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155 Cards in this Set
- Front
- Back
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Neurosensory retina
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Photoreceptors - rods and cones
ELM - not true BM, tight junctions of photoreceptors and mullers Outernuclear layer - photoreceptor nucleus Outer plexiform -synapse photoreceptors and bipolar Inner nuclear layer nucleus of bipolar, amacrine, horizontal, mullers Inner plexiform - synapse of bipolar with ganglion cells and amacrine Ganglion cell layer - where ganglion cell nuclei reside, multilayered in macula, 1 cell layer elsewhere Nerve fiber layer - unmyelinated axons of ganglion cells ILM - true BM, foot process of Mullers |
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attachments of retina
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optic nerve
vessels vitreous base macula |
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attachments of uvea
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scleral spur
optic nerve vortexs vein post ciliary vessels |
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attachments of choroid
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sclera
optic nerve scleral spur vortex veins post ciliary vessels |
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Function of RPE
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1. RPE development
2. Vit A cycle 3. nourish outer retina 4. waste management RPE 5. forms the outer blood retinal barrier 6. secretes BM 7. produce melanin granules 8. adhesion to sensory retina 9. ATP na/k maintain subretinal space |
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Components of ERG
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1. A-wave - photoreceptors
2. B-wave - bipolar and mullers 3. oscillating potential - amacrine cells 4. C-wave - RPE 5. Flicker - cone response 6. Photopic - cone function 7. scotopic - rod function |
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Indications for ERG
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1. help diagnose a retinal degeneration
2. assess family with hereditary disease 3. assess poor vision and nystagmus at birth 4. assess retinal function in opaque media, vascular occlusion 5. evaluate a functional vision loss |
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ERG with abnormal photopic but normal scotopic
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achromatopsia
cone dystrophy |
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ERG with normal A wave, decreased B wave
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CSNB
x-linked juvenile retinoschisis Central vein occlusion Central retinal artery occlusion myotonic dystrophy quinine toxicity |
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extinguished ERG patterns
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RP
ophthalmic artery occlusion DUSN metallosis RD drug toxicity (phenothizine, chloroquine) cancer assoc retinopathy |
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Fluorecein angiography
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Phases: choriodal filling --> arterial --> venous --> AV transit --> recirculating
- dye enters choroid via the short posterior ciliary artery (10-15sec) post injection. cilioretinal artery filled at time of choriodal filling Blue light (490nm) simulates fluorecein, and emit yellow green (530nm) -fluorecein 80% bound to albumin, 90% excreted by kidney hyperfluorecence- leakage, staining, pooling, window defect hypofluorecence- blockage, ischemia macular dark spot - due to xanthopyhll blockage in outer plexiform, and tall RPE cells |
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lesions no predisposing to RD
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1. Cobblestone degeneration (absent choriocapillaris, RPE, outer retina, adhesion between inner retina with bruchs)
2. retinal pigment epithelial hyperplasia (RPE hypertrophy due to chronic traction, inflammation 3. retinal pigment epithelial hypertrophy 4. peripheral cystoid degeneration |
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lesion predisposing to RD
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1. lattice
2. vitreoretinal tufts 3. meridional folds (redundant retina) 4. enclosd ora bays 5. peripheral retina excavations |
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Degerative retinoschisis
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occurs in adults >40 mostly bilateral, inferotemporal. precursor is peripheral cystoid degeneration. 2 types
1. typical- split at outer plexiform, due to coalese of cavities of cytoid degeneration. no risk of RD unless outer layer holes. layer whitens with laser of blanch with sclera depression. 2. retincular- splitting at NFL, posterior to peripheral cystoid. pathology-cavity contains hyaluronic acid. treat with laser barrier, RD, tears. Complication when holes in outer layer which cause RD |
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difference between RD and retinoschisis
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Retinoschisis
- no demarcation line - no RPE degeneration - no tobacco dust - absolute scotoma (RD is relative) - laser blanches while RD does not blanch |
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cystic retinal tufts
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nodular projection of fibroglial tissue, increased vitreous adhesions which predispose to tractional tears in PVD. In 5% population.
<1% risk RD. second to lattice as peripheral lesion causing RD |
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pars plana cyst
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cystoid space between pigmented and nonpigmented ciliary epithelium of pars plana. filled with mucopolysaccharides
not a true cyst. occur 17% eyes in autopsy. no RD risk, seen in multiple myeloma also |
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RD risk factors
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history RD in fellow eye
high myopia family hx lattice trauma cataract surgery (ICCE 1%, ECCE .1%) DM yag laser post capsulotomy AGE |
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Giant tears
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Tear of >90 degress or 3 clock hours
occurs in trauma, myopia 50% risk of RD in fellow eyes |
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traumatic retinal tears
list most common ones |
1. inferotemporal (most common)
2. superonasal 3. giant retinal tears 4. flap tears 5. lattice |
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Retinal tears with PVD
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most common at 2-10oclock when assoc with PVD.
PVD with vit heme, or pigment have 70% change retinal break. PVD only has 15% break |
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rhegmatogenous RD
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retinal break allows liquid vitreous access to subretinal space. 70% tears superior.
Risk: age, RD in fellows eye, high myopia, fhx, lattice, trauma, cataract surgery, DM yag capsulotomy, trauma. most common: dialysis > giant tears > flap tears>lattice 50% present with flashes/floaters Retina has break 97%, detached retina opaque, corrugated, undulating, tobacco dust, decrease IOP, vit heme, non-shifting subretinal fluid. |
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Repair for rhegmatogenous RD
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1. pneumatic retinopexy (best for superior RD, within 1-2 clock hours) Phakic better than aphakic. Inject gas or sterile air into vitreous cavity. The break is then sealed with cryo or laser. Have pt head doen to tamponade the break, RPE pumps subretinal fluid, allowing retinal to reattach.
