
Psoriaticarthritis
Sarcoidosis

Disease
Systemiclupus
erythematosus

Uveitis

Recurrentconjunctivitis,uveitis,keratitis,
arthritis(knee, sacroiliac),urethritis
Uveitis,episcleritis,peripheralulcerativekeratitis
Uveitis,conjunctivitis,keratitis

Uveitis,conjunctival nodules,cranialnerve
li
l
dl i l l d
i

Ocularmanifestations
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,visualfield
defects
Efferent:internuclear ophthalmoplegia,dysmetria,
nystagmus,cranialnervepalsies

Giantcellarteritis

Amaurosis fugax,diplopia,visionloss
Proptosis/exophthalmos,lidlagandretraction,keratitis,
decreasedvisualacuity,reducedvisualfields,relative
afferentpupillary defect,lossofcolorvision

Myastheniagravis

Diplopia,eyelidptosis

19

Disease
Ocular Manifestations
Wegener'sgranulomatosis Proptosis/exophthalmos,orbitalcellulitis,
uveitis,cornealulcers,opticneuropathy

Antiphospholipid
syndrome

Uveitis ,hypopion
Vasoocclusiveretinopathy,ischemic
opticneuropathy

Polyarteritis nodosa

Episcleritis,scleritis,opticneuropathy

Takayasu's arteritis

Vasoocclusiveretinopathy,ischemic
opticneuropathy,cataracts

Dermatomyositis

Eyelid/conjunctival edema,uveitis
retinopathy

Ankylosing spondylitis

20

ANTERIOR UVEITIS

21

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

22

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

UVEITIS ANTERIOR
= IRIDOSIKLITIS

Miosis

Production

Vasodilatation

23

UVEITIS ANTERIOR

Keratic
presipitat
hipopion

UVEITIS ANTERIOR

Synechia posterior

Iris bombans

24

UVEITIS ANTERIOR

Oclusio pupillae

UVEITIS ANTERIOR

Seclusio pupillae =
syn. post. perifer totalis

25

Secondary glaucoma mechanism

Production >>>

Post. synechiae,
occlusio pupillae,
seclusio pupillae
Viscosity >>>
Cells >>>
Resistance >>
Hypopion

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

26

DIAGNOSIS

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

27

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

28

Iris dan pupil pada iridosiklitis

Gambaran kripte iris tidak jelas,

warna : muddy appearance
Pupil kecil (miosis)

UVEITIS ANTERIOR

29

ACUTE IRIDOCYCLIITS

MUTTON FAT K.P.

FINE KERATIC PRECIPITATES

FINE K.P.:
pada non
granulomatous
iridocyclitis

MUTTON FAT K.P. : pada

granulomatous iridocyclitis

30

PEM. SLIT LAMP dan OCT

SeldiCOAdan
vitreus

Opticalcoherence
tomography (OCT).
(A)Normaleye. (B)uveitis

DIAGNOSIS BANDING

ENDOPHTHALMITIS

31

INTERMEDIATE UVEITIS

32

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).

33

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).

34

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).

35

Figure 6. Vitreous condensation with tractional force on the pars

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

POSTERIOR UVEITIS

36

VITRECTOMY

37

PANUVEITIS

PAN UVEITIS

38

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.

39

VOGT-KOYANAGI-HARADA
SYNDROME
Penyakit 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,
Foste CS, Vitale AT. Diagnosis and Treatment of Uveitis.WB Saunders Co.2002.
masalah
saraf pusat, LCS pleositosis.

40

ANKYLOSING
SPONDYLITIS
Uveitis 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.

41

PENGOBATAN

42

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 % diagnosis
dapat 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 ada clue untuk diagnostik walau
anamnesis & 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.

43

UVEITIS NON INFEKSI

Pastikan adanya keadaan Inflamasi non
Infektif pada mata Risiko Buta.

