BCSC Retina Flashcards
What is the ligament of Wieger?
A condensation of collagenous fibers attached to the posterior lens capsule.
How wide is the vitreous base?
2mm anterior and 3mm posterior to the ora serrate.
Where does the vitreous attach?
The vitreous base, lens capsule, retinal vessels, optic nerve and macula.
What is the vitreous made of?
Collagen fibrils separated by hydrated hyaluronan molecules.
What is the area of Martegiani?
The attachment of the vitreous to the disc.
Where is the macula clinically and how large is it?
The area between the disc and temporal vascular arcades, it is 5.5mm.
What defines the macula histologically?
The area with 2 or more layers of ganglion cells.
Why is the macula yellow?
Due to the accumulation of carotenoids, especially zeaxanthin and lutein.
What defines the fovea?
1.5mm area where the only photoreceptors are cones.
What defines the foveola?
0.35mm in diameter, where the INL and ganglion cell layer are displaced laterally.
What is the umbo?
150 micrometers in diameter, the central depression of the foveola, where cones are elongated.
What is the parafovea?
0.5mm ring around the fovea where ganglion cell layer, INL and OPL are thickest.
What is the perifovea?
1.5mm wide area around the parafovea.
What is the ora serrata?
The border between the retina and the pars plana.
Where do most retinal tears occur?
At the posterior border of the vitreous base, between the ora serrata and the equator.
What is a dentate process?
Jetties of retinal tissue extending anteriorly towards the pars plana.
What are ora bays?
Posterior extensions of the pars plana towards the retinal side.
What are meridonal folds?
Radially oriented thickening of retinal tissue extending to the pars plana,
What are the layers of the retina?
- Inner limiting membrane 2. nerve fiber layer 3. ganglion cell layer 4. inner plexiform layer 5. inner nuclear layer 6. middle limiting membrane 7. outer plexiform layer 8. outer nuclear layer 9. external limiting membrane 10. rod and cone inner and outer segments
Where are rods the most dense?
20 degrees from fixation.
How many cones does one midget bipolar cell synapse with?
One
Do bipolar cells synapse with one or many rods?
Many
What do amacrine cells do?
Help in signal processing by responding to changes in retinal stimuli like change in light intensity.
What is the ILM (internal limiting membrane)?
The foot pads of Muller cells, which attaches to the posterior cortical gel of the vitreous.
What is the XLM (external limiting membrane)?
Zonal attachments between photoreceptors and Muller cells, can be seen on OCT but not true membrane.
What supplies the inner retina?
The central retinal artery.
What supplies the outer retina?
The choriocapillaris.
What is the RPE?
Pigmented cells from the outer layer of the optic cup, continuous with pigmented epithelium of the ciliary body and iris.
Where is the apex of the RPE cell?
Facing photoreceptors, enveloping the outer segments.
What kind of junctions between RPE cells form the blood ocular barrier?
Zonulae occludentes near the apices.
What is the RPE function?
- absorb light 2. phagocytose rod/cone outer segments 3. fatty acid metabolism 4. form outer blood ocular barrier 5. maintain subretinal space 6. heal and form scar tissue.
Where is Bruch membrane?
Attached to the basal portion of the RPE.
What is the Haller layer of choroidal vessels?
The outer layer of large caliber vessels.
What is the Sattler layer of choroidal vessels?
The smaller diameter vessels and precapillary arterioles of the choroid.
What are the vortex veins?
Collect blood from the choroid.
Where are the vortex veins located and where do they drain?
Leave the eye at the equator, they drain into the superior and inferior ophthalmic veins.
Where is the sclera thinnest?
At the limbus, equator and peripapillary area.
What is the Hruby lens?
An external planoconcave lens with high negative optical power, gives upright image.
How is fluorescein eliminated?
Through the liver and kidneys
At what wavelength is fluorescein excited and at what wavelength does it fluoresce?
Excited at 465-490 nm (blue) and fluoresces at 520-530 nm (green).
What is autofluorescence?
Fluorescence prior to injection of fluorescein dye, such as optic disc drusen.
What are patterns of hypofluorescence?
- vascular filling defect 2. Blocked fluorescence
What are patterns of hyperfluorescence?
