- •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
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8 Ancillary Testing in the Management of Retinal Vein Occlusions |
8.3Optical Coherence Tomography and the Retinal Thickness Analyzer
OCT allows the quantitation of retinal thickening and assessment of morphologic changes. Some of the latter include cysts, presence of subretinal ßuid,
and preservation or absence of the IS/OS junction, which may have prognostic signiÞcance.50,75
There are many OCT instruments in use, and they use different segmentation algorithms for measuring thicknesses in the retina. The inner retinal boundary is the same Ð the internal limiting
8.3 Optical Coherence Tomography and the Retinal Thickness Analyzer |
203 |
membrane of the retina. However, the outer boundaries differ. The outer boundary for the Stratus OCT is the IS/OS junction. For the Cirrus OCT, the outer boundary is the apical surface of the RPE cell layer. For the Spectralis OCT, the outer boundary is the basal surface of the RPE cell layer.
Artifacts can be a problem in OCTs obtained in eyes with RVO (Fig. 8.6). There is some evidence that the rate of artifacts in OCT measurements is higher in RVO than in diabetic macular edema, for instance. Manual measurement of CPT by the Wisconsin Reading Center was performed in 29% of SCORE OCTs but only 19% of OCTs from a clinical trial of diabetic macular edema.26 Possible reasons include the effects of intraretinal and subretinal blood and of subretinal ßuid in RVO.26
OCT-measured macular thickness correlates modestly with visual acuity in nonischemic BRVO with macular edema with the correlation coefÞcient ranging between 0.232 and 0.591.7,45,73 OCT-measured macular thickness is routinely used as a primary and secondary outcome measure in studies of BRVO and as an important index to follow in the clinical care of patients with BRVO.94 Changes in OCT-measured macular thickness and changes in visual acuity correlate poorly in BRVO. In the SCORE BRVO study, the Pearson correlation coefÞcients between visual acuity changes and OCT CPT changes over 12 months were −0.19, −0.30, and −0.10 for the grid laser, 1, and 4 mg groups, respectively.94
Although some studies use center point thickness from the OCT as the outcome variable, most use CSMT because of its greater reproducibility. There are many outcome variables of interest including macular thickness, absolute and relative macular thickening, and logOCT. For eyes with marked macular thickening as is frequently the case with RVO, the best outcome variable is relative change in macular thickening.
Certain morphological characteristics of the OCT have predictive importance for Þnal visual outcome in RVO with macular edema. In branch retinal vein occlusion associated with macular edema persistent for at least 6 months, the Þnal visual acuity was not correlated with total foveal thickness (r = 0.336, P = 0.092). However, it did correlate with the thickness measured from the posterior surface of macular cysts and the RPE (termed the photoreceptor layer thickness) (r = −0.571, P < 0.0001) and with the integrity of the inner segmentÐouter segment junction. Eyes with a continuous IS/OS junction had signiÞcantly better Þnal visual acuity than eyes with an interrupted IS/OS junction (P < 0.0001).71,76,77 In cases where the foveal IS/OS junction cannot be seen at baseline, presumably due to swelling and misalignment of photoreceptors secondary to leakage from inner retinal capillaries, the parafoveal IS/ OS junction has also been found to predict Þnal visual outcome.76 The confounding effects of pretreatment visual acuity need to be controlled before IS/OS junction continuity is accepted as an important predictor of Þnal visual outcome in
Fig. 8.5 A 69-year-old woman with hypertension, hypercholesterolemia, and obstructive sleep apnea syndrome developed a left superotemporal BRVO. (a) Montage color fundus photograph shows the extent of the involved retina. Cotton wool spots are evident and the temporal fovea is impinged by the blood. (b) MagniÞed view of the involved arteriovenous crossing. The artery crosses the vein at the black arrow. The blue arrow denotes thrombus with white Þbrin marbling downstream of the involved arteriovenous crossing. The red circle encompasses a cotton wool spot. (c) A frame from the early-phase ßuorescein angiogram shows delayed Þlling of the superotemporal retinal vein. (d) Frame from the mid-phase ßuorescein angiogram. The thrombus downstream of the crossing is
hyperßuorescent due to pooling of stagnant ßuorescein trickling through the occlusion (blue arrow). The orange arrow shows speckled hyperßuorescence in a dilated upstream section of the obstructed vein, a sign of sluggish blood ßow. The green arrow denotes stained venules in the involved retina, a sign of ischemia. The yellow oval encircles a zone of poor capillary perfusion. The orange oval encircles the area of the cotton wool spot (compare (b)), which in the ßuorescein angiogram blocks the capillary detail. (e) Frame from the late-phase ßuorescein angiogram. Most of the involved retina shows extreme hypermeability of microvasculature (hyperßuorescence), but the nonperfused areas are relatively hyperßuorescent (yellow oval)
