Common characteristics of BRVO & CRVO.pptx

Common characteristics of BRVO & CRVO.pptx

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  Presented by:-Ranjita Amanatya 3rd yearPG VIMSAR, BURLA Common characteristics of BRVO & CRVO Work-up to consider in patients with BRVO & CRVO
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  Retinal vein occlusion wasfirst described in 1855 by Liebreich as retinal apoplexy In 1878 Julius Von Michel interpreted finding as Central vein thrombosis HISTORY BRVO was described by Leber in 1877 and Oeller in 1896
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  INTRODUCTION • RVO isan obstruction of retinal venous system involving central, hemicentral or branch retinal vein. • Retinal vein thrombosis is 2nd M.C. Retinal vascular disease after DR. • Incidence of retinal vein occlusions varies from 2 to 8 per 1,000 persons
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  INTRODUCTION Central retinal veinocclusion • CRVO results from thrombosis of CRV when vein passes through the lamina cribrosa. • CRVO can occur at all ages, with mean age between 60 and 70 years. • Prevalence of CRVO is around <0.1% to 0.4%. • CRVO is usually unilateral disease. • Occurs predominantly in elderly population (>65yrs). • Affects male & female equally.
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  Branch retinal veinocclusion (BRVO) • BRVO is 3 times more common than CRVO • BRVO (78%) is slightly more often seen than CRVO • An overall prevalence of BRVO of between 0.6% and 1.6% • Prevalence of BRVO varies between 0.6% and 1.6% • BRVO is unilateral in 90% of patients and occurs most commonly in 7th decade • Majority of patients superotemporal veinis affected. • 44–60% of patients with BRVO, superotemporal vein is affected and remainder (22–43%) occur in inferotemporal quadrant. • BRVOs can be subdivided into major BRVOs and macular BRVOs with different prognosis and management. • Risk of recurrence is low. Can occur in younger population. • Patients with BRVO are older than patients with CRVO at primary onset of disease. • First onset of disease 54% of patients with BRVO are 65 years or older, 41% are between 45 and 64 years old and 5% are younger than 45 year
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  • BRVO occursat an arteriovenous (AV) crossings or at edge of optic disk as hemicentral retinal vein occlusion (HCRVO). • Observation that BRVO occurs at AV intersections was made over 100 years ago by Leber. • HCRVO pathologically is a variant of CRVO, which affects half of retina. • BRVO can be subdivided with respect to extent and location of occluded area. • Major BRVOs involve one of major branch retinal veins usually near optic disk affecting a quarter or more of retina • Macular BRVOs involve one of the macular venules and a segment of the macular retina only. • BRVO is seen more often in females than males. • BRVO affects right eye more frequently than left eye. • Both eyes are involved equally. Branch retinal vein occlusion (BRVO)
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  CRVO BRVO Chief complaints •Sudden painless loss of vision • Pain & redness d/t NVG with high IOP  Sudden, painless DOV / Blurred vision/onset of field defect  Metamorphopsia indicating ME  Sudden onset floaters to complete loss of vision in VH H/O Present illness • Sudden painless loss of vision in one eye • Ischemic CRVO:-Marked deterioration of VA on waking in morning • NonIschemic CRVO:-No symptoms • Macular edema:-Decreased contrast sensitivity,micropsia,macropsia,metamo rphopsia,scotoma • Partially recovered CRVO:-Visual field loss/constriction • Complete documentation of onset duration & progress of visual complaints. Clinical Features
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  1. Cardiovascular 2. Atheroscleroticheartdisease 3. Arterial hypertension 4. Diabetes mellitus 5. Hyperlipidemia 6. Obesity 7. Smoking 8. Carotid artery occlusive disease (ischemic CRVO) 9. Rheological abnormalities 10. Increased hematocrit 11. Increased plasma viscosity 12. Increased red cell aggregation 13. Reduced red cell deformability 14. Thrombophilia 15. Hyperhomocysteinemia 16. Anti-phospholipid syndrome 17. Increased APC resistance / FV Leiden mutation (young patients) 18. Reduced plasminogen activator inhibitor 19. Oralcontraceptives Local risk factos:- 1. Glaucoma 2. Trauma 3. Retinal vasculitis 4. Central artery occlusion 5. Drusen, 6. papilledema 7. Arterio venous malformation 8. Hyper viscosity syndromes 9. Polycythemia 10. Macroglobulinemia 11. Myeloma 12. Leukemia Risk factors and associated diseases in CRVO • Crowding/Compression at the level of O.D. & systemic d/os predisposing to thromboembolic disease or disease of vascular wall M.C. risk factors. • Triggering mostly happens at night time in recumbent position probably by low B.P. ,and / or high central venous pressure. • Hyperviscosity and thrombophilia seem to facilitate development of CRVO. • Triggering mostly happens at night time in recumbent position probably by low B.P. ,and / or high central venous pressure.
