EyeWorld Asia-Pacific September 2018 Issue

Views from Asia-Paci c Lewis LEVITZ, MD Vision Eye Institute, Melbourne, Australia 27 Denmark Hill Road, Hawthorne East, 3123, VIC, Australia Tel. no. +61-(0)437224244 Fax no. +61-03-98823312 lewis.levitz@visioneyeinstitute.com.au I s there an association between pseudophakic cystoid macular edema and postoperative glaucoma drops? A recent article suggests an association with postoperative prostaglandin analogue (PGA) or beta-blocker (BB) usage and the finding of pseudophakic cystoid macular edema (PCME). The study 1 used the PharMetrics Plus database of over 150 million patients. 508 cases were assessed to have developed PCME following cataract surgery out of 19,979 eligible cases. These patients were matched with 5,080 post-cataract surgical patients of similar age and gender. The findings were interesting and unexpected. Patients on postoperative beta-blockers were found to have an increased relative risk ratio of 2.64 of developing PCME. The relative risk of PCME in the patients using postoperative prostaglandin analogues was 1.86. The postoperative use of either a PGA and beta-blocker was therefore reported as being associated with an increased finding of PCME. Is there a lesson to be extrapolated from this study which would change one’s clinical practice? A comprehensive contemporary review of the literature 2 , published in late 2017 found no convincing evidence that PGA should be withheld in the perioperative period. It also referenced four phase 3 trials that did not demonstrate a causal relationship between latanoprost and either aqueous flare or a cellular response in the anterior chamber. One way to reconcile the results from these two differing contemporary reports is to take into consideration that intraoperative complications were not accounted for in this study. Almost all reported cases on macular edema in pseudophakic patients receiving latanoprost have some risk factor for the development of CME, including ruptured posterior capsule, history of uveitis or complicated cataract surgery with vitreous loss. 2 An early study purporting to show that the blood aqueous barrier may be disrupted by PGA showed that half the patients had ruptured posterior capsules 3 . The ICD coding used in this retrospective study did not provide information as to whether the pseudophakic patients were on glaucoma medication due to high pressure associated with complicated surgery. These complications in themselves may also increase the risk of PCME. The preservative benzalkonium chloride (BAK) itself may have been responsible for the CME. In fact, the term “pseudophakic preservative maculopathy” has been proposed for CME caused by anti-glaucoma eyedrops. 4 The authors of the study must be commended on reporting on the largest cohort to assess for an association between PCME and postoperative beta-blockers or PGA. It is up to the clinician to realize that the study did not show any causality and may not therefore influence current clinical practice. References 1. Wendel C, et al. Association of postoperative topical prostaglandin analog or beta-blocker use and incidence of pseudophakic cystoid macular edema. J Glaucoma . 2018;27(5):402–406. 2. Razeghinejad MR. The Effect of Latanaprost on Intraocular Inflammation and Macular Edema. Ocul Immunol Inflamm. 2017:1–8. 3. Arcieri ES, et al. Blood-aqueous barrier changes after the use of prostaglandin analogues in patients with pseudophakia and aphakia: A 6-month randomized trial. Arch Ophthalmol. 2005;123(2):186–192. 4. Miyake K, et al. ESCRS Binkhorst Lecture 2002: Pseudophakic preservative maculopathy. J Cataract Refract Surg. 2003;29:1800–1810. Editors’ note: Dr. Levitz declared no relevant financial interests. continued on page 32 EWAP CATARACT/IOL 31 September 2018