Introduction

RETINA
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

Retina
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 (bipolar, 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

Thickness:
0.1 mm at the ora serrata 0.23 mm at the posterior pole

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

7 8 9 10

The Vitreous
Blood supply from two sources:
Outer third (outer plexiform and outer nuclear layers, the photoreceptors, and the RPE): choriocapillaris Inner two-thirds: branches of the central retinal artery

A clear, avascular, gelatinous body

99% water 1% collagen and hyaluronic acid

Fovea supplied entirely by the choriocapillaris Retinal blood vessels non fenestrated endothelium: inner blood-retinal barrier RPE: outer retinal-blood barrier

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, +90D):
Anterior segment (rubeosis iridis, cataract, etc) PVD (Weiss ring) Syneresis Vitreous hemorrhage Fibrovascular proliferation

Direct/Indirect Ophthalmoscope

Non-contact vs contact lens

Pupil dilation, topical anestetics, viscous solution Image resolution

B-scan Ultrasonography
diagnostic and prognostic, especially in media haze (corneal scar, small pupil/posterior synechiae, dense cataract or vitreous opacification)

Vitreous Disorders
Vitreous floaters Asteroid hyalosis: little/no effect upon vision Acute vitreous collaps: syneresis, photopsia
It should be assumed that patients with new floaters or photopsia have retinal tears or detachment until proved otherwise by thorough examination with an indirect ophthalmoscope

Fundus Fluorescein Angiography Electrophysiology Testing

Prolifrative vitreoretinopathy Vitreous loss due to trauma Vitritis Vitrectomy

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

Retinal Vascular Disease

1. Diabetic Retinopathy Lymphoma Malignant/choroidal melanoma Hemangioma Metastase tumor from kidney, lung and breast One of the leading causes of blindness in the western world Chronic hyperglycemia is the major determinant
Young patient with type-1 DM, DR does not occur for at least 3-5 years after the onset of the disease Type-2 DM, 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, consequences of prolonged hyperglycemia After 20 years of hyperglycemia, develop some degree of DR
nearly all in type I DM more severe proliferation 60% in type II DM older patients, visual loss due to macular edema

Type-1 should be referred at least 3 year after the onset, type-2 at the time of examination. Diabetic pregnant women should be examined in the first trimester. Any sign of severe NPDR or more should be treated. Re-examined every 3 months until parturition

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

Side effects and complications :

paracentral scotomas transient increased edema/decreased vision choroidal neovascularization photocoagulation scar expansion inadvertent foveolar burns

Vitrectomy in DME
A rare, 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 to surgical release of the traction clinically : prominent and thickened posterior hyaloid, VA <20/80
Smiddy WE, Flynn HW. Surv Ophthalmol 1999

If new vessels appear to be active and significant vitreous/preretinal hemorrhage are occuring, 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

venous obstruction venous pressure intraretinal hges macular edema decreased vision

capillary closure retinal ischemia intraocular NV

HCRO :
Ischemic (hemi-hemorrhagic retinopathy) Non-ischemic (hemi venous stasis ret.)

BRVO :
Major BRVO Macular BRVO

Systemic
Hypertension, DM, Cardiovascular disease (CAD), increased hematocrit and plasma viscosity Odds ratio for ischemic :
4.8 for hypertension 2.7 for DM 2.1 for CAD 2.1 for 1-globulin

Complications
Vitreous hemorrhage Neovascular glaucoma Retinal detachment

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

Macular Diseases

Age Related Macular Degeneration (ARMD)

Macular Hole

Treatment: Anti-VEGF Transpupillary Thermotherapy Photodynamic Therapy Macular Translocation Submacular Sx

Treatment: Vitrectomy + ILM Peeling

H/O DOV 6 mos Preop-REVA 20/200

Postop-REVA 20/40

Central Serous Chorioretinopathy (CSR)

Cystoid Macular Edema (CME)

Retinopathy of Prematurity (ROP)

Ind. Oph. Examination Stage 1

Stage 4a

Stage 4b

Stage 5 Stage 2 Stage 3

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

Mekanisme Perlekatan Retina Normal Aposisi: 1. Tekanan hidrostatik dari TIO 2. Perbedaan tekanan osmotik antara koroid dan rongga subretina 3. Transpor metabolik ion-ion oleh EPR Lain-lain: interdigitasi vili, MIP Melepas: 4. Gerakan bola mata 5. Gravitasi 6. Traksi vitreus 7. PVD

Laser Profilaksis
Retina robek, 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

Pemasangan Bakel

Sirkumferensial Sirklase Radial Sleeve

Bakel silikon: - Strip - Sponge - Tyre

Drainase cairan subretina

Prabedah

Pascabedah

Retinopeksi - Krio
- Diatermi - Laser

F. Indirek ulang

Penutupan luka operasi

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Color Vision Defects

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

THANK YOU

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