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  Risk factors inBRVO What to look Age >60yrs HTN Blood pressure Diabetes mellitus RBS,PPSB, HbA1c Coagulopathy I. Hyperhomocysteinemia II. Factor 5 leiden mutation III. Antiphospholipid Ab syndrome IV. Protein C/S deficiency I. Serum homocysteine II. Activated protein C resistance III. Antiphospholipid Ab IV. Free Protein C/S Ag Inflammatory a) Bechets b) Sarcoidosis c) Wegener’s a) HLA B51, Pathergy Test b) Serum ACE,Chest X-Ray,Chest CT c) C-ANCA,Chest X-Ray Infections i. TB ii. Syphilis iii. Lyme’s iv. HIV i. Mantoux test,Chest X-ray ii. VDRL iii. ELISA & Westetrn Blot iv. ELISA Chronic renal failure RFT Smoking,Oral contraceptive,Dehydration History
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  Pathogenesis can berepresented in three circles Transition into severe neovascular disease Development of retinopathy Triggering of venous outflow reduction by narrowing of vein and partial thrombosis 01 03 02
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  3 factors could lead to CRVO Compression bycentral retinal artery and cribriform plate Degenerative and/ or inflammatory disease within the vein. Hemodynamic disturbances leading to stagnation and primary thrombus formation AV intersection with hypertensive changes. AV crossing showing a common wall predisposing vein to degenerative changes in arterial wall
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  Pathogenesis of BRVO Causeof BRVO is multifactorial process:-  Mechanical obstruction by degenerative changes in arterioles  Abnormal blood constituents  Impedance of blood flow causing increased blood viscosity  Endothelial damage • Retinal veins are significantly influenced by pathology of neighboring retinal arteries d/t common wall at crossing sit. • BRVO may lead to partial occlusion of lumen,rarely to complete obstruction. • Inflammatory component in thrombus and vessel wall • Hypoxia stimulates increase of VEGF • Vitreous attachment at macula or at AV crossings may play important pathogenetic role. • Mechanical obstruction and others have suggested that BRVO is a result of arterial insufficiency. • BRVOs are typically located at arterial overcrossings suggests hemodynamic difference between arterial and venous overcrossings.
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  Pathological process atsite of occlusion consists of:-  Degenerative changes in vessel walls  Abnormal blood constituents  Blood flow (stasis) • These three classical components, known as Virchow’s triad, that play a role in thrombogenesis are interrelated. • Thrombus of branch vein was primary event and other vascular changes occurred secondarily. • Deviation of retinal vein at crossing sites lead to consecutive hemodynamic turbulence and thus predispose to thrombus formation at crossing sites. • Difference in distension of vein lying beneath artery within retina as opposed to between internal limiting membrane and artery explain disparity of risk between arterial and venous overcrossings. • Primary event of retinal vein occlusion includes endothelial cell proliferation in vein wall associated either with degeneration of endothelium and secondary thrombus formation. • Strong associations between BRVO and hypertension, focal arteriolar narrowing and arteriovenous nicking.