2. surgery, scleral buckle, vitrectomy with laser or cryp |
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exudative RD
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occurs with uveitis, tumors, glomerulonephritis, HTN, eclampsia/preeclampsia, hypothyroid, coats, nanophthalmos, scleritis,
CSR. Present with shifting fluid, smooth retinal surface, no retinal break, retinal is behind lens. |
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traction RD
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can occur after penetrating trauma, proliferative retinopathy, PHPV, toxoplasmosis, vitreous degeneration. Presents with taut retina, immobile, concave, no retinal break
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features of long standing RD
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thin retina
small breaks/dialysis demarcation lines RPE atrophy subretinal precipitates macrocyts |
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intraocular gases
rate of gas dissolution |
C3F8>C2F6>SF6>AIR
gas expansion is greatest for 100% C3F6 |
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Cilioretinal artery
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In 15-25% patients cilioretinal artery is perfusing macula
In CRAO cilioritinal artery can allow some preservation of central visual acuity |
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Ophthalmic artery occlusion
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Causes NLP vision with no cherry red spot entire retinal appears whitened, can occur in orbital mucor.
FA shows decrease in choriodal and reitnal filling. ERG- a wave absent |
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Branch retinal artery occlusion
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90% by emboli (cholesterol, calcium, fibrin, platelets)
occlusion most common at bifurcation 10% risk fellow risk |
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Central retinal artery occlusion
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Most common cause of cherry red spot.
etiology: atherosclerosis, at lamina cribosa, cholesterol emboli, GCA vasculitis, trauma, coagulopathy, ON drusen, increase IOP, collagen vascular disease, migraine, orbital mucor, fibromuscular hyperplasia, behcet's, leukemia. Presents with painless vision loss with cherry red spot, the retinal edema resolves in 4-6weeks, develop pales disk, attenuated vessels. Pathology shows atrophy inner retinal layers. Work up: work up GCA is patient >50, CBC, ESR, cardiac and coagulopathy work up, C-ANCA. FA shows delay filling. treatment: decrease IOP, paracentesis, ocular massage, carbogen |
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Branch retinal vein occlusion
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occlussion of AV crossing, artery compresses the vein.
most common superotemporal assoc: atherosclerosis, HTN, DM, old age, glaucoma, papilledema, increase IOP, ON drusen. types: nonischemic (<5dd nonperfusion) ischemis (>5dd nonperfusion). shows deep and superficial hemorrhage (do not cross mid raphe), CWS, CME, disc edema non-ischemic- macular edema ischemic- ME, ischemic maculopathy, neo, vit heme, TRD, 40% NVE (NVI is rare). treat with sector PRP when NVE develops. Grid laser for macular edema when <20/50 for 3 months and there is no evidence of macular ischemia |
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Hemiretinal vein occlusion
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risk factors: HTN, DM, glacoma
ischemic HRVO: high risk of NVD or NVE than both ischemic CVO and BVO |
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CRVO risk factors
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atheroclerosis
HTN optic disc edema glaucoma hypercoagulable state vasculitis drugs (OCP) retrobulbar compression migraine |
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CRVO
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blockage at level of lamina cribosa
non-ischemic- more common(70%) vision >20/200, 50% resolve ischemic(30%)- >10DD of nonperfusion. 60% develop NVI, 30% NVG have venous dilation, tortuosity, heme at all 4 quadrants, disc edema, Macular edema follow every 6 months look out for Rubiosis, PRP if present. Focal laser no help for macular edema RAPD, decrease B wave on ERG, VF constricton, VA worst 20/400 all signs to ischemis CRVO 8-10% risk of developing BRVO or CRVO in fellow eye |
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Study: Central vein occlusion study
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1. No benefits from early PRP in non-perfused CVO, wait for NVI then PRP
2. PRP when 2 clock hours of NVI 3. monthly follow up of gonio in 1st 6 months 4. no benefit from focal laser for macular edema |
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Study: Branch vein occlusion study
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Objective: evaluate PRP and grid in preventing neo, preveint vit heme, improving VA in eyes with macular edema
conclusions: grid laser recommended in BVO eyes 1. within 3-18mo 2. VA 20/40 or worst 3. FA documents macular edema without foveal heme Perform PRP when NVI develops |
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Rates of neovascularization in CRVO
HRVO BRVO |
CRVO- high rate of NVI
HRVO- has highest rate of NVI and NVE compared to BRVO and CRVO BRVO- NVE mostly |
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Ocular ischemic syndrome
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blood flow decrease to eye, common in >90% carotid occlusion. assoc with DM, HTN, CAD, stroke.
cause VA loss, dull eye pain, afterimages, prolong recovery after exposure to light, amarosis, conjunctivits, NVI, AC cells/flare, corneal edema, decrease IOP, vitreous cells, Neo, disc pallor, ON edema, mid peripheral heme, CME, attenuated vessels. FA: filling delay Perform carotid UA, ophthalmodynamometry Treat: decrease IOP to increase perfusion, carotid surgery. |
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Central Serous Choroidopathy
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Occurs in young males assoc with HTN, type A personality.
have a serous detachement of the macula Presents with blurry vision, micropsia, paracentral scotoma, induced hyperopia. fundus shows absent foveal reflex, yellow subretinal deposits when resolved, RPE changes. FA: expansile dot 80%, smokestack 10%. OCT: sesory elevation, PED. Treatment: observe. Laser indications: 1. persistent >4months 2. prevous CSR with permanent decrease VA 3. episode in fellow eye with vision loss 4. needs quick recovery due to job. *laser shortens recovery time but does not change final vision and CNV can be added risk. |
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Commotio retinae
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transient retinal whitening at the deep sensory retina from disruption of photoreceptor outer segments.
