Michael D. Ober, MD
Christina M. Klais, MD
Emmett T. Cunningham Jr., MD, PhD, MPH
New York City

Macular edema represents the pathologic accumulation of extracellular fluid within the retina, primarily in the outer plexiform and inner nuclear layers, as a nonspecific re­sponse to a breakdown in the blood-retinal barriers. ME is a frequent cause of vision loss in pa­tients with diabetes mellitus, retinal venous oc­clusion, uveitis, and following in­­traocular surgery. It oc­curs less frequently in the set­ting of vitreoretinal traction, choroidal neovascularization and a number of other con­­ditions. Many strategies have been employed to manage ME with varying success. This article reviews the available treatment options for this common condition.

Figure 1. A. Early phase fluorescein angiography of a patient with non-proliferative diabetic retinopathy. Microaneurysms are seen most prominently temporal to the fovea in addition to fluorescein leakage in the foveal avascular zone. B. Late-phase FA of the same patient showing diffuse leakage temporal to and within the foveal avascular zone corresponding to diabetic macular edema.


The clinical diagnosis of ME is best made using a contact lens and stereoscopic slit-lamp fundus bi­omicroscopy. ME typically manifests as an irregular elevation within the retina, often adjacent to intraretinal lipid, microaneurysms, and/or hemorrhages in cases secondary to diabetes mellitus, vascular oc­clu­sion, or is­chemia. In­tra­re­ti­nal fluid may also accumulate in cystic spaces lo­calized to the pa­ra­foveal retina with or without ad­jacent vascular ab­normalities. This cystoid macular edema (CME) results most commonly from inflammation, localized traction, or following surgery.

Fluorescein angiography is an essential tool in the diagnosis of ME. In the normal eye, fluorescein is prevented from passing into the retina by the blood-retinal barriers. In ME, however, fluorescein molecules leave the intravascular space to enter the retina. The effected sites show hy­perfluorescence in early to mid frames that increases in area and in­ten­sity in later frames (See Figure 1). FA not only highlights edema for easy visualization and treatment lo­cal­ization, but also creates a permanent record for future comparison. A four-grade quantitative scale was developed for ME, wherein grade 0 is no perifoveal hyperfluorescence, grade 1 is incomplete perifoveal hyperfluorescence, grade 2 is mild 360-degree hyperfluorescence, grade 3 is moderate 360-degree hyperfluorescence with the hyperfluorescent area being approximately 1 disc diameter across, and grade 4 is severe 360-degree hyperfluorescence with the hyperfluorescent area be­ing approximately 1.5 disc diameter across.1,2 While FA is a sensitive means of identifying the presence of ME, it pro­vides re­la­tively little information re­garding the an­a­tomical distribution of the fluid; i.e., dif­fuse vs. cystic vs. subre­ti­nal, and the severity of the leak over time. FA provides no quantitative information re­garding retinal thickening. It is not surprising, therefore, that overall this two-dimensional FA-based grading system correlates poorly with vision.3,4

Optical coherence tomography (OCT III, Carl Zeiss) is a non-contact, non­in­va­sive imaging technique that provides a useful adjunct in diagnosing ME. It di­rects a beam of near infra-red light (830-nm) perpendicular to the surface of the retina and analyzes the properties of the reflections. In 1.5 seconds, it produces a single linear high resolution cross-sectional image. These images can display and even measure the thickened, cystic retina found in edematous areas. It is also useful in visualizing the properties of the vitreoretinal interface and ef­fec­tive­ly demonstrates when vitreous traction plays a role in the formation of ME (See Figure 2).

One study used OCT to examine 84 eyes with ME secondary to uveitis, which provided the added benefit of re­vealing or confirming the presence of epiretinal membranes and serous retinal detachment in 41 and 20 percent of their cases, respectively.5 The study found a moderate correlation be­tween retinal thickness and decreasing visual ac­uity, although the degree of correlation has varied across studies with other investigators reported weak,6 mo­de­rate,7 and strong8,9,10 cor­relations using varying statistical methods in di­verse pa­tient pop­ulations, including pa­tients with diabetic retinopathy, uveitis and CME.

