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CME rate low after cataract surgery
The low incidence of postop CME was attributed to the use of NSAIDs.
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Acute cystoid macular edema occurs in a low percentage of patients after cataract surgery, according to a study.
Among 2,862 surgical cases, only three (0.1%) confirmed cases of postoperative cystoid macular edema (CME) occurred within 90 days after surgery, according to a retrospective chart review.
All patients who underwent phacoemulsification and IOL implantation at a private clinical practice in Eugene, Ore., between March 2007 and March 2012 were included in the study. In all cases, topical steroids and nonsteroidal agents were used as prophylactic treatment.
“We wanted to determine the amount of CME that is actually occurring in clinical practice when you do use nonsteroidals,” principal investigator Mark Packer, MD, told Ocular Surgery News.
Use of NSAIDs
Packer said using NSAIDs on a routine basis at the time of cataract surgery remains controversial.
“There is not a prospective, randomized controlled trial of adequate power to convince everyone that using these drugs actually reduces the incidence of CME as a consequence of postoperative inflammation after cataract surgery,” he said.
Packer believes that NSAIDs are helpful.
“They have been proven to be effective in reducing postop inflammation,” he said. “But as to whether or not they truly reduce the incidence of CME, I think the jury is still out.”
The study, which appeared in the Journal of Cataract & Refractive Surgery, noted that the gold standard for IOL approval is the U.S. Food and Drug Administration Grid of Historical Controls, which lists an acceptable cumulative incidence of 3% for pseudophakic CME.
“I attribute our lower rate to the use of nonsteroidals,” Packer said, because their use is a change in care that has taken place since the grid was established. “Previously, no one was using nonsteroidals. Everyone was just using a steroid.”
Cases with CME
Of the three study cases in which acute postop CME developed, case 1 involved implanting an anterior chamber IOL after capsule rupture.
“This is a classic case where you would expect to see some CME and perhaps be prepared by using a longer course than normal of topical anti-inflammatories,” Packer said. Poor patient compliance with the medication schedule may also have played a role.
Case 2 was a patient with a history of diabetic retinopathy.
“These patients are prone to get macular edema anyway and are more prone to macular edema after cataract surgery, so you should be on guard,” Packer said, adding that he often refers such patients for a retina exam before surgery. “They might need some laser or an Avastin (bevacizumab, Genentech) injection to get things under control.”
Case 3 was a routine case.
“This was a perfect, flawless case with no complications and yet [had] a significant course of CME. It is unclear as to what we might have done to prevent it. Some of these cases just happen, and we don’t know why,” Packer said.
“What is interesting, though, is that all three cases were initially treated prophylactically with an older drug, ketorolac, but once CME developed, they were treated with a more recent drug, bromfenac,” he said. “Hence, I think there is a perception that if someone develops CME, you want to use the latest and greatest drugs.”
Because the more modern, patented NSAIDs are more expensive, there is a tendency to use generic drugs, he said.
“When there is not a financial issue for the patient, I recommend the most potent agents,” he said.
Packer also advocated the use of more recently developed NSAIDs when implanting a premium lens or when there are risk factors such as a complicated case or diabetes. Extending the course of treatment from 3 weeks to about 6 weeks may also reduce the likelihood of CME, he said.
If resolution does not start within 2 weeks, Packer said that giving an intravitreal injection of an anti-VEGF is a reasonable treatment for eliminating CME. – by Bob Kronemyer