Dr. Behboudi. Ophthalmologist vitreoretinal surgeon 2016

CRVO CRVO is an important of visual loss among older adults throughout world. CRVO occurs due to thrombus within the central retinal vein at the level of the lamina cribrosa of the optic nerve.

That most forms of CRVO share a common mechanism: Thrombosis of the central retinal vein at and posterior to the level of the lamina cribrosa. In some cases, a thickened central retinal artery may impinge on the central retinal vein turbulence Endothelial damage thrombosis Histologic studies:

Evaluation of CRVO: non ischemic- ischemic Careful clinical examination  V.A  RAPD  SLE  Funduscopy (90-78 – indirect funduscopy)  Gonioscopy specially in F/U  Check IOP

Risk factors and causes of CRVO  Systemic-hypertension  Diabetes mellitus  Cardiovascular disease  Hyperlipidemia  Open-angle claucoma  Blood dyscrasias such as:  Leukemia  Lymphoma  Paraproteinemias  Waldenstrom macroglobulinemia  Multiple myeloma  Cryoglobulinemia Polycythemia vera

Risk factors and causes of CRVO  Oral-contraceptive  Diuretics  Hyperhemocysteinemia  protein S deficiency  Protein C deficiency

In CRVO vision loss is most commonly sudden:  Mild vision loss nonischemic CRVO  Severe vision loss ischemic CRVO  Less commonly, patients may experience premonitory symptoms of transient visual obscuration before overt retinal manifestations appear.

 Nonischemic CRVO (Mild)  Partial CRVO  Venous stasis retinopathy  Blurred –vision  No RAPD  Mild V-field defect  Mild dilation and tortuosity of all branches of central retinal vein.  Dot and flame shaped hemorrhages in four quadrant of retina.  Mild macular edema  Mild optic disc swelling

 Ischemic CRVO or severe CRVO  Complete CRVO  Non perfused CRVO  Hemorrhagic retinopathy Decrease V.A Decrease V.A RAPD: + RAPD: + Marked venous dilation Marked venous dilation Severe splinter and dot hemorrhage in four quadrant Severe splinter and dot hemorrhage in four quadrant Cotton-wool spots Cotton-wool spots Macular edema Macular edema

Hemi CRVO considered a variant of CRVO, is associated with a congenital variation in central vein anatomy; it may involve either the superior or inferior half the retina.

16% of nonischemic CRVO ischemic During 4.0 Ms 34% of nonischemic CRVO ischemic during 36Ms Conversion nonischemic to Ischemic CRVO In CVOS: Intermediate CRVO: when they are neither clearly ischemic nor nonischemic. More than 80% of intermediate eyes progress to ischemic disease.

Telangiectasias Telangiectasias Aneurysms Aneurysms Macular pigmentary changes. Macular pigmentary changes. Chronic changes of nonischemic CRVO:

Paraclinic ischemic CRVO Prolonged retinovascular circulation times. Prolonged retinovascular circulation times. Widespread CNP (at least 10 disc areas) Widespread CNP (at least 10 disc areas) OCT OCT Visual – field: dense central scotoma Visual – field: dense central scotoma ERG: decrease b-to a- wave amplitude ratio due to inner retinal- ischemia ERG: decrease b-to a- wave amplitude ratio due to inner retinal- ischemia Ultra wide field angiography Ultra wide field angiography F.A:

Differential diagnosis of CRVO:  Hyperviscosity retinopathy generally bilateral  Ocular ischemic syndrome

Ocular ischemic-syndrome  Conj-injection  Cataract  Rubeosis-iridis  Funduscopy: Venues dilation Venues dilation M.A M.A Mid pripheral intraretinal hemorrhages Mid pripheral intraretinal hemorrhages Attenuated arterioles Attenuated arterioles

F.A in ocular ischemic syndrome:  Prolonged arm –to-retina circulation time  Patchy choroidal filling pattern. Ophthalmodynamometer:  CRVO will have normal artery pressure.  Ocular ischemic syndrome will have low artery pressure.

Ocular ischemic syndrome

Current treatment is directed at secondary complications of CRVO that affect vision, including:  Macular edema  Retinal neovascularization  NVI  NVG  R.D Macular ischemia (CNP) another cause of visual loss in CRVO haven’t effective treatment. Treatment also involves management of predisposing risk factors, such as diabetes, hypertension and hyper- lipidemia.

Prognosis of ischemic CRVO: The central vein occlusion study (CVOS) showed:  Visual prognosis in generally poor  Only approximately 10% of eyes achieving vision better than 20/400.