Tegakkan Diagnosis Uveitis,

Tentukan: akut, intermiten, kronis
Rencana Pengobatan
Yeh S, Faia LJ, Nussenblatt RB. Semin Immunipathol; 2008;30:145-164
Daz-Llopis M, Gallego-Pinazo R, Garca-Delpech S et al. General Principles for the Treatment of NonInfectious Uveitis. Inflammation & Allergy - Drug Targets, 2009, 8, 260-265

AKUT

Pengobatan lebih agresif, fokus

pada efek jangka pendek untuk
mengontrol peradangan.

INTERMITEN
KRONIS Pengobatan perlu perspektif

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

44

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. Mycophenolatemofetil
2. Alkylatingagents:
a. Cyclophosphamide
b. Chlorambucil
3. Tcellinhibitor:
a. Cyclosporine
b. Tacrolimus
4. Cytokines:IFN

45

CYCLOSPORINE
11aminoacidpeptide membentukkompleks
dengancyclophilin,berikatankecalcineurin
hambattranslokasinukleussitosolyang
mengaktifkanTcells.
memotongprosestranskripsiTcell
danproduksisitokin(IL2&TNF).
inhibisiselektifpadaselT.
efeknyakecilpadaselB.

Metabolisme
Lipophilic.
Konsentrasipuncak:1 8jam.
Metabolismedihatilewatensim
sytochromeP450,diekskresidiempedu.
Interaksiobat:eritromicin,azole,
kontrasepsi,androgens,
methylprednisolone,calciumchannel
antagonists meningkatkankonsentrasi.

46

Effek samping
Palingsering:toksikpadaginjal
Padadosistinggi10mg/kg/duntuk
transplantasiorgan.
Padadosisrendahkurangtoksik(25
mg/kg/dunutkpenyakitautoimun).
Toxisitasdapatkembali(reversible)bila
obatdihentikan.

1
Disain:Randomised,doublemasked,
placebocontrolledclinicaltrial.Evaluasi:
minggu1,2,dan4dantiapbulansampai1
tahun.
Tujuan:menilaiefektifitas,keamanandan
tolerabilitascyclosporine.
Pasien:uveitisposterioridiopatik,
panuveitis/intermediateuveitis,kurang
responterhadapsteroid.
de Vries. J, Baarsma GS, Zaal, et al. Cyclosporine in the treatment of severe chronic
idiopathic uveitis. BritishJournal ofOphthalmology, 1990,74,344-349

47

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

TREATMENTSUCCES

Bulan1
Probabilitytreatmentsuccespada27pasienidiopathic
uveitis berat.
12
prednisonedancyclosporine
prednisonedanplacebo.
p>005. Wilcoxon'sranksumtest,twosided.
de Vries. J, Baarsma GS, Zaal, et al. Cyclosporine in the treatment of severe chronic
idiopathic uveitis. BritishJournal ofOphthalmology, 1990,74,344-349

48

VA dan Inflamasi

Meanvisualacuitydanmean inflammatoryactivitypada27pasien
idiopathic uveitis berat.prednisonedancyclosporine
prednisonedanplacebo.
p>005. Wilcoxon'sranksumtest,twosided.
de Vries. J, Baarsma GS, Zaal, et al. Cyclosporine in the treatment of severe chronic
idiopathic uveitis. BritishJournal ofOphthalmology, 1990,74,344-349

LOWDOSECYCLOSPORINEA

Pasienuveitisposteriorkronis:
Pasienrefrakterdengansteroid.
Rekurensaatdosisprednisolone
diturunkan<20mg/hari.
Pasiendiberisteroid1tahunsebelumnya.
Cyclosporindosisrendah(4mg/kgBB)
6 30bulan.,pada9pasien
Mathews D, Mathews J, Jones NP. Low-dose cyclosporine treatment for sight-threatening uveitis:
Efficacy, toxicity, and tolerance. Indian J Ophthalmol: 2010;58:55-58.

