- •Retinal Vein Occlusions
- •Preface
- •Acknowledgments
- •Contents
- •1.1 Anatomy and Histology
- •1.2 Microanatomy of the Retina
- •1.3 Vascular Anatomy
- •Bernoulli’s Principle and Deductions Concerning Changes in Central Retinal Vein Diameter at the Lamina Cribrosa
- •1.4 Pathologic Anatomy
- •1.4.1 Abnormalities of the Vessel Wall
- •1.4.2 Branch Retinal Vein Occlusion
- •1.4.3 Central Retinal Vein Occlusion
- •1.4.4 Hemicentral Retinal Vein Occlusion
- •1.5 Summary of Key Points
- •References
- •2.1 Abnormalities of the Blood
- •2.1.1 Thrombosis
- •2.1.2 Viscosity of Blood
- •2.2 Abnormalities of Blood Flow
- •2.2.1 Retinal Vascular Hemodynamics
- •2.2.1.1 Laplace’s Law
- •2.2.1.2 Poiseuille’s Law
- •A Misapplication of Poiseuille’s Law
- •2.2.1.3 Hemodynamics of Central Retinal Vein Occlusion
- •How Severe Must Central Venous Obstruction Be to Produce Symptoms?
- •The Central Retinal Artery in Central Retinal Vein Occlusion
- •2.2.1.4 Hemodynamics of BRVO
- •2.3 Macular Edema
- •2.3.1 Macular Anatomy and Its Relationship to Macular Edema in Retinal Vein Occlusion
- •2.3.2 Starling’s Law
- •2.3.3 The Retinal Pigment Epithelial Pump
- •2.3.4 Molecular Signaling in Macular Edema
- •Relevant Molecular Biologic Terminology
- •2.3.4.1 Vascular Endothelial Growth Factor
- •2.3.4.2 Other Retinal Cytokines with Lesser Roles
- •2.3.4.3 Molecular Signaling in BRVO
- •2.3.4.4 Molecular Signaling in CRVO
- •What Does the Response of RVO to Intravitreal Anti-VEGF Drugs Say About Pathophysiology?
- •2.4 Retinal Neovascularization
- •Spontaneous Venous Pulsations and CRVO
- •2.7 Animal Models of Retinal Vein Occlusion
- •2.7.1 Animal Models of BRVO
- •2.7.2 Animal Models of CRVO
- •2.8 Summary of Key Points
- •2.9 Future Directions
- •References
- •3.1 Background for Clinical Genetics
- •3.2 The Role of Polymorphisms in Genetic Studies
- •3.3 Types of Genetic Study Design
- •Why Are So Many Association Studies for Retinal Vein Occlusion Negative?
- •3.4 Studies of the Genetics of Retinal Vein Occlusion
- •3.4.1 Platelet Glycoprotein Receptor Genes
- •3.4.2.1 Pooled Retinal Vein Occlusion
- •3.4.2.2 Central Retinal Vein Occlusion
- •3.4.2.3 Branch Retinal Vein Occlusion
- •3.4.4 202210G > A Mutation of the Prothrombin Gene (Factor II Leiden)
- •3.4.6 Protein C
- •3.4.7 Protein S
- •3.4.8 Fibrinogen
- •3.4.9 Factor XII
- •3.4.12 Other Negative Genetic Association Studies
- •3.5 Summary of Key Points
- •References
- •4.1 Nosology of Retinal Vein Occlusions
- •4.2 Branch Retinal Vein Occlusion
- •4.3 Central Retinal Vein Occlusion
- •Central Retinal Vein Occlusion with Nonischemic and Ischemic Hemispheres
- •4.3.1 Conversion from Nonischemic to Ischemic Forms of Retinal Vein Occlusion
- •4.4 Summary of Key Points
- •References
- •Quantifying Risk
- •The Major Epidemiologic Studies of Retinal Vein Occlusion
- •5.2 Prevalence
- •5.2.1 Pooled Retinal Vein Occlusion
- •5.2.2 Branch Retinal Vein Occlusion
- •5.2.3 Central Retinal Vein Occlusion
- •5.2.4 Hemicentral Retinal Vein Occlusion
- •5.3 Incidence
- •5.3.1 Pooled Retinal Vein Occlusion
- •5.3.2 Branch Retinal Vein Occlusion
