- •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
132 |
6 Systemic and Ocular Associations of Retinal Vein Occlusions |
hyperlipidemia were similar for nonischemic and ischemic CRVOs (7.5% and 8.4%, respectively).75
In a meta-analysis of ten pooled case-control studies, the overall OR for systemic hyperlipidemia as a risk factor for CRVO was 2.9 (95% CI 1.5Ð5.8) and other studies since that meta-analy- sis have been in agreement.142,147 Other case-con- trol studies support an association of mean serum cholesterol, serum triglyceride, and VLDL triglyceride levels with CRVO.39 An elevated HDL cholesterol level has been reported to be protective for CRVO.181
6.2.4 Cardiovascular Disease
Because several risk factors for RVOs are also risk factors for arterial thromboembolic events, several studies have examined associations between RVOs and cardiovascular disease.196
6.2.4.1 Pooled Retinal Vein Occlusion
The relationship of cardiovascular disease and pooled RVO is inconsistent in the literature. If an association exists, it seems weaker than that for hypertension.
In a retrospective cohort study of insurance claims from Taiwan, no increased 5-year risk of myocardial infarction was detected in patients with pooled RVO compared to controls without RVO after adjusting for possible confounding factors except in patients in the age group 60Ð69.81 In one case-control study, there was no statistically signiÞcant association of coronary artery disease with pooled RVO compared to the control group. Another study found a marginally signiÞcant association that would vanish under correction for multiple statistical hypothesis testing.147,151
In the BDES, there was no statistical difference between the prevalence of a history of angina or myocardial infarction between subjects with and without pooled RVO.31 In the BMES, there was no statistical difference between the
prevalence of a history of myocardial infarction between subjects with or without pooled RVO.31 On the other hand, a history of angina was more prevalent in subjects with pooled RVO (26.3% vs. 12.2%, P = 0.001).31 In a population-based study from Japan, there was no association of cardiovascular disease or presence of electrocardiographic abnormalities and prevalence of pooled RVO.206
In the BMES, there was no association between cardiovascular disease and 10-year incidence of pooled RVO.32
In a study that combined data from the BDES and BMES, pooled RVO was not associated with cardiovascular mortality. However, in patients less than 70 years old, RVO was associated with higher cardiovascular mortality (hazard ratio 2.5, 95% CI 1.2Ð5.2).31
6.2.4.2 Branch Retinal Vein Occlusion
In various case series, the prevalence of cardiovascular disease in patients with BRVO has ranged from 7% to 23.4%.6,58,147,194 In a case series, the prevalence of ischemic heart disease was higher in the patients with major BRVO than in patients with macular BRVO.75 In a retrospective cohort study using insurance claims data, patients with BRVO had no higher risks of myocardial infarction than patients without BRVO (relative risk 1.07, 95% CI 0.73Ð1.57).196
In a case-control study of 84 patients with BRVO and 84 ageand gender-matched controls without RVO, the prevalence of coronary artery disease did not differ signiÞcantly (7.1% and 4.8% for cases and controls, respectively).194 In a case-control study of 35 patients with BRVO compared to an age-matched group of 19 subjects with hypertension and another with 17 healthy subjects, the group with BRVO had lower echographically deÞned aortic distensibility and largearterial elasticity indices determined from recording radial arterial blood pressure pulse waveforms.88
In the BDES, neither a history of myocardial infarction nor angina was associated with prevalence of BRVO.95 Likewise, there was no association of angina with 5-year incidence of BRVO
6.2 Systemic Associations |
133 |
nor of cardiovascular disease and 15-year incidence of BRVO.95,96
6.2.4.3Central and Hemicentral Retinal Vein Occlusion
In case series of patients with CRVO, the prevalence of cardiovascular disease has ranged from 11% to 36%.6,58,117,147 In a case series of 29 patients with HCRVO, 21.4% had ischemic heart disease.6 In a retrospective cohort study using insurance claims data, patients with CRVO had no higher risk of myocardial infarction than patients without CRVO (relative risk 0.97, 95% CI 0.55Ð1.72).196
A case-control study found that persons with a history of cardiovascular disease had a 40% higher risk of developing CRVO compared to persons without a history of cardiovascular disease.181 Patients with severe electrocardiographic abnormalities had a 60% higher risk of developing CRVO compared to persons without electrocardiographic abnormalities.181 A case-control study found that persons with a history of atrial Þbrillation had 2.47 times the risk of developing CRVO compared to persons with no history of atrial Þbrillation (P = 0.036).99
6.2.4.4 Stroke
Because they share common risk factors, several studies have examined associations between RVOs and stroke.196 However, evidence of an association of stroke and pooled RVO is inconsistent. In a retrospective cohort study of insurance claims from Taiwan, no increased 5-year risk of stroke was detected in patients with pooled RVO compared to controls without RVO, after adjusting for possible confounding factors, except in patients in the age group 60Ð69.81 A case-control study from Sardinia found no association of stroke and pooled RVO.147 In the BDES, there was no statistical difference between the prevalence of a history of stroke between subjects with and without pooled RVO.31 In the BMES, a history of stroke was more prevalent in subjects with pooled RVO than those without (15.8% vs. 4.9%, P = 0.002).31 In the BMES, there was no association between a history of stroke and 10-year
incidence of pooled RVO.32 In a study of combined data from the BDES and BMES, pooled RVO was not associated with stroke mortality.
Similarly, the evidence linking stroke and BRVO is inconsistent. In a large case series that compared prevalences of systemic associations to gender-, race-, and age-matched national cohort, cerebrovascular disease was more prevalent in BRVO than in the comparison group.75 In a casecontrol study of 84 patients with BRVO and 84 ageand gender-matched controls without RVO, the prevalence of stroke did not differ signiÞcantly (5.9% and 3.6% for cases and controls, respectively).194 In a logistic regression analysis, the OR for BRVO given the presence of stroke was 1.67 (95% CI 0.40Ð6.97, P = 0.484).194 The proportion of patients with BRVO having cerebrovascular disease was greater than the proportion of patients with pooled CRVO and HCRVO.75
6.2.4.5Carotid Artery Disease and Peripheral Vascular Disease
The literature on the relationship of carotid artery disease and RVO is scanty, reßects a low level of evidence, and is inconsistent. An uncontrolled case series of 223 patients having 225 pooled RVOs found that 6% had carotid stenosis greater than 70% as an associated abnormality. The rate in age, sex, and other risk factor-matched controls was unknown, and the results are therefore difÞcult to interpret.164 In another uncontrolled case series, the prevalence of obstructive carotid disease in patients with CRVO was not higher than in historical controls.22 An uncontrolled case series of 40 eyes of 39 patients with CRVO had carotid artery evaluation that detected carotid artery lesions in 49%, a proportion higher than the authors expected, but not speciÞcally checked against a control group.127 In a case series of 480 patients having carotid ultrasonography and ophthalmoscopic studies, a control group of patients without any retinopathy was described (n = 227). This group was compared to a group of 11 patients with CRVO and 71 patients with BRVO. There were no differences in intima-media thickness, average number of plaques, or degree of stenosis of the internal carotid artery.123 In a case