49

Visus, kadar kreatinin dan

inflamasi
Mathews D, Mathews J, Jones NP. Low-dose cyclosporine treatment for sight-threatening uveitis:
Efficacy, toxicity, and tolerance. Indian J Ophthalmol: 2010;58:55-58.

4
SeoulNationalUnversity: uveitisnoninfeksi
2001 2010.
Siklosporin(5mg/kb/hari)diberikanbila
steroidgagal,SEsteroid,imunosupresilain
gagal.
Siklosporin+steroid:161pasien
Siklopsorin+imunosupresi:46pasien
Aktifitas:inactive,slightlyactive,active
Lee SH, Chung H, Yu HG. Clinical Outcomes of Cyclosporine Treatment forNoninfectious Uveitis .
Korean J Ophthalmol 2012;26(1):21-25

50

Slightly active

Inactive

Waktu Klinis terkontrol setelah

pengobatan
Lee SH, Chung H, Yu HG. Clinical Outcomes of Cyclosporine Treatment forNoninfectious Uveitis .
Korean J Ophthalmol 2012;26(1):21-25

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.

51

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, dengan steroid-sparing
immunomodulary therapy (IMT).
Salah satu IMT adalah Siklosporin.

SIMPULAN
Kombinasi Siklosporin dengan kortikosteroid
atau imunosupresi lain merupakan pilihan
yang efektif pada pengobatan uveitis non
infeksi, karena mengurangi SE kortikosteroid
dan toxisitas imunosupresi.
Pada penggunaan siklosporin perlu
monitoring efek toksik.

52

SIMPULAN
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.

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

53

# 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.

54

#diagnosa:
klinis+lab aspirasihumoraquosusdan
vitreusuntukkulturdansensitivitytest
#terapi:
vitrektomi
ABintravitreal
kalauhebat,proginfaust eviscerasi
#prognosis:
tergantungsaatdatang,jenisendoftalmitis

HIVANDEYE

55

V.IMPACTOFHIVINFECTIONONTHEEYE
OccurinadvancedHIV,CD4+<200cellsx106 /l
Eyecomplications:70% 80%.HIVpatients90%
inSubSaharaAfricaandSEA,eyecomplications
differwithdevelopedcountries.
1. Opportunistic infections
2. Unusual neoplasm
3. HIV related inflammation
4. Antiretroviral toxicity
5. Immune recovery uveitis

Advanced HIV : marked

wasting, ("slim" disease)

Kaposi's sarcoma: multiple

skin nodules and plaques
KONAS 03

56

Hairy leucoplakia

Miliary tuberculosis

Oral candida

Cryptococcus
neoformans

Cerebral toxoplasmosis

KONAS 03

57

HIV VIRUS

HIV TRANSMISSION

Virus attached
to mucosal
receptors

Membrane
or skin
portal of
entry
Micros
copic
view of
proces

Dendritic cells
underlying skin
shelter and
amplify virus

Spread of virus to
lymphatic organ,
bone marrow,
circulation

58

Life cycle of HIV

HIV infection in vivo

59

Stages in HIV infection

Periode of infectiousness (virus present)
Antibody (-)

Antibody (+)

2 weeks
Infection

II

III

2 months

2- 15 years

IV

Incubation period

Months - years

Symptoms occur

Association between virological, immunological, and

clinical events and time course of HIV infection

60

Periocular Molluscum
contagiosum
Herpes zoster
ophthalmicus

Squamous cell carcinoma of the conjunctiva:

associated with HIV infection.
KONAS 03

61

Multiple Kaposis
sarcoma on the bulbar
conjungtiva

Conjungtival
microvasculopathy

Varicella-zozter keratitis in the absence

dermatitis

62

1. Microvasculopathy
2. CMV retinitis
3. HIV related retinitis

Retinal microvasculopthy with cotton-wool spots

63

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.