This is not retinal edema |
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epiretinal membrane
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proliferation at the vitreoretinal junction. if contract can cause retinal folds. assoc with DM, retinal occluson, PVD, myopia, retinal holes, ocular surgery, laser, aging
OCT - shows epiretinal membrane seen at surface of retina. treatment: consider surgery if vision <20/50 |
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ARMD
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Leading cause of central vision loss in adults >60 in US
Risk: old, white, female, smoker, HTN, poor nutrition, photic exposure, HTN, light iris, hyperopia. 2 forms 1. Dry- Drusen (PAS + between RPE and bruchs) 2. Wet- CNV classification drusen small <64 intermediate 64-124 large >125 risk CNV in fellow eye in soft pigmented drusent 60% (multiple soft drusen, RPE clumping, dense drusen, PED) |
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Signs of CNV
typed of CNV |
1. subretinal blood
2. fluid 3. lipid 4. RPE detachment 5. gray-green subretinal lesion Types of CNV defined by FA appearance 1. classic- early hyper, late leakage extending CNV margin 2. occult- 1. fibrovascular PED: early irregular mottled hyper, late stippled hyper not as bright as classic. 2. late leak of underteminate origin, early no leak, late strippled hyper |
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Study: ARED study
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evaluated the effect of supplement (Vit C, Vit E, b carotene, zinc, copper) on AMD progression, also cataract development.
Conclusion: Found that supplements where beneficial for category 3. extensive intermediate drusun or 1 large and 4. VA loss doe to AMD (foveal geographical atrophy, exudative). It does not affect cataract development of progression. Caution in smokers, beta carotine can increase lung Cancer |
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Study: Macular photocoagulation study (MPS)
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Objective was to evaluate laser treatment in preventing VA loss in CNV.
Conclusion: 1. treat extrafoveal CNV (200-2500) 2. juxtafoveal CNV benefit from krypton laser except HTN AMD patients. 3. AMD patients with subfoveal CNV benefit from argon or krypton laser 4. Classic juxtafoveal CNV, in AMD is beneficial. 5. Unilateral CNV with large drusen, focal hyperpigmentation is risk factor to develop CNV in fellow eye. |
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Study: Treatment of ARMD with photodynamic therapy trial (TAP)
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Objective to evaluate verteporfin photodynamic therapy in treating subfoveal classic CNV.
conclusion- PDT is recommended for subfoveal predominantly classic CNV. 34% more likely to retain vision |
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Study: Verteprofin in photodynamic therapy trial in photodynamic therapy pathologic myopia
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Objective to evaluate visudyne PDT in management of subfoveal CNV not included in original TAP sudy
Conclusion: Treatment is recommended in treating subfoveal occult but not classic CNV when there is progression. lesion size <4MPS DA Baseline VA < 20/50 |
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Definition of: extrafoveal, juxtafoveal, subfoveal
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extrafoveal: 200-2500microns from FAZ
juxtafoveal: 1-199microns from center of FAZ or CNV within 200-2500microns with assoc blood within 200microns FAZ Subfoveal - under the FAZ |
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parafoveal and juxtafoveal telangiectasia
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these are microaneurysmal and saccular dilatons of the parafoveal vessels
type 1- unilateral, middle age male, spectrum of coat's disease. 1a. congenital affect temporal fovea with macular edema and lipid. 1b. idiopathic, telangiectasia only 1 clock hours of FAZ, minimal leak on FA. vision good Type 2-most common, bil, aquired M=F, older. involve less than 1DD minimal ME. FA shows parafoveal capillary leak, ris of CNV Type 3-Bil, idiopathic M=F, capillary occlusion. Type 2 and 3 has similar structural abonormality to diabetes no risk of NVE complications: CNV, macular edema, exudation |
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Coats disease
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a non hereditary proliferative exudative disease. common males, unilateral, progressive. Present in child with leukocoria, strabismus.
Have telangiectatic vessels that leak --> subretinal lipid. 66% exudative RD <4yo. Pathology: retinal vascular abnomalies, subretinal and intraretinal cholesteral deposits, intraretinal PAS deposits. FA - show blood fluid levels, saccular aneurysm (light bulb dilations) of retinal arteries and venules. Small assoc with RP. TReat with cryo-laser to stop leaking vessels. |
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Diabetic retinopathy
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leading cause of new blindness in US. NPDR main cause VA loss --> macular edema. PDR main cause of VA loss --> PDR, Vit H, NVG, TRD
pathology: loss of pericytes, thickening capillary membrane, breakdown blood retinal barrier. Background BDR: mild retinal heme, exudate, CWS, MA, IRMA, venous beading Severe NPDR: 4-2-1 rule (one of these)(4 quads retinal heme, 2 quads MA, venous beading, 1 quad IRMA). very severe NPDR (two or more) Proliferative- NVD or NVE High risk PDR- >1/4 -1/3 NVD, any NVD with vit heme, NVE >1DD with vit heme |
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DM epidemiology
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Type 1 DM:
at dx no BDR. 5year- 25% BDR 20year- 98% BDR, 60% PDR, 30% CSME Type 2 IDDM at dx: 30% BDR 5year-40%BDR, 2%PDR 20year-90%BDR, 25% PDR, 40% CSME Type 2 NIDDM at dx: 20% BDR 5year- 30%BDR, 2%PDR 20year-50% BDR, 10%PDR, 20%CSME |
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other complications of
DM other than Diabetic retinopathy |
1. diabetic iridopathy- Iris neo, lacy vacuolization of iris pigment epithelium.
