 of proliferative diabetic retinopathy as our kind of our category. So the first one we were going to do was the DRS, which literally stood for diabetic retinopathy study. So we called it DOG. The main question for this was just in general is photocoagulation. So either argon or xenon, arg effective for treating diabetic retinopathy. So they're basically like, does pew pew plus sugar eyes, what is that, how does that, how does that help? Okay, so we're looking at PRP. So initially they enrolled patients that had PDR or bilateral severe NPR. And they had quite a large study of 1700 participants. And one eye got treated and the other eye did not. And their outcome they were looking for was severe vision loss at five years. They followed them for quite some time. So yeah, each patient had two diabetic eyes. One got pew pew, one got no pew pew. And then they looked at severe vision loss five years later. And the results, so at five years the PRP treated eyes had at least a 50% reduction rates of severe vision loss compared to their control eyes. And they found that those that fit the high risk PDR category achieved the greatest benefit from the treatment and that they had kind of advised at the end of the study that prompt treatment in that group was advised. And the complications that they had was that there was a decrease in visual acuity by at least one or more lines in 11% and loss of visual field and at least 5%. But this was more common in the xenon arc treated eyes. So our results were that the diabetic eyes that did get PRP had this is the symbol for vision severe vision loss had 50% less vision loss since that was their outcome than the eyes that did get did not get PRP five years later. So our conclusions are that treating diabetic eyes with PRP is a good treatment option and especially for high risk PDR. So that was the conclusion or the main kind of simplified breakdown of the DRS. We also had protocol S. What was the DRS study? Shoot, that's right. 1981 or 88? Yeah, a lot of the old. Older than some of us, right? Yes, except for Tyler. Okay, and then we also had protocol S since Brandon and Marshall are on vacation and on interviews. But we took some slides from last year, which was made easy. So the question, the main question was basically, again, a pretty landmark study is anti anti-vegeta specifically tested with Lucentus, an effective alternative to treatment of PRP for PDR. So this study again, like Catherine said, it was PRP versus Lucentus. And the primary outcome was vision loss, but they also looked at visual field changes, the development of DME and the rights of the tractomy may follow these patients for two years. And I just wanted to let everyone know, like, if you did have center evolving DME at baseline when you're enrolled, you were still allowed to be participate in this study. And they were traded treated with protocol I. So that was not something that they kind of ruled out patients for. Yeah, oh, this slide is from last year. But basically, the high points are that they had 394 eyes with active PDR and no prior PRP. And they were randomized either into six monthly injections of Lucentus, or they got immediate PRP with like from one to three sessions, whatever took to fill it in. And then the boxes on the far right just show that those with baseline DME got more injections of Lucentus. If you didn't have baseline DME, you got less. And that those that got PRP overall, I think it was like, received immediate nine injections. Whereas those that didn't have any DME didn't get any. So basically, there are two groups, one with Pew Pew, one with Owie. And again, they measured severe vision loss. But this time, two years later. And so what they found was that Lucentus was not inferior to PRP in the treatment of PDR. They also found some benefits of doing anti VEGF like they were less likely to lose visual field. They were less likely to develop DME and they didn't need the tractomy as often. And that those eyes that had DME at baseline that were treated with anti VEGF had a better improvement in vision than those that were just treated with PRP. Yeah, and that's that's including for treated with PRP for those patients that had baseline DME in the beginning of the study. Alright, so to summarize what the study said is that eyes diabetic eyes treated with laser are not inferior to the diabetic eyes treated with anti VEGF. And in fact, like we said that there may be benefits treating with anti VEGF and including no loss of visual fields and then also maybe less DME and then also less complications from protractomy. So like I said, and then no way, two years I'll come. Yeah, two years. I'm still working on the five years. Yeah, this one came out in 2018. Yeah, so pretty recent. 