64

Peripheral zone III inactive CMV retinitis in the left eye

Active varicella-zoster virus retinitis

65

Toxoplasmic retinochoroiditis

Multiple Pneumocystis carinii choroidtits

66

Papilledema due to cryptococcal meningitis

(A) Right and

(B) left colour
fundus
photographs
showing
bilateral optic
disc pallor

67

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

68

Gyrate atrophy

Angioid streak atrophy

VIII. UVEAL NEOPLASM

Hyperplasty epithelial
Naevus
Melanoma maligna
Neurilemmoma, neurofibroma,
hemangioma
Secondary tumor : Ca mammae, Ca pulmo

69

THANK YOU

PREVENTION OF
ENDOPHTHALMITIS

70

Infective endophthalmitis :
- infection of posterior segment
- rare complications.
- devastating, frequently results
in visual loss.
- even major advances in
asepsis, surgical technique
and antibiotic therapy.

71

ETIOLOGIC AGENT
Own bacterial flora :
eye lid margin, conjungtiva, pre ocular
tear film
microbiology
phage typing
DNA finger print

TO TREAT
OR

TO PREVENT

72

HOST AGENT RELATIONSHIP

ENVIRONMENT

AGENT

HOST

Pathogenicity
Virulence
Infective dose

Innate immunity
Adaptive immunity
Normal microflora

HOST AGENT RELATIONSHIP

Operating theatre

S. epidermidis
S. aureus
St. pneumonia
E coli

Immunocom
promise

ENDOPHTHALMITIS or NO

73

TO PREVENT

Primary line defence mechanism

Recovery ?
Intact

PRE OPERATIF

Damage

Intact ?

DURANTE OPERATIF POST OPERATIF

Risk of infection :
NONE

CLEAN

HIGH

HIGH ?

O PE RAT I O N

74

PROPHYLACTIC ANTIBIOTICS

PRE OPERATIF

DURANTE OPERATIF POST OPERATIF

PRE OPERATIF

PERI OPERATIF
POST OPERATIF

1. Risk factor :
a. local : bacterial flora.
infecton : dermatitis, blepharitis,
conjungtivitis, dacryocystitis, prosthesis.
b. systemic : DM, malignancies.
2. No infection and Good host immunity
PRE OPERATIF

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

75

Personnel : standard infection control measures

Operation 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
POST OPERATIF

1. Hygiene
2. Medication :
antibiotics

76

1. No infection
2. Good host
immunity
PRE OPERATIF

1. Personnel
2. Operation
condion

Wound leak

DURANTE OPERATIF POST OPERATIF

I. Reduce number of
bacteria :

1. Sterility

1. Antibiotics
2. Desinfection

2. Minimal
trauma

II. Avoid contami

nation : cilia,

3. Multiple op.

Replace old ED bottle

Postop. Care

1. Hygiene
2. Medication

4. IOL

PERI OPERATIF ANTIBIOTIC PROPHYLACTIC

TO TREAT

77

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

78

1. ANTIBIOTIC
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

2. ANTI INFLAMMATORY DRUGS

The uses : controversial.
Animal models : concomitant use of
dexamethasone beneficial and no SE.
Despite the conflicting results,
dexamethasone frequently used in
severe cases

79

3. VITRECTOMY
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

SUMMARY

80

PREVENTION
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.
2. Ocular surface :
Important role of :
aseptic procedures : desinfection, sterility,
draped lashes.
antiseptics : povidine iodine 5 %
topical antibiotics :
quinolone ciprofloxacin, ofloxacin,
levofloxacin, maxifloxacin, gatifloxacin.

3. Intraocular antibiotics :
a. subconjungtival injection : controversial.
b. intra cameral / infusate : controversial.
c. intra vitreal
d. Post operative care.
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.

81

TREATMENT = MANAGEMENT

1. Established diagnosis :
Clinical and microbiological
2. Antibiotics :
a. intra vitreal, second injection.
b. concomitant systemic ? quinolone
3. Vitectomy : depend on presenting VA
4. Anti inflammatory controversial.

82