2. diabetic cataract- excess glucose, glucose --> sorbitol which cause osmotic effect 3. papillitis-acute disc swelling, vision good >20/50, good prognosis 4. isolated CN palsies (3,4,6) 5. pupil abnormalies: light near dissociation 6. fluctuation refractive error- due to osmotic effect on lens due to unstable blood glucose |
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FA indications in DM
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identiy macular ischemia
localize the MAs to help guide focal laser treatment identify NVE identify capillary non-perfusion |
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follow up schedule for diabetic retinopathy
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Based on retinopathy
normal- 1 year mild NPDR-9mo mod NPDR-6mo severe NPDR-4mo CSME- 2-4mo PDR-2-3 Based on age and pregnancy 0-30 within 5 years dx: 1 year 31-over at dx: 1year pregnant- at first trimester, 3mo |
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Indications for pars plana vitrectomy in DM
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Most common indications
1. dense non clearing vit heme 2. TRD affecting macula 3. combo of TRD and RRD 4. CSME with posterior hyaloidal traction 5. significant recurrent vit heme Additional indications 1. progressive fibrovascular proliferation 2. ant. hyaloidal fibrovascular proliferation 3. ghost cell glaucoma 4. NVI with media opacity impeding PRP 5. dense subhyaloid heme |
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Study: Diabetic retinopathy vitrectomy study (DRVS)
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evaluated early surgical intervenstion vs. dealyed surgery in patients with severe NPDR or early PDR.
conclusion: early vitrectomy in eyes with severe VA loss due to nonclearing heme was helpful in type 1 DM patients. Also useful in eyes with useful VA and advanced PDR. Eyes with TRD not involving the fovea can be observed. |
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Study: Diabetic retinopathy study (DRS)
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evaluate whether laser prevents severe VA loss in diabetic retinopathy.
conclusion- laser decrease risk of severe Va loss. PRP patients with high risk PDR. (NVD 1/3-1/4 disc, NVD with vit heme, NVE 1DD with vit heme). There is no clear benefit in treating severe NPDR and PDR without high rick features. |
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Study: Early Treatment diabetic retinopathy study (ETDRS)
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Study designed to answer
1. laser effective for DME? 2. dose aspirin affect DR course 3. when to start PRP for DR? Conclusion: 1.Treat all patients with CSME becasue is decrease 50% mod vision loss. 2. immediate PRP for high risk PDR and positive severe NPDR in both eyes. 3. no benefit from ASA |
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Clinically significant macular edema
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1. retinal edema at fovea or within 500microns
2. retinal exudate at fovea or within 500microns with assoc retinal thickening 3. retinal edema 1DD size withing 1DD fovea *must grid laser with criteria for CSME met because there is a 50% decrease in VA loss according to ETDRS study |
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Study: Diabetes control and complication trial (DCCT)
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Evaluated tight vs conventional glucose control in type 1 DM
At 5 years- retinopathy was 50%less with intense therapy. Ha1c less than 8 decrease risk of retinopathy. But intense therapy increase hypoglycemic episodes 2-3x conclusion - tight control beneficial, but can lead to initial worsening of retinopathy in begining |
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Study: Epidemiology of DM interventions and complications (EDIC) trial
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A follow up trial of the DCCT. Found that tight control indeed is benficial
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Study: The United Kingdon Perspective Diabetes study
(UKPDS) |
Compared intense glucose control with oral hypoglycemic and or insulin control vs. conventional treatment with diet.
1. intensive treatment with either sulfonylurea, metformin, or insulin is all equally effective 2. intensive group have 11% decrease in ha1c compared to conventional 3. intense group decrease risks in DM 12%, 10% in DM related deaths, 6% all cause of mortality. 4. Type 2 diabetic patients benefit from intensive treatment just type 1 |
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Study: The United Kingdon Perspective Diabetes study - HTN in DM study (UKPDS-HDS)
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Does BP control affect type 2 DM complications?
- found that tight control of HTN decreased deaths related DM 32%. reduced vision loss. can use either captopril or atenolol it made no difference. conclusion: tight HTN control decrease risk of diabetic retinopathy complications |
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Radiation retinopathy
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microangiopathy that occurs with exposure to radioation. Threshold is 300 RADS
Brachytherapy is 15,000RADS EXT beam is 5000 RADS Finding similar to diabetic retinopathy. Pathology: loss of capillary endothelial cells and pericytes. Treatment: focal laser for ME and PRP for NV |
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Proliferative vitreoretinopathy
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Most common cause of failure in RRD repair.
Cells grow into the inner and outer retina. Vitreous form membrane wich on contraction can cause retinal folds, equitorial traction, detachement of non-pigmented epithelium of pars plana, retinal shrinkage. -It causes retinal breaks to reopen, new breaks, and TRD. can try fixing with scleral buckle. Risk: ocular perforation, rupture, penetration, FB. Three grades A,B,C (increasing severity) |
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Familial exudative vitreoretinopathy (FEVR)
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AD, x-linked recessive
A developmental abnormality in the temporal retina vasculature. Similar to ROP Stage 1. avascular peripheral retina Stage 2. fibrovascular proliferation with neovascularizaton, leads to disc and macular dragging Stage 3 - Scarring leads to RRD treat: laser to avascular retina, poor prognosis |
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Retinal arterial macroaneurysm
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common in old females.
assoc with HTN, atherosclerosis common along temporal arcades Causes blood in every retinal layer, lipid exudate, arterial occlusion, CME Pathology: thickening of vessel wall with hypertrophy of muscularis. Treatment: observe, consider focal laser |
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Hereditary hyaloideoretinopathies with optically empty vitreous
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vitreous liquifaction leading to a optically empty vitreous cavity. There can be thin cortical vitreous behind lens and a avascular membrane adhering to retina.
groups 1. Jansen - AD, RD Wagner - AD, no RD 2. Stickler - AD, mutation in type 2 collagen, have systemic abnormalies, marfanoid, pierre robin malformation, mid face, flattening, joint hyperextensiblity, arthritis. Very High rate RD. Weill-Marchesani variety- like sticklers, has short stature, stubby hands, feet |
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Asteroid hyalosis
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common in old and diabetic
unilateral. have calcium soap depostion in vitreous. usually does not affect vision pathology:grey spheres with maltese cross bifringence on polarizaton |
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synchisis scintillans
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Cholesterol crystals derived from old vitreous heme.