- •5.3.3 Central Retinal Vein Occlusion
- •5.4 Risk and Protective Factors for Retinal Vein Occlusion
- •5.4.1.1 Pooled Retinal Vein Occlusion
- •5.4.1.2 Branch Retinal Vein Occlusion
- •5.4.1.3 Central Retinal Vein Occlusion
- •5.4.1.4 Hemicentral Retinal Vein Occlusion
- •5.4.2 Gender
- •5.4.2.1 Pooled Retinal Vein Occlusion
- •5.4.2.2 Branch Retinal Vein Occlusion
- •5.4.2.3 CRVO
- •5.4.2.4 Hemicentral Retinal Vein Occlusions
- •5.4.3 Race
- •5.4.4 Laterality
- •5.4.5 Body Mass Index
- •5.4.6 Education
- •5.4.7 Physical Activity
- •5.4.8 Miscellaneous Factors Explored and Not Found Important
- •5.5.1 Pooled Retinal Vein Occlusion
- •5.5.2 Branch Retinal Vein Occlusion
- •5.5.3 Central Retinal Vein Occlusion
- •5.5.4 Hemicentral Retinal Vein Occlusion
- •5.6 Life Expectancy
- •5.7 Visual Impact of Retinal Vein Occlusions
- •5.8 Summary of Key Points
- •References
- •6.1 Introduction
- •6.2 Systemic Associations
- •6.2.1 Hypertension
- •6.2.1.1 Pooled Retinal Vein Occlusions
- •6.2.1.2 Branch Retinal Vein Occlusion
- •6.2.1.3 Central Retinal Vein Occlusion
- •6.2.2 Diabetes Mellitus
- •6.2.2.1 Pooled Retinal Vein Occlusion
- •6.2.2.2 Branch Retinal Vein Occlusion
- •6.2.2.3 Central Retinal Vein Occlusion
- •6.2.3 Hyperlipidemia
- •6.2.3.1 Pooled Retinal Vein Occlusions
- •6.2.3.2 Branch Retinal Vein Occlusion
- •6.2.3.3 Central Retinal Vein Occlusion
- •6.2.4 Cardiovascular Disease
- •6.2.4.1 Pooled Retinal Vein Occlusion
- •6.2.4.2 Branch Retinal Vein Occlusion
- •6.2.4.3 Central and Hemicentral Retinal Vein Occlusion
- •6.2.4.4 Stroke
- •6.2.4.5 Carotid Artery Disease and Peripheral Vascular Disease
- •6.2.5 Rheologic and Hematologic Abnormalities
- •6.2.6 Coagulation Abnormalities
- •6.2.6.1 Antiphospholipid Antibodies
- •6.2.6.2 Factor VII
- •6.2.6.3 Factor VIII
- •6.2.6.4 Lipoprotein a
- •6.2.6.5 Von Willebrand Factor
- •6.2.6.6 Other Coagulation Factors
- •6.2.7 Hyperhomocysteinemia
- •6.2.7.1 Pooled Retinal Vein Occlusion
- •6.2.7.2 Branch Retinal Vein Occlusion
- •6.2.7.3 Central and Hemicentral Retinal Vein Occlusion
- •6.2.8 Serum Folate
- •6.2.9 Serum B12
- •6.2.10 Smoking
- •6.2.11 Alcohol Consumption
- •6.2.14 No Underlying Vascular Risk Factor
- •6.3 Ocular Associations
- •6.3.1 Pooled Retinal Vein Occlusion
- •6.3.2 Branch Retinal Vein Occlusion
- •6.3.3 Central Retinal Vein Occlusion and Hemicentral Retinal Vein Occlusion
- •6.4 Practical Recommendations About the Systemic Workup of Patients with Retinal Vein Occlusion
- •History of the Standard Workup for Systemic Associations in Central Retinal Vein Occlusion
- •6.5 Retinal Vein Occlusion and Cardiovascular Disease Risk
- •6.6 Differences in Systemic Associations Between Ischemic and Nonischemic CRVOs
- •6.7 Summary of Key Points
- •References
- •7.1 Branch Retinal Vein Occlusion
- •7.1.1 Acute Phase
- •7.1.1.1 Symptoms
- •7.1.2 Clinical Signs
- •7.1.2.1 Visual Acuity
- •7.1.3 Chronic Phase
- •7.1.3.1 Clinical Signs
- •7.1.3.2 Visual Acuity
- •Why Does the Visual Outcome in Nonischemic, Macula-Involving Branch Retinal Vein Occlusions Usually Vary with the Size of the Involved Retina?
