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RETINAL DISEASES

Z A L D I

DEPARTEMEN ILMU KESEHATAN MATA FAKULTAS KEDOKTERAN UNIVERSITAS MUHAMMADIYAH SUMATERA UTARA MEDAN 2013

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Dengan menyebut nama Allah Yang Maha Pengasih Maha Penyayang.

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I. TUJUAN INSTRUKSIONAL UMUM


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Setelah Proses Belajar Mengajar mahasiswa mampu menegakkan diagnosa penyakit-penyakit retina dengan melakukan pemeriksaan sederhana yang akan dipelajari selama masa perkuliahan secara baik dan benar .

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II. TUJUAN INSTRUKSIONAL KHUSUS


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Setelah Proses Belajar Mengajar mahasiswa mampu mengetahui gejala-gejala penyakit retina , faktor resiko, menegakkan diagnosa , prinsip pengobatan, komplikasi, dan mengatasi komplikasi secara garis besar secara baik dan benar sesuai dengan kompetensinya

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ANATOMY OF EYEBALL
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FUNDUS ANATOMY
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Eyeball structure and retina

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The Ten Layers of the Retina


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1. Pigment epithelium layer 2. Layer of rods and cones 3. External limiting membrane 4. Outer nuclear layer 5. Outer plexiform layer 6. Inner nuclear layer 7. Inner plexiform layer 8. Ganglion cell layer 9. Nerve fibre layer 10.Internal limiting membrane
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HISTOLOGY
8 Internal limiting membrane Nerve fiber layer Ganglion cell layer Inner plexiform layer Inner nuclear layer

Outer plexiform layer

Outer nulear layer

External limiting membrane photoreceptor

RPE Bruchs membrane ZALDI RETINAL DISEASES

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NEUROCONDUCTION OF RETINA
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3 neurons:
Photoreceptor Bipolar Ganglion cell

rodscotopic vision conephotopic vision Connecting cell between photoreceptor and ganglion

Conduct to brain

Supporting tissue:
Mller cell

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VASCULATURE OF RETINA
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inner layer central retinal vascular system

outer layer choroidciliary vascular system


macula lutea choriocapillaries

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BARRIER OF RETINA
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Inner barrierbloodretina barrier


dense connection of retinal capillary endothelium

Outer barrierchoroid-retina barrier


zonula occludens between the RPE

RPE- Bruchs membrane- choriocapillaries complex

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Symptoms in retinal diseases


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Night blindness Peripheral visual disturbance Central visual disturbance Color visual disturbance Metamorphopsia Micropsia Macropsia Photopsia Muscae volitantes (floaters) Without symptoms
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Examinations
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Visual Acuity Dark Adaptation Color vision (Ishihara) Visual field :

Ophthalmoscopy

confrontation test Goldmann perimetry Bjerrum tangent screen Octopus perimetry direct ophthalmoscopy indirect ophthalmoscopy biomicroscopy + contact lens/ Hruby lens/ +90 D lens
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DIRECT OPHTHALMOSCOPY
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External Light

Fundus Reflex

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INDIRECT OPHTHALMOSCOPY

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DIRECT

INDIRECT

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BIOM

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Specific Examinations
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Fundus fluorescein angiography (FFA) Ultrasonography (USG) Electroretinography OCT

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Fundus Fluorescein Angiography (FFA)

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ULTRASONOGRAPHY of the NORMAL EYE

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Diseases of the retina


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Congenital anomalies Trauma Inflammation Retinal detachment Vascular disorders Degeneration Neoplasma

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Retinal diseases to be discussed


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Retinal detachment (ablatio retina) Retinal artery occlusion Retinal vein occlusion Diabetic retinopathy Hypertensive retinopathy Retinitis pigmentosa

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Retinal Detachment
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ablatio retina separatio retinae

A condition where the sensoric retinal layer seperates from the retinal pigment epithelium layer (RPE)

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Retinal Detachment
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Subjective symptoms
Photopsia,
due

floaters

to retinal traction, vitreous bleeding

Dark

shadow/curtain
peripherally

starts

Reduced
macular

Vision
involvement or vitreous bleeding involvement (detached)

Metamorphopsia
macular

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Retinal Detachment
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Objective signs
Low

IOP Relatively calm anterior segment Funduscopy


Detached

retina greyish in color, elevated towards the vitreous cavity, vessels also elevated, surface often multi-lobulated

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Retinal Tears Cryo/ Laser Prophylaxis

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Retinal Detachment

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Retinal Artery Occlusion


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A condition where the retinal artery is occluded by an embolus Symptom: sudden visual loss without pain Two types :
Central

(CRAO) - occlusion behind the lamina cribrosa Branch (BRAO) - occlusion in front of lamina cribrosa

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Retinal Artery Occlusion


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Causes : Arteriosclerosis Hypertension Carotid arterial disease Diabetes mellitus Valvular heart disease Others: oral contraception, trauma, coagulopathy, toxoplasmosis, etc.

