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Case 2: Treating nAMD With PED


Adrienne Scott, MD, presents a case of neovascular AMD with PED in a patient who experiences a stroke while on anti-VEGF therapy.

Arghavan Almony, MD: Let’s move on to the next case. Adrienne, if you could present this case for us.

Adrienne Scott, MD: Thank you very much. This is a patient whom I encountered in my clinic. He’s a 73-year-old man [with] a history of long-standing intermediate AMD [age-related macular degeneration]. He came in acutely, [presenting with] a new onset central scotoma in his right eye for [approximately] 1 week. No symptoms in the left [eye]. He has no positive past ocular history. He does have a past medical history, significant for hypertension and some psoriasis. He uses steroid cream occasionally, and he is [adherent] using his AREDS 2 oral supplementation as directed. He does have a family history of neovascular AMD.

He’s got 2+ brunescent cataracts at baseline, [and his] vision is 20/32 in each eye. This color fundus photo shows multiple large soft drusen throughout the macula and some drusenoid PEDs [pigment epithelium detachments]. I bring your attention to the central foveal PED that is most easily seen on the OCT [optical coherence tomography] scan encompassing the fovea. Not only is there a foveal PED that has a substantive height, [but] there’s also this hyperreflective material on the underside of the PED, which may be concerned for this being a fibrovascular PED.

After discussion with the patient, we decide to treat him with a course of anti-VEGF therapy. This fluorescein angiogram also helps confirm the presence of the PED with filling in the later frames. We started off with a course of aflibercept for his right eye; the subfoveal PED after serial aflibercept injections is imaged here. You can see very little anatomic response from the PED height. It seems about a similar height. There doesn’t appear to be much in the way of subretinal fluid at this point, and [his] vision remains stable, [at approximately] the 20/30 minus to 20/40 range throughout the course of treatment.

This is an excellent patient to treat because he is very much adherent to the treatment regimen recommended. He makes his appointments. He’s very clear about his response to vision after each injection. He feels like the vision does somewhat improve after each injection but wears off [approximately 1] week before it’s time for his next injection, so this is Q4 week treatment.

After several Q4 weekly treatments, we noticed something interesting about this PED—it’s growing in height. The vision is about stable at the 20/32 level, but the PED height has increased and you start to see these areas of subretinal fluid at the border of the subfoveal PED here, so we stay the course and continue to give monthly aflibercept injections. You can see in the subsequent frames [that] the PED is growing in height and the subretinal fluid tends to wax and wane. But for the most part, definitely higher PED and more subretinal fluid than was present at baseline, despite serial monthly treatments with aflibercept.

This is an image of his right eye. Again, this was after several treatments with serial aflibercept. [His] vision is dropped [to approximately] 20/50 plus. You can see at the border of the PED, which is also larger in size, an increase in subretinal fluid. Again, the patient’s very specific. He can outline the exact contour of the scotoma in his vision, [which is] enlarging when the subretinal fluid is present. We repeat the fluorescein angiogram, and [it] confirms [the] increasing size of the [PED] compared [with] baseline. You can see these pictures juxtaposed with the size of his PED at baseline, and then following 6 serial aflibercept injections.

At this point, we wanted to confirm it was truly choroidal vascularization we were treating, so we opted for an OCT angiogram. These are research images courtesy of our colleague Amir [Hossein] Kashani[, MD, PhD]. We see the fibrovascular PED on the right but no real choroidal neovascular net that’s imaged here, and certainly the drusen in the left without choroidal neovascularization, so we decide to continue treating with aflibercept monthly. [His] vision is fluctuating from the baseline of 20/30 all the way down to 20/50, but you can see the PED continues to grow in width and height. Similarly, the PED continues over the subsequent months of treatment, and we continue to give aflibercept monthly injections.

[In] August, [his vision is] 20/32 [and] PED is expanding almost to the area of the vascular arcades with extension of subretinal fluid. Then you can also see the image similarly, in September 2022 after several serial aflibercept injections, the subretinal fluid continues to expand. At the September [20]22 visit, 3 hours after the patient [received an] injection of intravitreal aflibercept, he acutely noticed a weakness in dysarthria and went to the emergency [department] and was diagnosed with a stroke. He was noticing an upper right quadrant anopia, and [magnetic resonance imaging] was confirmatory of a stroke with an acute infarction involving the left [posterior cerebral artery] territory. This was indeed an embolic stroke.

At this point, we were challenged by how to continue. We decided to hold any anti-VEGF injections. We did seek consultation with his neurologist, who was following him after the stroke, and neuro-ophthalmology, who we wanted to have input on the visual field defect. Both gave counsel to proceed with anti-VEGF with caution, if not discontinuing altogether. We can see here what happens after holding the anti-VEGF therapy for 2 months’ time. This PED has continued to grow and has grown even larger, with a large increase in the subretinal fluid. [His] vision is down to 20/80. You might notice the degradation of the image quality here, and that’s because his cataract is also worsening in density.

After the patient had the acute stroke, we had an in-depth consultation with both his neurologist and our neuro-ophthalmology team…. We did a deep dive and tried to best understand the risk-benefit alternative ratio in this patient with acute stroke and continued anti-VEGF therapy. It really came down to a conversation with the patient. You can see his vision has worsened to 20/80 after holding the anti-VEGF treatment for 2 months after the acute stroke. We’re watching the patient’s vision worsen. Most importantly, the patient is getting very concerned because not only does he have the visual field defect, [but] he’s [also] noticing worsening of his central vision after holding the anti-VEGF. At this point, he’s down to 20/80 and is very symptomatic from the central scotoma and the new onset visual field defect.

After our discussion, he wanted to proceed with anti-VEGF treatment. I decided to switch him to faricimab. At this visit we gave [his first] faricimab [injection]. After his first faricimab, we see slightly more consolidation of the PED and a decrease in the subretinal fluid. This was a promising treatment response to faricimab, and certainly there [are] data that suggest that faricimab performs very well with [PEDs]. I am convinced this patient had a better anatomic response with faricimab as opposed to the serial aflibercept we had him on earlier. While we’re treating him, [his] cataract is worsening. So, at this point, this is how he looks to this day. He’s had 4 serial faricimab injections, each monthly, and the PED is consolidated quite a bit more than it had been previously, with near resolution of the subretinal fluid. [His] vision is 20/125 and cataract surgery is pending. I plan to work with the anterior segment surgeon to make sure I inject faricimab within 1 or 2 weeks prior to the planned cataract surgery.

Transcript is AI generated and edited for clarity and readability.

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