- •7.2 Central Retinal Vein Occlusion
- •7.2.1 Acute Phase
- •7.2.1.1 Symptoms
- •7.2.1.2 Clinical Signs
- •When Retinal Venous Congestion and Optic Disc Edema Are Not Central Retinal Vein Occlusion
- •What Is the Relationship of Central Retinal Artery Pressure and Cilioretinal Artery Pressure?
- •Retinal Whitening Does Not Equal Infarction
- •A Clinical Picture Predicted by a Hypothesis
- •7.2.1.3 Visual Acuity
- •7.2.2 Chronic Phase
- •Why Are Optic Disc Collaterals Associated with Worse Initial and Final Visual Acuity After CRVO?
- •7.2.2.1 Visual Acuity
- •7.3 Hemicentral Retinal Vein Occlusion
- •7.3.1 Clinical Signs
- •7.3.2 Visual Acuity
- •7.4 Summary of Key Points
- •References
- •Which Measure of Reproducibility Is Best?
- •8.1 Color Fundus Photography
- •8.2 Fluorescein Angiography
- •8.2.1 Branch Retinal Vein Occlusion
- •8.2.2 Central Retinal Vein Occlusion
- •8.3 Optical Coherence Tomography and the Retinal Thickness Analyzer
- •Methods of Analysis of OCT in RVO
- •8.4 Visual Field Testing
- •8.5 Electroretinography
- •Electroretinography Essentials for Retinal Vein Occlusions
- •8.5.1 Branch Retinal Vein Occlusion
- •8.5.2 Central Retinal Vein Occlusion
- •8.5.3 Hemicentral Retinal Vein Occlusion
- •8.6 Indocyanine Green Angiography
- •8.7 Color Doppler Ultrasonographic Imaging
- •8.8 Laser Doppler Flowmetry
- •8.9 Ophthalmodynamometry
- •8.10 Scanning Laser Doppler Flowmetry
- •8.11 Laser Interferometry to Measure Pulsatile Choroidal Blood Flow
- •8.12 Vitreous Fluorophotometry
- •8.13 Summary of Key Points
- •References
- •9.1 Terminology
- •9.2 Branch Retinal Vein Occlusion
- •9.3 Central Retinal Vein Occlusion
- •9.3.1 Clinical Characteristics
- •In the Face of Evidence that Fluorescein Angiography Is Poorly Predictive of Ischemia in Acute Central Retinal Vein Occlusion, Why Is It Widely Used?
- •9.3.2 Conversion from Nonischemic to Ischemic Central Retinal Vein Occlusion
- •9.3.3 Outcomes by Ischemic Status
- •9.4 Interaction of Ischemia with Effects of Treatments
- •9.4.1 Branch Retinal Vein Occlusion
- •9.4.2 Central Retinal Vein Occlusion
- •9.5 Summary of Key Points
- •References
- •10.1 Branch Retinal Vein Occlusion
- •10.2 Central Retinal Vein Occlusion
- •10.3 Hemicentral Retinal Vein Occlusion
- •10.4 Treatment of Posterior Segment Neovascularization in Retinal Vein Occlusion
- •10.5 Summary of Key Points
- •References
- •11.1 The Pathoanatomy and Pathophysiology of Iris and Angle Neovascularization
- •11.2 Clinical Picture of Anterior Segment Neovascularization
- •11.4 Anterior Segment Neovascularization in Branch Retinal Vein Occlusion
- •11.5 Anterior Segment Neovascularization in Central Retinal Vein Occlusion
- •The Problem of Undetected Anterior Segment Neovascularization After Central Retinal Vein Occlusion
- •Why Is Anterior Segment Neovascularization Less Common in Central Retinal Vein Occlusion Than in Central Retinal Artery Occlusion?
