Pathophysiology of macular edema.
Macular edema is defined as an accumulation of fluid in the outer plexiform layer and the inner nuclear layer as well as a swelling of Müller cells of the retina. It consists of a localized expansion of the retinal extracellular space (sometimes associated with the intracellular space) in the macular area. Macular edema is a common cause of a sudden or chronic decrease in visual acuity occurring in many ocular diseases such as age-related macular degeneration, diabetic retinopathy and retinal vein occlusion. As a nonspecific sign of many intraocular and systemic diseases, macular edema represents a common final pathway. The existence of the blood-retinal barrier (BRB) formed by intercellular junctions is the precondition required to maintain this physiological status. This status may become severely disturbed by many diseases, finally resulting in macular edema. In this article, the development of macular edema will also be classified by its pathophysiological and pathobiochemical pathways. Vascular components, the dysfunctional BRB, the role of proteins and water fluxes as well as the role of several inflammatory mediators (e.g. angiotensin II, vascular endothelial growth factor, prostaglandins) in the retina will be discussed as responsible mechanisms leading to the development of macular edema.
Scholl
Stefan
S
Scholl & Augustin Augenärztliche Privatpraxis, Baden-Baden, Germany.
Kirchhof
Janna
J
Augustin
Albert J
AJ
D000804:Angiotensin II / Q000378:metabolism; D001813:Blood-Retinal Barrier / Q000502:physiology*; D006801:Humans; D008269:Macular Edema / Q000378:metabolism / Q000503:physiopathology*; D011453:Prostaglandins / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D011453:Prostaglandins; D042461:Vascular Endothelial Growth Factor A; D000804:Angiotensin II