Figure 2. A. Color fundus photograph of the left eye of a patient with non-proliferative diabetic retinopathy and lipid exudation in and around the fovea. B. Late-phase FA reveals macular edema in the central macula. C. Optical coherence tomography demonstrates the abnormal vitreoretinal interface as well as macular edema.

Another group reported that OCT was as effective as FA in detecting ME and superior to FA in describing the axial distribution of fluid.6 OCT also has the ability to identify some patients with ME not visualized on FA, as in certain cases of chronic CME where the sort of active leakage best visualized with FA is mi­nimal or even absent, or when fundus ex­­amination is compromised by the pre­sence of media opacities, such as in pa­tients with asteroid hyalosis.11

The retinal thickness analyzer (RTA, Ta­­lia Technology, Israel) is a similar non-contact imaging technique that allows for quantification of retinal thickness. It produces 16 parallel cross-sect­ion­al scans over a 3x3 square mm area of retina by analyzing reflections from an obliquely directed pulse of green light (540 nm) delivered over 0.3 se­­conds. Both OCT and RTA have shown ex­cellent precision in their individual mea­surements of retinal thickness, and a di­rect comparisons of the techno­lo­gies has demonstrated a statistically sig­ni­fi­cant correlation between their mea­sure­ments. While RTA has the ad­van­tage of rapid acquisition with perhaps fewer artifacts, it appears to be less ef­fective at measuring retinal thickness than OCT in the presence of me­dia opac­ities.12

An­other study compared fo­veal thickness with RTA and OCT in 30 healthy eyes. The mean foveal thickness in the normal eyes was measured at 181 µm and 153 µm for RTA and OCT, respectively. The authors concluded that RTA oc­casionally produces false high values, and thus has reduced reliability com­pared to OCT.13 In contrast, an analysis of pa­tients with mild non-proliferative di­abetic retinopathy found that RTA was more sensitive than OCT in identifying areas of retinal thickening during the initial stages of diabetic ME.14

Figure 3. A. Late phase fluorescein angiogram of a patient with cystoid macular edema. B. Optical coherence tomography showing the large cystic spaces at the fovea.

Treatments —Medical

Topical non-steroidal anti-inflammatory medications are the most common treatment for ME following cataract sur­gery (See Figure 3). These agents are di­­rected at decreasing intraocular pro­staglandin levels, which have been im­plicated in the path­ogenesis of ME. Dou­ble-masked, randomized, active and placebo-controlled studies including patients un­dergoing cataract surgery have re­ported anti-inflammatory effects from topically applied 1% in­do­meth­a­cin, 0.03% flurbiprofen, 0.5% ketorolac, and 0.1% diclofenac ophthalmic pre­pa­ra­tions.15,16 Diclofenac 0.1% and ke­to­ro­lac 0.5% ophthalmic solutions, however, are the only topically applied NSAIDs spe­cif­ically approved by the Food and Drug Administration for this in­dication. Therapy combining a topical corticoste­roid and NSAID drops has been found to have greater efficacy in treating ME than either medication alone.16 Al­though not FDA-approved, topical NSAIDs are often used prior to cat­aract surgery to prevent postoperative ME.

Oral acetazolamide is occasionally used in the treatment of ME secondary to inflammatory conditions and retinitis pig­mentosa, particularly when topical NSAIDs and corticosteroids fail. Several prospective, masked, crossover studies comparing ace­tazolamide and placebo in patients with ME due to a variety of causes. A five-cycle crossover study in 41 patients found a reproducible response, characterized as either partial or complete resolution of ME, in more than half of the patients with inherited or in­flammatory retinal disease, but no re­sponse from those with primary retinal vas­cular diseases.17 A 500-mg/day or oral acetazolamide was found to be more ef­fective than 250-mg/day in treating ME in patients with ME secondary to RP.18 This study ob­served improvement in 10 of 12 treated pa­tients.

