Treatment Of Cystoid Macular Edema Research Articles

Deep intramuscular methylprednisolone for the treatment of cystoid macular oedema in uveitis.

To study the use of intramuscular methylprednisolone in the treatment of cystoid macular oedema in patients with uveitis. A total of 32 patients with various types of uveitis with unilateral cystoid macular oedema were recruited. Patients received 160 mg of intramuscular methylprednisolone into the thigh and were reassessed 6-8 weeks later. In 17 patients in whom there had been no significant improvement, a further injection of methylprednisolone was given; a total of 49 injections. After a first injection a significant improvement in vision (an increase of > or = 2 Snellen lines) was seen in 15 of 32 eyes (47%), and 17 of 32 eyes (53%) showed no significant change. After the second injection 7 of 17 eyes (41%) showed a significant improvement but there was no change in 9 of 17 eyes (53%). Only one eye deteriorated more than 2 lines of Snellen acuity. There were minimal ocular or systemic side effects associated with this form of treatment. Despite limited success, deep intramuscular methylprednisolone may have a role as an alternative mode of treatment in uveitis patients with unilateral cystoid macular oedema, thus avoiding the potential hazards of periocular injections. In comparison with orally administered systemic corticosteroids, an injection ensures patient compliance and is associated with fewer side effects.

Cystoid macular edema following cataract surgery.

Cystoid macular edema (CME) remains a troublesome problem after cataract surgery and other types of ocular surgical procedures. It is recognized as the most frequent cause of decreased vision in patients following cataract surgery. Although the disease was first described more than 40 years ago, its cause is unclear, and all available therapeutic interventions, mainly based on theories regarding the pathogenesis of the condition, are of doubtful effectiveness and are still far from being satisfactory. Most published literature on the incidence and treatment of CME consists of small, retrospective case series and cannot provide reliable answers as to whether a given factor or intervention is associated with the occurrence or outcome of the disease.

Pseudophakic cystoid macular edema treated with high-dose intravenous methylprednisolone

Purpose To evaluate the efficacy of high-dose methylprednisolone in the treatment of pseudophakic cystoid macular edema (CME). Setting University-affiliated hospital. Methods Four patients with pseudophakic CME who reported decreased visual acuities were treated with oral prednisolone (20 mg daily for 5 days), oral acetazolamide (500 mg daily for 5 days), and topical dexamethasone 0.1% and diclofenac 0.1% (4 times a day for 14 days). The CME did not resolve. Next, they were treated with high-dose (1000 mg daily) intravenous methylprednisolone for 3 days. Results In 3 of 4 eyes, the CME resolved and visual acuity improved. Conclusion High-dose methylprednisolone may be effective in the treatment of pseudophakic CME.

Treatment of cystoid macular edema with non-steroidal anti-inflammatory drugs and corticosteroids.

Ophthalmologists are not infrequently confronted with reduced visual acuity due to cystoid macular edema (CME). In most cases the pathology can be managed in the outpatient office. In some cases, however, a graded and systematic therapeutic approach is necessary to prevent irreversible visual loss due to fluid accumulation in the macula.

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

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.

Medical prophylaxis and treatment of cystoid macular edema after cataract surgery: The results of a meta-analysis

Objective The study aimed to determine the effectiveness of prophylactic medical intervention in reducing the incidence of cystoid macular edema (CME) and the effectiveness of medical treatment for chronic CME after cataract surgery. Design The study design was a systematic review and meta-analysis of published reports of randomized clinical trials (RCTs). Participants Sixteen RCTs involving 2898 eyes examining the effectiveness of medical prophylaxis of CME and 4 RCTs involving 187 eyes testing the effectiveness of medical treatment of chronic CME were used in the study. Interventions Medical prophylaxis of treatment (cyclo-oxygenase inhibitors or corticosteroids) versus control (placebo or active treatment) was performed. Main outcome measures Incidence of angiographically diagnosed CME, incidence of clinically significant CME, and vision were measured. Results Thirty-six articles reported testing a prophylactic medical intervention for CME after cataract surgery. The incidence of CME varied extensively across studies and was related to the study design used. Summary odds ratios (OR) indicated that prophylactic intervention was effective in reducing the incidence of both angiographic CME (OR = 0.36; 95% confidence interval [CI] = 0.28–0.45) and clinically relevant CME (OR = 0.49; 95% CI = 0.33– 0.73). There also was a statistically significant positive effect on improving vision (OR = 1.97; 95% CI = 1.14– 3.41). A combination of the results of the four RCTs testing medical therapy for chronic CME indicated a treatment benefit in terms of improving final visual acuity by two or more Snellen lines (OR = 2.67; 95% CI = 1.35–5.30). Assessment of the quality of the 20 RCTs included in the meta-analyses indicated problems in the design, execution, and reporting of a number of trials. Conclusion A combination of the results from RCTs indicates that medical prophylaxis for aphakic and pseudophakic CME and medical treatment for chronic CME are beneficial. Because most of the RCTs performed to date have problems related to quality, a well-designed RCT is needed to confirm this result, using clinical CME and vision as outcomes.

