Nonpseudophakic Cystoid Macular Edema

Updated: Nov 03, 2023
Author: Hamoon Eshraghi, MD; Chief Editor: Hampton Roy, Sr, MD 



Although the most common cause of cystoid macular edema (CME) is due to Irvine-Gass syndrome of CME after cataract extraction or other intraocular surgery, numerous other conditions are associated with the clinical appearance of fluid-filled, cystoid spaces in the macular region. CME is a final common pathway of many intraocular diseases, usually involving the retinal vasculature. The appearance can differ somewhat, depending on the etiology; however, CME can appear as a nonspecific clinical finding. If the cause of CME is not obvious, detailed ophthalmoscopy and, occasionally, ancillary testing may be necessary to identify the cause.

Cystoid macular edema due to nonproliferative diabetic retinopathy is shown in the image below.

Fundus photograph of nonproliferative diabetic ret Fundus photograph of nonproliferative diabetic retinopathy with clinically significant macular edema and cystoid macular edema.


Macular edema is excessive fluid within the layers of the retina, distinct from the accumulation of fluid under or between the retinal layers (eg, subsensory fluid, serous retinal detachment). The amount of fluid normally present in the retina is maintained according to osmotic and hydrostatic pressures between the retina and the surrounding vasculature, which are compartmentalized by the blood-retinal barrier. A breakdown in the blood-retinal barrier allows for fluid to accumulate in cystoid spaces within the retina. Pathologic evidence of cell loss and Müller cell abnormalities may contribute to the resulting CME.

Several mechanisms have been proposed to explain how CME develops. The characteristic distribution of vascular leakage and retinal edema may be explained best by the diffusion of mediators (eg, prostaglandins) released in the eye. These mediators of inflammation cause increased permeability of retinal blood vessels, resulting in extravasion. This theory is supported by evidence that cyclooxygenase inhibitors (eg, indomethacin, other nonsteroidal anti-inflammatory drugs) reduce the incidence of angiographic CME. However, this finding has only been extensively reported on in pseudophakic CME associated with surgical trauma to the anterior segment. A 2013 case report described a phakic patient with idiopathic macular telangiectasia type 1 whose CME reacted robustly to the administration of NSAIDs and would reoccur in the absence of treatment.[1]

The major determinant of fluid movement in the retina is the Müller cell. Müller cells have bicarbonate-related transport mechanisms that control movement of potassium and sodium ions (and thus fluid), partly explaining the role for carbonic anhydrase inhibitors such as acetazolamide in the treatment of cystoid macular edema. Additional routes of ion control are achieved through the Kir2.1 and Kir4.1 channels that buffer changes in intracellular potassium.

In addition, evidence shows that the reduced outflow of fluid from the retina is responsible for the buildup of edema. In particular, reduced or absent flow to the deep vascular plexus of the retina has been described. This decreased flow can result from ischemia or inflammation and is mediated by integrins, selectins, and other adhesion molecules. Extravasated leukocytes have the ability to plug capillaries, thus blocking blood flow.[2]

Another mechanism emphasizes the role of mechanical factors, such as tractional forces on the macula from disruption of the normal vitreoretinal interface. Even according to this theory, it is believed that local forces induce a release of mediators that lead to a breakdown of the blood-retinal barrier, resulting in the clinical appearance of CME.

Photic injury has been implicated in the development of pseudophakic CME; however, there is no scientific evidence that light damage to the retina causes CME. 



United States

Frequency of CME that is unassociated with cataract surgery varies widely, both in the United States and internationally, depending on the etiology or underlying condition leading to CME. Incidence figures vary because of difficulty in observing subtle CME clinically, surgeon bias in reporting CME, and a lack in performing fluorescein angiography (FA) or optical coherence tomography (OCT) tests that would detect CME.


CME from any etiology often leads to significant central visual loss, typically in the 20/40 to 20/200 range.


No racial predilection has been associated with CME.


CME is distributed equally among males and females.


Age of incidence of nonpseudophakic CME varies according to etiology. Since diabetic CME is secondary to diabetic retinopathy, it occurs in persons aged 40 years and older.


Visual prognosis in eyes with CME depends on the etiology of the CME. If the CME resolves with treatment, visual acuity of 20/40 or better is common. However, in long-standing CME, vision is often 20/100 to 20/200.