Another group con­cluded that pa­tients under 55-years-old with ME at­tributed to chronic iridocyclitis were more like to respond to 500 mg acetazolamide b.i.d. than older patients.19 A re­cent study has suggested that ace­ta­zo­la­mide may also be effective for the treatment of diabetes induced ME as well.20

Corticosteroids are potent anti-in­flam­matory agents that are used frequently in the treatment of ME. They have multiple mechanisms of action, including stabilization of the blood-retinal barrier and inhibition of pro-inflammatory mediators. Delivery modes in­clude topical, periocular injection, intravitreal injection, and both oral and in­tra­venous administration. While oral and IV corticosteroids certainly reach the­rapeutic levels within the vitreous, they expose patients to the additional risk of systemic complications, and are therefore usually reserved for patients with sight-threatening uveitis in the setting of systemic disease. Topical corticosteroid drops are at the other end of the safety spectrum, but their ability to reach the posterior segment is limited.

Sub-Tenon's injections offer an alternative to deliver relatively high doses of cor­ticosteroids to the eye with lower risks of systemic complications.21 Though there have been no randomized, controlled trials, sub-Tenon's corticosteroid injection has been used effec­tive­­ly in treating macular edema for many years. The most common technique uses a short 25-ga. needle placed through the superotemporal bul­bar conjunctiva into the sub-Tenon's space while the patient looks inferonasally. The needle is ad­vanced posteriorly along the globe using a sweeping side-to-side motion to prevent inadvertent globe pe­ne­tration, until the hub reaches the conjunctival entry site, when the medication is delivered. One report included 20 con­secutive pa­tients with in­ter­me­di­ate uveitis associated with vision loss who were treated with sub-Tenon's injection of 40 mg triamcinolone acetonide.22 Although not all pa­tients demonstrated ME on FA, 67 percent improved by two lines of vision following one treatment. Risks of this procedure include persistently elevated intraocular pressure, cataract, ptosis and intraocular penetration among others.

Recently, the use of intravitreal in­jection of triamcinolone acetonide (Ken­a­log, 4.0 mg) has increased due to its po­tent ability to ameliorate refractory ME secondary to diabetes mellitus (See Fig­ure 4), retinal venous occlusions, inflammation, and other idiopathic causes.23-26 Pre­­liminary studies show dramatic re­duction in retinal thickening, decreased fluorescein leakage, and visual improvement, which may be marked in some pa­tients. Although the effect is temporary and typically lasts for three to six months or less, the ME usually re­sponds to re-injection. The use of intravitreal corticosteroids is associated with a 30- to 40-percent risk of persistently elevated intraocular pressure and an ap­proximate 10-percent risk of cataract re­quiring surgery, however. The National Eye Institute is currently enrolling pa­tients for SCORE, the standard care vs. corticosteroid for retinal vein occlusion study, which compares intravitreal in­jections of triamcinolone (1- and 4-mg dos­es) with standard care (observation and/or grid laser treatment) in patients with ME secondary to vein occlusion. The study will follow a total of 1,260 patients and continue treatment for 36 months.

ME also occurs in with age-related mac­ular degeneration (See Figure 5). Intravitreal injection of triamcinolone ace­tonide is currently under investigation for combined use with photodynamic therapy for the treatment of neovascular AMD (Visudyne with in­tra­vit­real Triamcinolone Acetonide, VisTA). One study emphasizes the im­portance of intravitreal triamcinolone preceding the application of PDT in patients with mac­ular edema and CNV.27 The authors theorize that ver­te­porfin may leak into cys­tic in­traretinal spaces leading to photoreceptor damage of adjacent, normal retina once the drug is photoactivated, while prior resolution of retinal edema may prevent this complication. Pre-ad­mi­nistration of corticosteroid may also serve to blunt any PDT-induced elevation in intraocular VEGF levels.

Intravitreal injections themselves are associated with small, but definite risks of serious, potentially blinding side effects in­cluding infectious endophthal­mi­tis, retinal detachment, hemorrhage, oc­­ular hy­pertension, cataract and hy­po­tony.28 Re­cently published guidelines for in­tra­vitreal injections attempt to establish a best-practices approach for this in­creasi­ngly used technique. The consensus pan­el's recommendations addressed pre-injection considerations including an­­tibiotics, glaucoma evaluation, glove use, and treatment of pre-existing eyelid abnormalities, as well as the importance of avoiding ex­ces­sive lid manipulation be­fore and during the procedure. The re­­commended peri-injection regimen in­­­cluded the use of topical and/or sub­con­junctival anesthetic, topical povidone io­dine, and an eyelid speculum. The authors stressed the importance of mo­­ni­toring IOP and direct fundus visualization following the injection to verify per­­fusion of the optic nerve, intravitreal location of triamcinolone, and the ab­sence of injection-associated hemorrhage or retinal detachment. They also stres­sed the im­portance of patient education vis-à-vis early symptoms of potential complications and thorough follow up.29

