retina pps dr arief
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Vitreo - Retina
Vitreo – Retina SubdivisionOphthalmology Department
Faculty of MedicineDiponegoro University / Kariadi 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 Vitreous Detachment
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 Vitamin A • Stimulation by light causes a biochemical cascade • Electrophysiological changes are transmitted and
modified through the layers of the retina to the ganglion cells that form the optic nerve
Central Vision:• The foveola has the most detailed vision • High density of cones • Reduction in the inner layers to reduce obstruction to
light • High (near 1:1) ratio of cones to ganglion cells
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Vision
Retinal Pigment Epithelium:• The RPE provides special metabolic and ionic conditions
necessary for the rods and cones and is essential for normal vision
• Aging changes in the RPE result in Age Related Macular Degeneration
• 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 family history
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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 may
minimize the toll of myopic macular degeneration on future visual function.
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Myopic degeneration
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ARMD
• The most common cause of central vision loss in persons older than 50 years of age in 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 wavy or 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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Dry ARMD
Wet ARMD
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Infection / Inflammation
• Chorioretinitis toxoplasma (toxoplasmosis)– intracellular protozoan Toxoplasma gondii.
• Mammal and bird hosts. – (The most common intermediate host is the cat).
– It is one of the most frequent causes of retinochoroiditis in humans, 75 % the world's general population possessing some seropositive findings.
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Toxoplasmosis
• Symptoms – unilateral, mild ocular pain, blurred vision and
new onset of floating spots.• Clinical findings
– granulomatous iritis, vitritis, optic disc swelling, neuroretinitis, vasculitis and retinal vein occlusion in the vicinity of the inflammation, in the actively involved eye.
– Funduscopically, • active toxoplasmosis presents with white-yellow,
choreoretinal lesions and vitreous cells. • There may be old, inactive lesions in the fellow eye.
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Treatment
• Eradicate the parasite and suppress the inflammatory response.
• Classic treatment regimen– pyrimethamine (a 75mg loading dose, followed
by 25mg PO BID administration) with sulfadiazine (2g loading dose, then 1g PO QID for 4 to 6 weeks).
– Concurrent folinic acid, 3 to 5mg PO twice weekly helps to minimize any bone marrow toxicity produced by the pyramethamine.
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Treatment
• Alternative treatments • clindamycin, tetracycline, trimethoprim /
sulfamethoxazole, • After beginning antibiotic therapy, add oral
steroids at a dose of 20 to 80mg PO daily for 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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NPDR
PDR
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Hypertensive retinopathy
• WHO definition– Systolic blood pressure >140 mm Hg – Diastolic blood pressure > 90 mm Hg
• HTN can affect the choroid, retina, and optic nerve
• Hypertension can cause:– Nerve Fiber Layer micro-infarcts, called Cotton
Wool Spots - due to disruption of axoplasmic 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 with
focal 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
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Retinal Detachment
• Detachment the nuero-sensory retina from the underlying pigment epithelial layer by subretinal 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