Eyeworld

JULY 2023 | EYEWORLD | 73 G Contact Eisengart: EISENGJ@ccf.org Kombo: ninani.kombo@yale.edu Tirpack: ATirpack@cvphealth.com Relevant disclosures Eisengart: None Kombo: None Tirpack: None so the normal flow of aqueous from the anterior chamber to the posterior chamber is obstructed, causing acute elevation of pressure." Dr. Kombo also addressed the use of laser procedures for uveitic glaucoma patients. There have been some studies that have shown that in well-controlled uveitis, this is a successful treatment. Cyclodestructive procedures may be used in select cases, but Dr. Kombo said you need to be careful because they can exacerbate inflammation, and the ciliary body can develop fibrotic membranes and result in hypotony. Dr. Eisengart said that while aqueous sup- pressants like beta blockers, carbonic anhydrase inhibitors, and alpha-2 agonists are effective in both typical glaucoma as well as uveitic glauco- ma, prostaglandin analogs are considered "last line" in uveitic glaucoma, as they may promote inflammation or macular edema. Miotic agents like pilocarpine are generally contraindicated in glaucoma, he added. "There is some emerging data that rho-kinase inhibitors may be effective in steroid-response glaucoma, but I think more data is needed to say this definitively." As for surgical options, Dr. Eisengart said that tube implants have traditionally offered the best success in patients with uncontrolled uveitic glaucoma. More recently, glaucoma doctors have come to understand that many of these patients with controlled anterior segment inflammation are best served with angle-based procedures such as goniotomy or GATT, he said. "These later procedures have made a tremen- dous impact in our practice because they are faster, safer, and often more effective than tube implants in these patients," he said. In patients with vision-threatening uveitis, preserving vision requires liberal use of topical, intravitreal, and/or systemic steroids, Dr. Eisen- gart said. "My job as the glaucoma specialist is to control the intraocular pressure so that my uveitis colleagues may apply these steroids as aggressively as needed to protect the patient's vision," he said. "If my uveitis specialist col- league can formulate an appropriate treatment plan for the patient without worrying about the intraocular pressure, I have done my job." Otherwise, Dr. Kombo said the treatment is similar to what is done for other types of glau- coma. You want to make sure you bring down the pressure. Aqueous suppressants like beta blockers and carbonic anhydrase inhibitors are the go-to medications, she said, and with more severe glaucoma, you would escalate to surgical options. While MIGS may be an option for these patients, Dr. Kombo said there is limited pub- lished data. Some has shown that Trabectome (MicroSurgical Technology) has about a 75% success rate, but we don't know what the safety profile is or what the long-term results are, she said. In pediatric patients, goniotomy is first line, she said. The concern with uveitic glau- coma and MIGS is that devices like the iStent (Glaukos) and Hydrus (Alcon) may become clogged from fibrin or affected by inflammation, making the device ineffective. Dr. Kombo added that for a well-controlled uveitis patient with no active inflammation, the jury is still out on the effectiveness, and more data on MIGS in these cases is needed. Tube shunts and glaucoma drainage devices have shown great results, she said. Depending on the study, there is a 70–80% success rate with tubes, and there is some long-term data (3–5 years), with the caveat being the better the control of the inflammation, the better the success. Success drops when there's active inflammation to about 50%. Similarly, with trab- eculectomy, Dr. Kombo said it will fail half the time if inflammation is present. In terms of the pressure that can be expect- ed after treatment, Dr. Kombo said it will vary from patient to patient. "You want the lowest or optimal pressure you can get to prevent progres- sion of optic nerve damage," she said. She added that it's important to realize that there are multiple mechanisms that create glaucoma in uveitis patients. "One of them is the treatment itself that we need to give the pa- tients to reduce inflammation, the steroids. This is called steroid-induced glaucoma," Dr. Kombo said. "Another mechanism is that the inflam- mation causes significant fibrin deposits and scarring, and the inflammatory cells can clog the trabecular meshwork, resulting in an open angle glaucoma type where outflow is dam- aged from inflammation. The other mechanism is where patients develop either anterior or posterior synechiae and there is angle closure,

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