- •Foreword
- •Preface
- •Contents
- •Contributors
- •Chapter 1
- •1.1 Introduction
- •1.2 Limitations of Time-Domain OCT
- •1.4 Conclusion
- •References
- •Chapter 2
- •2.1 Background
- •2.3 Clinical Application
- •2.4 Conclusions
- •References
- •Chapter 3
- •Fluorescein Angiography
- •3.1 Principles of Fluorescein Angiography
- •3.2 Procedures for Fluorescein Angiography
- •3.4 Time Course of Fluorescein Angiography
- •3.5 Interpretation of Fluorescein Angiography
- •3.5.1 Hypofluorescent Lesions
- •3.5.2 Hyperfluorescent Lesions
- •3.6 Fluorescein Angiography Today
- •References
- •Chapter 4
- •Wide-Field Imaging and Angiography
- •4.1 Introduction
- •4.2 History of Fundus Imaging
- •4.3.1 Fluorescein Angiography with a Scanning Laser Ophthalmoscope
- •4.3.2 Advantages of Imaging with a Scanning Laser Ophthalmoscope
- •4.4 Clinical Use of Wide-Field Imaging
- •4.4.1 Wide-Field Imaging in Uveitis
- •4.4.4 Wide-Field Imaging of Choroidal Tumors
- •4.5 Future Directions for Fundus Imaging
- •4.6 Conclusion
- •References
- •Chapter 5
- •Autofluorescence Imaging
- •5.1 Introduction
- •5.2 What is Fundus Autofluorescence?
- •5.3 Identification of Early Disease Stages
- •5.4 Phenotyping
- •5.5 Disease Markers
- •5.6 Monitoring of Disease Progression
- •5.7 Disease Mapping
- •5.8 Functional Correlation
- •References
- •Chapter 6
- •Imaging the Macular Pigment
- •6.1 Macular Pigment
- •6.1.1 Characteristics and Potential Functions
- •6.1.3 Spatial Distribution
- •6.1.4 Modifying the Macular Pigment
- •6.1.5 MPOD and Age
- •6.2 Measurement Techniques
- •6.2.1 Heterochromatic Flickerphotometry
- •6.2.2 Fundus reflectance
- •6.2.3 Autofluorescence
- •6.2.4 Raman spectroscopy
- •6.2.5 How do different techniques compare
- •6.3 Imaging
- •6.3.1 Heterochromatic Flickerphotometry
- •6.3.2 Fundus Reflectance
- •6.3.3 Autofluorescence
- •6.3.4 Raman spectroscopy
- •References
- •Chapter 7
- •7.1 Introduction
- •7.2 Origin of Near-Infrared Autofluorescence
- •7.3 RPE Melanin: Role and Aging
- •7.4 Clinical Cases
- •7.4.1 Age-Related Macular Degeneration
- •7.4.2 Retinal Dystrophies
- •7.4.2.1 Stargardt’s Disease
- •7.4.2.2 Best’s Disease
- •7.4.2.3 Retinitis Pigmentosa
- •7.5 Conclusion
- •References
- •Chapter 8
- •8.1 Introduction
- •8.3.1.1 Classic Choroidal Neovascularization
- •8.3.1.2 Occult Choroidal Neovascularization
- •8.3.1.4 Mixed-Type Choroidal Neovascularization
- •8.3.1.5 Retinal Angiomatous Proliferation
- •8.3.3 Fibrovascular Scar
- •8.5 Conclusions
- •References
- •Chapter 9
- •9.1 Fundus Cameras
- •9.1.1 Standard Images
- •9.1.2 Wide-Angle Images
- •9.1.2.1 Pomerantzeff Equator Plus
- •9.1.2.2 RetCam™
- •RetCam™ Camera Description
- •RetCam™ Technique of Image Capture
- •RetCam™ Problems
- •9.1.2.3 Panoret™
- •9.1.2.4 Optos™
- •9.2.1 Retinal Tumors
- •9.2.1.1 Retinoblastoma
- •9.2.1.2 Astrocytic Hamartoma
- •9.2.1.4 Retinal Cavernous Hemangioma
- •9.2.1.5 Retinal Racemose Hemangioma
- •9.2.1.6 Vasoproliferative Tumor
- •9.2.2 Retinal Pigment Epithelium Tumors
- •9.2.3 Choroidal Tumors
- •9.2.3.1 Choroidal Nevus
- •9.2.3.2 Choroidal Melanoma
- •9.2.4 Anterior Segment Lesions
- •9.2.4.1 Iris Lesions
- •References
- •Chapter 10
- •Metabolic Mapping
- •10.1 Aspects of Metabolism
- •10.4.1 Technical Solution
- •10.5 Clinical Results
- •10.5.1 Age-Related Macular Degeneration
- •10.5.1.1 Detection of Alterations in Early AMD
- •10.5.1.2 Lifetime Images in Late AMD
- •Non-Exudative AMD and Geographic Atrophy
- •Exudative AMD
- •10.5.2.1 Arterial Branch Occlusion
- •10.5.3 Metabolic Alteration in Diabetes Mellitus
- •10.5.3.1 Detection of Fields of Reduced Metabolism
- •References
- •Chapter 11
- •11.1 Diabetic Macular Edema
- •11.2 Examinations in Diabetic Macular Edema
- •11.3 Treatment of Diabetic Macular Edema
- •References
- •Chapter 12
- •12.1.1 Incidence and Natural History
- •12.2 Investigation of Diagnostic Accuracy of OCT for Detection of DME
- •12.2.2 Diagnostic Accuracy of OCT for Detection of DME: Are Photography or Biomicroscopy a Valid Gold Standard?
