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
 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
 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.