Clinical presentation

Cystoid macular edema (CME) typically presents with a complaint of painless visual loss in one eye. It can be bilateral, depending on the etiology. The onset of symptoms is usually gradual; however, patients often only notice it suddenly, when they check one eye separately. Different causes of CME have different clinical presentations. The most common entities are discussed below. 


Chronic uveitis, especially pars planitis, is associated with CME, most likely because of a breakdown in the blood-retinal barrier.[3]  The chronic inflammation disrupts the competence of the perimacular blood vessels, allowing for the development of the cystoid spaces. A clinical entity distinct from pars planitis has been described, characterized by CME, retinal periphlebitis, and vitreous inflammation. This condition typically is bilateral, affecting middle-aged women. Most patients maintain good vision over a prolonged time period.

Birdshot retinochoroidopathy, a severe form of posterior uveitis, presents with multiple, small, round or oval hypopigmented spots at the level of the choroid or RPE. Vitreous cells, disc edema, and leakage of fluorescein from retinal vessels are common features. CME can occur in conjunction with this condition.

CME has been reported in association with orbital pseudotumor, the swelling of tissues within the orbit. The edema resolved after treatment of the orbital condition.

CME has been associated with cytomegalovirus (CMV) retinitis in patients with the acquired immunodeficiency syndrome (AIDS) and immunocompetent patients. In some patients, CME develops specifically while the CMV retinitis resolves. A separate entity of CME has been described in patients with inactive CMV retinitis after immune recovery and improvement of their CD4 counts because of highly active antiretroviral therapy (HAART).

Diabetic maculopathy

Diabetic maculopathy affects the capillaries in the macular region, leading to macular edema. Occasionally, a CME component of the macular edema develops, with cystoid changes in the foveal region. This is more common in cases of diffuse and chronic diabetic macular edema, and the vision may be reduced to the 20/200 level.

When eyes with clinically significant macular edema (ie, edema overwhelming the homeostasis of the retina causing noticeable thickening) are treated early, before the onset of diffuse edema, CME possibly can be avoided if the patient maintains excellent control of the underlying medical problems.

CME, in association with diabetic macular edema, has also been correlated to the presence of an attached posterior hyaloid, whereas patients with a posterior vitreous separation are much less likely to develop a component of CME. This may support a mechanical mechanism of the development of CME, where tractional forces induce the formation of cystoid spaces in the macula. Alternatively, the traction on the macula may lift the retina away from the RPE pump, causing CME. Occasionally, even in the absence of an attached posterior hyaloid, a preretinal membrane can exert tractional forces and lead to CME.

Age-related macular degeneration

Age-related macular degeneration (ARMD) can present in 1 of 2 forms: atrophic or exudative (dry or wet). Atrophic macular degeneration without exudative changes does not generally lead to CME. The exudative form of ARMD, with choroidal neovascularization, can cause a serous detachment of the overlying retina and resultant CME.[4, 5]

CME is more common if the serous detachment of the macula has been present for 3-6 months or if the choroidal neovascular membrane has involved most of the subfoveal region. In such cases, the likelihood of restoring good vision is low.

Retinal vein occlusions

Retinal vein occlusion, a branch retinal vein occlusion (BRVO) or a central retinal vein occlusion (CRVO), can cause macular edema resulting from breakdown of the capillary endothelium associated with increased intravascular hydrostatic pressure.[6] The damaged vessels leak fluid into the intercellular spaces, and, eventually, intraretinal cystoid spaces can be seen. This form of CME can be associated with further visual loss and usually results in some permanent visual loss if the situation persists for more than 6 months. However, it can improve with earlier resolution of the macular edema.

Choroidal melanoma

Choroidal tumors, such as malignant melanoma, choroidal nevus, or capillary hemangioma, have been associated with CME. These cystoid changes can occur overlying the tumor and in the macula, even when the tumor is located some distance from the macula, a phenomenon known as the Wise theory of macular accentuation. The source of CME at the level of the retinal capillary network results from intraretinal microvascular abnormalities resembling endothelial cell proliferation. See Choroidal Melanoma.

Juxtafoveal macular telangiectasis

Perifoveal retinal telangiectasis or Coats disease typically presents with irregularly dilated and incompetent retinal vessels. These telangiectatic changes can occur at the level of the arterioles, venules, or capillaries. The closer the findings are to the macula, the earlier symptoms present. A clinical picture of CME may occur due to leakage from incompetent retinal vessels. Idiopathic juxtafoveal telangiectasis is a milder form of retinal telangiectasis, typically involving the temporal macula. CME is less common in this condition.

