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Vitreo-Retina

Vitreo-Retina Subdivision

Ophthalmology Department

Faculty of Medicine and Health Sciences

Jenderal Soedirman University / Margono Soekarjo General Hospital

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Vitreous

•  A water (99%) and Hyaluronic acid &

collagen (1%) mix

•  Optically clear, fills centre of globe

•  Firm adhesions to optic nerve, peripheral

retina at ora serrata and retinal blood

vessels can produce retinal detachment

when they tear loos

•  Normally shrinks somewhat with age

 – Sineresis, Posterior vitreous detachment

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Vitreous

•  Abnormality

 – 

Floater / turbidity

•  Degeneration, Haemorrhage, infection /

inflammation

•  Thin - dense

 – Flashes

• 

Traction to retina

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Posterior

VitreousDetachment

Traction Vitreous /

Retinal Break

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Retina

Normal retina • 

Optic disc

• 

Superior temporal arcades

• 

Inferior temporal arcades

• 

Macula

• 

Fovea

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 Anatomy

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 Anatomy

•  Retina layers

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Vision

Biochemistry of Vision:•  Visual proteins are based on Vit.A•

Stimulation by light causes abiochemical cascade

• 

Electrophysiological changes aretransmitted and modified through the

layers of the retina to the ganglioncells that form the optic nerve

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Vision

Central Vision:•  The foveola has the most detailed

vision

• 

High density of cones•

Reduction in the inner layers toreduce obstruction to light

• 

High (near 1:1) ratio of cones toganglion cells

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Vision

Retinal Pigment Epithelium:

•  The RPE provides special metabolic and ionic conditionsnecessary for the rods and cones and is essential fornormal vision

• 

 Aging changes in the RPE result in Age Related MacularDegeneration

•  Highly vascular portion of the uvea

•  Supplies the outer retina with much of its metabolic

requirements

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Examination

• 

Physical examiantion –

Slit Lamp Biomicrosopic with•  Condensing Lens

• 

Goldman three mirror – Ophthalmoscope

•  Direct

•  Indirect

• 

 Additional examination –

Fundus Photo Color

 – 

Fundus Fluorescein angiography

 – 

Ultrasonography

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Goldman Three Mirror Condensing Lens

Slit lamp Biomicroscopic

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Indirect Ophthalmoscope

Direct Ophthalmoscope

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Fundus Fluorescein angiography

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Ultrasonography

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Retinal Abnormality

•  Dystrophy

•  Degeneration

• 

Infection / Inflammation•  Vascular

•  Detachment

• 

Tumor

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Dystrophy

•  Retinitis Pigmentosa

•  Stargard’s Disease

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Retinitis Pigmentosa

• 

Hereditary degeneration

 – 

Fotoreceptor

•  Dysfunction, Loss and atrophy.

• 

 Autosomal recessive, autosomal dominant,x-linked rescessive and 1/3 no familyhistory

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Retinitis Pigmentosa

• 

Symptom :

 –  Niktalopia

 –  Constricted visual field

• 

Sign : –  Bone spicule – like

pigmentation in fundus

 –  Arteriolar narrowing

• 

Treatment

 – 

Low vision aid

 – 

No direct medical

treatment

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Stargardt disease

• 

Juvenile macular dystrophy•

Gen ABC4R on lp 21-22

•  Symptom

 – 

Presentation on second decades – Gradual impairment of central vision

• 

Signs

 – 

Geographic atrophy

 – 

Fovea may be normal or non specific

• 

Treatment

 – Low vision aid

 – 

No direct medical treatment

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Stargardt disease

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Degeneration

• 

Myopic degeneration

•  Age related macular degeneration

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Myopic degeneration

• 

Pathologic / high Myopia

 – 

Progressive elongation of the eye

•  Thinning RPE and choroid

•  > - 6.00 D

• 

 Axial length > 26 mm

•  Liable to glaucoma and cataract

•  Treatment

 – 

Limited to optical correction, intra-ocular pressure

control, and attention to complications that may occur. –

Scleral buckling can prevent axial extension and mayminimize the toll of myopic macular degeneration on

future visual function.

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Myopic degeneration

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 ARMD(Age Related Macular Degeneration)

• 

The most common cause of central visionloss in persons older than 50 years of agein developed countries.

