 I'm just gonna introduce myself. I'm Eileen Wong, I'm a third-year resident. So I'm gonna talk today about retinal pigment epithelial tears. I know this is a topic that really excites everyone, as I could tell by the turnout this morning. So I thought I'd throw in some travel photos. I recently got to go to Japan. My cousin had been a corporate lawyer for many years, and even though we're Chinese, she speaks Chinese, Japanese, and English fluently, but she recently quit her job as a corporate lawyer to work at the front desk at a hotel in a ski and ski out resort on the main island of Japan. So this is a photo from a nearby ski resort, and you can actually see the ocean from there, theoretically. So this is something I wanted to present at FA Conference when I was on retina, but I never got around to it because I kept getting assigned different other topics by the retina faculty. So that might indicate to you how interesting this is to them as well. Okay, so this is a case. It's a 45-year-old male. He had a mildly distorted central vision in his left eye. He had a history of keratoconus, for which he wore soft contact lenses, and dry AMD. So on exam, he was 2025 at the right, 2030 in the left. This was unchanged from baseline. With refraction, he had a significant amount of against role-sill, but this refraction didn't improve his visual acuity or the distortion he was experiencing. On AMSR grid, it's a little hard to, oops, the wrong thing. You can see he described a few swiggles here, centrally in that left eye. On slope-lamp examination, he had keratoconus with votes 3A in both eyes. He had moderate cataracts in both eyes. And on his dilated fundus examination, drusen and pigment changes were noted in both eyes. So what further testing would you like to get? I'll ask Rhys. A man for the RCT. Okay, any other testing that you'd like to get? Color fundus photos, auto fluorescence. Okay, so he saw his cornea specialist. So we got Topo, and you can see if you're seepening in both eyes. But he also did get a macular OCT, not all those other things you mentioned. And you can see some drusen in that right eye, and this is the left eye. I'll ask the next resident that I can see to describe the OCT in the left eye, that's Tara. There's a pointer over there, too. Oh, wow. Good, sounds like a beauty. Yeah, very good. So this hyporeflective area is a pigment epicellular detachment, or PEV, just as Tara said. So just to point out when there is hyporeflective stuff, it usually corresponds to fluid, and how do we tell that it's underneath the RPE? So we have these two lines here. This one's the ISOS junction, here's the RPE, and it's clear that the fluid is under the RPE. And you can kind of see post your hyalurve face here, and it's kind of attaching right at the phobia and kind of tenting it up a little bit, so a little bit of vitromacular attraction, as Tara said. Oh my God, what's my computer size today? Okay, here we go. So I'd like to pull the audience and see what you'd like to do next. Here are the options, and you could raise your hand with which one you want to go along with. So who wants to inject him for anti-veget? He's got some central distortion. He's got this pigment epithelial attachment. Raise your hand if you want to do that. Okay, no one wants to do that. How about observe? Who wants to observe? Okay, a lot of people want to observe. How about who wants to do a vitrectivine? He's got that vitromacular attraction, and you could fix it by releasing that. Anyone? Okay, seems like observing is pretty popular, and that is what his retina specialist, Dr. Bernstein, decided to do, and we'll talk about the rationale for that later. And then he followed up again four months later, saying that there were straight lines, like light poles, now have a wave to them, and that there's a spot in the middle of his vision that makes it hard to see. His visual acuity in that left eye has decreased from 2030 to 2060, and he's got a lot of squigglys, a lot more squigglys on his observe group. So here's the funnest photos from that visit. I'll call on the next resident that I see is we just Ashley. All right, so the other color from his photos are both eyes on the right eye, soft frozen, and then some more. Good. I love the left eye. The left eye, mostly just our key changes right here, and then barely, and some soft confluence. It doesn't show up that well here, but basically this round area is more yellow than the rest of the funnest. Here's the next photos, auto fluorescence and infrared. I think Renee is the next resident that I see. Can you describe them please? Yeah, so you have an auto fluorescent image on the left here, so you see the central area of hypo-auto fluorescence, some surrounding areas and central also, hypo-auto fluorescence, and then this halo of hypo-auto fluorescence in that area. You have your infrared image over here and basically you see hypo-reflectivity. Good, thank you. Renee, can you describe the OCTs as well? Yeah, sure, so the first thing that you're seeing is this hypo-reflective area that's represented by the PET, and then you see some overlying intra-repent cysts as well. Yeah, just in case you couldn't hear them, this is a PET, and now there's some cysts overlying it. I want to call on Rick's, because he's still getting Drake. How about back to Reese? Oh, Nico's back there. Okay, Nico, you're up. If you could describe this course. Yeah, I'll put it back. In the left lower corner, there's some early filling defects in the macular region, and then in the right lower corner, there seems to be late filling defects, that's like almost two minutes. Is there hyperfluorescence as well? Yes. Okay, yeah, so there's this round area of pulling of the dye that has kind of discrete margins. There are some hypo-fluorescent areas corresponding to the pigment clumps, and maybe this area's kind of darker, and this area's a little brighter, so it could be a notch in hot spot. Let's see, is Rick still getting