Eyeworld

85 EW RESIDENTS August 2014 appears sufficiently low as to raise concerns over the number needed to treat to prevent 1 case of CME. Supposing the addition of nepafenac could reduce the rate of CME by 1% (which would require a study of 3,600 patients to demonstrate, as discussed above), 100 patients would need to be treated to prevent one case of CME. This raises the issue of cost-benefit analyses. However, if one were to factor in calculations for the number needed to treat in order to reduce ocular discomfort and photophobia, the findings in this study support nepafenac use. Lastly, one must put the study's chosen medications in context of other available drugs. This study used dexamethasone as the control topical drug, which, while system- ically more active, has less ocular penetration than other topical steroids. Moreover, while this study evaluated nepafenac 0.1%, there are a number of commercially available NSAIDs—ketorolac, diclofenac, bromfenac—in existence and in various concentrations and formula- tions. All are proven to be useful in treating existing CME, but the subtle differences between these need to be better studied. In summary, this study adds helpful information regarding nepafenac as combination therapy when used with dexamethasone in preoperative cataract surgery care. It also provides important consider- ations that need to be better clari- fied, particularly regarding the use of macular thickness as a surrogate for risk of developing PCME. Given the relatively low rates of PCME in low-risk patients undergoing cataract surgery, further multicenter prospective studies investigating the occurrence of PSCME, subclini- cal PCME, and differences between the various commercially available NSAIDs would be helpful to give more compelling answers and to provide more guidance on preferred practice patterns. EW Contact information Challa: pratap.challa@duke.edu on preventing PCME, the rate of PCME in this study population is neither a primary nor secondary outcome measure. The authors do report the rate of PCME in their study populations—2 patients in the control arm of the study and 0 in the combination treatment arm— which was not statistically signifi- cant (p=0.5099). Given the low rate of postoperative CME in cataract surgery patients at baseline, the sam- ple size required to identify a mean- ingful change in CME rate would be large, as the authors acknowledge, which is a major limitation to many published studies on this topic. For instance, supposing a 2% basal rate of postoperative CME with the con- trol regimen, approximately 1,800 patients would be required in each arm of a study in order to detect a 1% decrease in CME rate with the addition of nepafenac at 80% power. The authors, recognizing the lack of PCME as a measureable out- come, argue for an increase in mac- ular thickness as a surrogate marker for developing PCME. However, this presumes that the chosen outcome measures 1) increased macular thickness at 3 and 6 weeks and 2) rate of macular swelling >10 µm at 3 and 6 weeks are indeed precursors to PCME in the postoperative cataract surgery patient. The results would carry greater weight and relevance if the threshold of 10 µm measured by Stratus TD-OCT arbitrarily chosen by the authors was justified in a clinical or basic research context in regard to PCME pathophysiology. This is es- pecially true given that the authors report the absence of corresponding differences in visual acuity or aque- ous flare at the same time points in OCT measurements were acquired. With reports that a reduction in contrast sensitivity can be seen with subclinical macular thickening, it would have been interesting if this were a reported outcome measure in this study. If the authors' primary outcome measures were proven to be precur- sors to PCME, the rate of conversion from these conditions to PCME 0.1% versus dexamethasone surgery" 19 TH ESCRS WINTER MEETING www.escrs.org 20 – 22 February 2015 ISTANBUL In conjunction with Turkish Ophthalmology Society Cataract & Refractive Surgery Section

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