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.
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.
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.
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.
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
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.
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
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.