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  • Arterial stiffnessis increased in patients with BRVO. • Localized arteriosclerotic processes contribute to stasis and occlusion in adjacent retinal veins. • In BRVO impedance of blood flow is virtually always at AV crossings where there is either pressure on the vein or a thickened wall due to arterial disease or endothelial proliferation, or both. • More eyes with BRVO develop partial vitreous separation. • Eyes with decreased axial length and hyperopia are at increased risk for BRVO because of the higher likelihood of vitreomacular attachment at AV crossings Pathogenesis of BRVO
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  OCULAR EXAMINATION:- Visual Acuity Ocular adnexa & globe Conjunctiva Sclera Nonischemic CRVO Ischemic CRVO Normal / >6/60 Marked deterioration of vision especially waking in morning <6/60  Proptosis in case of tumour  Skin examination for signs of coagulopathy,collagen vascular d/o & infection  Pt with Glaucoma have conjunctival bleb  In Coagulopathies conjunctival hemorrhage may be present  PUK in case of SLE & PAN Cornea  Nodular scleritis
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  OCULAR EXAMINATION Cont.:- A.C. IOP Pupil Lens  Shallow in ACG / Short axial length  KPs,cells & flare in vasculitis,sarcoidosis,HIV Iris  RAPD in suspected case of vascular occlusion  NVI OR NVA may be there  Complicated cataract in inflammatory conditions  Raised IOP d/t NVG, underlying open angle glaucoma
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  Anatomy and Histopathologyof BRVO • BRVO typically occurs at AV crossing sites. • Arterial overcrossings are at a higher risk of BRVO. • Adjacent artery is usually narrowed and sclerotic,obstructed branch vein dilated. • As branch retinal artery and vein converge on each other, at crossing sites outermost components of their walls, the adventitia, fuse • Common wall may be extremely thin • Lymphocytes infiltrate thrombus and vessel walls • Vein recanalizes, but with persisting retinal damage around it. • At the site of a BRVO an arterial overcrossing was present in 97.6% of eyes and a venous overcrossing only in 2.4%. • Arterial overcrossings are at higher risk of BRVO than venous overcrossings • The risk of BRVO in an eye is proportional to the number of arterial overcrossings in the eye and this type of overcrossing is most common in the temporal superior quadrant.
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  • The veindeviates around artery, dipping deep into retina in arterial overcrossing. • Ophthalmoscopic appearance of compression is caused by thickening of adventitial sheath and surrounding glial proliferation, both of which are less transparent tissues. • Fusion of vessel walls can continue until artery and veins share a common medium as they cross. • Common wall measured 4 μm at occlusion site. • Ischemic type represents hemorrhagic infarct of retina with extracellular edema in nerve fiber and ganglion cell layer, causing dilation and congestion of vein and rhexis hemorrhages from capillaries mainly in nerve fiber layer (scattered superficial) but also in deeper layers (spherical). • In both types of BRVO, retinal hemorrhages and ischemic necrotic areas reabsorb after months, resulting often in glial scar. • During recirculation affected capillaries reopen, and with dilation AV anastomoses develop bridging destructed area. • Later stages irreversible fibrotic alterations of vascular structure occur. Anatomy and Histopathology of BRVO
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  Fundus Early features ofCRVO Fresh CRVO:-  Mild changes with few superficial, flame-shaped bleedings,  Slight engorgement of the veins,  Hyperemia and swelling of the optic nerve head ,  Dense, and more extended bleedings,  Strongly dilated and tortuous dark blue veins  Gigantic papilledema with vitreous bleedings on top. Intraretinal bleedings are spread over the whole fundus and are mostly flame shaped in areas with a thick nerve fiber layer, i.e., around the optic nerve head. They can also occur as more deeply located dot and blot bleedings at the posterior pole or as spots in the periphery. Cotton-wool spots are signs of small capillary dropouts and hence of local ischemia.Found in all types of CRVO. Macular edema in all retinal vein occlusions with loss of vision, of the cystoid extracellular type. The swelling of the papilla is always marked, the margin often being obscured by cotton-wool spots and bleedings “papillophlebitis”
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  CRVO of amild type with heavy bleedings with few bleedings and engorgement of the veins with vitreous bleeding, all with macular edema CRVO with deeply located dot and blot bleedings CRVO with dominance of papilledema
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  Early Findings ofBRVO • Include edema and scattered superficial and deep retinal hemorrhages over a triangular retinal sector whose apex is located to occlusion site. • Obstructed vein is characteristically dilated and tortuous distal to occlusion, and associated artery is narrowed and sclerotic. • Dilated capillaries and microaneurysms are found in area of BRVO. • Cotton wool spots may be present indicating ischemia. • Nearer the occlusion occurs to optic disk,greater the extent of affected retina and more serious the complications. • Cystoid macular edema may be present. • Macular BRVO may show only subtle features, such as microaneurysms in limited sector.