Vitreoretinal Toxicity of Acetazolamide Following Intravitreal Administration in the Rabbit Eye

Acetazolamide, a carbonic anhydrase inhibitor, has been shown effective in the treatment of cystoid macular edema; however, chronic use of the drug is limited by its serious systemic side effects. Intraocular administration can eliminate these systemic complications. We evaluated vitreoretinal toxicity after intravitreal injection of acetazolamide in the rabbit eye. The right eye of each rabbit received a single acetzolamide injection; the left eye received balanced salt solution and served as a control. The effect of the drug was evaluated by clinical observation, electroretinography, and histopathologic study. Intravitreal injection of up to 0.5 mg acetazolamide did not cause vitreoretinal toxicity. Injection of 1 mg or higher doses depressed the b-wave amplitude of electroretinograms and damaged the outer segments of the photoreceptors, as determined by light and electron microscopy.

Potential Acuity Meter and Visual Outcome in Pseudophakic Eyes with Clinical Cystoid Macular Edema

OBJECTIVE: To establish whether or not the Potential Acuity Meter is a useful test to predict the visual outcome in patients about to undergo treatment for acute post-cataract surgery cystoid macular edema. STUDY DESIGN: Retrospective study of the final visual acuity after treatment for cystoid macular edema compared with pre-treatment potential acuity meter reading. SETTING: Sinskey Ophthalmic Center, Santa Monica, California. PATIENTS: 39 consecutive patients who had cystoid macular edema after phacoemulsification. MAIN OUTCOME MEASURES: Final visual acuity after treatment for cystoid macular edema and pre-treatment potential acuity meter readings. RESULTS: Of 39 patients considered in this study, we found 33 patients (26 reported 20/40 or better and seven reported 20/50 or worse) agreed in their PAM readings and final visual outcomes. The estimated Kappa statistic was 0.596. This indicates that the correction coefficient was significantly different from zero which shows that is not by chance alone. CONCLUSIONS: The potential acuity meter shows some correlation (kappa: 0.596) with the final visual acuity if we divide the patients into two groups: 20/40 or better and 20/50 or worse. This means that the patient with a better PAM reading before treatment tended to have a better final visual acuity than those with a poor PAM reading.

Hypothesis Concerning Carbonic Anhydrase Treatment of Cystoid Macular Edema: Example With Epiretinal Membrane

Acetazolamide has been shown experimentally to facilitate the transport of water across the retinal pigment epithelium (RPE) from the subretinal space to the choroid. 1 Cox et al 2 found that carbonic anhydrase inhibitors were effective in promoting the absorption of intraretinal fluid in some cases of cystoid macular edema (CME), and they proposed that these drugs would be most effective in disorders in which the leakage came from the RPE rather than from the retinal vasculature. However, Fishman et al 3 found them to be most effective against parafoveal retinal vascular edema in retinitis pigmentosa. There may be a simple explanation for these differing observations. Water is transported across the RPE in conjunction with a net movement of ions (particularly sodium chloride and bicarbonate), and the mammalian RPE membrane contains several active and facilitated transport systems that regulate traffic of those ions. 4 These drugs are presumed to work

Complications and after care in aphakic and pseudophakic patients

The aim of every cataract operation is optical rehabilitation. With the greater social demands made today by aphakic and pseudophakic patients, the recognition and treatment of diseases with early or late onset after cataract extraction assumes greater importance. The early aims are rapid mobilization, complete absence of irritation, and normalization of pressure. Regular administration of corticosteroids, essential in the post-operative treatment of pseudophakia, may mask a bacterial or mycotic infection. The sole indication for removal of an implant is the uveitis-glaucoma-hyphema syndrome. The prevention and treatment of cystoid macular edema is discussed: whether or not the posterior lens capsule is intact seems to play a major role in the pathogenesis of this early or late complication in both aphakia and pseudophakia.

Yag Laser Treatment of Cystoid Macular Edema

Fourteen eyes (some aphakic and some with implanted intraocular lenses) underwent neodymium-YAG laser treatment for cystoid macular edema with vitreous incarceration in the corneoscleral wound. Visual acuity improved in all 14 eyes; ten eyes improved at least three Snellen lines and 12 eyes improved at least two Snellen lines. After follow-up periods of one to nine months, 11 eyes had visual acuities of 20/40 or better (only two had had visual acuities of 20/40 preoperatively and none had had a better visual acuity). An additional eye, which had an intraocular lens implant, was treated prophylactically. Visual acuity in this eye remained stable during a nine-month follow-up period. YAG laser treatment produced no adverse side effects or complications in any of the 15 eyes.