Unilateral occurs after trauma crystals sink to bottom of globe |
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DDx Roth spots
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1. Ischemia (anemia, anoxia, CO poisoning)
2. elevated venous pressure (birth trauma, shaken baby, intracranial heme) 3. capillary fragility- HTN, DM 4. infection- bacterial endocarditis, HIV 5. leukemia 6. collagen vascular disease |
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Purtscher's retinopathy
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Occurs after head trauma, compressive injury. has retinal whitening, heme, CWS, papillitis, RAPD.
FA: shows leakage from retinal vaculature, late venous staining Can also occur with: pancreatitis, fat emboli, SLE, leukemia, amniotic fluid emboli, dermatomyositis |
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Terson's syndrome
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Retinal hemorrhage or vitreous hemorrhage with subarachnoid or subdural hemorrahge
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solar retinopathy
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photochemical damage of the retina by sungazing >90sec
assoc: solar eclipse, psych disorder, religieous ritual, use of hallucinogenics Decrease vision but improves cause yellow-white spot in the fovea, later causes red foveal depression and lamellar hole. FA: staining of damaged RPE, no leakage. window defect occurs later on. |
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Macular hole
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Occurs from tangential traction on the fovea by posterior vitreous. Occur more in Females.
Commonly causes: idiopathic (age), surgery, trauma, CME, inflammation. Risk of developing in fellow eye is <1%, no risk if PVD present Stage1-impending hole, foveal detachement, macular cyst. can close spontaneously Stage2-full thickness eccentric hole Stage3-Full thickness with operculum Stage4-Full thickness with PVD FA shows window defect, diagnose with OCT . Stage 1 observe, Stage 2-4 can try vitrectomy with posterior hyaloid peel and gas tamponade. |
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Traumatic macular hole
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Can result from commotio retinae in macula.
disruption and necrosis of retinal photoreceptors with subsequent loss of retinal tissues |
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chloroquine / hydroxychloroquine toxic retinopathy
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Binds to melanin
toxic dose chloroquine: >3.5mg/kg/day (300g total) hydroxychloroquine >6.5mg/kg/day (700g total) cause mottling of RPE causing a bull's eye. decreases vision, small scotoma to the red test object on targent *** the retinopathy progresses despite stopping medicaitons! |
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Chlorpromazine
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toxic 1200-2400mg/day x 12 months
can have blurred vision or symptomatic pigment deposit in lids, cornea, ant lens capsule, ant/post subcapsular cataract, retina |
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Thioridazine (mellaril)
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Toxic >800mg/day chronically, or >2000mg/day (get it quicker)
cause blurred brownish vision, RPE damage, nyctalopia ***Retinopathy can progress even after stopping medications! |
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Chloramphenicol
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Antibiotic that can cause atrophy of the maculopapullar bundle.
Visual defect- cecocentral scotoma |
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Quinine
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Cause RPE mottling, vessel attenuation, and disc pallor.
A single 4 gram dose can cause acute toxicity. Decrease vision, nyctalopia, hearing loss, dilated pupil, cherry red spot, dilated vessels. |
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Causes of drug induced crystalline retinopathy
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Tamoxifen >30mg/day
canthaxantine .35mg/day talc IV drug abusers nitrofurantoin methoxyflurane ethylene glycol |
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Tamoxifen
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Toxicity >30mg/day
cause a fleck like cystalline retinopathy, typically a ring around macula. can have retinal pigmentary changes and CME FA, macular edema |
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Digoxin
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Affect cones has minimal fundus changes, cause yellow changes and blurry vision
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Drug induced myopia
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Sulfa, tetracycline, promethazine, steroids, ampicillin, acetaminophen
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Gentamycin intraocular injection
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causes rapid macular ischemia
with 400mcg |
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sildenafil
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cause a transient blue vision. >100mg dose cause 50% ocular effect
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nicotinic acid maculopathy
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cause a non-leaking CME, blurry vision, metamophopsia.
FA causes CME but DOES not leak |
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Conditions that have typical CME appearance but do not leak on FA
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Nicotinic acid maculopathy
X-linked retinoschisis Goldmann-Favre some types of RP |
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Etiology of CME
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Diabetes
epinephrine pars planitis RP Irvine Gass Venous occlusion E2 Prostaglandins nicotinic acid maculopathy |
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Angiod Streaks
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Peripapillary cracks in the thick, denererated, calcified bruch's membrane
Minor trauma can cause choroidal rupture, subretinal heme. 50% idiopathic 50% systemic Think PEPSI 1. Pseudoxanthoma elasticum 2. Ehler's Danlos 3. Paget's disease 4. Sickle cell disease 5. Idiopathic |
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Pseudoxanthoma elasticum
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AR >> AD, females more
Patients have reduntant skin, waxy yellow papules in skin like plucked chiken have peau de orange in retina GI vascular malformation can bleed assoc with optic nerve drusen angiod streak 85% |
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Ehler's Danlos
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AD, hyperextensible skin due to deficient collagen matrix
have subluxed lens, myopia, keratoconus,blue sclera, RD |
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Paget's disease
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Increase in bone production and destruction.
increase serum phosphatase have skull and long bone fractures |
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Choriodal folds
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Results from shrinkage of the the inner choroid or bruch's, it will cause an undulation og RPE and retina.