Drug-induced and postoperative CME

Radiation retinopathy, a condition of vascular damage from prior radiation treatment to the eye or orbit, can mimic diabetic retinopathy in its appearance. A form of macular edema often develops that is quite similar to diabetic macular edema and may manifest as CME.

CME without leakage on FA has been reported in middle-aged men on high doses of niacin for treatment of hypercholesterolemia.

The presence of CME after successful retinal reattachment surgery has been reported to range from 30-43% during the first 4-6 weeks postoperatively. In aphakic eyes, incidence may be as high as 64%. Older patients are at a higher risk to develop CME after retinal detachment repair.

CME has been reported after corneal relaxing incisions for astigmatism.

CME after penetrating keratoplasty ranges from 20-43%. Aphakic eyes are at a much higher risk to develop postoperative CME. If an anterior vitrectomy was performed at the time of surgery, the risk of CME is 8-9 times more likely to occur.

Glaucoma treatment with latanoprost has been associated with the development of CME. The prostaglandin-like effect of latanoprost is believed to cause CME. CME typically resolves after discontinuation of the drug. In a study by Moroi et al of 7 patients with CME, after starting latanoprost therapy, all 7 patients had coexisting ocular conditions that may have placed these eyes at risk for prostaglandin-mediated blood-retinal barrier vascular insufficiency.[7]

CME inducing visual loss has been reported after the use of topical echothiophate iodide therapy.

Genetic disorders

Retinitis pigmentosa (RP) is associated with CME.[8, 9] Studies have found an increased permeability of the retinal pigment epithelium (RPE) and perifoveal capillaries to fluorescein in eyes with RP.A study found an increased presence of circulating antiretinal antibodies in patients who presented with RP and CME. This suggests a possibility of an autoimmune process mediating the development of CME in patients with RP.

Retinal neovascularization and CME have been reported in patients with punctata albescens retinopathy, a type of RP characterized by white retinal flecks. Dominantly inherited CME has been described as a macular dystrophy with an onset at middle age and a slow progression over ensuing decades. Pathologic studies of eyes with this condition suggest that the predominant changes occur in the inner nuclear layer and that this entity may present as a primary disease of the Müller cell.

Foveal X-linked retinoschisis has been mistakenly described as CME.

Epiretinal membranes

Epiretinal membranes can cause surface wrinkling of the underlying retina resulting from contracture of the membrane.[10]  Occasionally, macular edema may develop due to distortion and traction on the surrounding intraretinal vessels. If the edema persists, breakdown of the intraretinal architecture can lead to cystoid spaces. This breakdown may be related to mechanical traction leading to edema, or it may be caused by the loss of apposition between the retina and the RPE pump. Ideally, surgical removal of a significant epiretinal membrane causing surface wrinkling retinopathy and macular edema reducing vision to the 20/60 to 20/80 level should be performed before irreversible CME develops.


See History.


See History.





Laboratory Studies

Laboratory studies for cystoid macular edema (CME) vary depending on the presumed etiology of the edema.

If findings suggestive of diabetes are present, the patient should have blood glucose testing or a glucose tolerance test.

In the presence of uveitis, an appropriate evaluation for chronic uveitis should be initiated. See Uveitis, Evaluation and Treatment for details.

Imaging Studies

Optical coherence tomography (OCT) is the gold standard in the identification of CME. OCT is a noninvasive imaging modality that can determine the presence of CME by visualizing the fluid-filled spaces in the retina. The amount of CME can be monitored over time by quantifying the area of cystoid spaces on a cross-sectional image through the macula.

Studies have reported OCT to be comparable to FA in the evaluation of CME, especially with newer, high-resolution OCT scanners. OCT is beneficial by quantifying the thickness of the retina and by allowing quantitative measurements of macular edema over time. This noninvasive method is especially useful in monitoring the response to treatment.

Newer software for OCT has increased the resolution of this imaging modality and has led to the identification of specific patterns of CME.

Spectral domain OCT has increased the resolution of OCT imaging to as low as 2-3 microns and is more sensitive in detecting intraretinal fluid associated with CME.

OCT images are shown below.

Ocular coherence tomographic image of cystoid macu Ocular coherence tomographic image of cystoid macular edema in a patient with uveitis.
Ocular coherence tomographic image of cystoid macu Ocular coherence tomographic image of cystoid macular edema in an eye with nonproliferative diabetic retinopathy.