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Retinal Arterial Occlusion


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Symptoms and signs: Sudden blurred vision (HM - LP) Calm anterior segment Funduscopy
cherry-red

spot (greyish pale retina except at the fovea) small arteries, uneven caliber small veins, segmental

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Retinal Arterial Occlusion


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Branch RAO If macula not involved, vision relatively stable Retina pale only at the involved area A/v changes only at the occluded branch Complications: Papil atrophy NVI + NVG Prognosis: Poor. Visual recovery only if : 1. Occlusion overcome within 1-2 hours after onset, 2. Occlusion temporary (spasm), 3. Cilioretinal artery present

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CRAO

BRAO
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Retinal Arterial Occlusion


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Therapy: The aim of treatment is to quickly recover the arterial circulation by lowering the IOP :
paracentesis (AH aspirated 0.15 - 0.2 cc) Acetazolamide (Diamox) 500 mg. i.v. digital massage of eyeball inhalation of 95% O2 - 5% CO2 mixture

Look for cause

consult Internal Medicine

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Retinal Venous Occlusion


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Similar to RAO, painless sudden loss of vision as presenting symptom Two types:
central branch

(CRVO)
behind lamina cribrosa in front of lamina cribrosa

occlusion occlusion

(BRVO)

RVO 4-5 times more often than RAO

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Retinal Venous Occlusion


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Causes :

hypertension & arteriosclerosis (60%)

Common adventitial sheath at a-v crossing. Sclerosis --> vein compressed --> slowed flow --> thrombus --> occlusion

open angle glaucoma (40-70%) hyperviscosity (polycythemia, hyperli-pidemia, leukemia, etc) thromblophlebitis etc.

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Retinal Venous Occlusion


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Symptoms and signs :


sudden loss of vision calm anterior segment funduscopy :

dilated and tortuous vein edema, hemorrhage, soft exudate

Complication :

NVG

30-35% of CRVO, 1-3 months after onset

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CRVO

BRVO
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Retinal Venous Occlusion


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Branch RVO :
NVG seldom nasal branch --> no visual disturbance

Prognosis :

without NVG --> edema, hemorrhage, exudate slowly absorbed

Therapy :
medical therapy of no benefit laser photocoagulation look for cause --> consult Internal Medicine

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Diabetic Retinopathy
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DR is a retinal abnormality in a diabetic due to microangiopathy Almost always bilateral although the stages may be different incidence increased with duration of DM :
>

20 years > 30 years

50% retinopathy 80% more

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Diabetic Retinopathy
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Juvenile onset DM : delayed onset of DR. Mature onset DM (age > 40 yrs) : onset sooner Good metabolic control will delay the onset of DR Main cause of new blindness in the US

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Diabetic Retinopathy
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Signs :
microaneurysm retinal hemorrhage hard exudate soft exudate retinal edema collateral vessels (IRMA-IntraRetinal Microvasular Abnormalities) venous beading CNPA (Capillary Non Perfusion Area) neovascularization & gliosis

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Diabetic Retinopathy
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Complications :
vitreous

hemorrhage tractional retinal detachment

Classification :
nonproliferative

(background) = NPDR proliferative = PDR diabetic macular edema = DME

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Diabetic Retinopathy
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NPDR
early

: signs 1 to 8 severe = preproliferative

PDR
early

: + sign 9 severe : + complications

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Mild NPDR

Photo

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Severe NPDR

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Venous ZALDI Beading RETINAL DISEASES

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NVD

PDR

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Diabetic Retinopathy
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Therapy
metabolic

control laser photocoagulation


indicated

in

severe NPDR early PDR DME

vitrectomy
in

and retinal repositioning

Vitreous Hemorrhage and Retinal Detachment complications

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PRP

PRP

FOCAL
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PARS PLANA VITRECTOMY


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Hypertensive Retinopathy
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Changes in the retina of a hypertensive patient is due to hypertension and arteriosclerosis changes due to hypertension :

arteriole attenuation focal constriction/spasm hemorrhage and exudate papil edema


changes in arteriole light reflex changes in a-v crossing
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changes due to arteriosclerosis :


Hipertensive Retinopathy
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Changes due to hypertension :

arteriole attenuation

normal A:V ratio 2:3 or 3:4 attenuation < 3:4 (e.g. 1:2, 1:3)

focal constriction hemorrhage hard exudate soft exudate papil edema

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Hipertensive Retinopathy
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Changes due to arteriosclerosis


changes

in arteriole light reflex changes in a-v crossing

SCHEIE classification(1953)
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stages of hypertension and 5 stages of arteriosclerosis are used

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Attenuation Focal Spasm Venous Indentation

Hypertensive Retinopathy

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CWS Hemorrhage

Hypertensive Retinopathy

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SCHEIE classification
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Hypertension
Grade Attenuation Focal Hemorrhage Exudate Papil Spasm Edema

Arteriosclerosis
Light reflex A-v crossing

0
1 2

3:4
1:2 1:3

1:1 1:1 2:3 1:3 distal occl.


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(-) (-) (-) (+) (+)

(-) (-) (-) (+) (+)

(-) (-) (-) (-) (+)

Yellow line Widened Copper Silver Fibrous thread


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N V.Inden V.Inden Dist dilat Similar to 3

3
4

1:4
soft thread

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SCHEIE Classification
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Hypertension 0 Grade 1 Grade 2 Grade 3 Grade 4

Arteriosclerosis 0 Grade 1 Grade 2 Grade 3 Grade 4

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Hipertensive Retinopathy
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Therapy :
toward

the hypertension hypertensive signs may disappear; sclerotic signs persist


papil

edema, focal constriction quickly disappear hemorrhage, soft exudate disappear within several weeks-months hard exudate disappear within 4-6 months or more

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Retinitis Pigmentosa
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A hereditary disease in which a pigmentary degeneration of the retina occurs Characteristically there is a progressive degeneration of the photoreceptors and RPE most severe if X-linked recessive, least severe if autosomal dominant

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Retinitis Pigmentosa
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Subjective symptoms :
Nightblindness Gradual

reduction of visual acuity up to less than 6/60 within 4 - 10 years. In X-linked this occurs usually earlier (reading disturbance at age 20, blindness at age 40) often accompanied by hearing disturbance

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Retinitis Pigmentosa
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Funduscopy :
attenuation of retinal vessels in the midperiphery bone-specule pigmentation esp. along vessels; retina slightly dirty grey in color

Perimetry :

annular scotoma

Therapy :
untreatable low vision aids (LVA) genetic counseling

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Retinitis Pigmentosa

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