20 years apart. Yeah. Cool. All right. We have management of diabetic Macleodema coming up next. DME. Yeah, I think our entity that took a clinical practice right at more random. And I think so most at most academic center, we, we still we still use laser a lot to patient with high risk, PDR very often we do combine, you know, if they present with high risk PDR that already have like bleeding, active NBI, just you know, an angry looking I think we often start at least start with anti VEGF and then reschedule for laser or we do both at the same day we do laser first, you know, half session and then do the injection at the same day if they have like, you know, very angry looking high risk PDR at the time presentation. Okay, now diabetic Macleodema treatment. Yeah, so FGL isn't here today. So I'll be presenting on her behalf. I have the ETDRS and I actually didn't know there were multiple reports. But the one that was in the BCSC covered there is report nine. And this is for DME. So the questions here is how is fit of regulation effective for treating DME for diabetic retinopathy. And they also also want to take a look at aspirin, how that would affect progression if it would prevent it. So the methods are pretty similar to the previous presentation. They looked at patients with mild all the way from mild and PDR all the way to early PDR with visual acuity, better than 2200. And then they had in total about 3700 patients, one eye to fit of regulation versus one eye not but they also randomly assigned patients to 650 milligrams of aspirin versus a placebo. And the outcome was for at least four months vision or some of these were outcome measures they looked at visual acuity worse than 5200 for at least four months of visual acuity worsening by two times like 2040 to 2080. And then looking at how the DR progressed. Is 5 over 200 vision? Is that? Yes. I don't think so. So it's like, yeah, it's just the same math. So 2800 as long as it wasn't worse than 2800, right? That's what they're saying. I don't know how I didn't know that it transferred. I just from what I understand, it's the 2200 but you have to be five feet from that's the 25. That's at least what I got from the CSC, like visual acuity, like how you measure it. So really bad. So five feet from the 20 chart. Yeah. So macular dima results. So just jumping to the results they have the photo coagulation overall pretty good and decreased risk of moderate vision loss actually also increased chance of gaining vision and reduce retinal thickening. So both both functional and also in the retina better or decrease edema for scatter photo coagulation. So I think the scatter would be PRP and this there was a reduction in severe vision loss, but just a small risk reduction. It's not for mild to moderate diabetic retinopathy or more for a severe NPR and PDR. And then it's more effective for type two diabetes but not for type one. And then for the aspirin results, it didn't really affect diabetic retinopathy, but it didn't really make it worse in terms of vit heme. But overall, it was good for just cardiovascular health. So conclusions, this was from the report none that I was able to get from just reading online and overall I said that photo coagulation was pretty good at increasing visual acuity, lowering DME and did not have a lot of visual field losses in the cell for focal focal was better than scatter. And for DME and also you should consider if there was threat or presence of center involving DME. And overall aspirin was not too helpful, but just good for cardiovascular risk. That's it. When they talk about focal laser, they wouldn't manage that you know, the target at a specific macroaneurysm that you can visualize on FA. Okay, so that ETRS was probably in 1990s or 91. Yeah. And then now we're going to go on to the DCR, DCR protocol I and V with Mike and Cole. And V, right? Not yet. We're still doing on diabetic maledema with you want to make it though ahead of time? That's fine. I don't know. I thought you were already open. I'm sorry. Ars is really flashy. Okay, more DME stuff. So Tony talked about focal laser for DME. This is comparing anti veg of therapy to focal laser for DME. I think they just got the five year results in like 2018 for this one. They had a ton of groups that basically you either got prompt or deferred laser and deferred later was like six months later. Or you got Lucentus with that laser either prompt or deferred or you got Triumph Cine Lone, Intravitreal. And they found superior visual outcomes meaning you gained more EDTRS letters. If you had Lucentus compared to the focal and that was sustained over five years. And if you had adjunctive laser treatment, meaning in addition to Lucentus, that was didn't give you additional benefit, but it did reduce the number of injections that you got. So if you did both, it didn't change the visual outcome, but it reduced injections. And then if you deferred laser like in group three, that only showed benefit in folks with worse acuity at baseline. So you're not like hitting them with everything at once. In the steroid group, they did have similar visual outcomes, but that was only in pseudophagic patients and they had higher risks of IOP spikes need for glaucoma surgery. So steroid was considered second line based on this. And so the anti-vegeta is better than focal for treatment of DME, you can reduce injection burden by doing adjunctive laser. And then another key point from this is that both anti-vegeta and steroid kind of made your retinopathy severity better in all levels of NPTR. And this was the first algorithm where they did kind of PRN driven injections, meaning you got six monthly injections. And then you could start deferring once their acuity was stable and their OCT thickness was stable. So that was kind of a monumental thing for this one. All right. Then V, this one was looking at 2025 or