- Leakage 2. Staining 3. Pooling 4. Window defect 5. Autofluorescence
What are adverse effects of fluorescein angiography?
nausea/vomiting (10%), extravasation with tissue necrosis, urticarial reaction (1%), anaphylactic reaction (<1/100,000)
What does indocyanine green angiography (ICG) image?
Choroidal vessels.
What are indications for indocyanine green angiography (ICG) ?
CNV, PED, polypoidal choroidal vasculopathy, RAP, central serous choroiretinopathy, intraocular tumors, chronic inflammatory conditions
What allergy do you need to ask about prior to ICG angiography?
Shellfish (ICG has iodine).
What is basis for OCT imaging?
Optical reflectivity.
What is the axial resolution of SD-OCT?
7 micrometers.
What is the source of autofluorescence in the macula?
Lipofuscin, which has a pigment A2E.
What are the five different ERG responses?
- Rod response (dark adapted) 2. Maximal combined response (dark adapted) 3. oscillatory potentials (dark adapted) 4. single-flash “cone response” (light adapted) 5. 30-Hz flicker responses (light adapted)
What is the a wave on ERG?
Photoreceptor response, measured from baseline to a-wave trough.
What is the b wave on ERG?
Positive waveform measured from the a-wave trough to the b-wave peak which is generated by Muller/bipolar cells.
What is the ERG oscillatory potentials response?
Thought to be the result of feedback interactions between integrative cells of inner retina, reduced in retinal ischemia and some types of congenital stationary night blindness.
What does the ERG 30-Hz flicker response isolate?
It isolates cones, since rods can respond only up till 20-Hz.
Does full field ERG distinguish between macula and peripheral lesions?
No because 90% of cones are outside of the macula, so you can’t distinguish a macula lesion based on cone response.
What is the c-wave on ERG?
A late positive response occurring 2-4 min after stimulus generated by RPE.
What is multifocal ERG?
It tests cone generated responses that subtend 25 degrees from fixation, test for macular dysfunction.
What is bright-flash ERG?
Performed with a flash-stimulus brighter than usual to test for retinal function in eyes with opaque media.
How does the ERG change with retinal ischemia?
Abnormalities of b-wave and oscillatory potentials such as inversion of b-wave or delay in implicit time.
What does the EOG (electro-oculogram) measure?
The voltage differential generated across the RPE, which is measured as the voltage change as a patient looks from left to right with electrodes placed at both canthi.
What is a normal and abnormal Arden ratio?
Normal: 1.85
Abnormal: 1.30
What is visually evoked cortical potential (VEP)?
Occipital cortex response to stimulation of the retina, because the macula is highly represented in the visual cortex is a mainly test of macular function, can indicate abnormality anywhere along visual pathway from retina to cortex.
What can visually evoked cortical potentials be used to test?
Confirm diagnosis of optic neuropathy, estimate VA in infants, detect malingering
What are risk factors for AMD?
Family history, cigarette smoking, hyperopia, light iris color, hypertension, hypercholesterolemia, female sex and cardiovascular disease
What are druse?
Small yellow lesion at level of RPE, histologically are thickening of inner aspect of Bruch membrane, made of basal laminar deposits and basal linear deposits.
What are basal laminar deposits?
Granular, lipid-rich material and widely spaced collagen fibers between plasma membrane and BM of RPE cells.
What are basal linear deposits?
Phospholipid vesicles and electron-dense granules within inner collagenous zone of Bruch membrane.
What are the sizes of small, medium and large drusen?
Small: <64 micrometers diameter
Medium: 64-124 micrometers diameter
Large: 125 micrometers diameter
What are patterns of RPE abnormality in nonneovascular AMD?
Focal hyperpigmentation, nongeographic atrophy and geographic atrophy.
What is basal laminar drusen or cuticular drusen?
A clinical syndrome occurring in patients in their 30-40s consisting of innumerable, homogenous round drusen more apparent on angiography.
What was the orginal AREDS formulation?
500mg vit C 400IU vit E 15mg beta carotene 80mg zinc oxide 2mg cupric oxide
What were the recommendations of AREDS?
Patients with high risk of advanced AMD and vision loss(extensive intermediate drusen or 1 large druse or non-central geographic atrophy or advance AMD in 1 eye) should be recommended supplementation.
