The role of carbonic anhydrase inhibitors in the management of macular edema

Medical treatment of cystoid macular edema (CME) with carbonic anhydrase in hibitors has been known for over a decade. Initial observations were based on experimental data which suggested that acetazolamide can increase fluid absorption across the retinal pigment epithelium. Carbonic anhydrase inhibi tors (CAI) have also been shown to have other direct effects both on retina l and retinal pigment epithelial cell function by inducing an acidification of the subretinal space, a decrease of the standing potential as well as a n increase in retinal adhesiveness. It is thought that acidification of the subretinal space is finally responsible for the increase in fluid resorpti on from the retina through the RPE into the choroid. Several clinical studi es have suggested that patients with cystoid macular edema due to retinitis pigmentosa and uveitis may react more favorably to CAI treatment than othe r etiologies such as diabetic maculopathy or macular edema after retinal ve in occlusion. The present working hypothesis is that diffuse leakage from t he RPE responds more readily to CAI treatment than leakage from retinal ves sels. This may be due to the modulation of membrane- bound CA IV in the RPE which may have lost its polarised distribution in the presence of macular edema. A normal clinical starting dose of CAI is 500 mg/day which should be continued for at least one month to see an effect. This dose may be reduce d by the patients over the course of therapy. Metaphylaxis to the drug may occur with a rebound of the edema despite continuation of treatment.