Macular edema is a common cause of significant visual loss in a wide variety of ocular conditions. It is a nonspecific pathological response to the disruption of the normal permeability barrier protecting the retina. This permeability barrier, called the blood-retinal barrier,(1) restricts the free movement of plasma constituents into the retina and, in combination with active and passive transport systems, plays an important role in maintaining homeostasis within the neurosensory retina. The blood-retinal barrier is maintained at two anatomical locations: the tight junctions between the endothelial cells of the retinal blood vessels (inner blood-retinal barrier) and the tight junctions between adjacent retinal pigment epithelial (RPE) cells (outer blood-retinal barrier). The extracellular space of the retina normally constitutes a small proportion of its total volume. This relationship is maintained by the blood-retinal barrier and the active transport of electrolytes and larger molecules from the retina across the RPE to the choroidal space. Disruption of the inner or outer blood-retinal barrier allows unrestricted entry of plasma constituents, including plasma proteins and water, resulting in a significant expansion of the extracellular space of the retina. This expansion results in an accumulation of fluid in the macular area, with an accompanying increase in the normal thickness of the parafoveal retina. Increased fluid accumulation in cystic spaces, localized to the outer plexiform and inner nuclear layers of the parafoveal retina, results in cystoid macular edema (CME). The predisposition of the macula to develop cystoid edema is incompletely understood. In certain situations, including pseudophakic cystoid macular edema, CME is associated with localized leakage of the parafoveal capillaries. In other situations, such as diabetic macular edema, the vascular leakage may be more widespread, resulting in diffuse thickening of the posterior pole, with or without cystoid changes in the macula.