Causes: tumors, hypotony, inflammation, CNV, retrobulbar mass, papilledema, extraocular hardware appears as yellow elevated crest alternating with darker bands between crest. FA: light bands (thin RPE) hyperfluorece, while dark bands hypofluorese |
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Choroideremia
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X-linked. rod cone degeneration, affect males
progressive disorder of choriocapillaris onset childhood with nyctylopia, photophobia, and constricted VF. Find: degeneration of RPE and choriocapillaris in periphery (scalloped RPE atrophy). Late finding: absent RPE and choriocapillaris except the macula. ERG undetable in the late. female carriers have salk pepper fundus |
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Gyrate atrophy
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AR, deficient ornithine aminotransferase
Increase ornithine levels, decrease in lysine. Have decrease in vision, nyctalopia, constricted VF, scalloped absent choriocapillaris and RPE. assoc with myopia, cataracts, CME. test blood, Urine analysis treat by restricting arginine, protein, vit B6 supplementation |
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Best's disease
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AD, macular dystrophy
Stage1: previtelliform (yellow dot) Stage2:vitelliform (egg yolk= lipofusin) Stage3:scrambled egg Stage4:Cyst Stage5:pseudohypopyon Stage6:chorioretinal atrophy ERG normal , EOG abnormal vision much better than expected clinically |
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Stargardt's
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AR
most common hereditary macular dystrophy. Onset early life, cause decrease vision(before macular changes), nyctalopia. Present with BL pisciform, yellow flecks at RPE level. They can change with time. Fundus has beaten bronze look, foveal atrophy, bull's eye maculopathy Pathology:RPE thickening with lipofuscin accumulation. FA:classic dark choroid, hyperfluorecence does not correspond to flecks. ERG and EOG normal |
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DDx Bull's eye maculopathy
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Stargardt's
cone dystrophy chloroqine ARMD macular hole central aveolar choridal dystrophy olivopontocerebellar atrophy ceroid lipofuscinosis |
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Retinal pigment epithelial detachment
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discrete blister like elevation, can have orange pink rim of subretinal fluid.
patient<50 likely CSR (good prognosis) patient >50 likely PED w/drusen can les to CNV (poor prognosis) FA: discrete early hyperfluoresence of entire serous PED with late polling. 33% develop CNV |
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pathologic myopia
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axial length >26mm, >6Dmyopia. In 2% US population. Can have tilted disc, temporal cresent, post staphloma, tigroid fundus, lacquer cracks, fuch's spot, cataract, retinal holes, RRD
Lacquer cracks can cause decrease in vision, metamorphopsia, focal subretinal heme. complication: CNV 65% in fovea |
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Conditions associated with CNV
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Degenerative: ARMD, Myopia, angiod streaks
Heredodegenerative: vitilliform, stargardt's,ON drusen inflammatory: POHS, multifocal choroiditis, serpigenous, toxoplasmosis, toxocariasis, rubella, VKH, behcet's, SO Tumor: choroidal nevus, choroidal hemangioma, metastatic choriodal tumor, hamartoma RPE Trauma: choriodal rupture, laser Idiopathic |
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Siderosis
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Iron deposit in the epithelial tissues. Can be in iris muscles, non-pigmented ciliary epithelium, lens epithelium, RPE
RPE and photoreceptors susceptible to siderosis. Cause: nyctalopia, constricted VF, decrease VA, rust color stroma, iris heterochromia, pupil mydriasis, ant lens deposits, cataract, vitreous opacity, retinal pigmentation, attenuated vessels, optic dics atrophy, glaucoma from iron accum in TM |
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Congenital Stationary Night blindness
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Group of nonprogressive Rod disorder. have nytalopia. Can be x-linked, AD, AR.
Have normal vision, VF, and color vision. have parodoxic dialtion to light ERG shows decrease scotopic normal photopic 2 types: 1. Those with normal fundus: Nougaret AD, no rod function. Riggs AR, some rod function Schubert-burnschen x-link-myopia Type 2: Those with abnormal fundus Fundus albipunctatus- AR, mid peripheral yellow/white spots that spare macula. ERG scotopic normal after 4-8 hours in dark adaptation. Oguchi-Disease:Golden brown fundus in the light state, normal fundus in the dark adapted Kandori's flecked retina- AR, yellow white spots, spare macula |
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Retinitis pigmentosa Type 1
(ROD-CONE) |
Most common hereditary degeneration. Type 1 RP have multiple inheritance
AR most common AD least severe form x-linked rare most severe Have nyctylopia, decrease vision late. Finding: bone spicules, attenuated vessels, waxy pallor ON, retinal atrophy, vitreous cells, cataract Pathology:photoreceptor and outer retina layer atrophy. RPE invade retina casuing bone spicules. The VF is constricted in ring scotoma. Macula finding: can have Macular edema that does not leak on FA, ERM, atrophy. Carriers: can have bone spicules, salt pepper changes, bronze sheen in macula the most critical and constant finding is abnormal ERG |
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Retinitis pigmentosa Type 2
(CONE-ROD) |
Type 2 is cone-rod and can be AD, AR, xlink.
Findings have less pigment deposition. 50% are sin pigmento. ERG cone affected more. Treat with low vision, dark glasses, vit A. poor prognosis |
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RP variants
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Leber's congenital amaurosis- infantile RP
sector RP- focal RP, not progressive good prognosis unilateral RP- very rare inverse RP-posterior pole more affected than periphery, bone spicule in macula retinitis punctata albecens- small white dots in mid periphery, no bone spicules |
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Causes of pseudo RP
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Trauma
drug toxicity (chloroquine, phenothiazine) infection (syphillis, rubella) post CRVO resolved RD ophthalmic artery occlusion |
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Treatable RPs
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Abetalipoproteinemia (bassen-Kornzweig)
Refsum's (elevated phytanic acid) gyrate atrophy (elevated ornithine) |
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RP syndromes
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Usher's AR
Refsum's AR Bassen-Kornzweig AR Lawrence moon bardetbiedl AR spielmeyer vogt batten mayou CPEO olivopontocerebellar atrophy Alstrom |
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Refsum's
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AR, defienct phytanic acid oxidase
Phytanic acid increase in RPE cells, retina deteriorate. present with sine pigmento RP, cataract, prominent corneal nerves Diagnose: increase serum copper and ceruloplasmin, increase CSF protein and pleocytosis Treatment: diet restriction of: (animal fat, milk products, green veggies) |
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Usher's
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AR, most common syndrome assoc with RP
Have RP with deafness, ataxia, MR Type 1: deafness, unintellible speech, ataxia Type 2: partial deafness, intellable speech, no ataxia |
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DDx RP and deafness
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Usher's
Hallgrenn's alstrom's lawrence-moon-bardet-beidl cockayne's syndrome |
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Bassen-Kornzweig syndrome
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AR, hereditary abetalipoproteinemia
Cannot transport or absorb lipids due to absence of apolipoprotein B leads to malabsorption, steatorrhea. Deficient fat soluble vitamins (A,D,E,K) Findings are RP, bitot spot Diagnosis with CBC, cholesterol, stool sample Treat with Vit A, Vit E in the early stages the ERG can be reversible! |
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Lawrence-Moon-Bardet-Biedl
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AR
Have RP with flat ERG, mental retardation. Have short stature and hypogonadism B-B: obesity, polydactyly L-M: spastic paralysis |
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Alstrom's disease
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RP with profound vision loss early life.
