- •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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13 Spectral Domain Optical Coherence Tomography for Macular Holes |
has already been described in histopathological papers [31, 32].
Eckardt et al. demonstrated with SD-OCT that macular hole closure appears within 24 h of surgery in 54.5% of 13 the cases and in 48 h in 75.7%. Such fast closure of the macular hole after vitrectomy with ILM peeling may support the theory that ILM peeling is a type of refreshment of the edges of the macular hole, and allows for a similar situation to that observed in spontaneous macular hole closure, which is additionally supported by the gas bubble that provides a surface for cell migration so that the macular hole can close. According to Eckardt et al., if the macular hole does not close during the first 3 days, it will not close later on and will require repeated surgery [33].
The healing process does not end with macular hole closure. In the postoperative period, restoration of two hyperreflective lines, which are believed to be the ELM and the IS/OS junction, is observed [27, 34, 35]. Lee et al. presented three cases of restoration of the photoreceptor layer after macular hole surgery [34]. Chang et al. observed that 6 out of 7 eyes with macular hole closure had a decrease in the IS/OS defect size after the hole was closed. Visual acuity showed a trend towards improvement, but the improvement was not correlated with the change in the size of the IS/OS boundary defect [33]. Sano described 28 cases of healing of the IS/OS line. The visual outcomes were significantly better in eyes with a continuous IS/OS line than in those with a disrupted IS/ OS line [35].
Summary for the Clinician
■Elevation of the photoreceptor layer combined with asymmetric posterior hyaloid traction on the fovea can be considered an early step in macular hole formation.
■After successful surgery, various defects of the retinal layers in the fovea can be noted. Some of them may be influenced by surgical procedures.
■Visual acuity improves up to 12 months after surgery, as does the appearance of the fovea in SOCT.
13.9 Surgical Considerations
Vitrectomy as a method of treatment for macular holes was introduced in 1990–1991 by Kelly and Wendel [36]. During the 1990s, different adjuvants were used to improve the results of surgery. By the end of the 1990s
and the beginning of the 21st century, the increasing role of ILM peeling combined with vitrectomy and gas injection was observed. Various dyes are being used to improve the quality of ILM peeling. This kind of treatment is nowadays considered a standard procedure for the treatment of macular holes.
As this chapter is designed to present the diagnostics of macular hole with SOCT, surgical methods will not be widely presented or discussed. However, we recently presented a new method of treating large macular holes [37]with the use of an inverted ILM flap to cover the macular hole and to improve the closure rate of large macular holes. Postoperative SOCT examination after the use of the inverted ILM flap technique gave us the opportunity to demonstrate macular hole closure in those eyes. As can be seen, the ILM serves as a scaffold for tissue migration or proliferation with the aim of closing the macular hole. Without the use of SOCT, it would not be possible to observe this process. This mechanism may explain how full-thickness retinal defects close. Without a histopathological examination of the eyes after macular hole closure with the inverted ILM flap technique, one cannot be sure whether this process is due to glial proliferation or movement of the retinal cells [37]. Histopathological studies of the eyes operated on with vitrectomy but without ILM peeling show that glial proliferation (Muller cells) may be responsible for the healing process [31, 32]. A regeneration process of the photoreceptor cells, initiated by Muller glial proliferation, was recently described in zebrafish, and the same mechanism may take place in the above described situation. (Figs. 13.9, 13.10) [38].
Summary for the Clinician
■Vitrectomy with ILM peeling and gas injection is the method of choice in the treatment of macular holes.
■Spectral OCT demonstrates the mechanism of macular hole closure.
13.10 Lamellar Macular Hole and Macular
Pseudohole
The 1970’s, Gass described pseudomacular hole formation, as being caused by spontaneous contraction of an epiretinal membrane surronding but not covering the foveal area, and which may produce a biomicroscopic appearance simulating a full-thickness macular hole [39, 40]. Usually,
13.10 Lamellar Macular Hole and Macular Pseudohole |
151 |
Fig. 13.9 The images show an extremely large macular hole with a minimum diameter of 1,268 × 1,958 µm, which was operated on using the inverted internal limiting membrane (ILM) flap technique and air injection [37]. (a) Fundus view. (b) Fluorescein
angiography (Topcon Company, Tokyo, Japan). (c) Spectral domain OCT (Copernicus; Optopol, Zawiercie, Poland) demonstrates preoperative view of a macular hole. RPE retinal pigment epithelium, ERM epiretinal membrane
a |
b |
c
Fig. 13.10 (a) Spectral OCT picture demonstrates closure of the macular hole presented in Fig. 13.9 with the inverted ILM flap only. (b) However, the next picture, 1 month later, demonstrates that the
these patients have no or very few complaints and visual acuity is normal or almost normal.
Haouchine et al. confirmed this observation with OCT [41]. Differential diagnosis of macular pseudoholes
ILM flap serves as a scaffold for tissue migration or proliferation along the ILM to close the macular hole. (c) Further closure is visible after 3 months (Copernicus HR; Optopol, Zawiercie, Poland) [37]
(Fig. 13.11a) from lamellar macular holes (Fig. 13.11b) may be difficult, but it is possible on the basis of OCT, which shows the lack of dehiscence of the inner foveal retina from the outer foveal retina in the pseudoholes.
