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Purpose: To compare the clinical outcome of intravitreal dexamethasone implant versus oral acetazolamide in patients with cystoid macular edema (CME) secondary to retinitis pigmentosa (RP). Design: Multicenter, prospective, propensity-score-matched, comparative study. Methods: Eyes with RP and CME were treated either with intravitreal dexamethasone implant or with oral acetazolamide (500 mg/day). Patients were evaluated monthly and followed up for 12 months. Primary outcome measures were changes in central retinal thickness and best corrected visual acuity (BCVA). Adverse events were recorded. Results: Propensity score matching resulted in 2 groups of 30 eyes each. All patients completed 12 months of follow-up. Mean central retinal thickness decreased from 535 μm at baseline to 208 μm at month 12 in the dexamethasone implant group and from 519 to 339 μm in the oral acetazolamide group ( P  < 0.001, Student's t -test). Mean BCVA average change from baseline during the study (area-under-the-curve approach) was -0.084 logarithm of the minimum angle of resolution (logMAR) (+4.2 letters) in the dexamethasone implant group and -0.032 (+1.6 letters) in the oral acetazolamide group ( P  < 0.05, Mann-Whitney U test). Patients in the dexamethasone implant group required on average 1.7 treatments during 1 year of therapy. Conclusions: In this study, intravitreal dexamethasone implant produced better anatomic and functional improvements over oral acetazolamide in patients affected by CME secondary to RP. Larger, randomized clinical trials with longer follow-up are warranted to confirm these data.

Background : Intraretinal cystoid spaces (IRCS) are fluid-filled spaces seen in some retinal dystrophies and often treated with carbonic anhydrase inhibitors. The purpose of this study is to report an unexpected bilateral improvement in the IRCS after discontinuation of therapy. Material and Methods : We identified from our records 23 patients with retinal dystrophy and IRCS who had been treated with topical and/or oral carbonic anhydrase inhibitors. All subjects had regular follow-up with OCT and previous genetic testing. Results : We identified four (17%) patients who experienced a bilateral and symmetrical paradoxical improvement in IRCS size and visual acuity after discontinuation of carbonic anhydrase inhibitors. Two were mutations in RS1 , one in CLN3 and another in NR2E3 . All patients were followed for at least three years (range 39-63 months). None had systemic abnormalities. Conclusions : Patients with IRCS may exhibit a paradoxical response after discontinuation of carbonic anhydrase inhibitors. Although the pathophysiology of these phenomena is unclear, stopping treatment may be an option in patients who cease to improve or get worse on treatment.

Purpose: To determine the treatment effect of oral acetazolamide on refractory inflammatory macular edema., Methods: A retrospective review of identified patients with uveitic or pseudophakic macular edema treated using acetazolamide between 2007 and 2014. Visual acuity and central macular subfield thickness was determined at baseline and at first follow-up. Baseline optical coherence tomography features were analyzed as predictors of acetazolamide response., Results: Sixteen patients (19 eyes) of 61 screened met all criteria. Mean age was 57.9 years (19.7-81.1). The most common diagnosis was idiopathic uveitis (n = 6, 31.6%). Mean uveitis duration was 4.4 years (0.2-27.5). Average central macular subfield thickness decreased significantly (from 471.8 ± 110.6 μm to 358.3 ± 50.4 μm) (P < 0.0001). Average visual acuity (logarithm of the minimum angle of resolution) improved significantly from 20/54 (0.43 ± 0.25) to 20/37 (0.27 ± 0.16) (P = 0.003). Pretreatment optical coherence tomographies demonstrated intraretinal fluid (n = 19, 100%), subretinal fluid (n = 8, 42.1%), epiretinal membrane (n = 13, 68.3%), and vitreomacular traction (n = 1, 5.2%). No optical coherence tomography characteristic was predictive of a response to therapy., Conclusion: There is a significant benefit to vision and central macular subfield thickness after acetazolamide treatment in patients with inflammatory macular edema. In patients with refractory inflammatory macular edema, treatment using acetazolamide can provide anatomical and visual benefit without corticosteroid-related adverse effects.

