retina nss2013

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Page 1: Retina Nss2013

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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