better eyes with Centra involving DME is they sent us better laser or just observation. So this is 702 patients to your follow up. Big thing on results was it didn't matter. So whether you did individual injections, whether you did PRP, whether you did observation, only 16%, 70% or 19% of people got worse than 2025 or their baseline. And just as a side note, anyone who got worse did get additional treatment with Lucentus. And then one other thing just to know this kind of interesting is that the percentage of eyes that were 2020 or better was better with ILEA. But that was a statistical significant, not clinically significant because it was like two letters better. So just kind of like clinical pearls for us. If you have center involving DME, even if it looks pretty bad, and they're 2025 or better, you can be observed. And then you can inject it, the vision gets worse. And then kind of our paradigm unlike AMD, where you treat fluid in DME, you should let it be guided by a vision. Centra involving DME, how is that defined? In this one, I think they said there one millimeter. I think in mine, it was 500 microns from the photo. So yeah, to the class of the BCSC definition of Centra involved in me is the central subfield of the ETDS chart over the macular. So the very center is one millimeter. So that's a hundred. Yeah, that is small. That's smaller than the other optic nerve when you have the OCT scan. If you is the optic nerve on average is about 1.5 to 1.75 millimeter in diameter. So really late. So sometime when you got like, is that center involved? A lot of time it's not really like not at the under the phobia. Yeah, it doesn't fit the definition. Yeah, now we're looking at that the page in BCSC where it shows like what the center involving is and it shows the OCT. And there's literally like fluid that I would think is like right next to the phobia. But then when you look at the map, it's like not in that circle. Right. I was like, oh, we would have treated it. Right. But it's interesting to research things. And just to clarify, I mean, even if it if it's outside, then it's even more reason not to treat it right. Yeah. Cool. Okay, now we're going to move on to van occlusion. And Michael Adima secondary to van occlusion with Lydia. I found your colors. So you did not talk about the most and see both last year, right? Hush on last year. This is a very, very, very old study. I was 20 years. So I'm going to talk about van occlusions. And I put this picture of the canyon because that whenever the canyon gets occluded, that's surprisingly, it's not only occluded during ski season, but also doing a work that I just learned leaf peeping season. So van occlusions, I kind of did it a little bit different and then I looked through the BCSC and tried to give a few highlights before we move on to the studies. So for van occlusions, it's important to know that they are associated with age and hypertension. And that glaucoma, both open and narrow angle is a major risk factor. When we look at the funders, we see enterosin, hemorrhages, dilated torches, veins, and sometimes cotton wool spots. Macular edema is best detected with SDOCT and ischemia is best detected with fluosine angiography. Two important things for central retinal vein occlusions is that near vascularization occurs commonly in the anterior segment. And obtus ciliary shunt vessels, so vessels going from the core edge to the retina, like the small vessels that we have surrounding the optic nerve, they are dilated and commonly found in central retinal vein occlusions. And overall, it's important to know that the best visual acuity outcomes achieved by administering NTGF immediately when retinal vein occlusions are diagnosed when they have macular edema. For BRVO, it's important to note that they are commonly found in the subar temporal quadrant, so 63% of the branch retinal vein occlusions are in that quadrant. Risk factors are age, hypertension, smoking, glaucoma, and hyper coagulable conditions. And VCSC notes that diabetes is not a major independent risk factor for branch retinal vein occlusions. And we'll talk about the treatment later a little bit when we talk about the different studies. But as I mentioned before, the pharmacologic management is always the mainstream first land therapy, macular laser surgery, showed some benefit, and photo coagulation also shows regression of vessels and risk reduction of vitreous hemorrhage. And in central retinal vein occlusion, that can range between mild and for mild to severe disease, like mild is usually 2,200 which are purely or better. And is chemically disease is when it's like large areas at least 10 optic disc areas of non perfusion. Mostly central retinal vein occlusions have either thrombosis of the retinal vein at or posterior to the laminar composer. And we have a thickened or a thickened central retinal artery that can impinge the vein. And risk factors here diabetes is included. So I think that's important to know, as well as high hypertension, glaucoma, hyperliberidemia, hyper coagulable conditions. And we should monitor central retinal vein occlusions monthly in the first six months, as complications can include reverse hemorrhage, neurasculation and neurasculate glaucoma. And again, the treatments, pharmacologic treatment is the mainstay. Laser surgery