- •12.2.3 Diagnostic Accuracy of OCT to Detect CSME Using Time-Domain OCTs: How to Use OCT Retinal Thickness Cut-Offs?
- •12.3 Use of OCT When Compared with Photography: Beyond Diagnostic Accuracy
- •12.4 Appendix: Reproducibility of OCT Retinal-Thickness Measurement in Patients with DME
- •12.4.1 How Reproducibility is Reported
- •12.4.3 Spectral-Domain OCTs Reproducibility
- •References
- •Chapter 13
- •13.2 Clinical Features
- •13.3 Examination
- •13.4 Natural History
- •13.5 Ultra-High Resolution OCT and Spectral OCT Findings in Macular Holes
- •13.6 Macular Hole Formation
- •13.7 Postoperative Appearance
- •13.8 Theory of Macular Hole Closure After Vitrectomy
- •13.9 Surgical Considerations
- •13.11 Clinical Features
- •13.12 Treatment
- •References
- •Chapter 14
- •14.1 Introduction
- •14.2 Vitreous Biochemistry
- •14.3 Vitreo-Retinal Interface Anatomy
- •14.4 Anomalous Posterior Vitreous Detachment (PVD)
- •14.5 Spectral-Domain OCT (SD-OCT)
- •14.6 Vitreo-Maculopathies
- •14.6.1 Macular Pucker (MP)
- •14.6.2 Macular Hole (MH)
- •14.6.2.1 Lamellar Hole (LH)
- •14.6.3 Age-Related Macular Degeneration (AMD)
- •14.6.4 Vitreo-Macular Traction Syndrome (VMTS)
- •14.7 Conclusion
- •References
- •Chapter 15
- •15.3 Imaging the Choroid
- •15.4 Age-Related Choroidal Atrophy
- •15.5 Choroid in High Myopia
- •15.8 Volume Rendering
- •15.9 Summary
- •References
- •Chapter 16
- •16.1 Introduction
- •16.2 Optical Coherence Tomography
- •16.3 Role of Optical Coherence Tomography
- •References
- •Chapter 17
- •17.1 Background and Motivation
- •17.2 Three-Dimensional Imaging of the Choroid
- •17.3 In Vivo Cellular Resolution Retinal Imaging
- •17.4 Polarization Sensitive Retinal OCT
- •17.5 Doppler (Blood Flow) Retinal OCT
- •References
- •Chapter 18
- •Toward Molecular Imaging
- •Summaries for the Clinician
- •References
- •Index
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8 Near-Infrared Subretinal Imaging in Choroidal Neovascularization |
8.3.2 Idiopathic Polypoidal Choroidal
Vasculopathy
The term IPCV stands for a separate clinical entity that 8 differs clinically and demographically from AMD [47].