Which ingredient of AREDS increased risk of lung cancer in current smokers?
Beta carotene.
What is choroidal neovascularization?
Ingrowth of new vessels from the choriocapillaris into the sub-pigment epithelial space through a defect in Bruch membrane.
What is classic CNV?
An area of bright, uniform hyperfluorescence identified in early phase of FA that intensifies and demonstrates leakage in late phase.
What is occult CNV?
- Fibrovascular PED
2. Late leakage from undermined source on FA
What is polypoidal choroidal vasculopathy?
Variant of CNV characterized by multiple serosanguineous RPE detachments, peripapillary multifocal, orange, nodular lesions.
What is photodynamic therapy (PDT)?
Administration of photosensitizing drug followed by application of specific wavelength of light to generate reactive oxygen species to cause capillary endothelial cell damage.
What did the PDT in AMD studies show?
A benefit in treating predominantly classic lesions (TAP trial) and minimally classic lesions (VIM trial). VIP showed greatest benefit in eyes with occult CNV without classic component in small lesions.
What is vascular endothelial growth factor (VEGF)?
A homodimeric glycoprotein that is a heparin binding growth factor for vascular endothelial cells which can induce angiogenesis.
What is pegaptanib?
RNA oligonucleotide that binds VEGF165 near the heparin binding domain, does not target all active VEGF-A isoforms.
What did the VISION trial show?
Pegaptanib patients lost less vision than sham, and had small gains in vision.
What is ranibizumab?
Lucentis, humanized antibody fragment that binds and inhibits all active VEGF-A.
What did MARINA show?
Trial of ranibizumab vs sham in minimally classic or occult CNV treated monthly for 2 years, showed vision improvement/stabilization and greater gain of 15 letters compared to sham.
What did ANCHOR show?
Trial of ranibizumab and sham PDT vs sham injection and PDT in classic CNV with monthly injections for 2 years, found vision improved or maintained as compared to PDT.
What did PIER test?
Ranibizumab monthly for 3 months, then quarterly, demonstrated similar improvement in vision to monthly regimen in initial stage but then decline during quarterly dosing.
What are current clinical treatment regimens for wet AMD?
Treat and observe: treat till macula free of exudation then only treat for signs of recurrence
Treat and extend: continue treatment monthly till macula is dry, then extend intervals between treatment (will continue treatment even if appears dry).
What did PrONTO show?
Ranibizumab for monthly for 1st three months, then retreat during 1st year for thickening or loss of vision; 2nd year retreat for qualitative increase in fluid, found similar results to monthly regimens.
What is VEGF trap?
Soluble protein which combines ligand binding elements of VEGFR1 and VEGR2 extracellular domains.
What did VIEW1 and 2 show?
VEGF trap in monthly or bimonthly regimen compared to ranibizumab. Patients getting 2 mg monthly gained more letters than 0.5mg ranibizumab.
What is bevacizumab?
Avastin, Monoclonal antibody agains VEG with to antigen binding domains. Shorter half life than ranibizumab.
What did CATT show?
RCT comparing ranibizumab and bevacizumab for CNV in AMD, 1 year results showed no difference between two drugs in monthly or as needed delivery schedules.
What are the 4 signs of ocular histoplasmosis syndrome?
- Punched out chorioretinal lesions
- juxapapillary atrophic pigmentary changes
- no vitritis
- CNV
Where is ocular histoplamosis endemic?
Ohio and Mississippi River valleys
What are angioid streaks?
Dark red to brown bands radiating from optic nerve head representing breaks in Bruch membrane.
What conditions are associated with angioid streaks?
pseudoxanthoma elasticum, Paget disease, beta thalassemia, sickle cell anemia, Ehlers Danlos syndrome.
What are consequences of angioid streaks?
CNV, subretinal hemorrhage not associated with CNV, choriodal rupture from minor blunt injury.
What are signs of pathologic myopia?
Optic disc tilting, peripapillary chorioretinal atrophy, lacquer cracks, subretinal hemorrhages, Forster-Fuchs spots, posterior staphyloma, gyrate atrophy of RPE, cystoid, pavingstone and lattice degeneration, thinning or hole of retina, thinning of sclera, CNV
What is the chance of CNV in patients with high myopia?