- •11.6 Anterior Segment Neovascularization in Hemicentral Retinal Vein Occlusion
- •11.7 Summary of Key Points
- •References
- •12.1 Branch Retinal Vein Occlusion with Macular Edema
- •12.2 Central Retinal Vein Occlusion with Macular Edema
- •12.3 Summary of Key Points
- •References
- •Visual Acuity Measurement in Treatment Studies
- •OCT Measurement of Macular Thickness in Treatment Studies
- •13.1 Medical Treatment of Retinal Vein Occlusion
- •13.1.1 Anticoagulation
- •13.1.2 Systemic Thrombolytic Therapy
- •13.1.3 Isovolumic Hemodilution
- •Recipe for Isovolumic Hemodilution
- •13.1.4 Plasmapheresis
- •13.2 Treatment of Previously Unsuspected Risk Factors for Retinal Vein Occlusion
- •13.3.1 Treatments for Macular Edema
- •Relative Corticosteroid Potencies
- •13.3.2 Treatments for Intraocular Neovascularization
- •13.4 Results of Clinical Studies of Treatments for Macular Edema Secondary to Retinal Vein Occlusions
- •13.4.1 Branch Retinal Vein Occlusion
- •13.4.1.1 Grid Laser
- •13.4.1.2 Subthreshold Grid Laser Treatment
- •13.4.1.3 Sector Panretinal Laser Photocoagulation
- •13.4.1.5 Posterior Subtenon’s Triamcinolone
- •13.4.1.6 Intravitreal Corticosteroids
- •13.4.1.7 Combination Treatments Involving Intravitreal Triamcinolone Injections
- •13.4.1.8 Arteriovenous Sheathotomy
- •13.4.1.9 Vitrectomy
- •13.4.1.10 Intravitreal Injection of Autologous Plasmin
- •13.4.2 Central Retinal Vein Occlusion
- •13.4.2.2 Combination Regimen: Bevacizumab, Panretinal Laser, and Grid Laser
- •13.4.2.3 Systemic Corticosteroids
- •13.4.2.4 Posterior Subtenon’s Triamcinolone Injection
- •13.4.2.5 Intravitreal Corticosteroids
- •13.4.2.6 Vitrectomy
- •13.5 Treatment of Intraocular Neovascularization
- •13.5.1 Sector Panretinal Laser Photocoagulation for Retinal and Disc Neovascularization After Branch Retinal Vein Occlusion
- •13.5.2 Vitrectomy for Intraocular Neovascularization with Vitreous Hemorrhage
- •13.5.3 Laser Panretinal Photocoagulation for Anterior Segment Neovascularization
- •13.6 Economic Considerations
- •13.7 Future Directions
- •13.8 Summary of Key Points
- •References
- •14.1 Pooled Retinal Vein Occlusions in the Young
- •14.2 Branch Retinal Vein Occlusion in Younger Patients
- •14.3 Central Retinal Vein Occlusion in Younger Patients
- •14.4 Workup in the Younger Patient with Retinal Vein Occlusion
- •14.5 Summary of Key Points
- •References
- •15.1 Failed and Unadopted Treatments for Branch Retinal Vein Occlusion
- •15.1.1 Sector Panretinal Laser Photocoagulation for Serous Retinal Detachment in Branch Retinal Vein Occlusion