FA is an alternative imaging study to evaluate CME. Fluid accumulation may be delayed in certain conditions; thus, late phase fluorescein photos, sometimes as long as 20 minutes or more, may be required to properly evaluate the CME. Associated findings on FA may help determine the etiology of CME.

If leaking microaneurysms are present in the setting of diabetic retinopathy, then diabetes likely is the cause. This is shown in the images below.

Fundus photograph of nonproliferative diabetic ret Fundus photograph of nonproliferative diabetic retinopathy with clinically significant macular edema and cystoid macular edema.
Fluorescein angiogram of same eye as in the image Fluorescein angiogram of same eye as in the image above, revealing both cystoid macular edema and leakage from microaneurysms associated with diabetic retinopathy.

Vascular collaterals crossing the horizontal raphe on FA can help determine that the etiology of the edema (and retinal hemorrhages if present) is likely due to a vascular occlusion.

The absence of leakage from CME on FA suggests a diagnosis of nicotinic acid retinopathy, Goldmann-Favre disease, or X-linked juvenile retinoschisis.

FA also is helpful to verify the presence of CME when it is difficult to establish clinically.

Other Tests

In the appropriate clinical setting, an electroretinogram may be indicated to confirm a diagnosis of RP with associated CME.


Occasionally, in cases of uveitis with associated CME, a diagnostic vitreous biopsy or vitrectomy can aid in determining the correct diagnosis. The vitreous fluid can be sent for the appropriate laboratory tests based upon the clinical picture. It is beyond the scope of this article to discuss the full laboratory workup for uveitis.

In cases of orbital pseudotumor, an incisional biopsy for the purpose of confirming a diagnosis is indicated; however, CME rarely is associated with this condition.



Medical Care


Steroids are considered an effective treatment to uveitis, administered in 3 different ways: topical, oral, and injectable.[3]

Topical steroids and nonsteroidal anti-inflammatory agents have been used in the treatment of cystoid macular edema (CME), especially when associated with uveitis. Most studies have evaluated the efficacy of these drugs in the presence of pseudophakic CME after cataract surgery.[11] However, the effect of these medications in stabilizing the blood-retinal barrier may aid in the treatment of other forms of CME.

Oral steroids also are a commonly used modality of stabilizing the blood-retinal barrier for the treatment of inflammation and CME in patients with intermediate or posterior uveitis. Oral steroids should be avoided unless necessary because of the associated complications of systemic use (eg, aseptic necrosis of the femoral head).

Injections of long-acting depot steroids (eg, triamcinolone) into the sub-Tenon space usually are more effective and commonly are used in the treatment of noninfectious uveitis. Peribulbar injections have a greater risk of intraocular injection than a subconjunctival approach; however, the drug delivery to the retina is superior when administered into the posterior sub-Tenon space. These implants allow sustained release of the steroid, maximizing drug efficiency and minimizing toxicity. Three potential candidates are undergoing clinical trials: dexamethasone implant (Posurdex), triamcinolone acetonide implant (I-vation TA), and fluocinolone acetonide implant (Retisert, which is FDA approved).

Intraocular triamcinolone acetonide has been found to effectively, but temporarily, reverse CME in eyes with many conditions, including pseudophakic CME, retinal vein occlusions, diabetic macular edema, uveitis, and juxtafoveal telangiectasis. Clinical trials are underway to study the long-term benefit and safety of this treatment approach.

Many other causes of CME are treated by addressing the underlying condition. CME associated with CMV retinitis is treated by managing the retinitis with antiviral agents (eg, ganciclovir, foscarnet, cidofovir).

CME associated with immune recovery in patients with inactive CMV retinitis and a stronger immune system are also treated with steroids, either oral or posterior sub-Tenon injection of long-acting depot steroids.

Orbital pseudotumor is treated effectively with oral steroids, and, in the case reported to be associated with CME, the macular edema resolved with treatment of the orbital pseudotumor.

Diabetic maculopathy

As stated, intraocular triamcinolone acetonide is an effective treatment for diabetic macular edema.

Research implicates VEGF as an important mediator of vascular permeability and CME. Therefore, clinical trials are being conducted to evaluate the benefit of VEGF inhibitors in treating CME associated with different conditions, such as diabetic macular edema, retinal vein occlusions, and age-related macular degeneration.[12] Anti-VEGF treatments also stunt neovascularization.