Figure 4. A. Optical coherence tomography image of an eye with diabetic macular edema with corresponding retinal thickness mapB. generated by the OCT. C. OCT of the same patient one month following intravitreal triamcinolone acetonide injection withcorresponding retinal thickness map. D. Resolution of macular edema. Visual acuity improved from 20/200 to 20/80 following treatment.

Several trials are investigating alternative long-term corticosteroid delivery devices for use inside the eye. One study in­volves the surgical placement of a flu­o­cinolone acetonide pellet embedded on a plastic strut with controlled release of steroids over three years. Known as the Envision intravitreal implant, by Bausch & Lomb and Control Delivery Sys­tems, it is placed through the pars pla­na and sutured to the sclera. A Phase-II/III randomized, masked study compared Envision TD implant in 80 patients randomized to 0.5- vs. 2.0-mg fluocinolone acetonide vs. standard of care consisting of laser photocoagulation or observation. After six months, a statistically significant reduction in ME and severity of diabetic retinopathy was seen with the 0.5-mg implant compared to standard of care. In addition, there were no differences in the incidence of serious adverse effects. The 2.0-mg arm of the study was stopped early due to the results observed in a second study in which no advantage over 0.5 mg was noted. A second study enrolled 278 patients with non-infectious posterior uveitis randomized to receive either a 0.59-mg or 2.1-mg Retisert implant the affected eye or, in bilateral cases, in the more severely afflicted eye. After two doses and 34 weeks, there was a significantly lower recurrence rate in eyes with the implant (10 vs. 55.7 percent, p<0.0001) with a decrease in use of systemic cor­ti­co­steroid/­im­mu­no­sup­pres­sive therapy (59.0 percent at baseline vs. 13.7 percent at 34 weeks) as well as sub-Tenon's and topical steroid use. There was a significant improvement in visual acuity (p<0.05). The most common adverse events included cataract progression and increased intraocular pressure which required a filtering procedure in 8.6 percent. (Jaffe G. Invest Ophthalmol Vis Sci. 2004; 44 ARVO E-Abstract #3369.)

Another trial involves Allergan's Pos­ur­dex, a bioerodable dexa­meth­asone pel­­let injected into the vitreous space that releases medication over 50 to 160 days. Results of a Phase-II trial revealed that both a 350-µg and 700-µg pellet significantly improved the percentage of pa­­tients with two lines or greater im­provement in vision (27.2 percent and 35.7 percent 350 µg and 700 µg, respectively) as well as a three line or greater im­provement in vision (13 percent and 19.4 percent, for 350 µg and 700 µg, re­spectively) at 180 days compared to pla­cebo. Thus far, there has been no in­creased incidence of cataract reported, though IOP increases were seen in about15 percent of patients.


Treatments —Laser

Most recently, Eyetech's and Pfizer's Mac­ugen was studied in a randomized, double-masked, multicenter, dose-ranging, controlled Phase II trial of 172 pa­tients with diabetic ME. The study in­vestigated three doses (0.3 mg, 1.0 mg, 3.0 mg) verses sham injections given every six weeks for three injections. While prior focal/grid laser investigators were asked only to enroll patient in whom they felt comfortable deferring focal/­grid laser for at least 12 weeks. Ad­di­tional injections and/or focal/grid photocoagulation were given at the investigator's discretion from week 18 to 30. Final assessments were conducted at week 36, six weeks after the last planned in­jection. Overall, subjects assigned to re­ceive Macugen had better vision outcomes, were more likely to show reduction in central retinal thickness, and were deemed less likely to need additional laser therapy as compared to sham patients.31 A confirmatory Phase III study is currently planned.