CNV may develop in 5-10% of eyes with axial length >26.5.
What is high myopia?
Axial length >26.5 and spherical equivalent of -6.00 or greater
What is pathologic myopia?
Axial length >32.5 and spherical equivalent of -8.00 or greater.
What are broad categories of conditions that lead to CVN?
Degenerative (AMD, angioid streaks), Heredodegnerative (Vitelliform mac dystrophy, drusen), Inflammatory (histoplamosis, MCP, toxoplasmosis, VKH, Behcet), tumor, trauma (photocoagulation), idiopathic
What is NPDR?
Intraretinal vascular changes without the presence of extraretinal fibrovascular tissue.
What is PDR?
Ischemia-induced neovascularization.
What did WESDR (Wisconsin Epidemiologic Study of Diabetic Retinopathy) show?
The prevalence of diabetic retinopathy is associated with duration of diabetes in type I and type II DM, mainly in white population.
What did NHNES III (National Health and Nutritional Examination Survey III) who/
It showed the frequency of diabetic retinopathy among blacks and Mexican Americans was higher than non-Hispanic whites.
What did DCCT (Diabetic Control and Complications Trial) show?
Intensive control of diabetes reduced retinopathy as well as neuropathy and nephropathy in type I DM.
What did UKPDS (United Kingdom Prospective Diabetes Study) show?
Intensive control of blood sugar and blood pressure reduced slowed progression of retinopathy in type II DM.
Is pregnancy associated with worsening diabetic retinopathy?
Yes, pregnant women need more frequent examination.
What are causes of vision loss in diabetic retinopathy?
- Macular edema
- Capillary occlusion (macular ischemia, diabetic papillopathy
- Sequelae from ischemia induced neovascularization (vitreous hemorrhage, tractional RD, neovascular glaucoma).
What is the definition of clinically significant macular edema (CSME)?
- retinal thickening at or within 500 micrometers of the center of the macula
- hard exudates at or within 500 micrometers of center with associated thickening of retina
- zone of thickening 1 DD if within 1 DD of center of macula.
What study defined CSME and what was recommended treatment?
ETDRS defined CSME and recommended focal laser photocoagulation if met criteria, treated patients had less risk of moderate visual loss and increased chance of visual improvement.
What are different options for treatment of diabetic macular edema?
Anti-VEGF drugs, corticosteroids (sub-Tenon’s, intravitreal, implant), focal or grid macular laser.
What is focal laser treatment?
Green or yellow wavelength spots applied to leaking microaneurysms, 50-100 micrometer spot size, 0.1s duration.
What is grid laser treatment?
Green or yellow wavelength laser applied to areas of diffuse leakage more than 500 micrometers from disc or center of macula. 50-100 micrometer spot size, 0.1s duration, spots 1 burn width apart.
What are risks of focal laser?
paracentral scotoma, transient increase in edema, CNV, subretinal fibrosis, foveolar burns.
What defines severe NDPR?
One of any of the following
4 quadrants of diffuse intraretinal hemorrhages and microaneurysms
2 quadrants of venous beading
1 quadrant of IRMA.
Who should be considered for early treatment with PRP?
Patients with severe NPDR, they are at 15% risk of progression to high risk PDR within 1 year.
What is high risk PDR?
Any of the following:
- NVD with vitreous hemorrhage
- 1/3-1/4 disc area of NVD
- 1/2 disc area of NVE with vitreous hemorrhage
What study defined high risk PDR and what did it show?
Diabetic retinopathy study, showed eyes treated with PRP had less risk of severe vision loss compared to no treatment, high risk PDR had greatest benefit.
What are risks associated with anti-VEGF in PDR?
Precipitation of retinal detachment
What are the goals of PRP?
- destroy ischemic retina, reducing production of VEGF
2. increase O2 tension by decreasing consumption by retina and increasing diffusion of oxygen from choroid.
What is full PRP as defined by DRS?
1200 or more burns, 500micrometer spot size, 1/2 burn width apart, argon green or blue/green laser.
What are risks of PRP?
increased vitreoretinal traction, tractional RD, vitreous hemorrhage, decreased night vision/color/contrast, loss of accommodation, photopsias, worsening macular edema.
What areas should be spared if possible when treating with PRP?
