- •Contents
- •Preface
- •Abstract
- •Morphological Lesions
- •Visual Impairment in Diabetic Retinopathy
- •Conclusions
- •References
- •Abstract
- •Physiology of the Retinal Vascular Network
- •Physiology of the Blood-Retinal Barrier
- •Macular Edema
- •Assays for Studying the Permeability of the Blood-Retinal Barrier
- •Conclusions
- •References
- •In vivo Models of Diabetic Retinopathy
- •Abstract
- •Animal Models of Diabetic Retinopathy
- •Neovascularization
- •Conclusions
- •References
- •Pericyte Loss in the Diabetic Retina
- •Abstract
- •Pericyte
- •Retinal Pericyte Function
- •Pericyte Loss in Diabetic Retinopathy
- •Mechanisms of Pericyte Loss
- •Conclusions
- •References
- •Neuroglia in the Diabetic Retina
- •Abstract
- •Microglial Cells
- •Astrocytes
- •Müller Cells
- •Conclusions
- •Acknowledgements
- •References
- •Regulatory and Pathogenic Roles of Müller Glial Cells in Retinal Neovascular Processes and Their Potential for Retinal Regeneration
- •Abstract
- •Control of Extracellular Matrix Deposition by Müller Cells
- •Neuroprotective Role of Müller Glia
- •Müller Glial Cells as a Source of Retinal Neurons in the Adult Eye
- •Potential Barriers for Stem Cell Transplantation to Regenerate Retinal Neurons in the Diabetic Retina
- •Potential of Müller Stem Cells for the Development of Human Therapies to Restore Retinal Function Damaged by Disease
- •References
- •Growth Factors in the Diabetic Eye
- •Abstract
- •Vascular Endothelial Growth Factor
- •Insulin-Like Growth Factor 1
- •Platelet-Derived Growth Factor
- •Fibroblast Growth Factor
- •Hepatocyte Growth Factor
- •Angiopoietins
- •Connective Tissue Factor
- •Stromal Cell-Derived Factor 1
- •References
- •Balance between Pigment Epithelium-Derived Factor and Vascular Endothelial Growth Factor in Diabetic Retinopathy
- •Abstract
- •VEGF and PEDF in the Eye
- •PEDF/VEGF in the Diabetic Retinopathy
- •Anti-VEGF Therapy for Diabetic Retinopathy
- •References
- •The Renin-Angiotensin System in the Eye
- •Abstract
- •History of the Renin-Angiotensin System
- •The Circulating Renin-Angiotensin System
- •Tissue Renin-Angiotensin Systems
- •The Renin-Angiotensin System in the Eye
- •Conclusions
- •References
- •Interactions of Leukocytes with the Endothelium
- •Abstract
- •Multistep Process of Leukocyte Recruitment
- •Leukocyte Transendothelial Migration
- •References
- •Stem and Progenitor Cells in the Retina
- •Abstract
- •Niches
- •Characteristics of a Stem Cell
- •Types of Stem and Precursor Cells
- •Methods for Studying Stem/Progenitor Cell Behavior
- •CD34+ and CD14+ Cells in Diabetes
- •Conclusion
- •References
- •Role of Pericytes in Vascular Biology
- •Abstract
- •Pericytes Are Cells with a Unique Position in the Microvascular Wall
- •Identification of Pericytes
- •Functions of Pericytes
- •Acknowledgements
- •References
- •Current Approaches to Retinopathy as a Predictor of Cardiovascular Risk
- •Abstract
- •Diabetic Retinopathy and Mortality
- •Diabetic Retinopathy and Heart Disease
- •Retinal Venules and Cardiovascular Disease
- •Pathogenic Links between Retinopathy and Cardiovascular Disease
- •Genetic Links between Retinopathy and Cardiovascular Disease
- •Implications
- •Conclusion
- •References
- •From Bedside to Bench and Back: Open Problems in Clinical and Basic Research
- •Abstract
- •References
- •Author Index
- •Subject Index
fact that red dots is the initial funduscopically visible lesion implies that the presence of white lesions occuring alone are not hard exudates. This may be an important diagnostic parameter especially in older type 2 diabetic patients where white lesions may represent drusen secondary to age-related maculopathy. Small sharply delimited whitish drusen that are difficult to differentiate from exudates may also occur in younger persons. However, these lesions can be identified by repeating the examination after more than 1 month where drusen will be unchanged, whereas the dynamic nature of exudates implies that this lesion will always have a changed size, location or configuration.