Assoc: deafness, DM, obesity, renal failure, baldness, acanthosis nigrcans, hypogenitalism |
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Cockayne's syndrome
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RP with profound vision loss in the 2nd decade. Have deafness, dwarf, MR, premature aging, psychosis, intracranial calcifications
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Olivopontocerebellar atrophy
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cause retinal degeneration, bulls eye maculopathy. Tremor, ataxia, dysarthria
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Speilmeyer-vogt-batten-mayou
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AR, lysosomal storage disease, neuronal ceroid lipofuscinosis. Occurs in young jewish females has progressive demantia, seizures and RP with bulls eye maculopathy. Shows characteristic curvilinear or fingerprint inclusions on electron microscopy of peripheral blood conj vessels.
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CPEO
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Mitochondrial inheritance
Have salt and pepper fundus, progress to RP like disease, Ptosis, ophthalmoplegia, strabismus Kearn-sayre: have heart block |
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Pattern dystrophies
1. sjogren's reticular 2. butterfly 3. adult vitelliform |
Group of disease w/ central pigment disturbance.have good vision, normal ERG, abnormal EOG (like best's). Can develop CNV
1. Sjogren's-reticular fishnet configuraton. have fishnet hypofluorescence on FA 2. butterfly - gray-yellow butterfly lesion. slight vision decrease 3. Adult vitelliform- yellow lesion in the macula like Best's but smaller and does not break up. EOG is normal. CNV more common than Best's! |
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Goldmann favre disease (enhance S cone)
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AR, chromosome 15,
A vitroretinal dystrophy presents with nyctalopia, increase sensivity to blue light, pigmentary degeneration, empty vitreous, preipheral VF loss, has yellow sheen-like round lesions around arcade. Macular schisis does not leak with FA. decreae in ERG and FA. |
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Progressive cone dystrophy
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AD, less x-linked
Progressive dysfunction of cones with normal rods. Onset 30s, decrease vision, dyschromatopsia, photophobia, nystagmus, macular degeneration, bulls eye maculopathy. VF is normal. ERG absent photopic, normal scotopic, EOG normal. prognosis poor |
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Colorblindness
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X-linked - red-green
AD - tritan congenital usually a red-green defect while acquired is a tritan defect. Deuteranomalous trichromats most common at 5% Color vision does not decrease vision except in rod monochromatism and blue cone monochromatism, Anomalous trichomatism have all three cones but asymmetric proportions. congenital dichormatism- lacks one cone. Diagnosis with: farnsworth munsell 100 hue test, D15, city univerity test, hardy rand ritter, ishihara. Kollner's rule: Optic nerve diesase: red green defect. retinal disease --> tritan defect |
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Kjer's syndrome (dominant optic neuropathy)
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AD (OPA1), most common hereditary optic atrophy.
onset 4-8. BL symmetric, mild decrease vision, have tritan defect, dyschromatopsia. temporal wedge disc pallor. suspect when there is tritan color defect with decrease in vision. |
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Rod monochromatism (congenital achromatopsia)
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AR, A Stationary cone dystrophy, present at birth, nonprogressive. Absent or abnormal cones.
Have severe decrease vision less 20/200. complete color blindness, nystagmus. have normal retinal exam. Vf have central scotoma. ERG normal scotopic but abnormal photopic |
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Blue cone monochromatism
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X-linked, have only blue cones. severe vision loss, nystagmus, photopsia. ERG, absent cone response and normal rod
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Retinal cavernous hemangioma
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vascular tumor. assoc with CNS, skin vascular lesion.
unilateral, unifocal Have cluster of red intraretinal vascular sacs. (looks like bunch of grapes) can have overlying gliosis. Does not have exudates or RD but can have vit heme. FA shows fluid levels within the vascular sacs. treat with vitrectomy is non clearing Vit heme |
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Eales disease
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idiopathic, retinal perivascularitis and peripheral non perfusion with NVE. Vitreous heme most common cause of vision loss. Occurs in healthy men, bilateral. common in middle east and india. increase risk of BVO. Will have NVD, NVE, NVI, NVG, vit heme, cataract, vascular sheathing that leaks on FA. vessel tortuosity and collateral formation, peripheral nonperfusion. Can also have ac rxn, vitritis, CME
Stage1- sheathing vessels, retinal edema, heme stage2-more severe, vit heme stage3-peripheral NV stage4-proliferative retinopathy, Vit heme, TRD can have hearing loss, vestibular dysfunction, cerebral vasculitis, +PPD |
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Bietti's crystalline retinopathy
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decrease in vision in 5th decade
yellow-white, refractile spots throughout the fundus. can have crystals in peripheral retina. systemic disease with pigmentary retinopathy |
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cystinosis
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A amino acid metabolic disorder, lysosome cannot excrete cysteine.
types: infantile (fanconi) AR, salt pepper fundus. no visual abnormality, polyuria, growth retardation, renal failure, rickets, crystals seen in conjunctiva, cornea, iris, lens, retina Adolecent: AR less severe Adult: benign, no renal disease. deposits in the anterior segment only. Treat with cystamine |
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Study: Endophthalmitis Vitrectomy Study
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To evaluate acute post op endophthalmitis with immediate vitrectomy vs. tap and inject and also if IV antibiotic help.
