1. Hemi Central Retinal Vein Occlusion
Grand Rounds March 11, 2005
John Nicolau, M.D.
Leo Dominguez, M.D.

2. CRVO/BRVO Findings
Most common retinal vascular problem second to Diabetic Retinopathy
Dilated and tortuous veins in all 4 quadrants
ONH Edema
Diffuse retinal hemorrhages at all levels and possibly cotton-wool spots
Largely divided into ischemic vs. nonischemic by Fluorescein Angiography
BRVO Similar but segmental distribution of findings – morbidity related to area of blockage

3. Clinical Presentation
Abrupt decrease in vision/Resolution?
TVOs
Redness and Photophobia
Pain – usually advanced with NVI, NVG and increased IOP
Classic clinical picture on dilated examination

4. CRVO

5. BRVO

6. Pathophysiology CRVO BRVO
Thrombosis at level of lamina cribosa possibly 2’/2 vessel narrowing and turbulent flow – relation to increased IOP?
Occlusion of arterial and venous components producing differing clinical pictures
BRVO
Compression of vein by artery sharing common adventitial sheath causing turbulence and thrombosis
Location of occlusion affecting clinical appearance

7. Risk Factors CRVO BRVO Hypercoaguable States Systemic Hypertension
Cardiovascular Disease
Diabetes Mellitus
POAG
BRVO
Glaucoma
Increased Body Mass Index at 20 yrs old
NOT Diabetes Mellitus
Hypercoaguable States

8. Causes of Vision Loss CRVO/BRVO Macular Edema
Macular Hemorrhage with RPE damage
Macular Nonperfusion
Neovascular Glaucoma (CRVO)
Retinal Neovascularization and complications (BRVO)
ERM
Macular Hole RD
Subretinal Fibrosis

9. Prognosis and Statistics
CRVO
Approximately 30% ischemic (10 DD on FA)
NVG 40% to 60% of these eyes vs 5% Nonischemic
<10% developed retinal neovascularization
CVOS – 83% of undetermined developed ischemia or NVI
BRVO
1/3 to 1/2 recover VA of 20/40 or better w/o therapy
50% Ischemic (5 DD) of which 40% develop neovascularization; 60% of these develop VH
NVI Rare; 1%

10. Treatment of CRVO
Early studies with poor definition of ischemia, non randomization, lack of controls, small number of subjects, etc.
CVOS founded and attempted to answer two main questions:
1. Whether PRP prevents NVI and NVG in ischemic eyes
2. Whether grid treatment improves VA in eyes losing vision from macular edema

11. Perfused and Indeterminate Groups
34% of initially perfused eyes converted to nonperfused and thus became eligible for the study
Final VA depended on initial VA
16% developed iris/angle neovascularization
Strongest risk factors were degree of nonperfusion and VA < 20/200
20/52 of indeterminate group developed neovascularization

12. Macular Edema
Eyes with initially 20/50 VA or worse showed no difference in final VA after grid-pattern treatment compared to control eyes which received no treatment. Macular edema was however reduced in these eyes angiographically.

13. Nonperfused Group
Set out to determine if prophylactic PRP would prevent neovascularization or it was more appropriate to wait for its development
Neovascularization developed less in treated eyes but not with statistical significance
Regression was prompt when treated in both controls and treated eyes

14. Recommendations
There is no indication for PRP in ischemic or nonischemic eyes without neovascularization if patient available for follow up
Grid treatment not shown to improve VA in eyes with decreased VA due to macular edema
Progression towards ischemia greater in early months following CRVO with VA <20/200 best indicator
Monthly follow up for first 6 months with prompt PRP when any neovascularization observed
No systemic anticoaugulation

15. BRVO Treatment
BVOS
Found that 63% of treated eyes with perfused macular edema, no foveal heme, and other minor criteria gained two or more lines of VA when compared to controls at 3 years.
PRP reduced VH in half (60% to 30%) when neovascularization present

16. BRVO Recommendations
Wait 3 to 6 months before beginning laser therapy in an eye with VA < 20/40 and perfused macular edema
No treatment for macular nonperfusion
PRP at first sign of NVD, NVE, or NVI

17. BRVO

18. BRVO

19. HCRVO CRVO with two trunks behind lamina cribosa (20%)
Thought to be variant of CRVO but with complications and findings of both types of vein occlusions
Also divided into ischemic and nonischemic

20. CRVO Anatomy

21. Anatomy of HCRVO

22. Fluorescein Angiography HCRVO

23. HCRVO/CRVO Similarities
Hayreh and Hayreh found BRVO artery crosses over vein in 91% whereas in HCRVO only 1/3 showed this and >1/3 had no crossing
Collateral vessels in BRVO feed at crossing whereas in CRVO they form at disc or more posterior as found in HCRVO
In HCRVO about 1/3 showed increased IOP as did CRVO unlike BRVO where increased IOP not > general population
ONH edema seen in HCRVO/CRVO but not usually in BRVO
Lack of NVI/NVG in BRVO not found it HCRVO/CRVO

24. Clinical Features

25. CRVO Shunting

26. BRVO Collaterals

27. Further Evidence
Appiah, Clement Trempe found increased IOP when comparing HCRVO and CRVO but not BRVO and the above
Also found HTN and Hyperopia in BRVO but not CRVO or HCRVO
Hayreh, Zimmerman et al. compared HCRVO and CRVO and found increased prevalence of glaucoma and OHT when compared to general population

28. Treatment Implications
HCRVO (ischemic) 13% NVI (Hayreh) thus NVI being > BRVO and < CRVO;
Nonischemic showed no neovascularization
NVD 29% and NVE 42% in ischemic HCRVO > CRVO and BRVO
Question arises as whether to pre-treat ischemic HCRVO with PRP and whether or not to treat macular edema in light of recommendations in BRVO but not CRVO

29. HCRVO

30. References 1. BCSC. Retina and Vitreous. Section 12 pp 136-145., 2004.
2. Spalton, David. Atlas of Clinical Ophthalmology; Retinal Vascular Disease I. pp
3. Weinberg, David V., Venous Occlusive Diseases of the Retina. Principles and Practice of Ophthalmology. pp
4. Clarkson, John G. Central Retinal Vein Occlusion. Retina. Vol 2. pp
5. Finkelstein, Daniel and Fekrat, Sharon. Branch Retinal Vein Occlusion. Retina. Vol 2. pp
6.Hayreh, S.S., Zimmerman, M. Bridget, Beri, Meena. Intraocular Pressure Abnormalities Associated with Central Retinal Vein Occlusion. Ophthalmology. Vol 111. Number 1. Jan
7. Appiah, Aaron, Trempe, Clement. Differences in Contributory Factors among HCRVO, CRVO, and BRVO. Ophthalmology. Vol 96 Number 3 March pp
8. Hayreh, S.S. and Hayreh M.S. HCRVO: Pathogenesis, Clinical Features, and Natural History. Archives of Ophthalmology. Vol 98. Sept pp
9. Alexander, J. Larry. Primary Care of the Posterior Segment. Retinal Vascular Disease. Pp