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  • The firstophthalmoscopic signs are fine retinal hemorrhages at AV crossing site. • Distal from crossing site vein appears dilated, congested and tortuous. • Retinal edema in involved area is usually present. • Involved retina demonstrates variable degrees of scattered superficial and deep retinal hemorrhages which respect the horizontal midline. • Superficial hemorrhages are located in nerve fiber layer and follow nerve fiber layer course in an arcuate wedge of retina having its apex at site of obstruction. • Resorption of hemorrhages takes several months upto a year. • Retina involved depends on size and location of affected vein. • Macular BRVO is a subgroup that show only subtle clinical and angiographic clues, such as microaneurysms in a limited sector of macular region. Early Findings of BRVO
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  • Visual acuityadversely affected due to macular edema or central ischemic damage. • Nearer the occlusion occurs to optic disk, greater the extent of affected retina and more serious the complications. • When ischemia results in nerve fiber infarct, cotton wool spots develop. • Retinal vein thrombosis causes increased venous pressure and lead to retinal capillary decompensation with macular edema, which is the most frequent cause of loss of vision in BRVO. • At macula, edema is clinically recognized by thickening of the macular retina that is often accompanied by cystoid spaces. • Microvascular abnormalities of BRVO include dilated capillaries and microaneurysms that develop within area of vein occlusion. • Chronic leakage from these abnormal vessels contribute to macular edema and cause deposition of lipid exudates in retina. • Large capillary or venous macroaneurysms may develop within the territory of BRVO as well. • Serous retinal detachment with massive macular hard exudates are rare complications of BRVO. Early Findings of BRVO
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  Major BRVO ofthe left eye affecting the superotemporal vein with superficial flame hemorrhages distal to the occlusion site. Associated artery appears narrowed and sclerotic Macular BRVO with fine superficial hemorrhages BRVO involving supero temporal vein with flame- shaped retinal hemorrhages radiating in wedge
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  Late features ofCRVO • The streaky bleedings become blurred or begin to slowly disappear. • Engorgement of the veins becomes less, and the vessel walls lose their transparency and whiten. • Cilioretinal collaterals on the papilla are a very characteristic sign of a several-weeks-to-months-old CRVO. • Macular edema first increases and with the ensuing reduction after months and years,a dry, pigmented scar may be the clue indicating an old CRVO. • Serous retinal detachment over wide areas with hard exudates may then develop. • The first sign proving an ischemic CRVO is neovascular disease of the iris. • Untreated rubeosis iridis may lead to occlusion of the chamber angle with secondary glaucoma and hyphema
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  CRVO with many cotton-woolspots CRVO of the perfused exudative type after 1 year CRVO after months to years with a collateral typical macular scar
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  CRVO: Intermediate type Ischemictype with widespread capillary occlusion
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  Progression of non-ischemicCRVO after 2 months Largely non-perfused ischemic CRVO
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  • Occluded, sheathedretinal venules in affected area. • Chronic leakage leading to chronic cystoid macular edema and lipid exudate deposition. • Collateral vessel formation at edge of affected area located temporal to fovea draining into uninvolved quadrant. • Retinal neovascularizations (NVEs) develop in one-third of patients with major BRVO. • NVEs occur at border of perfused and non perfused retina; neovascularization at disk (NVD) is rare. • Significant risk for neovascularization exists when the area of capillary non perfusion exceeds 5 disk diameter. • Neovascularization of iris is extremely rare. • Complications of neovascularization include VH and fibrovascular membranes with consecutive TRD. • Late complications are epiretinal membranes, hard exudates, chronic cystoid macular edema, retinal pigmentary dispersion, subretinal fibrosis and macular hole formation. • Older BRVOs are characterized by occluded and sheathed retinal venules in affected sector. Late Findings and Complications of BRVO
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  • Weeks tomonths after onset of BRVO, collateral vessel formation observed characteristically located at edge of involved area. • Collaterals are usually small tortuous venous channels that cross horizontal raphe mostly temporal to fovea and drain into venous circulation of uninvolved quadrant from retinal neovascularizations. • Collaterals pass from territory of occlusion to a point proximal to site of occlusion or to an uninvolved vein. • Take the form of vein to vein anastomosis, bypassing occluded segment and then exiting through central retinal vein. • Reversal of blood flow toward arterial system can also occur in response to elevated venous pressure. • AV shunts that bypass capillary bed may occur at AV crossing site, whereas in some instances unrelieved venous pressure can result in rupture of vein wall. • Risk of complications can be attributed to location of BRVO, extent and severity of damage, and adequacy of compensatory mechanisms. • Retinal neovascularization may occur at border of perfused and non-perfused retina. Late Findings and Complications of BRVO
