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Kelainan-kelainan vitreoretina
dr. H. A. K. Ansyori, SpM (K) MKes
Ophthalmology DepartmentMohammad Hoesin Hospital
2011
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CORPUS VITREUM/VITREUS BODY=BADAN KACA
Benda cair berkonsistensi “jelly”, berkonstruksi “spongeus” , bagian tengah lebih cairTerdiri atas : - air 99%
- zat lain : 1. mucoplysacharide2. protein3. lemak organik4. elektrolit;Na,K,Biknat,glukosa5. Gel effects of collagen and
hyaluronan - Mengisi 4/5 volume bola mataMempunai indeks refraksi sama seperti humor aqueous, lebih rendah dari indek refraksi lensa, Vitreous sehat tidak bercampur dengan air, Memunyai peranan pada penyembuhan retina
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Primary roles•maintain clarity in optical axis & maximizing photon transmission to retina
• anti-migratory & anti-proliferative properties
•Important at vitreoretinal interface
•Viscoelastic gel Provides shock absorption
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1.Gel Liquefaction/syneuresisdevoid of liquid during infancy begins
to liquefy in childhoodprogresses throughout life molecular
re-arrangement of structural macromolecules hyaluronan and collagen.
alteration involves cross-linking and aggregation of the collagen fibrils of vitreous
accelerated in myopia, one manifestation of myopic vitreopathy
Phatobiology
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weakening of vitreo-retinal adhesion Concurrent with vitreous gel liquefaction
critical levelseparation of the posterior vitreous cortex from the retina, with displacement of the liquefied vitreous into a developing cleavage plane between the posterior vitreous cortex and the internal limiting lamina of the retinaposterior vitreous detachment (PVD).
2.Posterior Vitreus Detachment(PVD)
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Age-related vitreous liquefaction and PVD. Pockets of liquid appear within the central vitreous that gradually coalesce. There is a concurrent weakening of postoral vitreoretinal adhesion. Eventually, this can progress to PVD, where the liquid vitreous dissects the residual cortical gel away from the ILL on the inner surface of the retina as far anteriorly as the posterior border of the vitreous base.
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EMBRIOLOGI RETINA1.OPTIC VESICLE, OPTIS CUP
2.a. LAPISAN SENSORI RETINA1.Membran limitan interna2.Lapisan serabut saraf3.Lapisan sel ganglion4.Lapisan fleksiform dalam5.Lapisan nukleus dalam6.Lapisan fleksiform luar7.Lapisan nukleus luar8.Membran limitan eksterna 9.Lapisan sel kerucut dan batang
b. LAPISAN PIGMEN EPITELIUM RETINA
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PATOLOGI RETINA
1.KELAINAN VASKULER2.ABLASIO RETINA3.INFLAMATORY4.DEGENERASI5.RUDA PAKSA (TRAUMATIS RETINOPAHIES)6.KELAINAN KONGENITAL7.NEOPLASMA
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PENYAKIT VASKULER RETINA
1. GANGGUAN PD ARTERI RETINA2. GANGGUAN PD VENA RETINA3. GANGGUAN PD KAPILER RETINA
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1 GANGGUAN PD ARTERI RETINA, antara lain:a. oklusi arteri retina sentralb. oklusi arteri retina cabangc. retinopati hipertensi
2 GANGGUAN PD VENA RETINA, antara lain :a. oklusi vena retina sentralb. oklusi vena retina cabangc. retinopati berhubungan dengan
hiperviskositas3 GANGGUAN PD KAPILER RETINA, antara lain :
a. retinopati diabetika
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oklusi arteri retina sentral (CRAO)• Often sixth decade of life• Causes : embolism (most common
cause)from ulcerated atheromatous plaque in carotid artery thrombosis: arterial spasm : carotid obstruction
• Sudden monocular visual loss with acute ischemic withening due to swelling in inner retina
• Cherry red spot : normal retinal transparency returns in 2-3 weeks
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CRAO
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• Types of emboli : platelet, fibrin, cholesteril, calcific
• 30% of patients retain 20/10 vision. Most maintain light percetion due to presenceof small cilioretinal arteries
• 1% develop rubeosis• optic athropy• FFA show delayed filling of retinal vessels• treatment : reduces IOP with paracentesis,
CAI.• Promote vasodilation by rebreathing CO2
from paper bag
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oklusi arteri retina cabang (BRAO)
• associated with arteriosclerosis, emboli, collagen, vascular disease, rheumaric heart disease
• acute whitening of retinal supplied by arteriole
