J. Michael Jumper, MD, a retina specialist, described how retina treatments relate to glaucoma–not only injections, but also vitrectomy and laser treatments can trigger glaucoma.
Anti-vascular endothelial growth factor (anti-VEGF) and corticosteroid injections are adding to the increased prevalence of glaucoma, according to J. Michael Jumper, MD. “We’re talking about glaucoma caused by retina specialists,” he said.
Dr. Jumper, a retina specialist and assistant clinical professor of ophthalmology, University of California, San Francisco, described how retina treatments relate to glaucoma–not only injections, but also vitrectomy and laser treatments can trigger glaucoma–during the Glaucoma Symposium CME at the 2016 Glaucoma 360 meeting.
Among Medicare fee-for-service patients, ophthalmologists will perform three times as many intravitreal injections as cataract surgeries in 2016, Dr. Jumper said. Most of these will be anti-VEGF injection therapy, but the number will also include injected corticosteroids, mainly triamcinolone, as well as implanted dexamethasone (Ozurdex, Allergan), and fluocinolone (Retisert, Bausch + Lomb, and IIluvien, Alimera Sciences).
Dr. Jumper cited a meta-analysis (Surv Ophthalmol. 2013 Jul-Aug;58(4):291-310) showing that the different drugs cause ocular hypertension at different rates.
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In that study, the researchers found that 32% of patients develop ocular hypertension following a 4-mg intravitreal triamcinolone injection, 66% following a 0.59-mg fluocinolone implant, 79% following a 2.1-mg fluocinolone implant, 11% following a 0.35-mg dexamethasone implant and 15% following a 0.7-mg dexamethasone implant.
Ocular hypertension was defined as either intraocular pressure (IOP) ≥ 21 mm Hg or ≥ 10 mm Hg from baseline or IOP ≥ 25 mm Hg or ≥ 10 mm Hg from baseline.
“You can get a hint that fluocinolone is going to create higher rates of ocular hypertensions,” said Dr. Jumper. “It’s important to note that the Retisert implant requires incisional surgery in about 45% of patients who receive it.”
The reason some corticosteroids are more likely to provoke ocular hypertension than others could be that they stimulate different kinds of gene expression within cells. “Their steroid response also definitely relates to the strength of the drug, the length of time it works, and the dose,” Dr. Jumper added.
Sometimes, Dr. Jumper has tried to gauge a patient’s response to corticosteroids by challenging them with topical difluprednate or prednisolone acetate. But given the variability from one corticosteroid to another, he wondered if this is an effective test.
Corticosteroids also are not the only substances that can raise the risk of glaucoma as a result of an intravitreal injection. Anti-VEGFs have also been associated with both transient and sustained pressure elevation, said Dr. Jumper.
The transient elevation is common, she said. In some of his patients, it reaches 40 mm Hg, but it resolves quickly. Research has shown it drops below 25 mm Hg within 30 minutes in 97% of patients, he added.
Risk factors for a significant pressure elevation include smaller gauge needles, Dr. Jumper said. “It turns out that using a small gauge needle allows less reflux after the injection and therefore you have a higher pressure rise,” he said.
Patients with pre-existing glaucoma also are likely to have sustained or a higher transient and long-lasting transient pressure rise, Dr. Jumper added.
Sustained IOP elevation has been reported in 2.4% of eyes receiving intravitreal injections of any chemical, excluding steroids, Dr. Jumper said. Some studies have reported an incidence as high as 11% in case series of patients receiving anti-VEGF injections, including significant elevations.
Such findings highlight the importance of referring patients who receive these injections to glaucoma specialists or general ophthalmologists to monitor their risk of glaucoma, he said.
Though the definitive reason why anti-VEGF medications trigger pressure elevation has not been found, researchers have proposed several mechanisms. These include the pharmacological effects of VEGF blockade itself; inflammatory mechanisms, such as trabeculitis; and obstruction caused by particulate matter, such as silicon, particularly in compounded medicines.
“Then just repeated intermittent spikes may have something to do with long-term glaucoma,” Dr. Jumper pointed out.
Glaucoma and retinal disorders also can go hand-in-hand, Dr. Jumper said. He cited reports of patients with open angle glaucoma and rhegmatogenous retinal detachment.
“These often were low-lying detachments,” Dr. Jumper said. “It was felt that there was some communication between the subretinal space and the anterior chamber that led to this kind of reaction in the anterior chamber.”
One possible mechanism is that photoreceptors are being shed and getting into the anterior chamber.
Retina specialists also treat other conditions associated with inflammatory glaucoma, Dr. Jumper said. He mentioned herpes, toxoplasmosis, Posner-Schlossman syndrome, sarcoidosis, and syphilis.
“In central vein occlusion, IOP may be lower in the affected eye at the time of diagnosis so that you may not discover the glaucoma until you check the other eye,” he pointed out.
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Turning to hypotony-related conditions that affect the retina, Dr. Jumper mentioned choroidal detachment and hypotony maculopathy. “The thing I want to point out for those is that I’m able to drain serous choroidal detachments,” he said. “But these tend to come back unless we do something to get that pressure just a little bit higher.
“And what pressure is required to keep the choroidals from coming back, or the hypotony maculopathy, is variable from one patient to the next, and that’s a conundrum that I work out with our glaucoma colleagues,” Dr. Jumper added.
Dr. Jumper said he enjoys working with glaucoma specialists on combined glaucoma and vitreous surgery. “Sometimes at the time of vitrectomy I will do endocyclophotocoagulation,” he said. “But much more effective is tube shunt surgery with vitrectomy.”