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  • Neovascularization ofdisk is less common, and it tends to be concurrent with retinal neovascularization. • Risk for development of retinal neovascularization exists when area of capillary nonperfusion exceeds 5 disk diameters. • In ischemic type of BRVO, risk for neovascularization is 36%, whereas it is 22% overall. • 28.8% incidence of retinal neovascularization following major BRVO. • Majority of untreated eyes with retinal neovascularization will develop VH. • Advanced stages, preretinal hemorrhage and vitreous hemorrhage, & rarely fibrovascular membranes with consecutive TRD, may develop. • Rhegmatogenous RDis rare complication of BRVO, but when breaks occur they tend to be located posterior to equator and result from traction exerted by fibrovascular proliferation or secondary to ischemic retinal degeneration with hole formation. • VH occur in approximately 7–20% of patients with BRVO. • Complications in later stages include macular pucker, chronic cystoid macular edema, retinal pigmentary dispersion, subretinal scarring, macular hole and atrophy of inner retinal layers. • Permanent and vision-limiting RPE changes can develop from long-standing edema. Late Findings and Complications of BRVO
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  blockage at siteof cotton wool spots and cystoid macular edema Macular BRVO with intense cotton wool spot formation. Cystoid changes Early phase Late phase
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  Chronic long-standing BRVOwith deposition of lipid exudates and small tortuous collateral vessels crossing horizontal raphe Long-standing mid peripheral BRVO with associated serous retinal detachment, lipid exudates and foveal pigmentary dispersion Long-standing BRVO affecting supero temporal vein with sheathed retinal venules and massive hard exudates Occluded and sheathed retinal venules in longstanding BRVO affecting supero temporal quadrant with neovascularization Retinal neovascularization secondary to BRVO in superior mid periphery and at optic disk causing subhyaloidal hemorrhage BRVO with secondary neovascularization, consecutive preretinal hemorrhage involving macula, retinal edema, lipid exudates and sheathed venules long-standing HCRVO affecting superior quadrants.
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  leakage of newvessels Extensive capillary non perfusion and neovascularization Neovascularization Long-standing HCRVO affecting the superior quadrants.
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  Complications a/w CRVO Complications a/w BRVO Macular edema  Macular ischemia  NVG  VH  TRD  Optic atrophy  Macular edema  Macular ischemia  NVG  NVI (rarely) Complications
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  D/D of CRVOD/D of BRVO (For intraretinal hemorrhages)  Ocular ischemic syndrome  DR  Papilledema  Radiation retinopathy  Retinopathy d/t anemia  CRAO with CRVO  Venous stasis retinopathy  DR  CRVO  AION  CNVM  Coat’s disease  Vasculitis  Retinitis
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  INVESTIGATION:- a. SYSTEMIC WORK-UP:-  Routine Blood Pressure  Fasting Blood Glucose  Lipid profile Investigations for hypercoagulable condition Complete hemogram with peripheral smear ESR Plasma homocysteine level Chest X-Ray C-reactive protein Thrombophilia screening Autoantibodies Serum angiotensin converting enzyme Treponemal serology Carotid Doppler Scan
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  OCULAR INVESTIGATIONS b . Ultrasonograph y ERG & Perimetry FUNDUS FLUORESCEIN ANGIOGRAPHY WIDE-FIELD ANGIOGRAPHY OPTICAL COHERENCE TOMOGRAPHY
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  FFA to r/o Macular ischemia  Determine type of CRVO  Detect NVD & NVE CRVO Non ischemic Ischemic Capillary nonperfusion <10 disc areas Capillary nonperfusion >10 disc areas non-ischemic CRVO after 2 months largely non-perfused ischemic CRVO FUNDUS FLUORESCEIN ANGIOGRAPHY
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  wall staining oflarge veins of mild type cystoid macular edema in a non-ischemic CRVO after 6 months  Marked delay in AV transit time  Blocked fluorescence/t retinal hemorrhage  Vessel wall staining  Areas of non-perfusion  Collaterals  NVD  NVE  Macular edema Angiographic Features of CRVO
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  Angiographic Features ofBRVO  Delayed filling of the occluded retinal vein  Blocked fluorescence d/t intraretinal hemorrhage  Microaneurysms  Dye extravasation secondary to macular edema  Telangiectactic collateral vessels  Cpillary non perfusion  Retinal neovascularization Macular edema Perfused Non perfused (ischemic) Areas of macular leakage with normal FAZ Distorted & enlarged FAZ
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  Early phase delayed venousfilling as well as venous dilation and tortuosity distal from the occlusion site, and retinal edema Late phase
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  Angiographic Features ofBRVO • In BRVO reflect changes in permeability, caliber, and patency of retinal vessels. • Fluorescein angiography (FLA) distinguish leakage without capillary nonperfusion from leakage with capillary nonperfusio. • Intact perifoveal capillary perfusion is prerequisite for macular grid laser photocoagulation • FLA maps out extent of ischemia assisting in detection of patients at higher risk of neovascularization and those requiring closer follow-up examinations • Peripheral FLA helpful to detect whole extent of avascular area. • FLA distinguish collateral vessel formation (which do not leak) from retinal neovascularization. • Later stages, diagnosis of BRVO established with help of FLA • Macular edema are associated with disruption in BRB at level of retinal capillaries. • Changes in the permeability, caliber, and patency of retinal vessels.