Background: Pseudophakic cystoid macular edema (PCME) is a common complication of cataract surgery. We report the management of a case presenting with PCME in his left eye complicated by a full-thickness macular hole (MH). Four weeks after a cataract surgery on his left eye, a 75-year-old man presented with a vision loss on the same eye (best-corrected visual acuity: 20/64). A PCME complicated by a full-thickness MH was diagnosed. After oral acetazolamide treatment, the PCME completely regressed and the full-thickness MH closed after medical treatment., Conclusion: Macular edema may rarely lead to MHs, by inducing mechanical changes and probable inflammatory mechanisms as well as a thinning of the fovea. We report a case of spontaneous closure of MH complicating a PCME, with medical treatment.

Monozygotic twins with glutathione synthetase deficiency, progressive retinal dystrophy and cystoid macular edema were followed for foveal changes on optical coherence tomography under different treatment modalities. The purpose of the study is to show the effect of topical dorzolamide in conjunction with systemic acetazolamide in terms of decreasing macular edema in this specific disease. The results showed that systemic acetazolamide alone or in combination with topical dorzolamide decreased CME in both patients for a certain period of time. The result can be temporary sustained after treatment discontinuation. In conclusion, topical dorzolamide, in conjunction with systemic acetazolamide, could reduce cystoid macular edema in GSSD., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Objective: We present an interesting case of accidental overdose of latanoprost eye drops., Case Report: A 71-year-old patient underwent an uncomplicated cataract surgery in his right eye. During the first postsurgical week he mistakenly used latanoprost eye drops six times daily instead of the prescribed tobramycin/dexamethasone eye drops. The patient experienced gradually decreasing visual acuity and was diagnosed with cystoid macular edema seven weeks after surgery. The cystoid macular edema resolved 4 weeks later after treatment with nepafenac 0.3% eye drops and oral acetazolamide. The cystoid macular edema recurred 2 weeks after rechallenge with latanoprost. The rechallenge-induced cystoid macular edema once again resolved after cessation of latanoprost and retreatment with nepafenac eye drops. A Naranjo assessment score of 7 was obtained, indicating a probable relationship between the patient's symptoms and the suspect drug., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Background: Carbonic anhydrase inhibitors (CAI) are often used in the treatment of cystoid macular edema (CME) in retinitis pigmentosa (RP) patients. The aim of this meta-analysis is to gain a better understanding of the overall efficacy of CAI treatment., Methods: Databases including PubMed, EMBASE, and Cochrane Library were searched to identify relevant studies. Eligible studies were clinical trials of patients with RP assigned topical or oral CAIs such as dorzolamide and acetazolamide. Changes in central macular thickness (CMT) by OCT in μm and best-corrected visual acuity (BCVA) in log MAR equivalents were extracted and results compared between baseline and after treatment., Results: 11 clinical reports were identified which included a total of 194 patients (358 eyes) available for analysis, with 59 patients (115 eyes) assigned oral CAI treatment and 135 patients (243 eyes) assigned topical CAI treatment. The combined results showed a significant reduction of macular edema, as calculated by baseline and final central macular thickness (CMT) based on OCT examination (46.02μm, 95%CI: -60.96, -31.08, I2 = 65%). However, the effect on visual acuity was inconsistent across studies., Conclusion: Based on non randomized controlled clinical studies, RP patients with CME who were treated with CAIs had better anatomical outcomes, but the effect on visual acuity was contradictory across studies. Multicenter prospective randomized controlled trials would be ideal to definitively test its clinical efficacy in RP patients.

