Dr Behboudi Ophthalmologist vitreoretinal surgeon 2016 CRVO is

Dr. Behboudi. Ophthalmologist vitreoretinal surgeon 2016

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.

Histologic studies: 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 damage thrombosis turbulence Endothelial

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

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

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

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

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

v. Ischemic CRVO or severe CRVO v. Complete CRVO v. Non perfused CRVO v. Hemorrhagic retinopathy üDecrease V. A üRAPD: + üMarked venous dilation üSevere splinter and dot hemorrhage in four quadrant üCotton-wool spots üMacular 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.

Conversion nonischemic to Ischemic CRVO In CVOS: 16% of nonischemic CRVO During 4. 0 Ms 34% of nonischemic CRVO ischemic during 36 Ms Intermediate CRVO: when they are neither clearly ischemic nor nonischemic. More than 80% of intermediate eyes progress to ischemic disease.

Chronic changes of nonischemic CRVO: üTelangiectasias üAneurysms üMacular pigmentary changes.

Paraclinic ischemic CRVO F. A: üProlonged retinovascular circulation times. üWidespread CNP (at least 10 disc areas) üOCT üVisual – field: üERG: dense central scotoma decrease b-to a- wave amplitude ratio due to inner retinal- ischemia üUltra wide field angiography

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

Ocular ischemic-syndrome v. Conj-injection v. Cataract v. Rubeosis-iridis v. Funduscopy: üVenues dilation üM. A üMid pripheral intraretinal hemorrhages üAttenuated arterioles

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

Ocular ischemic syndrome

Current treatment is directed at secondary complications of CRVO that affect vision, including: u. Macular edema u. Retinal neovascularization u. NVI u. NVG u. 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 hyperlipidemia.

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

Iris-neovascularization in CRVO 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 v. Large areas of CNP v. Massive intraretinal and preretinal hemorrhage v. Cotton wool spots

Follow up: In the absence of treatment, should be monitored on a monthly for at least 6. 0 Ms üFor the progression of CRVO üFor 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: u. Intravitreal anti-VEGF agents is currently first line therapy for macular edema u. Intravitreal steroid therapy is considered an alternative for patients with edema refractory to anti. VEGF monotherapy.

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

Anti VEGF agent administration strategies for CRVO treatment include monthly dosing, asneeded 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. üRanibizumab üBevacizumab üaflibercept

Based on CRUISE study GALILEO COPERNICUS üRanibizumab üBevacizumab üaflibercept Are effective for macular edema in CRVO patients.

In CRUISE study (efficacy and safety of ranibizumab) at 6. 0 Ms Patients gained V. A 15 or more ETDRS letters Ranibizumab monthly injection 0. 5 mg 47. 7% Ranibizumab monthly injection 0. 3 mg 46. 2% Sham group monthly injection 16. 9%

CME secondary to CRVO before and after IVB

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

Anterior segment neovascularization: upatients with anterior segment neovascularization are at risk of neovascular glaucoma. u. 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).

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

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

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

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

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

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

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