[Therapy of cystoid diffuse macular edema after uveitis and cataract surgery with the carbonic anhydrase inhibitor acetazolamide (Diamox)].

BACKGROUND

Observations made by Cox, Bird et al. (1988), who first used acetazolamide (Diamox) for treatment of macular edema of various origin in a higher number of patients, let assume a positive effect of this therapy on fluid accumulation specifically inside the inner retinal layers. Based on these studies 15 patients (20 eyes) with cystoid or cystoid-diffuse macular edema were treated with acetazolamide in a pilot-study.

MATERIALS AND METHODS

Eleven patients (fifteen eyes) had postuveitic macular edema, four other patients (five eyes) had cystoid edema following cataract surgery. Patients with additional diseases causing macular edema of retinal vascular origin were excluded. The initial dose was 500 mg daily. In one patient responding to therapy the dose was gradually reduced after three weeks down to a minimum of 125 mg every second day. For evaluation of the therapeutical results fluorescein angiography and visual acuity were taken into account.

RESULTS

Eleven patients (fourteen out of twenty eyes) showed a distinct therapeutical effect with decrease of macular edema in repeatedly controlled fluorescein angiography. All these patients had a subjective improvement of vision which correlated with an increase of visual acuity in exactly one half of all patients. Therapy was stopped, when the macular edema had still appeared unchanged in angiography after three weeks or when--in spite of fluid reduction in angiography--no improvement of visual acuity could be obtained in the next two months. The maintenance dose showed large individual variation with a minimum of 125 mg every second day and a maximum of 250 mg per day. Attempts to stop therapy resulted in a early reappearance of the edema of original extension with corresponding deterioration of visual acuity and sensitivity of central visual field. In a few patients even the reduction of the dose below the individual maintenance dose could be demonstrated angiographically. All patients were under continuous internal medical control, permanent side-effects of acetazolamide with the doses used in this study were not seen.

CONCLUSIONS

The results show that acetazolamide is a basically effective agent against cystoid macular edema and that a therapeutical trial is justified based on the treatment criteria of this study. The factors limiting the therapeutical effect of acetazolamide cannot yet be evaluated on the basis of the small amount of patients in this pilot-study. Considering the patient data a time factor depending on the period between onset of edema-related symptoms and begin of treatment is likely. In the group of unsuccessfully treated cases we had the patients with the longest period of preexisting edema (more than one year) of the study.