does not improve visual QD and photo-curriculation does not decrease neurascularization. So important studies, the BVOS and the CDOS are the two that we focused on. And they are relatively old studies. So BVOS was published in 1984. It's the Branch Rain Occlusion Study, multi-centered or randomized control trial. And the two things that wanted to figure out is the efficacy of argon macular laser. So argon macular laser therapy and treating macular edema secondary to the vein occlusion, and then the argon scattered PRP to prevent neurascularization and hemorrhage. And it's important to note that these gold standards that were defined in these trials were before introdutorial injections were available. So the first outcome when we look at the argon macular good laser therapy is basically looking at like patients that were treated versus non-treated. And it showed that it was highly significant that the argon good laser was helpful. And that was established as the gold therapy at that time. And as I said, like 139 eyes follow up for three years and there was a significant benefit of the argon laser therapy. And then the argon laser PRP similar story we had treated eyes and non-treated eyes and there was a significant benefit of treatment and was basically established as a gold standard to prevent neurascularization and hemorrhage. And then the CVOS was published in 1995. So a little later, and the purpose was to evaluate good laser macular edema associated with central vaginal vein occlusion. And there was no significant difference between treated and non-treated eyes, which is why laser is not recommended for central vaginal occlusion. And visual acuity not OCT was the main outcome measure for both of those trials. I think when we look at what VCSC says, those studies are not even really mentioned much in VCSC because they're outdated. So I think the important things that came out of those studies are really the risk factors that I mentioned earlier that go along with the RVO and C-RVO and they just have them up here again. But when we go to the next group that is presenting the pharmacologic treatment is the mainstay. And I think that's an important point. We sometimes do do focal laser for branch renovated occlusion where there is a good area of MA outside of the central macular. You see the clinics doing that. Is it like they come in, they get diagnosed and it's like the FAA is like pretty amenable to that or do they always start with anti-vegetary? We always start with anti-vegetary. We always start with anti-vegetary. And he usually is the fellow who like push for because it is, you know, it does take more effort and coordination to do focal laser than to do the ejection right. But if you see this refractory multiple like earlier even try steroid and refractory, then I think it's a good time to try focal laser. And I've seen that, you know, being effective for some patients. We just sometimes we forget about this option because we saw you use just to eject, eject, eject. And then one important thing to get from the presentation is that, you know, the frequent monitoring for the first six months. And you know, this wasn't the time when you guys present to me case of the VA. I always ask when was the onset of the vein inclusion so that we documented so that we be more diligent about follow up early on. And then after six months, we can relax if they don't have magladema that require monthly treatment. Well, and then the up to similar shot and vessel. Oftentimes, it could be tricky to try to distinguish between that, which is positive findings, right? Versus NVD, which is a negative findings. And sometimes it's hard to distinguish. So FA is your answer. Just get an FA and then document that, you know, the FA done on this day, confirm that is, you know, after the shot vessel and not NVD so that we don't keep repeating the FA with each of the new resident. Okay, let's move on to Bravo and Cruz. Sean and Tyler, Sean's not here. All right. Like when my kids bring their dates over in high school for like school dances and stuff is like be so cringe worthy. So I got to practice now. I don't know if I'm mundane. Is someone Gmail on, open on this server? I logged out. Did you log out of your channel? Did you log out? So the Bravo study was looking at the safety and efficacy of randomism and in patients with macular edema secondary to a branch retinol vein inclusion. Busy slide, but phase three, multi center randomized control trial, looking at randomism versus sham inclusion criteria include macular edema, central subfield thickness created 250 microns, and then best corrected visual acuity between 2040 and 2400 participants were randomized to either six month injections of two doses of renovism at point three versus point five versus sham. And they were eligible for rescue laser within that certain criteria. Primary outcome was mean change from baseline best corrected visual acuity to six months. And then they had secondary outcomes as well. The 397 patients were randomized. The mean gain was at six months was 6.16.6 letters and the point three milligrams 18.3 and the point five milligram and 7.3 in the sham. Showing that randomism map for branch retinal vein inclusion leading to macular edema was better than sham. And then their secondary outcomes also went