1. IV antibiotic don't help 2. If vision is better than LP than Tap an Inject (.4mg amikacin and 1.0mg vancomycin) If vision worst than LP then immediate vitrectomy |
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Mucopolysaccaridosis
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Retina and cornea: Hurlers and Scheie
Retina Only: Hunter's and San Filippo Cornea Only: Morquio and Maroteaux Lamy None: Sly All are AR except hunter's (x-linked). Only those accumulating heparan sulfate have retinopathy |
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Sphingolipidoses
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AR, accumulation of sphingolipids due to lysosomal enzyme defect. Sphingolipid accumulate in retinal ganglion cells.
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Cherry red spots in Sphingolipidoses
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Tay sach- most common, hexosaminidase deficiency
Sandhoffs- visceral involvement neimann-pick- no MR gaucher's (remember mnemonic TSNG) |
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No Cherry red spots in Sphingolipidoses
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Fabry's and krabbe's
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Fabry's
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x-linked, sphingolipidosis
mutaton of alpha galactosidase A ceramide trihexoside accumulates in smooth muscle, blood vessels, kidney, skin,GI, CNS, heart, reticuloendothelial system - first symptom may be burning paresthesia or pain on extremities - ocular signs. corneal verticillata, tortous conjunctival and retinal vessels. Lens changes. Diagnosis, test tears to confirm the absent enzyme |
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Acute macular neuroretinopathy
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Occurs in young, healthy women. Can be unilateral or bilateral. present with decrease vision, paracentral scotomas. Retina has petalloid lesion around the fovea, appear dark red or brown surrounding normal macula.
FA: normal, VF paracentral scotoma no effective treatment, usually self limited. |
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DDx for blood in all retinal layers (subretinal, intraretinal, preretinal)
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Macroaneurysm
trauma (shaken baby) sickle cell choroidal melanoma capillary hemangioma vein occlusion (rare) CNV (rare) |
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Laser settings for focal and grid for diabetic macular edema
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Use FA to guide treatment
Focal- yellow-green apply to MA's 500-3000 from center of macula. spot: 50-100 duraton:0.1sec titrate power until whiten or darken MAs Grid: yellow-green wavelength apply to area of diffuse leakage 500 from center of macular and 500 from temporal margin. Spot: 50-100 duration:0.1sec space spots 1 burn width apart |
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Laser setting for PRP as per DRS, ETDRS
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Spot: 500microns
duration:0.1 sec power: until blanch #shot >1200 burns separated 0.5 burn width apart |
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Absorption of key pigments of eye
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Melanin absorbs yellow, green, red, infrared
Xanthophyll absorbs blue, minimal yellow, red RBC: absorbs blue, green, yellow. does not absorb red |
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Laser wavelength advantages
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Green- absorbed well by melanin and RBC
Red- penetrates cataracts and vit heme well, minimal absorption by macula. great for CNV lasering next to fovea Infrared: like red laser but penetrates deeper. Yellow: mininal scatter through NS cataract, low absroption at macula, little photochemical damage. Good for retinal vascular or chroidal lesions |
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side effects of PRP laser
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paracentral scotoma
transient edema CNV subretinal fibrosis scarring foveal burn choriodal swelling, and detachment exudative RD permanent mydriasis vit heme |
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Optic pit
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a grey-white depression of optic disc usually inferotemporal. 85% unilateral. can develop serous RD. No treatment for isolated pit, is serous detachment, laser to temporal margin of disc.
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Risk of Wet AMD vision loss
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old age, hyperopia, blue eyes. family hx, soft drusen, focal pigmentation, RPE detachment, HTN, smoking
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Sickle cell retinopathy
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proliferative retinopathy of equitorial or pre-equitorial,
severity SC>Sthal>SS>SA have salmon patches (intraretinal heme after retinal arteriolar occlusion), Black sunburst (chorioretinal scar and RPE proliferation after old heme), sea fan(peripheral Neo),refractile dots(old heme), angiod streaks, vascular occlusions, coma shape conj vessels, Vit heme, RRD. Stage1-peripheral arterial occlusion Stage2-Peripheral anastemosis Stage3-sea fan neo Stage4-Vit heme Stage5-Vit with traction RD Diagnosis with sickle cell prep and electrophoresis FA show capillary non-perfusion, AV anastemosis, neo TReat with PRP, surgery for RD and chronic VH. |
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differentiating Choriodal melanoma from a choriodal nevi
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TFSOM
Tumor size >2mm Subretinal fluid Symptoms Orange pigment Margin touching Optic disc Risk of transformation in 5 yrs 0 - 3% 1 - 38% 2 or more -50% |
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Study: The Studies of Ocular Complications of Aids (SOCA)
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reported patiented treated with ganciclovir had 79% higher mortality than those with foscarnet, both drugs equal in controlling CMV retinitis and which tolerable side effects. Retinitis progression best controlled with combo of treatments. Color photography is gold standard in following the diease progression
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Pneumatic retinopexy
indications |
Principle is to create a intraocular tamponade of the reitnal breaks to allow sufficient time for subretinal fluid to be resorbed and chorioretinal adhesion to form around break.
1. retinal breaks confined to superior 8 clock hours 2. retinal breaks with 1-2 clock hours 3. absence of PVR grade C,D 4. ability to maintain head position 5. clear media |
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Study: Pneumatic retinopexy
trial comparing Pneumatic retinopexy with scleral buckle |
no statistical difference between repairs made with pneumatic retinopexy vs scleral buckle. function outcome equivelent in macula on detachments. for patients with macula off RD <14 days, pneumatic retinopexy was superior to scleral buckle in regards to visual outcome.
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Pneumatic retinopexy
complications |
subretinal gas migration
anterior chamber gas migration endophthalmitis cataract new retinal break formation |