Very ischemic CRVO ant-segment. Neovascularization (iris and angle) 60% of cases NVG 3-5 months after the onset of symptoms Risk factors for NVG Iris-neovascularization in CRVO  Large areas of CNP  Massive intraretinal and preretinal hemorrhage  Cotton wool spots

In the absence of treatment, should be monitored on a monthly for at least 6.0Ms Follow up: For the progression of CRVO For the progression of CRVO For the development of Ant-Seg-neovascularization and NVG For the development of Ant-Seg-neovascularization and NVG In the patients treated with anti-VEGF agents should be observed for a similar duration after D/C of the drugs.

Treatment of macular edema:  Intravitreal anti-VEGF agents is currently first line therapy for macular edema  Intravitreal steroid therapy is considered an alternative for patients with edema refractory to anti- VEGF monotherapy.

Intravitreal anti-VEGF therapy in patients with:  Anterior segment bleeding.  Elevated IOP and corneal edema  P.S formation and miosis  Vit-hemorrhage and preretinal-hemorrhage Laser cannot be performed, only anti VEGF is effective. Laser cannot be performed, only anti VEGF is effective.

Anti VEGF agent administration strategies for CRVO treatment include monthly dosing, as- needed treatment and treat-and – extend approaches. Anti VEGF drugs reduce Iris neovascularization and NVG. ophthalmology 2011: 118(10)

A 2015 technology assessment for the A-A.O found that intravitreal anti-VEGF was safe and effective for treatment of macular edema associated with improved visual out comes. Ranibizumab Ranibizumab Bevacizumab Bevacizumab aflibercept aflibercept

Based on CRUISE study GALILEO GALILEO COPERNICUS COPERNICUS Ranibizumab Bevacizumab aflibercept Are effective for macular edema in CRVO patients.

Patients gained V.A 15 or more ETDRS letters Ranibizumab monthly injection 0.5mg 47.7% Ranibizumab monthly injection 0.3mg 46.2% Sham group monthly injection 16.9% In CRUISE study (efficacy and safety of ranibizumab) at 6.0Ms

CME secondary to CRVO before and after IVB

Intravitreal triamcinolone 4mg reduced macular edema and, in some patients improved vision. Many studies report a treatment effect lasting about 6.0 Ms. Repeat injection often being necessary. Side effects of triamcinolone: Macular edema in CRVO Cat. Increase IOP 33% of cases

A dexametasone injectable intravitreal implant Ozurdex Has been approved by FDA for the treatment of macular edema associated with RVO. Ozurdex improved V.A outcome over a 6 – month Clinical trials are currently assessing a fluosinolone acetonide intravitreal insert with longer-term steroid delivery for the treatment of RVO.

Intravitreal corticosteroids in CRVO 27% of eyes treated with 1mg of triamcinolone 27% of eyes treated with 1mg of triamcinolone 26 of eyes treated with 4mg of triamcinolone 26 of eyes treated with 4mg of triamcinolone 7% of eyes is the sham group 7% of eyes is the sham group Had an improvement of V.A 15 ETDRS letters. Archive ophthal 2009 based on CRVO arm of the SCORE study at 1 year:

Anterior segment neovascularization:  patients with anterior segment neovascularization are at risk of neovascular glaucoma.  Prophylactic scatter retinal photocoagulation is recommended to reduce this risk in patients with NVI ( the effect of laser take 2 to 4 weeks to develop).

Grid-pattern macular laser photocoagulation of mac- edema was evaluated in the CVOS. Even though grid laser treatment reduced angiographic evidence of macular edema, but V.A did not improve. Laser treatment of CRVO

Macular edema and subsequent permanent macular dysfunction occur in virtually all patients with ischemic CRVO and in some patients with Non schemic CRVO.

Although macular grid photocoagulation conclusively reduced angiographic macular edema, the study didn’t find a difference in V.A between the treated and untreated eyes at any stage of the F/U period. As a result: it is not generally recommended that macular grid photocoagulation be employed in CRVO

In CVOS prophylactic PRP did not result in a statistically significant decrease in the incidence of NVI NVI developed in 20% of CRVO who had received prophylactic PRP. Therefore close monitoring of high risk patients is necessary. Laser surgery for CRVO: PRP

CVOS recommendation: Waiting until undilated gonioscopic examination revealed at least 2 clock-hours of Iris neovascularization before performing PRP. PRP is often performed at the first sign of NVI, particularly when close F/U in not possible CVOS the central vein occlusion study Laser surgery for CRVO

Nonclearing Vit after 3Ms Vit-H +N.V.I or NVG Need P plana vit X + ELP Persistent NVG: glaucoma surgery (glaucoma valve) PARS PLANA Vit X

 Create an anastomotic connection between the retinal vein and choroidal circulation.  Using a high-power laser application.  Radial optic neurotomy sectioning of the posterior scleral ring to decompress the central retinal vein.  Retinal vein cannulation with an infusion of tissue plasminogen activator (tpa). Another surgical approaches

Thank you for your attention