in there that more people gained three lines, or 15 letters in their best corrected visual acuity with randomism app compared to sham. And then crews was it's twin only for central rate of main inclusion. So everything was the same. Except for the results. And the fact that they included central revenue inclusion. So 392 patients were randomized. At one six 12.7 letters were gained on average for the point three milligram group 14.9 for the point five milligram group and point eight for the sham. And more patients gained three lines or better with the randomism app compared to sham. So the conclusions of the crews C for central Bravo B for branch was that introvertial injections of randomism have showed a statistically significant improvement in visual acuity compared to sham. Remaining questions that Bravo crews did not answer is when patients present with the retinal vein inclusion. And they ask us what will my visual acuity be after treatment. We can't say based on these results score I think tried to answer that but didn't but showed that presenting visual acuity was the most important predictor of final visual acuity. And then can an alternative dosing strategy of anti veg so they did one injection every month for six months. Can we do for example treat and extend with AMD as we do with AMD can that be applied retinal vein inclusion. But Bravo crews did not answer those questions. But they came up at the end. So the question of you know the different efficacy among the different regimen you have PRN you have monthly and you have treat and extend right. That question is being answered for AMD. And the answer is that the outcome in general all the same whether you chose those three one of those three regimen. I guess the only difference is like you know we rather multiple visit which rather multiple injections and let's visit. So that that's why sometimes we offer a patient you know the option. Practically in clinical practice we approach vein inclusion similarly to AMD treat and extend versus in diabetic macadamia is more of a PRN. So good job. You got to take a little break. I'm going to go upstairs because I forgot the bells. Can you feel it? Yeah. Let's say it doesn't work. That's always the answer. I'm just as tired. How do I do this? Do I just put plug it into the Mac? Oh, McDonald's. I think you have to get admitted. No, this was like not known at the time. It's like intramuscular stuff. They came to the ER. I was in a pizza clinic and they're like our kids. I was like, no, no, no, you go see him on her ketamine and I was like, yeah, I don't know why. His main symptoms were at night and he like wouldn't sleep without a light on. Intramuscular. It's crazy. I think you get a loading dose weeks later or something. It's funny because like I feel like all our cold cereals are fortified. So like, you're going to go so hard. I'm surprised they don't fortify me. I know maybe they should. It's like you just put, you know, pouring in the water, pool and cycle beer in there. Act positive visual minutes that by nothing's in our. This TV static. Visual snow is diagnosed in our clinics. I don't know, Jock. I have this TV static and these floaters that I can see through and I've been present for more than three months and I see these trailing after images. We have a resident who has that. You have visual snow. We have a resident that has that. I've had a lot of people ask me about what it's like to have visual snow. Wait, Catherine. If you have visual snow, do you overgrade cell and flare? Uh, no, Brad, not exactly. People have also sent a lot of up and coming research my way. Catherine, I just found another paper on how patients with visual snow have hyper excitable visual courtesies. Are you hyper excitable? We have a resident who has that. Um, I just opened up my email. My laptop was in function six residents. So instead of having the group of three, four, four team, let's just do two. You guys can just have them. So let's divide by PTOI level. That's really good. We'll take the bar when he goes back. He's clutch. It's clutch. Such a cool thing about these belts. So these are the exact same question like last year. I didn't change it because Catherine told me not to change them. So if you pay attention last year, you should know. The dollar store and left the tag on us. Little ringers. And if you guys this year, I know, can it throw out pride? Their prizes. Oh, it's not really a prize by bus. You got to try. I feel like the prize is Hong-Yam hugging us up with like $50 sushi and $25 dollars. I put it in my order. So putting is an Asian drink. I feel like we always love sugar stuff. Prize and link. Come on, the winning team. What's Jeopardy-ish? I don't know. I'm a buzzer. You're a two. Ignore the rule. All right. I'm not when I'm that reading the question. She's that reading. Okay. I think you should wait longer. What is Google Laser? That was the problem. And every watch not shown here, but when you see. A certain ring outside of the fovea. That's a telltale side that there may be an AMA here. Leaking, right? So this is a good patient with especially VA patient poor follow up. He basically hit three criteria for for Google Laser. VA patient. It's a criteria. So CSME, you know, this is the, the, um, this is in the which study that we talk about today for