• plaque may be seen• fluorescent shows delayed perfusion of
retina• treatment : reduce IOP if macula involved
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BRAO
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retinopati hipertensi
• mild to moderate hypertensives : asymptomatic with arteriole narrowing
• severe hypertension : marked arteriolar constristion, cotton wol patches,microaneurysms
• malignant hypertensions burred vision, headaches, macular star, swollen optic nerve head
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CENTRAL RETINAL VEIN OCCLUSION (CRVO)
• Otherwise healthy patients : elevation of
venous and intracapillary pressure and
arterial blood flow.• Impending : mild blurring of vision, few
scattered hemorrhages, mild venous dilation.• Mild (better than 20/200 vision) : minimal
capillary endothelial damage, some return of
retinal function.• Severe (less than 20/200 vision) :
hemorrhagic infaretion, extensive loss of
capillary bed, swelling of optic nerve, cotton-
wool patches, permanent changes
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Macular findings : cystoid macular edema,
macular hole, or epiretinal membrane can
develop.Less chance of neovascularization than with
branch vein occlusions (less than 20%)hemorrhagic glaucoma : may develop 3 or 4
month post-CRVO.Photocoagulation if ischemic to reduce risk
of neovascularization and rubeosis
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BRVO
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DIABETIC RETINOPATHY
Klasifikasi :1. non proliferative diabetic retinopathy
(NPDR)2. proliferative diabetic retinopathy (PDR)
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Non proliferative diabetic retinopathy, dibagi menjadi :
1. Mild to moderate NPDR, tanda-tandanya
a. Microaneurysms b. Intraretinal hemorrhages : mild to
moderatein fewer than four quadrants
c. Hard exudates d. Macular edema e. Foveal avascular zone abnormalities
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2. Moderate to severe tanda-tandanya :
a. Cotton wool spotsb. Intraretinal hemorrhages : mild to
moderate in four quadrantsc. Intraretinal microvascular abnormalities
(IRMA)
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3. Severe “Nonproliferative Retinopathy (ETDRS), Any
one of the following : a. Severe intraretinal hemorrhages in four
quadrant b. Venous beading in two quadrants
c. Moderately severe IRMA in one quadrant
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4. Very severe “Nonproliferative Retinopathy (ETDS) Any two of the following : a. Severe intraretinal hemorrhages in four
quadrants b. Severe intraretinal hemorrhages in four
quadrants
c. Moderately severe IRMA in one quadrant
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NPDR
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Proliferative diabetic retinopathy, dibagi menjadi :1. Early Proliferative Retinopathy a. Neovascularization of the disc b. Neovascularization of the retina
elsewhere c. Preretinal hemorrhage d. Vitrous hemorrhage e. Tractional retinal detachment f. Neovascularization of the iris of angle, or
both
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2.High Risk Retinopathy Any three of the followinga. Presence of new vesselsb. Location of new vessels on the discc. Severity of new vessels; If NVD one-quarter
to one third disc area or standard photograph 10 A; If NVE one half disc area; If both NVD and NVE, count severity of NVD
d. Presence of pre retina or vitreous hemorrhage
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PDR with vitreus hemorrhage
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Ablasio Retina
Keadaan dimana lapisan sensoris retina terlepas dari RPE
Penyebab:◦Robekan retina rhegmatogen, vitreus yang
mencair masuk melalui robekan mengisi ruang potensial antara retina & RPE
◦Tarikan dari jaringan di badan kaca traksional◦desakan cairan, tumor atau darah
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Gejala◦Visus menurun ◦Floaters◦Photopsia◦TIO menurun◦Tobacco dustRPE di vitreus◦Seperti melihat tirai
Tanda Undulasi, demarcartion line,
tears/hole
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Ablasio retina
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RETINITIS PIGMENTOSA
Disebut distrofi primer pigmen retinaPembuluh darah retina menyempitPapil saraf optik pucatPigmentasi retina di ekuator bone
corpuscleBilateralGejala: buta senja,↓lap pandang perifer,
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Retinitis pigmentosa