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  • Venous fillingin area of occlusion is delayed and fluorescein column is narrowed at site of occlusion. • Small area of early hyperfluorescence observed just proximal to occlusion site. • Macular edema with good capillary perfusion is associated with fluorescein leakage on fluorescein angiogram since edema is of vasogenic type, with leakage of fluorescein molecule occurring through break in BRB. • FLA maps out extent of ischemia assisting in detection of patients at higher risk of neovascularization and those requiring closer follow-up examination. • Later stages, after reabsorption of hemorrhages, diagnosis of BRVO established with help of FLA. • Peripheral angiography is helpful to detect whole extent of avascular area. • FLA distinguish collateral vessel formation from retinal neovascularization at edge of affected area. • In neovascularizations, shunt vessels do not leak. • Angiographic findings of BRVO are vascular abnormalities including capillary dilatation, microaneurysms and retinal edema. Angiographic Features of BRVO
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  Early phase Latephase Cystoid macular edema Associated retinal and macular edema extending to foveal center together with cystoid spaces
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  WIDE-FIELD ANGIOGRAPHY  UWAgives 200 degrees field of vision. Use:- 1. Determine extent of peripheral capillary non-perfusion 2. Helps in targeted laser 3. Pick up neovascularization
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  Optical Coherence Tomographyin BRVO • OCT determine presence of macular edema, foveal thickness and cystoid changes, but delivers 2D morphologic information. • Demonstrate vitreofoveal adhesions. • Important and sensitive tool with which to assess extent of macular edema in patients with BRVO and their response to t/t. • Cross-sectional OCT image of macular edema associated with BRVO shows intraretinal cystic spaces delineating uninvolved and affected area. • Serous detachment distinguished from intraretinal and subretinal fluid accumulation. • Exact evaluation of vitreoretinal interface visualizing vitreofoveal adhesions, macular thinning, in complete or full thickness ruptured cysts. • Foveal retinal thickness measured by OCT in pts with BRVO correlated with VA and multifocal ERGs from central retinal area
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  Optical Coherence Tomographyin CRVO Use:-  Assessment of macular edema  Detect cystic spaces,retinal thickening,serous RD  Detect ERM & VMA in long standing cases
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  MANAGEMENT of CRVO Macular edema Ocular neovascularization Other modalities Vitrectomy
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  Macular edema Mechanism of intravitrealsteroid:- 1) Reducing vascular permeability 2) Inhibiting expression of VEGF gene  Ozurdex FDA approved for t/t of macular edema secondary to CRVO  Intravitreal anti-VEGF are the 1st line therapy for macular edema
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  Ocular neovascularization  PRP shouldbe delivered after development of NVI/NVA to prevent secondary complications  Laser should be delivered as anterior as possible  Prophylactic PRP in cases of ischemic CRVO Scatter LC pattern covering involved segment, sparing area within two disk diameters of fovea
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  Vitrectomy Indication:-  Non-resolving VH TRD secondary to retinal neovascularization surgical arteriovenous decompression with dissection of the commonadventitial sheath at the occlusion site using a bent microvitreoretinal blade
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  Other modalitie s 1 2 3 4 5 Systemicanticoagulants (Prevent non ocular thrombotic events) Oral pentoxifylline (hemodilultion/vasodilator) Recombinant tissue plasminogen activator (r-Tpa) Chorioretinal venous anastomosis between nasal branch of retinal vein & choroidl circulation using Nd:YAG laser in nonischemic CRVO Radial optic neurotomy
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