44 EyeWorld Asia-Pacific | December 2024 CORNEA trabeculectomy or tube placement, may have associated endothelial compromise, she said. Possible mechanisms of endothelial cell loss include altered circulation patterns of aqueous humor, intermittent tube-cornea touch, or elevated oxidative and inflammatory markers.2 Along similar lines, chronic inflammation in patients with a history of anterior uveitis can impact endothelial cell health.3 When evaluating patients preoperatively, Dr. Syed said certain features forecast further endothelial decompensation after cataract surgery. Preoperative microcystic edema, stromal thickening on the slit lamp, low central endothelial cell density (<1,000 cells/mm2), and/or increased central corneal thickness (>640 microns) predict deteriorating postoperative endothelial function.4 Dr. Syed said that some intraoperative variables that may aggravate endothelial cell loss include the length of surgery, inappropriate use of instruments, excessive phacoemulsification energy, toxicity from intracameral medications, vitreous loss, and IOL endothelial touch. Phacoemulsification may damage endothelial cells by the production of free radicals,5 and patients with compromised endothelium are vulnerable to potentially detrimental effects. “Strategies to reduce the risk of endothelial damage during cataract surgery include use of technology such as femtosecond lasers that may reduce phacoemulsification energy requirements, increased use of mechanical chopping, or frequent reapplication of viscoelastic to protect the corneal endothelium from phacoemulsification energy.” Dr. Price said one of the basic things physicians can do is manage viscoelastic. He prefers the softshell technique, where you lightly fill the anterior chamber with a dispersive viscoelastic. “Then you go in with a little bit of cohesive viscoelastic and put it on top of the lens, and that helps prevent iris prolapse during hydrodissection and hydrodelineation,” he said. “If it’s all dispersive, it can build up the pressure, and you could pop the iris out.” “The other thing you need to be careful with,” Dr. Price said, “are shallow anterior chambers because there’s not as much working space. You want to carry out the surgery, while keeping the phaco as much as you can in the posterior chamber and not the anterior chamber.” “With a dense nucleus requiring extra energy, consider reapplying a dispersive viscoelastic a few times to protect the cornea.” “You might even want to consider a different approach to cataract surgery if the nucleus is dense. While not commonly done in the U.S.,” Dr. Price said, “for a rock-hard cataract, you might consider using manual small incision surgery, which includes making a 7–8 mm incision and expressing the nucleus manually.” After surgery, for those with endothelial damage and/ or cell loss, Dr. Price said it’s important to treat the inflammation to try to minimize the amount of damage. At this point, there isn’t anything to inject to help cells regenerate, but there are a number of medicines being looked at that may stimulate endothelial cells to recover better. Dr. Price elaboated that his course of action is to increase steroids to decrease inflammation in the eye and use hyperosmotics, like sodium chloride ointments and drops, to pull out excess fluid while the remaining endothelial cells cover areas that were damaged. “We know from Descemet’s stripping only (DSO) that you can remove central Descemet’s membrane and endothelial cells, and peripheral endothelial cells will migrate over time and cover the denuded area,” he said. After cataract surgery, you’ll see this around the wound, and those damaged areas usually clear up in days to weeks after endothelial cells cover areas that were damaged. The left panel shows a pseudophakic eye with Fuchs dystrophy prior to DMEK. The view of the IOL is obscured by the thickened Descemet’s membrane and guttae. After removal of Descemet’s membrane (right panel), it became obvious that the eye had a multifocal IOL. Source: Matt Feng, MD
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