Dr. Gilbert WS Simanjuntak Bagian IP Mata FK-UKI SMF IP Mata RS PGI Cikini

while they were saying among themselves it COULD NOT be done, BEHOLD IT WAS DONE
Helen Keller


Thin, semitransparent, multilayered sheet of neural tissue Lines the inner aspect of the posterior two-thirds of the wall of the globe Anterior ending point: ora serrata The retina and and retinal pigment epithelium are easily separated: subretinal space


Ten layers of retina, starting from inner aspect:
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Internal limiting membrane Nerve fiber layer Ganglion cell layer Inner plexiform layer Inner nuclear layer y (bipolar, ( p amacrine, horizontal cell bodies) Outer plexiform layer Outer nuclear layer of photoreceptor cell nuclei External limiting membrane Photoreceptor layer Retinal pigment epithelium


Sepuluh Lapisan Retina
1. Lp. Epitel pigmen 2. Lp. Batang dan kerucut 3. Membran limitans eksterna 4. Lp. Nukleus luar 5. Lp. Pleksiform luar SelBipolar 6. Lp. Nukleus dalam 7. Lp. Pleksiform dalam Sel Amakrin 8. Lp. Sel ganglion 9. Lp. Serabut saraf 10.Membran limitans interna

2 3 4

5 6

7 8 9 10

• 0.1 mm at the ora serrata • 0.23 mm at the posterior pole

Area 1.5 mm in diameter, yellowish pigmentation resulting l i from f the h presence of f luteal l l pigment i (xanthophyll): macula


avascular. topical anestetics. Blood supply from two sources: • Outer third (outer plexiform and outer nuclear layers. +90D): • • • • • Anterior segment (rubeosis iridis. and the RPE): choriocapillaris • Inner two-thirds: branches of the central retinal artery Fovea supplied entirely by the choriocapillaris Retinal blood vessels – non fenestrated endothelium: inner blood-retinal barrier RPE: outer retinal-blood barrier The Vitreous A clear. cataract. gelatinous body • 99% water • 1% collagen and hyaluronic acid Comprises two-thirds of the volume and weight of the eye Outer surface: the hyaloid membrane Vitreous base: firm attachment throughout life to the pars plana epithelium and the retina immediately behind the ora serrata Also attach to the lens capsule and optic disc Examination Slitlamp/biomicroscope examination (+60D. +78D. viscous solution • Image resolution 3 . the photoreceptors. etc) PVD (Weiss ring) S neresis Syneresis Vitreous hemorrhage Fibrovascular proliferation Non-contact vs contact lens • Pupil dilation.

photopsia • It should be assumed that patients with new floaters or photopsia have retinal tears or detachment until proved d otherwise th i by b thorough th h examination i ti with ith an indirect ophthalmoscope Prolifrative vitreoretinopathy Vitreous loss due to trauma Vitritis Vitrectomy 4 . dense cataract or vitreous opacification) Fundus Fluorescein Angiography Electrophysiology Testing Vitreous Disorders Vitreous floaters Asteroid hyalosis: little/no effect upon vision Acute vitreous collaps: syneresis.Direct/Indirect Ophthalmoscope B-scan Ultrasonography • diagnostic and prognostic. small pupil/posterior synechiae. especially in media haze (corneal scar.

lung and breast 5 . photocoagulation and/or chemotherapy Lymphoma Malignant/choroidal melanoma Hemangioma Metastase tumor from kidney. cryotherapy. exophytic extend through the optic nerve to the brain • Large tumor: enucleation. Photocoagulation diathermy or cryotherapy are treatment modalities Retinoblastoma • Life-endangering of childhood • The normal retinoblastoma gen. present in every individual. small: radiotherapy.Intraocular Tumors Retinal angioma • Vision affected by uxudation or bleeding from the tumor vessels • Photocoagulation. is a supresor gene or anti-oncogene • Exophytic and/or exophytic.

Any sign of severe NPDR or more should be treated. Re-examined every 3 months until parturition 6 . develop some degree of DR • nearly all in type I DM → more severe proliferation • 60% in type II DM → older patients. type-2 at the time of examination. DR d does e not t occur for at least 3-5 years after the onset of the disease • Type-2 DM. consequences q of p prolonged g hyperglycemia yp g y After 20 years of hyperglycemia. DR occur at a longer period Diabetic retinopathy is worsening in pregnant women 25% of diabetic population have some degree of diabetic retinopathy (DR) 5% are affected by more severe disease (proliferative retinopathy) Prevalence increases with the duration of diabetes. visual loss due to macular edema Type-1 should be referred at least 3 year after the onset.Retinal Vascular Disease 1. Diabetic Retinopathy One of the leading causes of blindness in the western world Chronic hyperglycemia is the major determinant • Y Young patient tie t with ith type-1 t e 1 DM DM. Diabetic pregnant women should be examined in the first trimester.