When CME is associated with diabetic macular edema, focal laser photocoagulation according to the guidelines of the Early Treatment of Diabetic Retinopathy Study (ETDRS) should be followed (see Diabetic Macular Edema). However, CME in the setting of diabetic macular edema often suggests chronicity of the condition and will not respond adequately to laser treatment. Some physicians advocate the use of posterior sub-Tenon or intraocular injection of triamcinolone with or without macular laser photocoagulation to treat diabetic macular edema associated with CME. A randomized, sham-controlled trial testing the efficacy and safety of a dexamethasone intravitreal implant showed that it was safe and efficacious in correcting best corrected visual acuity.[13]

A 5-year randomized controlled trial showed that eyes receiving ranibizumab with prompt or deferred laser treatment had better long-term vision improvements than eyes managed with laser or triamcinolone with laser follow by deferred ranibizumab.[14]

Age-related macular degeneration

CME associated with choroidal neovascularization in ARMD is a secondary response to the presence of subretinal neovascularization.[4, 5] It is present most commonly in eyes with significant subsensory fluid in the macula and a poor prognosis for central vision. Fortunately, current treatments of exudative ARMD reduce the incidence of disciform scarring and associated CME.

FDA-approved treatments for ARMD include the following:

  • Ranibizumab (Lucentis)
  • Aflibercept (Eylea)
  • Pegaptanib sodium (Macugen)
  • Verteporfin (Visudyne)
  • Implantable telescope

Retinal vein occlusions

Intraocular triamcinolone acetonide and VEGF inhibitors have been found to reverse CME in eyes with retinal vein occlusions.[15]

Currently, anti-VEGF agents are the primary treatment for retinal vein occlusion, specifically ranibizumab. Alongside, the Posurdex Study is evaluating the benefit of an injectable dexamethasone implant for the treatment of macular edema in retinal vein occlusions.

Intravitreal triamcinolone has been reported to be effective in reversing CME in branch retinal vein occlusion and nonischemic central retinal vein occlusion.[16, 17] The Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) Study, a clinical trial sponsored by the National Institutes of Health (NIH), is evaluating the benefit of preservative-free intraocular triamcinolone acetonide in retinal vein occlusions.

Macular edema is a common cause of visual loss in eyes with branch retinal vein occlusion or central retinal vein occlusion. CME also can be associated with this form of macular edema. Macular laser photocoagulation has been shown to be effective in improving vision in patients with branch retinal vein occlusion for greater than 4 months’ duration and a visual acuity of 20/40 or worse. However, the Central Vein Occlusion Study (CVOS) did not show any visual benefit from laser photocoagulation in eyes with central retinal vein occlusion and macular edema, although it did reduce the macular edema.

Choroidal melanoma

When malignant intraocular tumors are associated with CME, the priority is to treat the tumor. Systemic malignancies, such as multiple myeloma, have been observed to be associated with CME. Systemic treatment of the myeloma is the priority and usually addresses the CME. However, sub-Tenon injection of steroid may enhance resolution of the CME in such cases. Depending on the nature of the disease, CME associated with intraocular tumors requires treatment of the tumor (eg, laser photocoagulation, cryotherapy, radiation, thermotherapy, enucleation).

Juxtafoveal macular telangiectasis

Treatment of CME associated with juxtafoveal telangiectasis has been undergoing preliminary trials with steroids, VEGF antibodies, and laser photocoagulation. Results show that intraocular triamcinolone acetonide temporarily lessens CME, but it recurs less than 6 months after treatment. Both bevacizumab and ranibizumab are being tested to reduce CME. Results show success in improving vision and CME for up to 12 months.[18]

CME secondary to juxtafoveal telangiectasis in Coats disease has been shown to respond to laser photocoagulation, with resolution of the edema and improvement in visual acuity, and remains the prevalent form of treatment.

Drug-induced and postoperative CME

Macular edema secondary to radiation retinopathy is often treated with laser photocoagulation.

CME after surgical interventions such as retinal reattachment surgery, corneal relaxing incisions, and keratoplasty usually resolve with time.

In drug-induced cases, such as CME associated with latanoprost, echothiophate iodide, or nicotinic acid, discontinuation of the drug usually causes reversal of CME.