Purpose: To evaluate changes in cystic-appearing macular lesions and visual acuity in patients with X-linked retinoschisis while being treated with a carbonic anhydrase inhibitor., Methods: A retrospective analysis of 68 eyes from 36 patients between the ages of 5 years and 61 years with X-linked retinoschisis were monitored while on a carbonic anhydrase inhibitor. Macular cystic-appearing lesions were monitored with optical coherence tomography. Snellen visual acuity measurements were converted to logarithm of the minimum angle of resolution equivalent Early Treatment Diabetic Retinopathy Study letters for analysis. Analyses for changes in both visual acuity and macular cysts included comparisons between treatment and pretreatment segments., Results: Forty-five eyes (66%) had a reduction of their cysts while on a carbonic anhydrase inhibitor. Twenty eyes (29%) showed no cystic change, whereas 3 eyes (4%) demonstrated worsening of their cysts with treatment when compared with pretreatment. There was a statistically significant improvement in logarithm of the minimum angle of resolution visual acuity while on treatment relative to pretreatment (P < 0.0001). The estimated average Early Treatment Diabetic Retinopathy Study equivalent improvement was 0.09 (slightly less than one line on the Early Treatment Diabetic Retinopathy Study chart) with a 95% confidence interval of 0.08 to 0.11., Conclusion: Considering the entire 36 patients in this cohort, while statistically significant, the average improvement in visual acuity was modest. Nonetheless, in individual patients, the improvement was more substantial. Improvement in the extent of cystic macular lesions was observed in a high percentage of cases.

Background: Hydroxychloroquine (HCQ) retinopathy can accompany other retinal complications such as cystoid macular edema (CME), which leads to central visual loss. We report a case of CME with HCQ retinopathy that improved with the use of oral acetazolamide, and discussed the possible mechanisms of CME in HCQ retinopathy using multimodal imaging modalities., Case Presentation: A 62-year-old patient with systemic lupus erythematosus (SLE) and HCQ retinopathy developed bilateral CME with visual decline. Fluorescein angiography (FA) showed fluorescein leakage in the macular and midperipheral area. After treatment with oral acetazolamide (250 mg/day) for one month, CME was completely resolved, best corrected visual acuity (BCVA) improved from 20/50 to 20/25, and FA examination showed decreased dye leakage in the macular and midperipheral areas., Conclusions: In cases of vision loss in HCQ retinopathy, it is important to consider not only progression of maculopathy, but also development of CME, which can be effectively treated with oral acetazolamide.

Purpose: Little is known regarding the therapeutic effect of carbonic anhydrase inhibitors (CAIs) in the management of cystic macular lesions in children with X-linked juvenile retinoschisis (XLRS) despite the fact that this disease often manifests during childhood. Therefore, our goal was to determine the efficacy of CAIs in the treatment of cystic macular lesions in children with XLRS., Methods: We used CAIs to treat cystic macular lesions in 18 eyes of nine children with XLRS. We evaluated the therapeutic effect of CAI treatment with the best-corrected visual acuity and foveal zone thickness (FZT) with spectral-domain optical coherence tomography. A reduction of at least 22.4% in FZT was defined as objective evidence of response., Results: Five of nine (55.6%) XLRS patients showed a significant reduction of FZT in both eyes over a median treatment interval of 6.8 months (range, 1-23). In four of five (80.0%) patients, this reduction was already apparent after 1 month of treatment. An improvement of visual acuity was observed in five eyes (27.8%) of three patients (33.3%). Six patients (66.6%) reported minor side effects., Conclusions: Treatment with CAIs decreased FZT in more than half of the children with XLRS. This effect was observed within 1 month in the majority of patients. Carbonic anhydrase inhibitor treatment restores retinal anatomy and may contribute to creating optimal circumstances for gene therapy.

Unlabelled: Fingolimod is a potent drug in relapsing forms of multiple sclerosis. Visual impairment due to fingolimod-associated macular edema (FAME) usually leads to discontinuation of fingolimod therapy., Methods: We report on a 24-year old woman with bilateral FAME., Results: We continued fingolimod and added oral acetazolamide, which led to recovery of visual acuity and regression of macular edema. However, fingolimod had to be discontinued when fluorescein angiography revealed an enlarged foveal avascular zone., Discussion and Conclusion: Oral acetazolamide might be a treatment option for FAME, while ischemic conversion may be limiting. Ophthalmologic assessments are mandatory for follow-up when fingolimod therapy is continued after onset of FAME., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Bietti crystalline retinal dystrophy is a rare, inherited disorder whose hallmark is the presence of retinal crystal deposits associated with later chorioretinal degeneration. This condition may rarely be complicated by the development of cystoid macular oedema leading to rapid visual decline. Currently, treatment options for this complication of Bietti dystrophy are limited and the visual prognosis is poor. Here, we present a case of cystoid macular oedema associated with Bietti dystrophy that was successfully diagnosed using multimodal imaging techniques including optical coherence tomography and fluorescein angiography. These modalities confirmed the diagnosis of macular oedema and excluded other possible causes of oedema such as choroidal neovascularisation. In this patient, cystoid macular oedema was resolved with oral acetazolamide therapy, a treatment that has not been previously reported in this context. Acetazolamide treatment resulted in oedema resolution and improvement in visual function, and can be considered a therapeutic option for other patients with Bietti dystrophy who develop cystoid macular oedema.