The fact that exudates often arrange in rings around a leakage point with a microaneurysm and/or a haemorrhage in the centre demonstrates an interdependence between these two lesion types with the red dot being the immediate response and the hard exudate the more sustained response to a localised vascular abnormality. The radius of the exudate ring will represent the diffusion distance from the leakage point to the point of plasma protein precipitation.
The presence of haemorrhages and retinal oedema without exudates may be observed in diabetic maculopathy of the ischaemic type. Ischaemic maculopathy may be difficult to diagnose without fluorescein angiography to show the typical capillary occlusion.
Visual Impairment in Diabetic Retinopathy
The general purpose of the management of diabetic retinopathy is to prevent impairment of central vision secondary to the two complications diabetic maculopathy and proliferative diabetic retinopathy. However, several other types of visual impairment may occur in diabetic patients. Generalised changes such as subclinical perturbations in the electroretinogram [2] may not be appreciated by the patient, whereas
changes in contrast sensitivity, dark adaptation and the peripheral visual field induced by retinal photocoagulation may be serious adverse effects that limit normal activities [61, 62]. However, the individual retinopathy lesions may also affect visual function, the severity of symptoms depending on the size and the location of the retinal area involved. Table 2 gives an overview of these different types of visual impairment in diabetic retinopathy [23, 63].
It appears that individual retinal lesions can affect visual function through a variety of mechanisms and may contribute to the visual dysfunction experienced by diabetic patients. The fact that the morphological lesions correlate with functional pathology in diabetic patients is important for understanding how the disease leads to visual loss.
Conclusions
The diagnosis and management of diabetic retinopathy depends on both the correct detection of morphological lesions related to impaired retinal vascular supply, and the correct interpretation of the dynamics, the relative occurrence, and the spatial distribution of these lesions in the ocular fundus. The pathological correlates of these changes include anatomical changes that can be studied by clinical inspection and by histopathological techniques, and functional changes that can be studied by electrophysiological or psychophysical examination techniques. Therefore, these approaches are necessary in order to distinguish the disease patterns that are unique for diabetic retinopathy from those seen in retinal vascular diseases in general. This is crucial for gaining a deeper insight into the pathophysiology of diabetic retinopathy and for improving screening, diagnosis and treatment of diabetic retinopathy in the future.
16 |
Bek |
Table 2. Overview of different types of visual impairment in diabetic retinopathy
Lesion type |
Visual impairment |
Clinical course |
|
|
|
Microaneurysms |
none |
|
|
|
|
Haemorrhages |
blocking of retinal photoreceptors, foveally and |
partly reversible |
|
extrafoveally |
|
|
|
|
Exudates |
blocking of retinal photoreceptors, foveally and |
partly reversible |
|
extrafoveally |
|
|
|
|
Barrier leakage |
none |
|
|
|
|
Retinal oedema |
gradual reduction of visual function |
almost always irreversible |
|
|
|
Cotton wool spots |
local relative scotoma that regresses partly; longer |
Partly reversible |
|
lasting lesions may result in arcuate scotoma |
|
|
|
|
Arterial changes |
none |
|
|
|
|
Venous changes |
none |
|
|
|
|
Retinal ischaemia |
localised defects in visual field |
irreversible |
|
|
|
Neovascularisations |
blocking of retinal photoreceptors |
reversible |
|
|
|
Vitreous haemorrhage |
blocking of retinal photoreceptors |
reversible |
|
|
|
Tractional retinal detachment |
retinal damage |
almost always irreversible |
|
|
|
Photocoagulation |
retinal damage |
irreversible |
|
|
|
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Prof. Toke Bek
Department of Ophthalmology
Århus University Hospital, Norrebrogade 44 DK–8000 Århus C (Denmark)
Tel. +45 8949 3223, Fax +45 8612 1653, E-Mail toke.bek@mail.tele.dk
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