- •15.1.2 Laser Chorioretinal Venous Anastomosis for Branch Retinal Vein Occlusion with Macular Edema
- •15.1.3 Intravenous Infusion of Tissue Plasminogen Activator
- •15.1.4 Intravitreal Injection of Tissue Plasminogen Activator
- •15.1.5 Macular Puncture for Branch Retinal Vein Occlusion with Macular Edema
- •15.2 Failed and Unadopted Treatments for Central Retinal Vein Occlusion
- •15.2.1 Grid Laser for Macular Edema in Central Retinal Vein Occlusion
- •15.2.2 Chorioretinal Venous Anastomosis for Nonischemic Central Retinal Vein Occlusion with Macular Edema
- •15.2.3 Radial Optic Neurotomy for Central Retinal Vein Occlusion
- •15.2.4 Retinal Endovascular Surgery with Intravenous Injection of Tissue Plasminogen Activator
- •15.2.5 Intravitreal Injection of Tissue Plasminogen Activator
- •15.2.6 Intravitreal Tissue Plasminogen Activator and Triamcinolone
- •15.2.7 Systemic Acetazolamide for Central Retinal Vein Occlusion with ME
- •15.2.8 Combined Central Retinal Vein Occlusion and Central Retinal Artery Occlusion
- •15.2.9 Optic Nerve Sheath Decompression
- •15.2.10 Section of the Posterior Scleral Ring
- •15.2.11 Infusion of High Molecular Weight Dextran
- •15.3 Failed and Unadopted Treatments for HCRVO
- •15.4 Summary of Key Points
- •References
- •16.1 Case 16.1: An Asymptomatic Central Retinal Vein Occlusion with Asymmetric Hemispheric Involvement
- •16.1.1 Discussion
- •16.2 Case 16.2: Chronic Macular Branch Vein Occlusion with Subtle Ophthalmoscopic Signs, More Obvious Fluorescein Angiographic Signs, and Macular Edema
- •16.2.1 Discussion
- •16.3 Case 16.3: Old Hemicentral Retinal Vein Occlusion with Late Vitreous Hemorrhage and Hyphema
- •16.3.1 Discussion
- •16.4 Case 16.4: Spontaneous Improvement of a Nonischemic Central Retinal Vein Occlusion
- •16.4.1 Discussion
- •16.5 Case 16.5: Conversion of a Nonischemic Hemicentral Retinal Vein Occlusion to an Ischemic One
- •16.5.1 Discussion
- •16.6 Case 16.6: Nonarteritic Ischemic Optic Neuropathy Following Branch Retinal Vein Occlusion
- •16.6.1 Discussion
- •16.7 Case 16.7: Differentiating Central Retinal Vein Occlusion from the Ischemic Ocular Syndrome
- •16.7.1 Discussion
- •16.8 Case 16.8: Late Development of Neovascularization Elsewhere After Ischemic Branch Retinal Vein Occlusion
- •16.8.1 Discussion
- •16.9 Case 16.9: Nonischemic Central Retinal Vein Occlusion with Secondary Branch Retinal Artery Occlusion
- •16.9.1 Discussion
- •16.10 Case 16.10: Nonischemic Central Retinal Vein Occlusion with Macular Edema or Asymmetric Diabetic Retinopathy with Diabetic Macular Edema?