The purpose of this paper was to describe a patient with pericentral retinitis pigmentosa (RP) and cystoid macular edema (CME) refractory to oral acetazolamide alone who was successfully treated with adjunctive pegaptanib sodium. A 33-year-old man presented with decreased vision and a best-corrected visual acuity (BCVA) in his left eye of 20/200 due to CME secondary to RP. Although he had been treated daily for 1 month with 500 mg of oral acetazolamide, the edema was unresponsive. When informed of the available treatment options, the patient requested adjunctive intravitreal pegaptanib sodium. One month after receiving an injection of pegaptanib sodium 0.3 mg and continued daily acetazolamide, the patient's BCVA had improved to 20/40. At the 4-month follow-up visit, no recurrence of CME was found on fundus biomicroscopy, fundus-related perimetry, and optical coherence tomography. We conclude that intravitreal pegaptanib sodium combined with daily doses of acetazolamide appears to provide benefits in CME refractory to oral acetazolamide alone with regards to the improvement of visual acuity.

Purpose: Although uncommon after phacoemulsification surgery, cystoid macular edema (CME) is an important cause of postoperative reduction of vision after cataract surgery. To demonstrate an optical coherence tomography (OCT) measurable, dose-related response to orally administered acetazolamide in a patient presenting with pseudophakic CME., Methods: A 76-year-old woman with reduced vision in right eye due to cataract had uneventful phacoemulsification. Surgery was complicated by early onset endophthalmitis that was treated with intravitreal antibiotics with good visual recovery. At 6 months follow-up, she presented with further reduction of vision (0.5 LogMAR) due to CME and a central foveal thickness (CFT) of 587 microm., Results: Acetazolamide treatment was started in combination with topical ketorolac. At a daily dose of 500 mg, CFT and visual acuity were 262 microm and 0.34 LogMAR, respectively. Dose reduction of acetazolamide to 250 mg/day was associated with worsening of the CFT to 335 microm. CFT was subsequently measured at 230 microm on increasing the acetazolamide dose to 500 mg/day and measured 353 microm when acetazolamide dose was halved. CFT was 478 microm when acetazolamide was ceased.CONCLUSIONS. In this report, the authors have shown a dose-related response of pseudophakic CME to oral acetazolamide. This would suggest that the clinical response to oral acetazolamide may be titrated to the extent of CME and monitored by OCT.

Docetaxel (Taxotere) is an anticancer agent used to treat a wide range of malignancies including breast, lung, and prostate cancer. In this report, we describe a patient with bilateral vision loss due to cystoid macular edema (CME) associated with docetaxel therapy. This report documents for the first time the optical coherence tomography (OCT) findings of CME despite the lack of leakage with flourescein angiography and its association with the Fluid Retention Syndrome (FRS). Successful management of CME with oral acetazolamide is also discussed.

Cystoid macular edema (CME) is the most frequent cause of visual deterioration in uveitis patients. Intraocular inflammation disturbs the blood-retina barrier and leads to retinal edema. The basis of successful treatment is the anti-inflammatory and immunosuppressive therapy of uveitis. Restoration of the blood-retina barrier is mediated by corticosteroids and nonsteroidal anti-inflammatory agents. Resorption of extracellular fluid is improved by systemic carboanhydrase inhibitors. Despite aggressive therapy loss of visual acuity is frequent. Therefore, early diagnosis of CME and initiation of treatment, even if visual acuity is not yet impeded, is mandatory.