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8 Ancillary Testing in the Management of Retinal Vein Occlusions |
Fig. 8.6 Fundus images of a 75-year-old woman with an old hemicentral retinal vein occlusion of the right eye developed sudden blurring of the left eye from an acute superotemporal branch retinal vein occlusion. (a) Glaucomatous cupping of the right optic disk is seen. The inferotemporal retinal veins are sheathed and the inferotemporal retinal arteries are narrowed. (b) Glaucomatous cupping of the left optic disk is seen along with fresh hemorrhages of the superotemporal retina. (c) Frame from the mid-phase ßuorescein angiogram of the right eye. Areas of capillary nonperfusion are present inferior to the macula. (d) Frame from the mid-phase ßuorescein angiogram of the left eye. Capillary perfusion is good. (e) Optical coherence tomography of the left eye 9 months before the left branch retinal vein occlusion. An artifact of the segmentation algorithm renders the nasal false-color map artifactitious (red ovals). (f) OCT scan at the time of the acute BRVO of the left eye. No artifacts are present. Note the marked increase in the superior inner and outer paracentral sectors compared to the scan from December 15, 2010 (compare purple and blue arrows from (e) and (f). The variation in thickness of
the inferior paracentral sectors (blue arrows, 219 vs. 222 m) exempliÞes the intersession agreement of OCT measurement because nothing has changed in this sector. The variation in thickness in the superior paracentral sectors (purple arrows, 229 vs. 255 m) represents a real change, in excess of the intersession variability of OCT measurements. (g) OCT of the right eye from December 15, 2010, shows a segmentation artifact (red oval). In this display, without the segmentation lines shown, only the false-color maps indicate that an artifact has occurred. (h) OCT of the right eye from August 11, 2011, showing a different segmentation artifact from the December 15, 2010 study. In this case, the display shows the segmentation lines, and it is clear that the algorithm mistook the posterior hyaloid face for the internal limiting membrane (red oval). The artifact has not compromised the central subÞeld measurement (compare yellow arrows from (g) and (h) both 197 m), but the difference in the outer paracentral subÞeld measurements in (g) and (h) (279 vs. 215 m) is artifactitious (compare blue arrows from (g) and (h))
8.3 Optical Coherence Tomography and the Retinal Thickness Analyzer |
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Fig. 8.6 (continued)
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Fovea: 267,67 |
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8 Ancillary Testing in the Management of Retinal Vein Occlusions |
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|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Central subfield |
Cube volume |
Cube average |
|
|
|
|
|
|
thickness (µm) |
(mm3) |
thickness (µm) |
|
ILM - RPE |
|
232 |
8.6 |
240 |
||||
|
|
|
|
|
|
|
|
|
Fig. 8.6 (continued)
8.3 Optical Coherence Tomography and the Retinal Thickness Analyzer |
207 |
g
500
400
300
200
100
0 m
Overlay: ILM - RPE transparency:50 %
High-definition mode
|
|
221 |
|
|
|
|
255 |
|
|
279 |
235 |
197 |
244 |
227 |
|
|
195 |
|
|
|
|
222 |
|
|
ILM-RPE thickness (µm) |
Fovea: 242,70 |
ILM - RPE
12-15-2010 Right eye
|
|
|
|
|
|
|
ILM |
|
|
Distribution |
|
|
|||||
|
|
|
|
|||||
|
of normals |
|
|
|
||||
|
|
|
|
99% |
|
|
|
|
|
|
|
|
|
|
|
||
|
|
|
|
95% |
|
|
|
|
|
|
|
|
5% |
|
|
|
|
|
|
|
|
1% |
|
RPE |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Central subfield |
Cube volume |
Cube average |
|
|
|
|
|
|
thickness (µm) |
(mm3) |
thickness (µm) |
|
|
|
|
|
|
||||
ILM - RPE |
|
197 |
8.4 |
234 |
||||
|
|
|
|
|
|
|
|
|
Fig. 8.6 (continued)
208 |
8 Ancillary Testing in the Management of Retinal Vein Occlusions |
08-11-2010 Right eye
h
500 |
|
|
222 |
|
|
|
|
400 |
|
|
|
|
|
||
|
|
|
|
|
|
||
|
|
|
25 |
|
|
|
|
300 |
215 |
234 |
197 |
244 |
225 |
|
|
|
|
||||||
200 |
|
|
196 |
|
|
|
|
|
|
|
|
|
|
||
|
|
|
170 |
|
|
|
|
100 |
|
|
|
|
|
|
|
ILM-RPE thickness (µm) |
Fovea: 271,77 |
||||||
|
|||||||
0 m
Overlay: ILM - RPE transparency:50%
ILM - RPE
|
|
|
|
|
ILM |
|
|
|
|
|
|
|
|
Distribution |
|
|
|
|||
of normals |
|
|
|
|||
|
|
|
99% |
|
|
|
|
|
|
|
|
|
|
|
|
|
95% |
|
|
|
|
|
|
5% |
|
|
|
|
|
|
1% |
|
RPE |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Central subfield |
Cube volume |
Cube average |
|
|
|
|
thickness (µm) |
(mm3) |
thickness (µm) |
ILM - RPE |
232 |
8.6 |
240 |
|||
|
|
|
|
|
|
|
Fig. 8.6 (continued)
eyes with BRVO and macula edema.42 Similar |
cyst size and presence of subretinal ßuid did not |
Þndings were reported in a study employing intra- |
correlate with visual acuity outcome.41 |
vitreal tissue plasminogen activator injection to |
In CRVO, baseline central retinal thickness |
treat macular edema associated with BRVO.71 |
was predictive of visual acuity outcome (r = 0.41, |
Intraretinal cysts of diameter >600 m were associ- |
P = 0.018).41 Intraretinal cyst size and presence of |
ated with longer duration of BRVO and less mac- |
subretinal ßuid did not correlate with visual acu- |
ular thinning in response to treatment. Intraretinal |
ity outcome.41 |
