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Abstract
Macular edema is an accumulation of fluid in the outer plexiform (Henle’s) and inner nuclear layers of the retina centered about the foveola. It is a common macular disorder that has many diverse etiologies (Kanski, 1997).
The first clinical description of macular edema was published by Jaeger in (1956). In (1872) Nettleship proved the retinal vascular origin of diabetic macular edema. The discovery of macular edema in retinitis pigmentosa (RP) in 1896 was followed by the publication of radiation induced macular edema few years later.
Vogt in Zurich described macular edema in iridocyclitis and central retinal vein occlusion (CRVO). Then Irvine and Hurby in (1953) investigated macular edema after intracapsular cataract extraction (ICCE), and in (1966) Gass demonstrated finally the cystoid spaces using fluorescein angiography.
It is known that extracellular fluid accumulation resulting in edema is well tolerated in most tissues of the body, but in the retina it results in dysfunction of the retinal neurons. When the fovea is involved it results in decrease visual acuity.
Macular edema is considered as one of the most prevalent causes of vision loss in the developed countries, although in short-term it is usually innocuous, long standing cases usually lead to coalescence of the fluid-filled microcystic spaces and subsequent formation of lamellar holes at the fovea with irreversible damage to the central vision (Kent et al., 1984).