Purpose: To assess the long-term effect of acetazolamide treatment on patients with cystoid macular edema (CME) in the course of intermediate or posterior chronic uveitis and to define those patients who may particularly benefit from the drug., Methods: Fifty-two eyes (45 patients) with chronic uveitic CME were treated with acetazolamide at an initial dosage of 500 mg/d. The effect of treatment was assessed by fluorescein angiography, ophthalmoscopy, visual acuity, and Amsler testing. Therapy was withdrawn when CME did not improve at 3 weeks. In cases with CME improvement, the dosage was gradually tapered., Results: The mean follow-up was 3.1 years (minimum, 1.5 years). Two subgroups were identified: group 1, quiescence of uveitis with acetazolamide as the single therapeutic agent (33 eyes); and group 2, chronically active uveitis requiring additional systemic antiinflammatory drugs (19 eyes). In both groups, visual acuity improvement was statistically significant (group 1, P = 0.012; group 2, P = 0.025). In 12 patients with a stable visual acuity gain, the medication dose could be tapered off completely without any recurrent edema shown by fluorescein angiography after a minimum follow-up of 1 year. Sixteen patients required a maintenance dosage, ranging from 125 to 500 mg daily. No major adverse effects of the medication were observed., Conclusions: During long-term follow-up, low-dose acetazolamide can be a useful therapeutic option for chronic CME in uveitis. The effect was better in patients with quiescence of uveitis than in those with chronically active uveitis. Permanent therapy is not imperative in every case.

Cystoid oedema of macula is the most frequent problem following non-complicated cataract surgery, which leads to weakening of visual acutity. We have studied the treatment outcomes of the topical therapy with corticosteroids and nonsteroid antirheumatics during prospective randomized study in comparison with orally applied acethazolamide. However, 8 weeks later in treatment was observed a positive effect in both groups, on the eyes of patients, treated with acetazolamide, resorption of the oedema was faster, more intensive and ultimate visual acutity was statistically significantly better. Results demonstrated a benefit of combined therapy with antiinflamative drugs and orally prescribed acetazolamide in pseudophakic macular oedema.

Medical treatment of cystoid macular edema (CME) with carbonic anhydrase inhibitors 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 inhibitors (CAI) have also been shown to have other direct effects both on retinal and retinal pigment epithelial cell function by inducing an acidification of the subretinal space, a decrease of the standing potential as well as an increase in retinal adhesiveness. It is thought that acidification of the subretinal space is finally responsible for the increase in fluid resorption from the retina through the RPE into the choroid. Several clinical studies have suggested that patients with cystoid macular edema due to retinitis pigmentosa and uveitis may react more favorably to CAI treatment than other etiologies such as diabetic maculopathy or macular edema after retinal vein occlusion. The present working hypothesis is that diffuse leakage from the RPE responds more readily to CAI treatment than leakage from retinal vessels. 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 reduced by the patients over the course of therapy. Metaphylaxis to the drug may occur with a rebound of the edema despite continuation of treatment.

Purpose: To compare the effectiveness of topical dorzolamide hydrochloride (Trusopt, Merck and Co., Inc., West Point, PA), a carbonic anhydrase inhibitor, with that of oral acetazolamide (Diamox; Lederle Laboratories, Pearl River, NY) for the management of chronic cystoid macular edema in patients with retinitis pigmentosa., Methods: A prospective, double-masked, crossover study was conducted in five patients with retinitis pigmentosa who had chronic cystoid macular edema. After baseline visual acuity was measured and a fluorescein angiogram was obtained, each patient was randomly assigned to receive either topical dorzolamide or a placebo for 4 weeks, followed by a crossover for the same period. Oral acetazolamide then was given separately to each patient for 2 weeks. Each phase of the study was followed by a washout period of 4 weeks, during which the patient was taken off all medications. At each visit, best corrected visual acuity was measured, a fluorescein angiogram was obtained, a subjective assessment of the effects on visual function, and any side effects of the medication or placebo were recorded in the form of a questionnaire by an independent observer., Results: Compared with baseline or placebo values, there was no measurable improvement in visual acuity on the Early Treatment Diabetic Retinopathy Study charts with dorzolamide in any of the patients. The visual acuity in three of five patients, however, improved by seven letters or more with acetazolamide. Compared again with baseline or placebo values, fluorescein angiograms of two of five patients showed improvement in macular edema in both eyes with the use of dorzolamide, whereas all five showed improvement with acetazolamide. The improvement in macular edema was more marked with acetazolamide than with dorzolamide. The effect of dorzolamide given three times a day was the same as that when it was given five times a day. One patient indicated that dorzolamide was more effective than acetazolamide in improving visual function, three of five patients believed that acetazolamide was more effective, and one felt that both were equally effective., Conclusion: Dorzolamide provided improvement in cases of macular edema on fluorescein angiograms and subjective improvement of visual function in some patients with retinitis pigmentosa with cystoid macular edema. However, there was no measurable improvement in visual acuity with the topical use of this drug. Oral acetazolamide was found to be more effective than dorzolamide in managing macular edema and improving visual acuity.

