Macular Edema of Choroidal Origin

Abstract

Macular edema is most often clinically defined as an accumulation of serous fluid within the neurosensory retina with increased thickness of the central retina. In exudative age-related macular degeneration the leakage of fluid from the choroidal new vessels may be the origin of macular edema. Their abnormal permeability and the inflammatory reaction are mechanisms involved in this accumulation of fluid, which occurs in all layers. Cystoid macular edema is more often associated with subepithelial occult choroidal neovascularization (CNV) than it is with pre-epithelial classic CNV. The simultaneous presence of choroidal new vessels and ME implies a number of cellular dysfunctions especially of Müller cells and subsequently metabolic alterations. The leakage from the choroidal new vessels, predominantly vascular endothelial growth factor (VEGF)-induced, may produce a large accumulation of fluid under the neurosensory retina. It is also likely that the key signaling steps occur prior to the upregulation of VEGF either initiated by, or facilitated by, cytokines, which act under normal basic conditions to counterbalance the integral VEGF effects and, in pathologic circumstances, may either counteract or serve to amplify the process.

Association between Inflammatory Factors in the Aqueous Humor and Hyperreflective Foci in Patients with Intractable Macular Edema Treated with Antivascular Endothelial Growth Factor

“…ME is clinically defined as an accumulation of serous fluid within the neurosensory retina, with increased thickness of the central retina. Some researches have shown that the leakage from the choroidal new vessels, predominantly VEGF-induced, may produce a large accumulation of fluid under the neurosensory retina [ 15 ]. Anti-VEGF has now become the cutting-edge treatment choice for ME, due to its excellent visual and anatomic improvement [ 16 ].…”

Mechanisms of macular edema

“…Although the choroid sits outside the site of the outer BRB, together with Bruch’s membrane, it may still influence fluid homeostasis across the barrier. For instance, the hydraulic conductivity of Bruch’s membrane decreases with age ( 80 ), which is a possible factor in the accumulation of subretinal fluid in exudative age-related macular degeneration ( 81 ). Changes to the choroid are also likely to affect processes of retinal fluid absorption across the RPE cells.…”