Genetic disorders

Other forms of CME have been reported to respond to treatment with acetazolamide. CME after scleral buckling procedures, CME in some forms of uveitis, and CME associated with RP may respond to acetazolamide therapy.[15]


Complications associated with the treatment of CME are infrequent. When a posterior sub-Tenon injection of triamcinolone is given, patients can occasionally experience a transient ptosis or subconjunctival hemorrhage. Retinal arterial occlusion after sub-Tenon steroid injections has been reported due to intravascular injection of the drug.

Intravitreal triamcinolone has been associated with ocular hypertension, cataract progression, retinal tear or detachment, infectious and noninfectious endophthalmitis, and lens damage.

Long-Term Monitoring

Typically, patients with cystoid macular edema (CME) are evaluated 1-3 months after intervention to evaluate the efficacy of treatment.



Medication Summary

The most common drugs used to treat cystoid macular edema (CME) include steroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and acetazolamide.


Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli. Used to stabilize the blood-retinal barrier and to induce resolution of macular edema.

Prednisone (Deltasone, Orasone, Meticorten)

Used rarely for severe inflammatory conditions with associated CME. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Prednisolone acetate 1% ophthalmic solution (Pred Forte)

Occasionally used in CME; however, poor penetration to the macula via topical route. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.

Triamcinolone (Amcort, Kenalog)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Posterior sub-Tenon injection of steroid to reduce CME. Depending on etiology of edema, it is often DOC.

Dexamethasone (Posurdex)

Dexamethasone is an intravitreal implant used to treat macular edema associated with retinal vein occlusion. The pellet is injected through the pars plana, and through sustained-release, delivers the drug slowly over a month. Increased intraocular pressure and conjunctival hemorrhaging are the 2 main complications associated with the implant.

Fluocinolone acetonide (Retisert, Iluvien)

The fluocinolone acetonide implant uses the drugs low solubility for its sustained-release effect. However, the effect is temporary (results diminish within a year) and risks increases in intraocular pressure. It is FDA-approved to treat certain types of uveitis.

Iluvien, an intravitreal implant with sustained release of fluocinolone acetonide, has been FDA-approved to treat diabetic macular edema.

Nonsteroidal anti-inflammatory agents (NSAIDs)

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell membrane functions.

Ketorolac ophthalmic (Acular)

NSAID; often used in conjunction with steroids in treating CME. Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.

Diclofenac ophthalmic (Voltaren)

NSAID; often used in conjunction with steroids in treating CME. Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which in turn decreases formation of prostaglandin precursors. May facilitate outflow of aqueous humor and decreases vascular permeability.

Bromfenac ophthalmic (Prolensa, Bromday)

Often used in conjunction with steroids in treating CME. Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation. Reported to have better penetration into the posterior segment.

Nepafenac ophthalmic (Nevanac)

Often used in conjunction with steroids in treating CME. Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation. Converts from prodrug into active amfenac inside the eye by ocular tissue hydrolases.

Carbonic anhydrase inhibitors

Class Summary

Active in drying macular edema in select situations. Usually of minimal benefit with undesirable systemic side effects.

Acetazolamide (Diamox)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which in turn reduces intraocular pressure (IOP). Second-line drug for CME.

Vascular endothelial growth factor inhibitor

Class Summary

Inhibitor of vascular endothelial growth factor, a potent mediator of angiogenesis and capillary permeability.

Bevacizumab (Avastin)

Bevacizumab, an inhibitor of vascular endothelial growth factor (VEGF), was approved originally in the treatment of colorectal carcinoma. It is now used commonly via intravitreal injection to treat disorders such as exudative macular edema and retinal vein occlusion.[7, 8] Its use has been reported in treating nonpseudophakic CME as well.

Pegaptanib (Macugen)

Pegaptanib sodium is a stable RNA aptamer that binds to an isoform of VEGF. It is FDA-approved to treat age-related macular degeneration through intravitreal injection, and is awaiting approval as a treatment for diabetic macular edema. It has also been used with photocoagulation treatment to improve results.

Ranibizumab (Lucentis)

Ranibizumab is an antibody that blocks the entire VEGF family of proteins. It is FDA-approved to treat age-related macular degeneration.

Aflibercept intravitreal (Eylea)

Aflibercept intravitreal is a fusion protein to treat diabetic macular edema, and potentially central retinal vein occlusion. In the DA VINCI study, it was found more effective than laser photocoagulation in showing long-term improvement in visual acuity and reduction in central retinal thickness. It is FDA-approved to treat age-related macular degeneration.

Photosensitizing Agents

Verteporfin (Visudyne)

It is FDA-approved to treat age-related macular degeneration.