Background: Fluorescein angiography with a scanning laser ophthalmoscope allows the quantification of morphologic and dynamic changes in the retina. In two patients with central retinal vein occlusion we monitored the progression of the cystoid macular edema (CME) and changes of microcirculation with a follow up of 4 to 6 months., Materials and Methods: Two patients with central retinal vein occlusion and CME were examined by means of digital fluorescein angiography. Arteriovenous passage times and macular capillary blood velocities in combination with quantifications of the macular angioarchitecture and the extent of the CME were evaluated., Results: Hemodilution therapy improved retinal circulation, whereas macular circulation and the severity of the CME remained unchanged. With persisting CME oral acetazolamid therapy was initiated. Oral Acetazolamide led to resorption of the cystoid edema in tandem with improved macular circulation. The capillary density was altered but remained unchanged over time., Conclusions: By means of digital analysis of fluorescein angiograms a detailed monitoring and retinal and macular dynamics, macular morphology is possible. In these two cases CME improved after Acetazolamide and moreover retinal circulation returned to normal conditions.

Unlabelled: Eight patients (four men, four women), with low visual acuity caused by autosomal dominant cystoid macular dystrophy, were treated daily with oral 250 mg dose acetazolamide. Treatment ranged from two to 17 months. None of these eight patients had improvement of visual acuity of more than 0.1., Conclusion: Treatment with 250 mg acetazolamide appears not to be an effective therapy for cystoid macular oedema in dominant cystoid macular dystrophy. The electroretinography b-wave/a-wave ratio was normal. The primary lesion in dominant cystoid macular dystrophy remains obscure.

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.

Twenty-five eyes (23 patients) with inflammatory cystoid macular edema (CME) (11 after cataract surgery and 14 eyes (12 patients) with uveitis) were followed in a prospective open study. The aim was to determine the efficiency of a combined treatment of Diamox (acetazolamide), Voltaren Ophtha (diclofenac, a NSAID) and Ultracortenol (prednisolone acetate) and in the case of treatment failure, the usefulness of posterior subtenon's injections of corticosteroids (Kenacort 40 mg (triamcinolone)). Seven eyes (all pseudophakic CMEs) responded successfully to the initial therapy. Their mean visual acuity improved from 0.31 +/- 0.13 to 0.93 +/- 0.08 after 18 +/- 5 days (p less than or equal to 0.001). Of the sixteen of 18 evaluable eyes that were additionally treated with a mean of 3.28 +/- 1.07 three-weekly posterior subtenon's injections, 15 eyes including all uveitis CME responded to treatment. Their mean visual acuity improved from 0.49 +/- 0.20 to 0.96 +/- 0.31 (p less than or equal to 0.001). Two patients were excluded; in 22/23 eyes the sequential treatment was successful with an overall success rate of 95% of cases (improvement of five lines on the Snellen chart or final visual acuity of 0.8 or better). Initial angiographic cystoid macular edema was comparable and significantly improved after therapy in the two treatment groups. No mean intraocular pressure rise was noted after steroid injections. Measurement of anterior chamber inflammation with the laser flare-cell meter (Kowa FC-1000) showed elevated flare in all cases which significantly decreased in both treatment groups and represented a good follow-up parameter for the effect of antiinflammatory treatment and restoration of blood-ocular barrier.(ABSTRACT TRUNCATED AT 250 WORDS)