Managing Geographic Atrophy in 2026

When Talia R. Kaden, MD, examined the images of an 82-year-old patient, there was a lot to consider. In both the near-infrared and optical coherence tomography (OCT) b-scan images of the patient’s right eye, she observed subretinal drusenoid deposits (SDDs)—also known as reticular pseudodrusen—alongside atrophic lesions of the retina, the retinal pigment epithelium (RPE), and the choriocapillaris. These findings were indicative of one thing: geographic atrophy (GA). There are many questions to answer when managing GA patients, but even considering them requires a solid understanding of the condition.

In this session, Dr. Kaden, an associate professor of ophthalmology and director of the vitreoretinal fellowship at Northwell Health, breaks down everything practitioners need to know about managing GA in 2026.

First described in 1885 by Otto Haab,¹ and named nearly 90 years later by Don Gass,² GA is the most advanced form of age-related macular degeneration (AMD), not neovascular or dry in nature. As Dr. Kaden’s case highlights, GA is characterized by complete RPE and outer retinal atrophy (cRORA), which is diagnosed using the following OCT biomarkers:

“Incomplete RPE and outer retinal atrophy (iRORA) has a five times greater risk of progression to GA (cRORA),” Dr. Kaden highlights.³ “Hyperreflective foci and SDDs, both of which can also be seen on OCT, also each carry a five-times greater risk of progression over a two-year period. So it's important to pay attention to what we're seeing when we look at the OCTs of our patients.” Regarding the lesions themselves, multifocal and larger lesions, a lack of subfoveal lesions, and SDD are all associated with higher rates of progression.

At present, there are two FDA-approved drugs for treating GA: pegcetacoplan and avacincaptad pegal (ACP). Both of these therapeutics work to inhibit the complement system, a signaling cascade well-documented as playing a role in GA development and progression.⁴ There are also several investigational agents being studied. “These include a single injection gene therapy, the subretinal delivery of human RPE cells, and an intravitreal trial currently in phase 3. There are exciting things coming down the pipeline,” she notes.

But, as with all treatment modalities, there’s lots to ask beyond simply what to prescribe. “It's important to think about how we counsel GA patients—do we suggest complement inhibitors? Assuming both eyes are similarly impacted, do we treat them both; if so, do we do so on the same day? What if one eye has ‘counting fingers’ vision with central atrophy? Does that change which drug we use—and do we try it in the poor-seeing eye first? These are all important questions to think about.” And once the treatment regimen is decided, patients still need to be carefully monitored.

Two months after starting her 82-year-old patient on complement inhibitors, Dr. Kaden noticed evidence of a little subretinal fluid. “Seeing that, the question became, ‘what’s going on?’” explains Dr. Kaden. “Is it actually evidence that she’s converted to neovascular AMD—a common risk with these drugs?” To clarify this, she obtained a fluorescein angiogram, but there wasn’t any leakage consistent with a neovascular membrane—but what if there had been? “Do we offer the patient simultaneous treatment—which is how it was done in the clinical trials, have them come back on another day for the complement inhibitor injection, or stop treating with the complement inhibitor and just continue treating the neovascular membrane?” Dr. Kaden asks. “None of these options are wrong or right, but it's good to think about them in advance of seeing these patients so you're prepared.”

However, not all atrophy is GA. For example, Dr. Kaden saw a 78-year-old patient referred for possible complement inhibition therapy; but when she considered his OCT images, although she observed atrophy, there weren’t any other AMD hallmarks. Through genetic screening, she demonstrated that he instead had an inherited retinal disease, and wasn’t a good complement inhibition candidate. “This is a reminder to always look at all atrophy and ensure we know we're treating GA for macular degeneration and not atrophy from another disease.”

But that still leaves the question of when patients with potential GA should be referred in the first place. “I would argue that any patient today with any kind of atrophy should be seen by a retina specialist so that, if they're a good candidate for complement inhibition, they can have that conversation with their doctor,” advises Dr. Kaden. She points to one final patient as an example of the potential impact late referrals can have. This patient was referred to Dr. Kaden in 2024, at which point she began complement inhibition therapy—however, when she looked back at his retinal nerve fiber layer images that had been taken going back eight years, there were already areas of atrophy, which had continually grown in size—something that an earlier referral might have stopped.

Because unmanaged GA can greatly impact patients’ quality of life. “100% of GA patients report difficulty reading, 75% report difficulty with driving, and 63% report having difficulty with activities of daily living (ADLs),” Dr. Kaden highlights.⁵ “GA patients have a higher risk of developing depression and anxiety from the loss of independence and difficulties with ADLs—this may actually be more pronounced in patients with unilateral blindness, often due to fear over losing the vision in their functioning eye.⁶ GA patients are also often more likely to suffer a fall,⁷ and in a prospective cohort study from the late '90s, Medicare patients who had AMD with GA often had a higher rate of hip fractures compared with patients who did not have AMD.”⁸

This is why early, effective intervention is crucial, not just in limiting the ocular impacts patients might experience—but also those that can grow to limit the quality of the rest of their lives.