The horizontal meridians to preserve the long ciliary nerves/vessels and nasal and superior retina to preserve inferior and temporal peripheral vision.
What did the DRVS (Diabetic Retinopathy Vitrectomy Study) show?
RCT, showing patients with type I DM and severe vitreous hemorrhage or patients with severe PDR benefitted from early (1-6 mo after onset) vitrectomy compared to late (1 year).
When should DM type I patients first be screened?
3-5 years after diagnosis.
When should DM type II patients first be screened?
At diagnosis.
When should pregnant patients with DM be screened?
First trimester or prior to conception.
How often should patients with CSME be followed?
Every 2-4 months.
How often should patients with NPDR be followed?`
Every 2-4 months.
How often should patients with PDR be followed?
Every 2-4 months.
What are Elschnig spots?
Hyperpigmented lobule-sized patches surrounded by hypopigmentation which are signs of hypertensive choroidopathy.
What are Siegrist streaks?
Linear hyperpigmentation following meridional course that are signs of acute, uncontrolled hypertension.
What are signs of hypertensive optic neuropathy?
Linear peripapillary flame-shaped hemorrhages, blurring of disc margin, florid disc edema and macular exudates
Which type of sickle cell disease results is more likely to result in ocular complications?
Sickle cell hemoglobin C (SC) and sickle cell thalassemia.
What are signs of nonproliferative sickle cell retinopathy?
Salmon patch hemorrhages, refractile deposits, black “sunburst” lesions.
What are salmon patch hemorrhages?
Intraretinal hemorrhage occurring after peripheral retinal occlusion.
What is a black sunburst lesions?
Areas of RPE hypertrophy, hyperplasia and pigment migration, due to subretinal extension of hemorrhage.
What are the five stages of proliferative sickle cell retinopathy?
- Pripheral arteriolar occlusion
- Peripheral arteriovenular anastamoses
- Sea fan neovascularization
- Vitreous hemorrhage
- tractional retinal detachment
What are signs of sickle cell disease found outside of the retina?
Segmentation of blood in conjunctival blood vessels, comma shaped thrombi in conjunctiva, dark red spots on disc from intravascular occlusions, angioid streaks.
What are patients with sickle cell retinopathy at risk for with treated with PRP?
Higher riskof retinal tears and rhegmatogenous retinal detachment.
What are steps to avoid anterior ischemia in surgical management of RD in sickle cell patients?
Avoid epinephrine, avoid buckle, do not remove extraocular muscles, judicious laser use, ensure pt hydration, use supplemental nasal oxygen.
Where do BRVOs usually occur?
At an arteriovenous crossing.
What should you consider if BRVO occurs away from an arteriovenous crossing?
Underlying retinochoroiditis or retinal vasculitis.
Which quadrant is most commonly affected in BRVO?
Superotemporal (63% of time).`
What is mean age for occurrence of a BRVO?
Seventh decade.
What are risk factors for BRVO?
- history of HTN
- cardiovascular disease
- increase BMI at age 20
- history of glaucoma
What is the prognosis for BRVO?
50-60% of eyes maintain vision 20/40 or better after 1 year
In what percent of eyes with BRVO does NVI develop?
1%.
What did the Branch Vein Occlusion Study (BVOS) show regarding macular edema?
Argon laser improved treatment in patients with macular edema with vison 20/40-20/200 and intact foveal vasculature.
What did the Branch Vein Occlusion Study (BVOS) show regarding PRP?
PRP reduced risk of neovascularization in patients with at least 5 DD of ischemia, and reduced risk of hemorrhage by 1/2 in patients with neovascularization but recommended observing patients with ischemia till they develop neovascularization.
What did SCORE (Standard Care Versus Corticosteroid for Retinal Vein Occlusion) show for BRVO?
RCT of laser vs 1mg vs 4 mg triamcinelone showed no difference in visual acuity for patients and increased risk of cataract or high IOP with steroid.
What did Branch Retinal Vein Occlusion study (BRAVO) show?
RCT of sham vs 0.3mg vs 0.5mg ranibizumab, found improvement in visual acuity with ranibizumab.
What is the pathophysiologic cause of BRVO?
Thickened arterial wall at arteriovenous crossing leads to narrowed vein and turbulent flow leading to endothelial cell damage and thrombus.