Drake? Rick, is there anything notable on this ICG? So there's that area of hypo-reflectivity, the superior macular? Are you talking about these little guys, or that this guy? I'm not sure, you know, how significant that is. The main thing is we can see that on this ICG, the funnest details are obscured in this area that kind of corresponds to where the pigment epithelial detachment is. But it doesn't get, it doesn't really stay in or leak. So the patient was then started on a flivercept based on the findings of the previous imaging. But on his visit for the third injection, he hadn't noticed any changes, but his visual acuity had actually decreased to 20 over 250 from 20 over 40. Finally? Yeah. In this patient with wet AMD, I guess what is the utility and cost benefit of ICG? I mean, if it's an African-American patient who can take the polyphoto, I can see that. But I guess I'm just unaware of the benefit. So in this case, I think, you know, when you have a serious PED as you see in this photo, I think that is a really good question. You know, we don't often get ICGs. Why did Dr. Bernstein decide to get an ICG in this case? I can't read his mind, but he could speak for himself. But, you know, one thing is that serious PEDs don't always correspond to wet AMD. They don't always correspond to neobascularization. They could just be, you know, kind of a degenerative change without choroidal neobascularization. And in those cases, the ICG can, if there is hyperfluorescence, indicate that there is a skin need. You can see, you know, how big it is, et cetera. And then, you know, on this OCT, you know, those are probably intrametinal cysts. So this is probably a CMD, but I don't think it's so much fluid that it's so obvious that it's definitely an active process. What's your thought on that? So the other things I would add is, I would get it in these atypical AMD because they may be polyfoil. We talked about African-Americans, but here in this population, I do see it in Caucasians. And so that could be different. We might use PDT. We might use total laser. If I saw a hotspot sometimes, you see an extra provial hotspot on these things. And that, you know, conventional laser or PDT can be useful. So thank you. Yep. I'd say in this case, you know, it wasn't super obvious that this was definitely active, wet AMD. All right, so now we have his four-month follow-up where his vision has dropped in that left eye. Reese, can you describe that? This is his four-month follow-up and this is the previous visit. You see any differences in those photos? So in the current picture on the left, there's a little bit less yellow here instead of in the area that we need to put more hyperpigments here. Yeah, it's difficult to appreciate. You can see the funness details better here and this area is darker. Next, we have the autosluorescence. And this is again, the four-month follow-up visit and the previous visit. Tara. So it looks like in the current picture, there is a hypo-autopressin. Correct. With pretty sharp borders, too. And here's the OCT. This is actually a vertical skin. Ashley, do you mind describing this? Sure. So in that large PD, at this point you really have a large area of ISOS function drop out. And right lower, you're just going to see the Coroid well. Correct. So the main finding here is that you can see the RP here and you can see the RP here, but there's no really, not any RP present here. And you can see the Coroid in more detail because that RP is not reflecting the light. And this RP is kind of scrolled up and scrunched up. So this is a retinal pigment epithelial tear and that's what this patient was diagnosed with. Here's another photo. This is from the backside of the mountain. You can see that there are kind of a lot of ski resorts here, some beautiful lakes and the trees are mostly birch trees. So I'm going to just give a little background on pigment epithelial detachments and RP tears when they occur and how they should be treated. So back to the pigment epithelial detachments. We talked about the cirrus PEDs as being, they may or may not be a sign of Coroidal Neobascularization. And those are the ones that have more uniform filling with discrete edges. There's also fibrovascular PEDs, which on fluorescein have the stipple hyper fluorescence with late leakage. Druzenoi PEDs, this is actually a photo of the patient's right eye that are more just a sign of confluent Druzen. They're definitely not a sign of Coroidal Neobascularization. And then when you do have a cirrus PED, we talked about trying to distinguish, is it a sign of active Coroidal Neobascularization that needs to be treated? If it is associated with CND, it is treated with anti-veg F. However, recent studies have shown that the PEDs get smaller with a Flibersev compared to a Renovizumab. However, that doesn't necessarily correspond to better visual acuity in these patients, but it might be a better idea if you're gonna start something to start a Flibersev. And then how about those cases where like at this patient's first presentation where he had the PED, but he didn't have any sub-retinal or intrametinal fluid on the OCT. So our suspicion that there was Coroidal Neobascularization was low. It can still cause visual symptoms. He did have a little bit of central distortion, maybe that was from this PED. In the past, they did do some studies where they treated these PEDs with grid laser, even though they didn't show signs of CFP and there was no visual benefit, as you can imagine. Grid laser immaculate might not, for mild symptoms might not be the best. However, for anti-veg F, I'm not aware of any studies that tried to treat PEDs that were not associated with Coroidal Neobascularization. I think the reason for that is because there's gris and possibly no benefits. So how about retinal pigment epithelial tear as like this patient had? So they often occur in PEDs that have CNB and they're thought to be due to contraction of the CNB as well as hydrostatic forces