1. In the name of
GOD

2. Dr. Behboudi. Ophthalmologist vitreoretinal surgeon 2016
Central Retinal Vein
Occlusion
Dr. Behboudi. Ophthalmologist vitreoretinal surgeon

3. 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.

4. 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 turbulence Endothelial damage thrombosis

5. 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

6. 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

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

8. 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.

9. 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

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

11. 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.

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

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

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

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

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

26. 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.

27. Ocular ischemic syndrome

28. 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.

29. 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.

30. 3-5 months after the onset of symptoms
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
Large areas of CNP
Massive intraretinal and preretinal hemorrhage
Cotton wool spots

31. Follow up:
In the absence of treatment, should be monitored on a monthly for at least 6.0Ms
For the progression of CRVO
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.

32. 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.

33. 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.

34. 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)

35. A 2015 technology assessment for the A-A
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
Bevacizumab
aflibercept

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

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

38. CME secondary to CRVO before and after IVB

39. Macular edema in CRVO
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:
Cat.
Increase IOP 33% of cases

40. 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.

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

42. 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).

43. Laser treatment of CRVO
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.

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

45. 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

46. Laser surgery for CRVO: PRP
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.

47. Laser surgery for CRVO 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

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

49. Another surgical approaches
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).

50. Thank you for your attention