ICG and OCT studies revealed that polypoidal vascular lesions of the choroid are associated with serous and hemorrhagic RPE detachments [48, 49]
The variable presentation of IPCV gives rise to equally variable NIR images. RPE detachments and serous retinal elevations have a similar aspect as vascularized RPE detachments in AMD (Sect. 8.3.1.3). However, the localization and the source of the underlying subretinal structures separate IPCV from a regular AMD-associated RPE detachment on NIR imaging (Fig. 8.10). The polypoidal structures can be identified by their increased signal on NIR that collocates with their position on ICGA. The bright reflex represents the typically elongated, large vessel -like structures, as opposed to the adjacent smallsized signals of RPE alterations and the large, round reflexes of RPE detachments.
8.3.3 Fibrovascular Scar
Following treatment or in the later stages of a wet AMD, a degenerative process will lead to vessel occlusion and the development of scar tissue within the neovascular lesion. This scar consists of dense fibrous tissue, possibly surrounded by fibrinous exudations [50]. Higher levels of collagen fibers will lead to increased scattering and reflectance within the tissue, consequently enlarging the NIR signal [51]. Therefore, fibrovascular scars can be identified by their exceedingly bright appearance on NIR imaging (Fig. 8.11). Depending on a residual elevation of the overlying retina, a dark halo may be observed in the vicinity of the scar. In addition, there may be co-existing active parts of a CNV with the typical NIR manifestations as described in Sect. 8.3.1.1 through 8.3.4.
Summary for the Clinician
■The location of the neovascular membrane in relation to the RPE has its effects on the resultant NIR image.
■A dark, often poorly defined halo around the lesion is a frequent finding in the NIR of exudative macular degeneration and correlates with active CNV leakage on fluorescein angiography.
■On the NIR image, a bright corona surrounding a dark core is the characteristic sign of a welldefined, classic CNV.
■Occult CNV lesions show poorly demarked areas of scattered NIR increase with an underlying dark halo.
■In RPE detachments, a thin, lighter corona encircles an area of normal to low reflectivity, including scattered NIR increase at the area of the CNV.
■The darkened halo in RAP often exceeds the leakage zone on fluorescein angiography, possibly as a result of pre-edematous Müller cell disease. The RAP lesion itself appears as an irregular, increased NIR signal.
■Abnormal vessels in IPCV are mirrored by relatively high-reflective, elongated structures on NIR imaging.
■In the end stage of CNV membranes, the densepacked collagen fibers in fibrovascular scars produce a very strong NIR signal.
8.3.4 Choroidal Neovascularization
Not Associated with AMD
A variety of other disorders like high myopia, retinal dystrophies, uveitis, or idiopathic genesis may account for the development of CNV [52–54]. The majority of these neovascularization appear to be of the well-defined classic type. Coexisting retinal changes associated with underlying disorder, however, may confuse the interpretation of the NIR image. For instance, non-neovascular fundus lesions like inflammatory spots may also have increased fluid content and cause a locally elevated retina, giving rise to NIR abnormalities not unlike CNVs.
8.4 Evaluating Therapeutic Effects
with Near-Infrared Reflectance Imaging
The evolving new therapeutic strategies in CNV treatment require repeated imaging of the fundus to monitor the treatment effects and to aid in the appropriate timing for re-treatment [55]. Besides fluorescein angiography as the gold-standard for the assessment of CNV activity, OCT has become a widely accepted noninvasive tool in the evaluation of AMD therapy [56]. However, OCT data are not directly comparable with fluorescein angiography results due to their essential differences. Besides the static character of the anatomical OCT image, the huge memory capacity needed for modern three-dimensional OCT may be a drawback. Fluorescein angiography evaluates the functional aspects of the CNV by dynamic imaging
8.4 Evaluating Therapeutic Effects with Near-Infrared Reflectance Imaging |
89 |
Fig. 8.10 Idiopathic polypoidal choroidal vasculopathy. In idiopathic polypoidal choroidal vasculopathy vascular structures may be detected in NIR (upper panel, arrow), typically located nasally from the macular area. These structures correlate with the polypoidal vessel abnormalities identified on ICGA in the early phase (lower panel, open arrow). A corresponding RPE detachment causes characteristic NIR affections comparable to those in Fig. 8.8
90 |
8 Near-Infrared Subretinal Imaging in Choroidal Neovascularization |
8
Fig. 8.11 Fibrovascular scar. After treatment a fibrovascular scar remains as leftover of the CNV. This formerly classic lesion has partially kept the appearance of a bright ring on NIR (upper panel). Some parts of the membrane still show some perfusion on FA (lower panel), however others do not (open arrow). These avascular components appear highly reflective on NIR due to their increased content of collage fibers (arrow)
