CYSTOID MACULAR EDEMA AND CYSTOID MACULAR DEGENERATION AS A RESULT OF MULTIPLE PATHOGENIC FACTORS IN THE SETTING OF CENTRAL SEROUS CHORIORETINOPATHY. Issue Volume 11:Issues 1(2017:Winter) (2017)

• Record Type: Journal Article
• Authors: Astroz, Polina; Balaratnasingam, Chandrakumar; Yannuzzi, Lawrence A.
• Is Part Of: Retinal cases & brief reports. Volume 11:Issues 1(2017:Winter)
• Publication Date: 2017
• Subjects: anti–vascular endothelial growth factor -- central serous chorioretinopathy -- cystoid macular degeneration -- cystoid macular edema -- microaneurysm -- multimodal imaging; Retina -- Diseases -- Periodicals; Retina -- Periodicals; Retinal Diseases -- Periodicals; Retina -- Case Reports; Retinal Diseases -- Case Reports; 617.7
• DOI: 10.1097/ICB.0000000000000443
• Languages: English
• ISSNs: 1935-1089

Abstract

Abstract : Purpose: To report the pathogenic factors that account for cystoid macular edema and cystoid macular degeneration in chronic central serous chorioretinopathy (CSC). Methods: The clinical course and multimodal imaging findings, including fundus color photography, fundus autofluorescence, spectral-domain optical coherence tomography, and fluorescein angiography, of one eye with cystoid macular edema due to chronic CSC was documented. Results: A 44-year old woman with a history of chronic CSC presented with progressive visual decline in the right eye. Best-corrected visual acuity was 20/40. Funduscopic examination revealed diffuse retinal pigment epithelial changes and macular edema. Fluorescein angiography demonstrated perifoveal microaneurysms and leakage in a petaloid configuration. Spectral-domain optical coherence tomography demonstrated cysts at the level of the inner nuclear layer, an epiretinal membrane, vitreomacular traction, and an attenuated retinal pigment epithelial band. Central subfield thickness was 486 μ m. Three intravitreal injections of aflibercept were administered over 16 weeks following which there was resolution of leakage, release of vitreomacular traction, and resolution of microaneurysms. Central subfield thickness reduced to 379 μ m, but persistent intraretinal cysts were observed. There was subjective improvement in visual symptoms, but Snellen acuity remained at 20/40. Conclusion: Intraretinal cystic changes in chronic CSC may be the result of multifactorial pathogenic factors and may represent the coexistence of cystoid macular edema and cystoid macular degeneration. Anti–vascular endothelial growth factor may play an important role in the treatment of cystoid macular edema caused by CSC. Abstract : This case report defines anatomical changes associated with cystoid macular edema caused by central serous chorioretinopathy. It provides evidence that intraretinal cysts can be the result of the coexistence of cystoid macular edema and cystoid macular degeneration and that the cystoid macular edema component can be resolved with anti–vascular endothelial growth factor therapy.