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Lattice degeneration
Vitreoretinal abnormality6-10 % general populationCommonly in myopic eyesPredisposed to retinal breaks & detachmentHistopathologic features
◦Discontinuity of ILM◦Liquefied vitreus◦Atrophy of inner layers retina
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Lattice degeneration
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Commotio retina
Damage of outer retinal layer Cause by shock wave (blunt trauma)Sheenlike retinal whiteningCommon in posterior poleCalled Berlin edemavisual recovery 3-4 weeks
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Berlin edema
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Toksoplasmosis
Infeksi retina paling seringDisebabkan protozoa toxoplasma gondii
protozoa parasitik intraselulerBisa congenital / aquiredAkut lesi putihKronik jaringan parut berpigmen
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toxoplasmosis
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retinoblastoma
Tumor pada anak2/3 kasus muncul sebelum usia 3 thnBilateral pada 30% kasus Herediter kromosom 13q14LeukokoriaTampak spt mata kucing
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leukokoria
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retinoblastoma
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MAKULA
Makula atau fovea merupakan struktur yang sangat kompleks. Kelainan pada makula menyebabkan penurunan tajam penglihatan yang berat. Terletak pada daerah temporal dari papil antara arcade superior dan inferior, Makula sama dengan diameter papil yaitu 1.500 mikron
Foveola adalah suatu depresi dalam makula seluas 350 mikron ditandai oleh suatu refleks disebabkan berbedanya ketebalan membrana limitan interna di daerah ini
Umbo adalah pusat foveola
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Jenis penyakit makula yang sering ditemukan:1. Central Serous Retinopathy2. Retinal Pigment Epithelial detachment3. Degenerasi makula/Senila Macular
Degeneration4. Macula Hole5. Drusen
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Central Serous Retinopathy (CSR)
Central Serous Retinopathy adalah suatu pelepasan dari retina sensoris di daerah macula akibat adanya cairan di bawahnya.
Berbagai konsep mengenai penyebab CSR antara lain adalah :1. Gangguan sirkulasi daerah makula2. Akibat toksik3. Gangguan stabilitas vasomotor4. Gangguan pada khoroid
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• Penyebab gangguan sirkulasi daerah makula, stabilitas vasomotor dan pada koroid menyebabkan gangguan nutrisi pada Epitel Pigmen Retina (EPR)
• pada pemeriksaan histology tampaknya penyebab utama CSR adalah disfungsi dari EPR
• Pada keadaan normal EPR melekat secara erat pada membrane Bruch dan antara sel-sel EPR sendiri dengan adanya tight junction diantaranya
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“tight junction” ini rusak sehingga cairan serosa dari khoroid mengalir melalui EPR ke bawah retina sensoris.Gejala :• penurunan tajam penglihatan dapat dikoreksi
dengan lensa konveks• penderita mengeluh mengenai daerah gelap di penglihatan sentralnya (skotoma sentral)
• metamorphopsia dan mikropsia• pada keadaan CSR lanjut yaitu setelah
lebih dari 2 minggu akan terlihat adanya bercak-bercak presitat kuning
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Retinal Pigment Epithelial (RPE) detachment
• RPE detachment dalah pelepasan lapisan EPR akibatnya adanya cairan dibawahnya
• Sering dianggap sebagai tingkat yang lain CSR
• Watzke menemukan RPE detachment pada 40% penderita CSR
• Gass menduga bahwa cairan berasal dari pembuluh darah yang tumbuh pada permukaan dalam membrana Bruch
• Pada funduskopi tampak suatu penonjolan pada makula berbatas tegas dengan warna kuning keruh
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Age Related Macular Degeneration
Degenerasi makula pada usia lanjut atau dahulu disebut degenerasi makula senilis sekarang lebih sering disebut sebagai Age Related Macular Degeneration (ARMD)
ARMD merupakan salah satu penyebab utama kebutaan pada orang-orang berusia 65 tahun ke atas
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Gejala awal dari ARMD adalah Drusen
Ada 3 bentuk Drusen yaitu :1. Drusen keras terdiri dari jaringan hialin2. Drusen lunak adalah badan koloid3. Drusen Granular dikaitkan dengan
membranneovaskular subretina
Uyama membagi ARMD dalam 5 bentuk :1. Pelepasan retina oleh cairan serosa2. Bentuk disiform3. Perdarahan subretina4. RPE detachment5. Tahap fibrosis sampai sikatriks
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