The pathogenesis and clinical presentation of macular edema in inflammatory diseases

Cystoid macular edema (CME) is a classical complication of ocular inflammat ion. This syndrome was already described by Irvine in 1953 but the pathogen esis of this condition remains unclear. Cystoid macular edema can result ei ther from a rupture of the inner or from the outer blood ocular barrier. Cl inical CME that is responsitble for a low visual acuity must be differentia ted from angiographic CME that can be present even without any decrease in visual acuity. Fluid progressively accumulates into the outer plexiform lay er of the retina and pools into cystic spaces. Fluid accumulation can now b e better seen with optical coherence tomography (OCT). In chronic CME fluid accumulation is associated with thinning of the retina and fibrosis. At th is stage irreversible lesions are present and CME does not respond to medic al therapies. Inflammatory CME must be differentiated from CME resulting fr om irreversible vascular damage such as in diabetic CME or due to vein occl usions. Experimental research on cystoid macular edema has been hampered by the lack of animal model: most of laboratory animals have no macula, monke ys appear to be highly resistent to macular edema. Five major causes have b een suspected to be at the origin of CME: (1) photic retinopathy, (2) traum a of ocular tissue, (3) secondary irritation of the ciliary body, (4) vitre ous traction and (5) pharmaceutically induced CME. Clincial experience has shown that pseudophakic CME usually responds well to local therapy of stero ids and non-steroidal antiinflammatory drugs (NSAIDs) and/or in association with systemic acetazolamide. Acetazolamide is increasing fluid resorption through the retinal pigment epithelium. Postoperative CME rarely needs addi tional posterior subtenon's injections to resolve. But in CME occurring sec ondary to uveitis additional posterior sub-Tenon's steroid injections or sy stemic steroids may be necessary to decrease the constant release of inflam matory mediators.