- •16.10.1 Discussion
- •16.11 Summary of Key Points
- •References
- •Index
7.1 Branch Retinal Vein Occlusion |
167 |
retinal vessels after BRVO lack tight junctions.109 The clinical correlate of this is leakiness to ßuorescein during ßuorescein angiography, a discriminating point from collateral vessels within the retina (Figs. 7.7 and 7.11). Proliferation of new vessels with accompanying Þbrous tissue can lead to traction, vitreous hemorrhage (Fig. 7.11), traction retinal detachment, retinal breaks, and rhegmatogenous retinal detachment.6,24,33,103,119,137
Iris neovascularization is not common after BRVO but can occur, especially if the area of capillary nonperfusion is large.57,119 Extrafoveal vitreous traction detected by OCT has been reported in 24% of cases with BRVO.102 Vitreous
attachment to the retina in BRVOs with extensive capillary nonperfusion is a risk factor for development of retinal neovascularization.65 Ischemic BRVO evolves with thinning of the ganglion cell and nerve Þber layer and sectoral optic disc atrophy.44
7.1.3.2 Visual Acuity
Older retrospective series with imperfect comparability provide a rough idea of the natural history of BRVO visual acuity outcomes.74,94 Based on a combined sample of 135 eyes followed for at least 1 year, the weighted averages for visual
Fig. 7.8 A 51-year-old woman developed a superotemporal branch retinal vein occlusion in the left eye with macular edema. Visual acuity was 20/50. (A) Monochromatic fundus photograph shows optic disc collateral vessels (yellow arrow). (B) A frame from the latephase ßuorescein angiogram shows that the disc collaterals do not leak ßuorescein dye (the yellow arrow). Macular edema is present. (C) A false-color map from time domain
optical coherence tomography (OCT) shows macular edema. (D) A line scan from time domain OCT shows macular thickening with cysts. (E) Follow-up color fundus photograph shows a macular hole (the green arrow) with a cuff of subretinal ßuid (the black arrow). (F) Spectral domain OCT shows a macular hole with cysts of edema in the border tissue. (G) False-color map from spectral domain OCT shows persistent macular edema superiorly
168 |
7 The Clinical Picture and Natural History of Retinal Vein Occlusions |
Fig. 7.8 (continued)
Fig. 7.9 Fundus image of a chronic branch retinal vein occlusion involving the right eye. The visual acuity is 20/32. Lipid exudates are present at the border of edematous and normal retina and tend to be heavier closer to the horizontal raphe and the macula (the black arrow) and lighter peripherally (the green arrow). A cluster of leaking microaneurysms is present within the oval area deÞned by the interrupted lipid ring
outcomes suggest that 42% of eyes end with visual acuity better than or equal to 20/40, 27% with visual acuity in the 20/50Ð20/100 range, and 31% with visual acuity of 20/200 or worse (Table 7.2).74,94 One older meta-analysis of natural history studies of BRVO found that 53% of patients with BRVO end with a Þnal visual acuity of 20/40 or better.103 A meta-analysis of more recent studies reported that the mean change in visual acuity during follow-up ranged from 1 Early Treatment Diabetic Retinopathy Study (ETDRS) letter at 6 weeks to 28 ETDRS letters at 12Ð24 months.117
The most reliable data on the natural history of visual acuity data in BRVO comes from popu- lation-based studies of incident cases. In the Beaver Dam Eye Study (BDES), 61 eyes suffered incident BRVO during 15 years of follow-up. For these, the average drop in visual acuity caused by the BRVO was 12 ETDRS letters.72 The BDES
7.1 Branch Retinal Vein Occlusion |
169 |
Fig. 7.10 A 77-year-old man with hypertension had a history of bilateral branch retinal vein occlusions (BRVO). The left BRVO occurred in 1997 and was associated with macular edema treated by grid laser, but the eye never regained better than 20/200 visual acuity. In 2007, examination showed a macular epiretinal membrane and chronic cystoid macular edema. (a) Frame from the middle-phase ßuorescein angiogram shows the irregular telangiectasia superotemporal to the fovea. (b) Frame from the late-phase of the ßuorescein angiogram shows petalloid hyperßuorescence surrounding a
hypoßuorescent area (yellow oval) that was a large cyst (see (c)). (c) A linear SD-OCT scan shows the large central cyst (the green arrow) and a macular epiretinal membrane (the yellow arrow). (d) Four linear SD-OCT scans that straddle the central scan of C from the Þve-raster display show different cuts through the large macular cyst and the overlying epiretinal membrane (the yellow arrow). Surgery was not offered to the patient in view of the 10-year history of the problem and poor vision and the low probability of improving visual function even with technically successful surgery