! 

Symptom!  In the early stages!  central vision may be blurred or distorted,with objects looking an unusual size or

shape and straight lines appearing wavyor fuzzy (quickly or over several months).

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Dry ARMD

• 

Dry ARMD (90%) – Drusen (yellowish deposits of debris in retina)

 –  Atrophic

• 

Treatment –

eat a diet rich in leafy green vegetables,antioxidants,zinc, lutein and zeaxanthin.

 – avoid excessively bright sunlight (ultraviolet

(UV) rays and blue light) – don't smoke

 – contact a low vision specialist if vision worsens

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Wet ARMD

• 

Wet Armd (10%), More progressive – Choroidal neovascularization

•  Treatment

 – 

Laser photocoagulation –

Photodynamic therapy

 – 

Macular translocation

 – Sub macular surgery

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Infection / Inflammation

• 

Chorioretinitis toxoplasma (toxoplasmosis) – intracellular protozoan Toxoplasma

gondii

• 

Mammal and bird hosts. – (The most common intermediatehost is the cat).

 – It is one of the most frequent causes of

retinochoroiditis in humans, 75 % theworld's general population possessingsome seropositive findings.

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Toxoplasmosis

• 

Symptoms –

unilateral, mild ocular pain, blurred vision andnew onset of floating spots.

•  Clinical findings

 – 

granulomatous iritis, vitritis, optic disc swelling,neuroretinitis, vasculitis and retinal veinocclusion in the vicinity of the inflammation, inthe actively involved eye.

 – 

Funduscopically:

• 

active toxoplasmosis presents with white-yellow, choreoretinal lesions and vitreouscells

• 

There may be old, inactive lesions in thefellow eye

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Treatment

• 

 Alternative treatments•  clindamycin, tetracycline, trimethoprim /

sulfamethoxazole,

• 

 After beginning antibiotic therapy, add oralsteroids at a dose of 20 to 80mg PO dailyfor four or six weeks

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 Active toxoplasmosis

Inactive toxoplasmosis

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Retinal vascular disease

• 

Diabetic retinopathy•  Hypertensive retinopathy

•  etc

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Diabetic Retinopathy

• 

Hyperglycaemia•  Loss of pericyte•  Thickening of basement membrane•  Alteration of coagulation state

• 

Non-proliferative DR – Microaneurism –

Dot & blot intraretinal hemorrhage

 – Hard exudates

 – 

Dilatation and beading of retinal vein

•  Proliferative DR – Neovascularization

•  On the disc or else where

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Diabetic Retinopathy

• 

Treatment – Glucose and other systemic abnormality control –

Laser photocoagulation

 – Vitrectomy

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PDR

NPDR

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Hypertensive retinopathy

• 

WHO definition – Systolic blood pressure >140 mm Hg

 – Diastolic blood pressure > 90 mm Hg

• 

HT can affect the choroid, retina, and opticnerve

•  Hypertension can cause:

 – 

Nerve Fiber Layer micro-infarcts, calledCotton Wool Spots - due to disruption ofaxoplasmic transport

 – Dot/Blot and flame shaped hemorrhages

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Hypertensive Retinopathy

Modified Scheie Classification – Grade 0 No changes

 – 

Grade 1 Minimal arteriolar narrowing

 – 

Grade 2 Obvious arteriolar narrowing withfocal irregularities

 – 

Grade 3 Grade 2 + retinal hemorrhages and/or exudate

 – 

Grade 4 Grade 3 + swollen optic nerve(Malignant hypertension)

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Hypertensive Retinopathy

• 

Management – Lower the blood pressure gradually to

decrease risk of blindness and stroke

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Grade III

Grade IV

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Retinal Detachment

• 

Detachment the nuero-sensory retina fromthe underlying pigment epithelial layer bysubretinal fluid – Exudativa

• 

Uveal effusion (infection or inflammation)•  Treatment : Underlying disease

 – 

Rhematogenous•  Retinal break

• 

Treatment : Scleral Buckling, Vitrectomy – Tractional

•  Proliferative DR•  Treatment : Vitrectomy

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Rhegmatogen RD

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Tractional RD

Exudative RD

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Tumor

• 

Retinoblastoma•  Hemangioma choroid•  Tumor sub division

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Thank you