46-year-old Asian patient underwent cataract extraction due to posterior subcapsular opacities. The right eye was first, with a visual acuity on the first day post-op of 20/30 by pinhole. All post-op elements were unremarkable except for a 3+ anterior chamber (AC) reaction. He was to continue the standard medication regimen (Zymar [0.3% gatifloxacin, Allergan]), Pred-Forte [1.0% prednisolone acetate, Allergan]) and Nevanac [0.1% nepafenac, Alcon]) q.i.d. for one week. At this visit, the AC had quieted to 1+. BCVA was 20/25 with +0.75 -2.00 x015. We prescribed Pred-Forte and Acular LS (ketorolac 0.4%, Allergan) t.i.d. for the next three weeks.

The patient returned two months post-op and noted he'd discontinued all topical medications approximately six weeks earlier. BCVA was only 20/50 with the same prescription lens. Optical coherence tomography (OCT) indicated that the central macular thickness was 337μ, which is consistent with cystoid macular edema (CME) (the normal value is about 150μ). Other OCT images were also consistent with the diagnosis. This was a case of acute CME rather than chronic CME, which typically occurs about three to four months post-op.

We resumed t.i.d. treatment with Pred-Forte and Acular LS. The anterior chamber was quiet. The patient underwent cataract extraction with IOL placement in the left eye and returned for evaluation one week following the procedure. This visit coincided with the threemonth visit for the right eye. BCVA was 20/25 OU.

The patient was using the topical drops as directed (standard post-op regimen as above, OS). OCT indicated that the central macular thickness had resolved 156μ. The left eye was showing some signs of macular thickening, but VA remained good. We decided to continue the Pred-Forte and Acular LS OU. We'll follow the patient on the standard postop schedule for the left eye (two months) and we'll evaluate the right eye for resolution of CME.

CME was considered a thing of the past with the application of clear corneal incisions. The gold standard for definition was fluorescein angiography. With newer non-invasive imaging such as OCT or with confocal scanning laser ophthalmoscopy (HRT III with macular module, Heidelberg Engineering), perhaps we'll discover more post-op CME. However, we'd have no reason to perform such a test on an asymptomatic patient. In our case, with reduced VA, imaging demonstrated the cause. Treatment with NSAIDs and steroids is generally effective with b.i.d. or t.i.d. dosing over four to six weeks.

There's controversy over the etiology of CME following cataract surgery. Clinicians believed prostaglandins played a role and prophylactically administered oral NSAIDs many years ago. These became unnecessary with refined cataract procedures.

The contemporary model for CME involves breakdown of the blood-retinal barrier potentiated by preservatives. It may make sense to reduce the topical preservative load for patients undergoing cataract surgery.

With current imaging capabilities, we may discover the true prevalence of CME. In the meantime, pre-operative treatment with topical NSAIDs may prevent symptoms from occurring.