Upload
regina-leonard
View
215
Download
1
Tags:
Embed Size (px)
Citation preview
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.