What are the two types of CRVO?
Nonischemic (good visual acuity, minimal nonperfusion) and ischemic (poor visual acuity, extensive nonperfusion, risk of NVI).
What is the ERG pattern associated with CRVO?
Decreased bright flash, dark adapted b-wave:a-wave amplitude ratio.
What percent of eyes with ischemic CRVO achieve better than 20/400 vision?
10%
What percent of ischemic CRVOs develop NVI?
Up to 60%.
When do ischemic CRVOs develop NVI?
Mean of 3-5 months after onset of symptoms.
What are risk factors for CRVO?
Hypertension, diabetes mellitus, glaucoma
What are conditions/drugs associated with CRVO?
Oral contraceptives, diuretics, polycythemia vera, hypercoagulable conditions (Protein S and C deficiency, hyperhomocysteinemia), vasculitis (sarcoid, lupus), dysproteinemias.
What are the complications of CRVO?
Vitreous hemorrhage, anterior segment neovascularization and neovascular glaucoma.
What did SCORE (Standard Care Versus Corticosteroid for Retinal Vein Occlusion) show for CRVO?
Patients treated with 1mg or 4mg of triamcinolone demonstrated greater improvement in visual acuity with macular edema than observation.
What did the Central Retinal Vein Occlusion (CRUISE) trial show?
Patients receiving 0.5 or 0.3mg of ranibizuman demonstrated greater improvement in visual acuity with macular edema than observation.
What did CVOS show?
- No benefit in visual acuity for patients with macular edema treated with grid laser.
- No statistically significant decrease in NVI with prophylactic PRP, recommend waiting till 2 clock hours of NVA on gonio prior to PRP.
What are symptoms of ocular ischemic syndrome?
Vision loss over weeks to months, aching pain in orbital area, prolonged recovery after exposure to light.
What are signs of ocular ischemic syndrome?
Iris neovascularization (2/3 of eyes), AC cellular response (1/5 eyes), low or high IOP
What is the definitive treatment for ocular ischemic syndrome?
Endarterectomy.
What is the risk with carotid reperfusion in ocular ischemic syndrome?
Reperfusion in eyes with decreased ciliary body perfusion causing decreased aqueous production can lead to rebound high IOPs once the ciliary body is reperfused.
What is zone I in ROP?
The area included in a circle centered on the optic nerve whose radius is 2x the distance from the optic nerve to the foveola.
What is zone II in ROP?
The area included in a circle centered on the optic nerve with radius from the optic disc to the nasal ora serrata.
What is zone III in ROP?
The remainder of the fundus outside of zone I and II.
What is stage 1 ROP?
Presence of a demarcation line between vascular and avascular retina.
What is stage 2 ROP?
Presence of a ridge demarcating vascular and avascular retina.
What is stage 3 ROP?
A ridge with extraretinal fibrovascular proliferation.
What is stage 4 ROP?
Partial retinal detachment, A extrafoveal, B including fovea
What is stage 5 ROP?
Total retinal detachment with funnel configuration.
What is plus disease in ROP?
The presence of retinal vascular dilation and tortuousity in the posterior pole.
What is threshold disease?
5 contiguous clock hours of extraretinal NV or 8 cumulative clock hours with plus disease in zone I or II.
What is prethreshold disease type 1 ROP?
- Zone I any stage with plus disease
- Zone I stage 3 without plus
- Zone II stage 2 or 3 disease with plus
What is prethreshold disease type 2 ROP?
- Zone I stage 1 or 2 without plus disease
2. Zone II stage 3 without plus disease
When is retinal vascularization completed?
At 36 weeks of gestation nasally and 40 weeks of gestation temporally.
What are conditions associated with eyes with regressed ROP?
myopia with astigmatism, strabismus, amblyopia, cataract, glaucoma, macular pigment epitheliopathy, tractional RD, anomalous foveal anatomy, angle closure glaucoma and pupillary block glaucoma.
Which babies need to be screened for ROP?
Babies born 30 weeks or less of gestation or birth weight less than 1500g, or if unstable clinical course and believed to be at risk.
When should the first examination for ROP be performed?
At 4-6 weeks of postnatal age or at 31-33 weeks of postmenstrual age, whichever is later
When can screening be discontinued for ROP?
