By Shlomit Schaal, Henry J. Kaplan
Written for finished ophthalmologists and vitreoretinal surgeons, this ebook discusses cutting-edge scientific and surgical administration of cystoid macular edema (CME) and explains the present knowing of the pathophysiology of the situation and techniques of analysis. The administration process is obviously exact for every capability presentation, together with CME taking place in organization with uveitis, diabetes mellitus, vitreoretinal interface adjustments, retinal vascular occlusions, and lens-induced pathology. The information takes complete account of the ongoing growth in clinical therapies end result of the improvement of recent medications and the elevated availability of minimally invasive surgeries. also, considering the fact that healing ways to CME depend upon a transparent figuring out of pathophysiologic mechanisms and the structural alterations within the vitreous and neurosensory retina published via imaging reports, those points are rigorously regarded as well.
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Extra resources for Cystoid Macular Edema: Medical and Surgical Management
CME seen by OCT in patients with juvenile idiopathic arthritis (JIA)-associated uveitis has been reported in 84 % of eyes , a figure higher than that observed in previous ophthalmoscopy-based reports [127, 128]. JIA-associated uveitic OCT changes include perifoveal thickening, CME, foveal detachment, and atrophic changes. Duration of JIA-uveitis correlated with the development of CME . Central subfield thickness is an important endpoint for various clinical trials and is an important parameter in the clinical management of uveitic CME.
3 Diagnosis of Cystoid Macular Edema: Imaging 45 Role of Fundus Autofluorescence Imaging in CME Fundus autofluorescence (FAF) is determined by the lipofuscin distribution in the RPE and is also influenced by macular pigments in the INL, ONL, and OPL [150, 151]. RPE autofluorescence depends on outer segment renewal and can be affected by the RPE’s ability to clear lipofuscin. Lipofuscin accumulation leads to reduced RPE phagocytic capacity which in turn can lead to RPE cell death and photoreceptor loss.
Jaffe Fig. 9 Lack of visual acuity improvement in an eye (stable at 20/60) with CME associated with non-ischemic CRVO (top) despite near-complete resolution of CME following treatment with anti-vascular growth factor injections attributed to ellipsoid layer disruption at the central fovea (bottom) Fig. 10 Hyperreflective foci in an eye with BRVO and CME (top) with increased subretinal lipid exudates 8 weeks later (bottom). It has been suggested that these foci could be small intraretinal protein and/or lipid deposits and precursors of hard exudates Various anatomical characteristics have been evaluated as potential prognostic indicators in RVO-associated CME.