Hemi Central Retinal Vein Occlusion

Grand Rounds March 11, 2005

John Nicolau, M.D.

Leo Dominguez, M.D.

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

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

CRVO

BRVO

Pathophysiology

CRVO 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

Risk Factors

CRVO Systemic Hypertension Cardiovascular Disease Diabetes Mellitus POAG

BRVO Systemic Hypertension Cardiovascular Disease Glaucoma Increased Body Mass Index at 20 yrs old NOT Diabetes Mellitus

Hypercoaguable States

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

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%

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

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

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.

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

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

BRVO Treatment

BVOSFound 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

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

BRVO

BRVO

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

CRVO Anatomy

Anatomy of HCRVO

Fluorescein Angiography HCRVO

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

Clinical Features

CRVO Shunting

BRVO Collaterals

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

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

HCRVO

References 1. BCSC. Retina and Vitreous. Section 12 pp 136-145., 2004. 2. Spalton, David. Atlas of Clinical Ophthalmology; Retinal Vascular Disease I. pp 233 -243.

2004. 3. Weinberg, David V., Venous Occlusive Diseases of the Retina. Principles and Practice of

Ophthalmology. pp. 1887-1987. 4. Clarkson, John G. Central Retinal Vein Occlusion. Retina. Vol 2. pp. 1368-1374. 2001. 5. Finkelstein, Daniel and Fekrat, Sharon. Branch Retinal Vein Occlusion. Retina. Vol 2. pp.

1376-1381. 2001. 6.Hayreh, S.S., Zimmerman, M. Bridget, Beri, Meena. Intraocular Pressure Abnormalities

Associated with Central Retinal Vein Occlusion. Ophthalmology. Vol 111. Number 1. Jan 2004. 133-139

7. Appiah, Aaron, Trempe, Clement. Differences in Contributory Factors among HCRVO, CRVO, and BRVO. Ophthalmology. Vol 96 Number 3 March 1989. pp 364-366.

8. Hayreh, S.S. and Hayreh M.S. HCRVO: Pathogenesis, Clinical Features, and Natural History. Archives of Ophthalmology. Vol 98. Sept 1980. pp 1600-1608.

9. Alexander, J. Larry. Primary Care of the Posterior Segment. Retinal Vascular Disease. Pp 219-221. 1994.