- Full retinal vascularization
- Zone III vascularization attained without previous Zone I or II ROP.
- Postmenstrual age of 45 weeks and no prethreshold disease
- Regressing ROP
How closely should prethreshold type II ROP (zone I stage 1 or 2 without plus or zone 2 stage 2 or 3) be followed?
1 week or less follow-up
What did Early Treatment of ROP (ETROP) show?
Compared early ablation of retina to cryotherapy for threshold disease, found that patients with high risk prethreshold disease (similar to type 1 ROP classification) benefited from treatment.
Which patients with ROP should be considered for ablative laser treatment?
Threshold disease or prethreshold type I.
What are risk factors for ROP?
Low birth weight, short gestational age, sepsis, slow weight gain.
What did Bevacizumab Eliminates the Angiogenic Threat of Retinopathy of Prematurity (BEAT-ROP) show?
RCT for infants with zone I or II stage 3 disease with plus, bevacizumab versus laser, found significant treatment effect for zone I ROP for anti-VEGF, zone II no difference between laser and anti-VEGF.
What is central serous chorioretinopathy?
An idiopathic condition characterized by a well-circumscribed serous detachment of the sensory retina.
What is the demographic of patients affected by central serous chorioretinopathy?
25-55 year old males, common in whites, Asians and Hispanics, uncommon in African Americans.
What kind of refractive change is associated with central serous chorioretinopathy?
Hyperopic.
What conditions are associated with central serous chorioretinopathy?
Exogenous steroid use, endogenous hypercortisolism, organ transplantation, systemic lupus erythematosus, HTN, sleep apnea, GERD, pregnancy.
What are the fluorescein angiography patterns noted in central serous chorioretinopathy?
- Expansile dot pattern
- Smokestack pattern
- diffuse pattern
What is seen in OCT of central serous chorioretinopathy?
Subretinal fluid and pigment epithelial detachments, patients may have increased choroidal thickness.
What is the prognosis of central serous chorioretinopathy?
Generally good, 80-90% of patients experience spontaneous resorption of fluid in 3-4 mo.
What are treatment options for central serous chorioretinopathy?
Observation, laser photocoagulation at site of leakage, PDT.
What are causes of choroidal vascular abnormalities?
Venous outflow issues (CC fistula), hypertension (malignant, eclampsia, cocaine), inflammation (GCA, Wegener, lupus), thromboembolic disease (TTP, DIC), iatrogenic.
What are treatment options for choroidal hemangioma?
Laser photocoagulation, PDT, cryopexy, radiation.
What are complications of choroidal hemangiomas?
Cystic retinal edema, neurosensory detachment, epichoroidal membranes.
What causes uveal effusion?
Nanophthalmos, scleritis, idiopathic uveal effusion syndrome.
What are the findings of bilateral diffuse uveal melanocytic proliferation (BDUMP)?
Diffuse thickening of the choroid, red or brown choroidal discoloration, serous RD and cataracts.
What cancers are associated with bilateral diffuse uveal melanocytic proliferation (BDUMP)?
Most common are ovarian, uterus and lung, also found with colon, pancreas, gallbladder and esophagus.
What are the demographics of patients affected with APMPPE?
Young adults in 2nd to 3rd decade of life, no sex predilection.
What is APMPPE?
Acute posterior multifocal placoid pigment epitheliopathy, a bilateral inflammatory disease presenting with yellow placoid lesions at RPE level in macula.
What does fluorescein angiograpy show in APMPPE?
Early blockage, late staining.
What is the visual prognosis for APMPPE?
Good, no specific treatment indicated.
What are other names for serpiginous choroidopathy?
Geographic choroiditis or helicoid peripapillary choroidopathy.
What is serpiginous choroidopathy?
A recurrent bilateral inflammatory disease with gray-yellow lesions spreading centrifugally from posterior pole.
What is the prognosis for serpiginous choroidopathy?
Poor.
What is the fluorescein angiography pattern for serpiginous choroidopathy?
Early hypofluorescence of lesions, late hyperfluorescence, may appear similar to APMPPE.
What is the treatment for serpiginous choroidopathy?
Immunosuppresion.
What is MEWDS?
Multiple evanescent white dot syndrome, characterized by multiple white dots in deep retina and RPE.