Cystoid Macula Edema Following Cataract Surgery

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 by Sadiqa Stelzner, MD, FACS on May 8, 2023.

Disease Entity


Cystoid macular edema (CME) involves retinal thickening in the outer plexiform and inner nuclear layers. These cystic changes arise due to fluid accumulation from breakdown of the perifoveal capillaries. This condition is typically associated with ocular inflammation, which can be precipitated by cataract surgery, a process known as pseudophakic CME.[1]

Risk Factors

Any patient undergoing cataract surgery is at risk for developing CME, a frequent postoperative complication that results in reduced vision. In particular, there are certain demographics that are considered higher risk developing CME. These include patients with diabetes, diabetic retinopathy, uveitis, posterior capsule rupture, vitreous prolapse, and prior retinal vein occlusions.[2] Old age and male gender have also been shown to be risk factors.[3]


Inflammation is believed to play a large role in the pathogenesis of CME.[4] Pro-inflammatory mediators such as Vascular Endothelial Growth factor (VEGF), prostaglandins, nitric oxide, cytokines, and several others are implicated in the inflammatory cascade that may arise after cataract surgery.[1] This inflammation leads to the destruction of the blood-retinal barrier and increases vascular permeability, which in turn leads to inner nuclear edema, outer plexiform edema, subretinal fluid and ultimately retinal thickening.[5] [6] While the exact pathophysiology of CME has yet to be fully understood, many factors have been implicated in its pathogenesis, such as vascular traction, vascular instability, and relative ocular hypotony.[7] CME may lead to permanent vision loss, even after the resolution of the edema.[8] This is thought to occur due to changes in photoreceptor architecture which is more common in chronic cases of CME.[9]



Symptoms typically present as decreased or blurred central vision, with best-corrected visual acuity (BCVA) less than 20/40, as well as mild photophobia and ocular irritation.

Clinical diagnosis

Clinically, pseudophakic CME is diagnosed by decreased visual acuity post-cataract surgery.[10]

Diagnostic procedures

The two main ways to diagnose pseudophakic CME are fluorescein angiography (FA) and more commonly, optical coherence tomography (OCT). In cases of CME, FA details a perifoveal petaloid stain with or without leakage from the optic disc. On OCT, pseudophakic CME will display macular thickening as well as cystic spaces in the outer plexiform layer.[11]



Practice patterns on CME vary given that spontaneous resolution of symptoms can occur following most uncomplicated cases.[12] No official FDA-approved preventative strategy for pseudophakic CME currently exists. One randomized controlled trial conducted in Europe led by the ECRS PREMED study group compared the efficacy of topical NSAIDS (0.09% Bromfenac), topical corticosteroid (0.1% dexamethasone), and a combination of both drugs to prevent the occurrence of CME after cataract surgery in non-diabetic patients.[12] This study found that a combination of both of these drugs was more effective at preventing CME than any of the drugs alone. Guidelines from the American Academy of Ophthalmology (AAO) indicate that NSAIDs should only be used in high-risk cases, such as patients who have diabetic retinopathy or uveitis.[13] A randomized, double-blind study showed that use of preoperative ketorolac for 3 days prior to surgery improved short term visual outcomes and incidence of CME, but there was no evidence that it affected long term outcomes.[14]

Medical Therapy

Treatment for CME varies from topical NSAIDs, topical steroids, intravitreal anti-VEGF, intravitreal steroids, posterior subtenon steroids, and systemic steroids.[3] Corticosteroids have been used to treat CME due to their anti-phospholipase-A2 activity, which prevents the release of arachidonic acid, thereby curtailing the inflammatory cascade. NSAIDs on the other hand, prevent prostaglandin synthesis by inhibiting the COX enzyme. Common ocular side effects of topical NSAIDs include burning, stinging, and conjunctival hyperemia.[7] Clinicians should also be cognizant of steroid-associated adverse effects, such as IOP elevation, delayed wound healing, and infection.[11] The latest treatment algorithm for CME comes from the Jampol lab where they used a combination of a topical NSAID and a topical corticosteroid, such as diclofenac and fluorometholone. If no improvement in vision is noted after 4-6 weeks, an alternate NSAID, such as nepafenac or bromfenac, may be used. If no improvement comes after 4-6 weeks of nepafenac/bromfenac, then an intravitreal corticosteroid may be considered.[7] In addition to this algorithm, it has been documented that in cases of treatment-resistant cystoid macular edema subtenon triamcinolone should be considered as a therapeutic option.[15]


CME tends to be a self-limiting disorder that resolves within 3-4 months. Chronic CME can persist for over 6-9 months and may produce permanent retinal fibrosis.


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