from the fluid within the PED. And they're characterized by scrolling and retraction of that free RPE edge and then an RPE free area like we saw in our patient's treatment. So if we go back to the imaging, you can see that clearly on the OCT and also in the auto fluorescence, this very discreet hypo-autofluorescence area corresponds to a total lack of an RPE in that area. So the RPE normally has these floor floors like lipofusion but there's none here and it's kind of bunched up here so it's a little more fluorescent. So what are the risk factors for tears? One of the better-studied ones is larger PEDs are more likely to tear. Other things are, it may be more common in cirrus PEDs and fibrovascular PEDs and it usually occurs in a cult without classic and hemorrhagic CNB. There are some studies where they looked at the people who tore and looked at their imaging before the tear and they found that some of them have radial hyper-reflective lines on the infrared and they think that corresponds to the coronal vascular membrane kind of pulling traction on that surface of the RPE. Another sign is non-homogenous spilling on the FAA which our patient kind of had and another sign would be leakage into the PED on ICG. So in our patient, he got the tear after getting two injections. This is a pretty common pattern. Tears are most frequently seen in the few months to several months after the first injection but do the injections cause the tears? So this was a study that looked at the major clinical trials that were first done for ranivismab and there were similar rates of tears in the injection group and in the control group about two to three percent but the median time to tear was a lot sooner. Three months in the injection group compared to 12 months in the control group. So it's not clear to me whether the injections cause tears but they are more likely to happen after you start injecting. It may just be that the tear happened sooner if you inject. So visual prognosis, it's very variable. As you can imagine if that RPE free zone is far from the fovea, patients could have no decrement to their visual acuity but if like in this patient that RPE free area is right under his fovea your vision can really drop dramatically at the time of the tear. Over time, patients can experience a small gradual decline in their acuity and then they can develop either a fibrotic scar or an atrophic area and the fibrotic scars are correlated with worse vision. So how should these tears be treated? So there is a possible thought that maybe the injection might have caused the tear. However, these patients probably do better off if you keep treating them with injections to dry up their fluid. Although it hasn't been studied in a very controlled manner if you get a tear that's thought to be from an injection whether you should observe or treat but I think in general treating is correlated with better outcomes. So a follow-up in this case he continued to get monthly injections. His PED became a lot smaller. The sub-retinal fluid resolved and his intra-retinal cyst mostly resolved. The central retina, as you can see here, became pretty atrophic. He used to be an accountant and one of his complaints this whole time was he has to use two computer monitors so and it's very difficult for him. So he retired from his accounting job and moved down to St. George where theoretically he might be seeing Dr. Jacoby or Dr. Teske. His visual acuity was 2080 at his last visit here but he reported having some disabling that diplopia. So in conclusion, pigment epithelial detachments when they occur without any intra-retinal or sub-retinal fluid they may not be a sign of what AMD and they should probably be observed so you can see that everybody else was on the same page with that. And RPE Terrace can be a pretty serious cause of vision loss in patients with AMD that have PEDs. Imaging, they generally demonstrate a bare area without RPE adjacent to an area with retracted RPE. Patients with large PEDs are more likely to get them and they frequently occur after a few anti-veg F injections but continued injection is probably helpful. So this is another picture from the top of that mountain. As you can see the trees are really close together in Japan so that was exciting for us to see. Questions, comments, Dr. Zuggs? So your last line there is that assuming that after the RPE Terrace you continue to treat them? Correct. So in the original trials that approved retivismab like marina, et cetera they looked at the patients that got tears in the injection group and the patients that got tears in the control group and the patients that got injections did better. So, and they continued to get injections after they got their tear. But I don't think that's really a perfect comparison since the control group was getting no injections at all and I wonder if their vision was worse than the people who got injections. And they've looked at retrospectively in modern times where everybody with AMD gets injected and the number of injections correlates with better visual acuity and people that have tears. But they could be being treated because their visual prognosis is better compared to the other. So I don't think that's proof either but. Yeah, they, just to add, there is still an act of neobascularization and that's scrolled up RPE so that's why you keep treating these to dry out. We used to see these a lot too when we did photodynamic therapy. I mean, almost anything, these are just, when you see a patient like this, I tell them from the start, there's a risk that this may tear and everything's, you may lose your vision permanently centrally. It's a bad situation from the start. Yeah, they definitely, if they have active neobascularization, they'll do better with injections then. Yeah, I think, in fact, for the great presentation, I always wondered what the consequence of an RPE tear was. And a woman by old retina techniques would always say, dipovia is better than no-povia. Thank you.