Focal/grid laser photocoagulation remains the standard of care for the treatment of diabetic ME. The Early Treat­ment Diabetic Retinopathy Study showed that patients treated with grid laser had a 50-percent reduction in moderate visual loss, defined as a doubling of the visual angle or a three-line decrease in vision, when compared with observation.30 Although the exact mechanism by which laser decreases ME is unknown, it is believed to promote the formation of tight junctions between RPE cells as well as reduce oxygen demand from photoreceptors and in­crease oxygen perfusion from the cho­roid.31 The EDTRS identified pa­tients eligible for focal laser photocoagulation as having clinically significant ME. This was defined as meeting one of the following three criteria: 1) retinal thickening located within 500 µm of the fovea; 2) hard exudates less than 500 µm from the fovea associated with adjacent retinal thickening; or 3) an area of edema 1 disc diameter or greater, any part of which located less than 1 disc diameter from the fovea. The EDTRS did not, however, distinguish between focal ME, which corresponds to local thickening of retina adjacent to microaneurysms, and diffuse ME, which refers to a generalized thickening of the posterior pole. An­ecdotal evidence shows that focal diabetic ME responds well to focal/grid laser while the diffuse variety more frequently fails laser treatment and re­quires alternative management.

Figure 5. A. Early fluorescein angiogram showing classic subfoveal neovascularization. B. Corresponding optical coherence tomography reveals areas of subretinal and intraretinal fluid accumulation as well as demonstrating the neovascularization (arrow).

Treatments —Surgery

The first group that reported the benefits of vitrectomy and posterior hyaloid separation in patients with diabetic ME suggested that a subgroup of patients exists in whom vitreous traction and shal­low macular detachments contribute to retinal thickening.32 This has sub­sequently been confirmed with OCT, leading to refinement of the indications for this technique.33,34 The three largest series35,36,37 of patients undergoing vi­trectomy for diabetic ME unresponsive to less invasive treatments analyzed 59, 58 and 65 patients, respectively. They reported 47 percent, 53 percent and 45 percent, respectively, of their patients improved in vision by two lines or greater. The last of these reported serious postoperative complications de­veloped in a minority of patients including retinal detachment (1.5 percent), rubeosis iridis (4.6 percent) epiretinal membrane (13.8 percent), recurrent vitreous hemorrhage(1.5 percent), and fo­veal hard exudate deposits (4.6 percent) while the complications revealed the second group included epiretinal membranes in 10.2 percent and cataracts in 63.2 percent of phakic eyes. Several other case series have shown similar re­sults, however, all were nonrandomized, without placebo control, and using diffe­rent inclusion and exclusion criteria. Fur­­­ther, surgical techniques have also dif­fered, leaving the exact indications for vitrectomy in patients with CME open to interpretation.

ME remains a major cause of visual loss despite the variety of available treatments. Laser photocoagulation remains an integral part of the management of ME due to diabetes, ischemia and vascular occlusions. Topical NSAIDs and cor­ticosteroids are currently the primary method to control postoperative ME, while acetazolamide remains an effective means to treat in selected patients with ME secondary to uveitis and retinitis pigmentosa. The role of intravitreal cor­ticosteroids in ME therapy is ex­panding, but remains limited by side ef­fects and duration of effect. Re­fine­ments in surgical techniques will continue to add a new dimension to ME unresponsive to less invasive treatment while advances in pharmacotherapy and ocular drug delivery promise to play a role in the prevention and management of all causes and types of ME. 


Dr. Ober is a fellow in vitreoretinal surgery at the Edward S. Harkness Eye Institute at Columbia University College of Physicians and Surgeons, and the LuEsther T. Mertz Retinal Research Center at Manhattan Eye, Ear, and Throat Hospital. Contact him at 210 East 64th St., 8th Fl, New York, NY 10021; e-mail: obermike@aol.com; or (212) 605 3777 or fax (212) 605 3795.

Dr. Klais is a retina fellow at the LuEsther T. Mertz Retinal Research Center. Contact her at the same address, phone or fax numbers, or by e-mail at cmcKlais@cswebmail.com.

Dr. Cunningham is a clinical professor of ophthalmology and director of the Uveitis Service at New York University, School of Medicine. He is also an employee of Eyetech Phar­ma­ceuticals Inc.Contact him at Vitreous-Retina-Macula Con­sultants of New York, 460 Park Ave., New York, N.Y. 10022, by e-mail emmett_cunningham@yahoo.com, or by phone/fax at (212) 861 9797.


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