one spot width apart • Duration <100 ms • Power adequate to obtain definite whitening around the m. Technique : • Spot size 50-100 microns. or leakage site 7 .a.

more subtle traction-induced complication with macular edema induced by the contraction of a taut. persistently attached posterior hyaloid • does not respond to focal or grid laser • respond d to t surgical i l release l of f the th traction t ti • clinically : prominent and thickened posterior hyaloid. VA <20/80 Smiddy WE. Surv Ophthalmol 1999 8 . Side effects and complications : • • • • • paracentral scotomas transient increased edema/decreased vision choroidal neovascularization photocoagulation scar expansion inadvertent foveolar burns Vitrectomy in DME A rare. Flynn HW.

9 .

10 .

additional PHC strongly considered LIO is useful to ‘fill-in’ the far periphery in cases continued NV activity after good PRP Artery Occlusions Classifications of Retinal Vein Occlusions CRVO : • Ischemic • Non-ischemic HCRO : • Ischemic (hemi-hemorrhagic retinopathy) • Non-ischemic (hemi venous stasis ret. If new vessels appear to be active and significant vitreous/preretinal hemorrhage are occuring.) BRVO : • Major BRVO • Macular BRVO 11 .

8 for hypertension 2.1 for CAD 2.1 for α1-globulin Complications Vitreous hemorrhage Neovascular glaucoma Retinal detachment 12 .7 for DM 2. increased hematocrit and plasma viscosity Odds ratio for ischemic : • • • • 4. Cardiovascular disease (CAD).venous obstruction venous pressure intraretinal h’ges macular edema decreased vision capillary closure retinal ischemia intraocular NV Systemic Hypertension. DM.

Results : • Intraoperative decompression achieve in all 15 patients • 80% VA postoperative ~ preoperative • 67% VA improved. average 2 lines 13 . with average gain i 4 lines li of f vision • 20% had worse VA.

Macular Diseases 14 .

Age Related Macular Degeneration (ARMD) Treatment: • Anti-VEGF • Transpupillary Thermotherapy • Photodynamic Therapy • Macular Translocation • Submacular Sx Macular Hole Treatment: Vitrectomy + ILM Peeling 15 .

H/O DOV 6 mos Preop-REVA 20/200 Postop-REVA 20/40 16 .

Examination Stage 1 Stage 2 Stage 3 17 . Oph.Central Serous Chorioretinopathy (CSR) Cystoid Macular Edema (CME) Retinopathy of Prematurity (ROP) Ind.

Stage 4a Stage 4b St Stage 5 Pl Di Plus Disease RETINAL DETACHMENT Ablasio Retina Regmatogen Lapisan retina sensorik/neuroretina terpisah dari lapisan EPR Akibat adanya robekan retina Cairan dari vitreus melalui robekan pindah ke rongga subretina retina terangkat Terapi : operasi 18 .

Gravitasi 6. Perbedaan tekanan osmotik antara koroid dan rongga subretina 3. Transpor metabolik ion-ion oleh EPR Lain-lain: interdigitasi vili.Mekanisme Perlekatan Retina Normal Aposisi: 1. Traksi vitreus 7. Tekanan hidrostatik dari TIO 2. belum terjadi pelepasan retina [1] Bibir robekan dan daerah sekitarnya difotokoagulasi laser [2] Terjadi sikatriks korioretina yang tidak dapat dilalui oleh cairan ablasio retina tercegah [3] Dapat juga dengan kriopeksi [4] [1] [4] [3] [2] Persiapan Daerah Operasi 19 . Gerakan bola mata 5. PVD Laser Profilaksis Retina robek. MIP Melepas: 4.

Tyre Drainase cairan subretina Retinopeksi p .Sponge .Pemasangan Bakel Sirkumferensial Sirklase Radial Sleeve Bakel silikon: .Krio .Laser F.Diatermi . Indirek ulang Penutupan luka operasi Prabedah Pascabedah 20 .Strip .

green and red) Congenital: most red-green Acquired: blue blue-yellow yellow Affects both eyes equally Protanopia: red-sensitive pigment loss Deutranopia: green-sensitive pigment loss Tritanopia: blue-yellow color blindness THANK YOU 21 .Color Vision Defects Spectrum wavelength 400-700 nm is capable of being absorbed by visual pigment of cone photoreceptors (blue.