Fig. 7.11 Fundus images of a 47-year-old man with unsuspected hypertension and a right inferotemporal branch retinal vein occlusion with retinal neovascularization and a subhyaloid hemorrhage. (a) Monochromatic fundus photo-
graph showing the subhyaloid hemorrhage (the turquoise arrows) and neovascularization (the yellow arrow). (b) Frame from the middle-phase ßuorescein angiogram showing the leaky neovascularization (the yellow arrow)
170 |
|
7 The Clinical Picture and Natural History of Retinal Vein Occlusions |
||
Table 7.2 Natural history of visual acuity outcomes in branch retinal vein occlusion |
|
|||
Study |
N |
20/40 or better (%) |
20/50Ð20/100 (%) |
20/200 or worse (%) |
Michels and Gass94 |
91 |
51 |
26 |
23 |
Foster Moore, cited in Krill74 |
15 |
13 |
33 |
53 |
Jensen, cited in Krill74 |
29 |
31 |
28 |
45 |
Weighted average |
135 |
42 |
27 |
31 |
|
|
|
|
|
Visual acuity outcomes in untreated branch retinal vein occlusion followed for at least 1 year
identiÞed 31 persons with BRVO at baseline. Twenty-three were alive and examined 5 years later. In these subjects, best corrected visual acuity did not change.71
The untreated arm of the Branch Vein Occlusion Study (BVOS) provided natural history data on 35 eyes with BRVO of duration 3Ð18 months excluding cases with macular ischemia and foveal hemorrhage. For such eyes, over 3 years, the average change in visual acuity was 0.23 Snellen lines of improvement.138 Thirtyseven percent of eyes gained two lines of visual acuity, and 34% had vision better than or equal to 20/40 at 3 years of follow-up.138 The sham arm of the Ranibizumab for the Treatment of Macular Edema Following Branch Retinal Vein Occlusion (BRAVO) study provided natural history information on visual acuity for an initial 3 months in mostly BRVOs (13% were HCRVOs) with durations of 0Ð16 months.18 In the Þrst 3 months after diagnosis, 17% of 132 eyes in the sham group gained greater than or equal to three lines of visual acuity.18
The prognosis for visual outcome depends on the extent and severity of the initial obstruction, the extent of involvement of the FAZ border, the initial visual acuity, the extent and timing of collateral vessel formation, the age of the patient, and comorbidities of the involved retina.94,115 Of eyes with initial visual acuity greater than or equal to 20/50 and followed without treatment, 90% end with visual acuity greater than or equal to 20/50. Of eyes with initial visual acuity less than or equal to 20/200, 14Ð33% end with visual acuity greater than or equal to 20/50.43,115 Of eyes with initial visual acuity greater than or equal to 20/50, 0Ð5% end with visual acuity less than or
equal to 20/200. Of eyes with initial visual acuity less than or equal to 20/200, 50Ð83% end with visual acuity less than or equal to 20/200.43,115
Extent of capillary nonperfusion may inßuence the natural history of visual outcome. The smaller the sector of the foveal avascular zone border involved, the better the visual prognosis.25,94 Presence of subretinal blood is a negative prognostic sign as it leads to RPE metaplasia. Causes for poor Þnal vision in BRVO are foveal lipid deposition, submacular scarring, severe cystoid macular edema, and a combination of superior and inferior BRVO.74,94
A case series of 45 BRVOs found that eyes that developed collaterals had statistically signiÞcantly better visual outcomes than eyes that did not.63 Because eyes with BRVOs usually develop venous collaterals Ð and reproducibility of grading collaterals has not been demonstrated Ð this conclusion is an interesting hypothesis in need of further testing, but not a consensus.
For macular BRVO, three studies provide information on the course of visual acuity in untreated cases.5,64,106 In a series of 35 patients followed without treatment for 24 months, the average baseline visual acuity was logMAR 0.42 ± SD 0.13 (Snellen equivalent 20/50) and improved without treatment by an average of 10 ETDRS letters at 3 months and 14 ETDRS letters by 12 months.106 No further visual acuity improvement was noted between 12 and 24 months.106 In a second study of 64 patients, 20% of eyes experienced an improvement of greater than or equal to two lines.64 In a third series of 35 patients, the mean visual acuity over 2 years improved from 20/50 to 20/30.4