CSME. It is right. This is the definition of CSME was defined in ETRS. No longer relevant in clinic. We no longer describe these three criteria. Why? Before OCT, how do ophthalmologists grade the CSME? I'm looking at the looking with what lens? Oh, so we don't use that anymore. Right? So you can't really make this judgment with a 90 or super view or 78 lens for that matter had to do with the contact lens for you to appreciate the depth. Right? With focal laser, we start a much lower, um, they say here 100 million watts, but I probably will start at like, you know, even 50 80 and then crank up instead of 200 micrometer, which we use in PRP. We use 100 and instead 100 duration. We use 50 million second duration and can title it up. So start as low and crank up. Hang up. I've never done focal. How well can you see the spots where you've treated? Can you see them well? No, that's the thing. You start, um, so you start very, um, low and then the moment that you see the spot, you low it again. So you shouldn't see your spot. You should not. Okay. Joan, I have looked at, um, patients like a couple of the VA and like, their scars become like massive. Yes. So once you start to see, like, let's say if you were at 100, um, million watt and you see the spots, you see a light spot, then go down to 80. Go down, go back. Can we do a retinopathy for 100? Retinopathy does this patient have. Tell us about what you see here on this pack slide. So you get these, the thickening of the posterior epithelium with cysts and then there's probably some NVI there. I can't really tell. Hey, I just, uh, somehow okay. Okay. Get back again. And then what about the black arrow? Iris, new basalization, lacy vascularization of iris pigment epithelium. That's what we'll talk about for the red arrow. Um, different of the basement membrane of pigmented epithelium. Okay. Yes. Yes. It has not looked up twice. Yeah, but it's also like, you know, like terrible quality. It looks like it's like that, but like really blurry. Are we getting dragged? I'm getting dragged. I have an Excel, especially. All right. All right. Did we do a arterial occlusion disease for 100? Yeah. What is the diagnosis? Answer, anti-dumbbell. Answer, anti-dumbbell. Answer, anti-dumbbell. So what make you say that when you first see the picture? So some mid-peripheral hemorrhages and then I also thought there's delayed filling there on the FA. 25.6 second. What is a normal arm to write in a time in a healthy eye? Like 10 to 12. It's, but the technician has to be good, right? And the person who pushed had to try to push that within 10 seconds. One time at a certain clinic that I was at, they, we thought they were totally delayed and the technician was like, oh, but there might have been a kink and I like me and pushed a little bit late and we were like, so like it totally, totally matters. Then we did it again and they're normal. Yes, more dark blood hemorrhage. Splinting him is what splinting him is in the retinal nerve fiber layer. That's also known as, you know, flame shade, feather. That is more commonly in hypotensive retinopathy. Okay. Other vascular disease for a hundred. Sequel cell hemoglobinopathy is most commonly associated with liver, sequel cell retinopathy. No. You guys can see the most common thirty three percent. Half of that is ester and very small SS three percent bonus question here. What complications would you see more often after laser PRP for proliferation of sequel cell retinopathy compared to diabetic proliferative diabetic retinopathy? Yeah. There's detachment. That's why we don't go aggressive on this patient. Although, you know what? In my more than a year and a half, almost a year and a half yet, so like sitting, I haven't seen a patient with sequel cell retinopathy. Yeah. Oh, yeah. We do other vascular disease for two hundred. Retinal arterial microanerism Ram. There must be a picture here. Oh, what? Oh, it's five hundred answer from category three. Go back. Go back. Go back. Something's wrong. Two. Sorry about that one. We'll just skip that one. Okay. Vision changes. What are the fighting scenes below? I say we just do. Okay. The top picture is alchemy spot because they spot, right? And then the bottom picture is linear configuration. So that's the street reverse. Yeah. This reverse. Why do these happen? Yeah. So it's been hypotensive. Quarantopathy. Lava non-profusion of the core capillaries early phase. They look more like 10 color deep within the retina and then that time go on become pigmented and has a little bit of a halo hyperpigmentation around it. Okay. And the same pathology, but it's up in a more linear configuration along the quarter arteries. The streaks are the, is it linear hyperpigmentation? Hyper, hyper. Same pathology though. I see. Just linear configuration. But it's what condition that this patient likely have. Otherwise we're just going to be sitting there being like. How about you guys just hit as soon as, I don't have to read. Just get it. That was slow reader. Okay. Let's do, why not? Let's do fake metastasis for 100. Oh, yeah. The picture tear it off. 27 year old man with this fighting. His father was also adopted by the same syndrome. What is the most likely cause of death in this syndrome? Most likely cause of death in this syndrome. Yes. We're going to renal cell curbs. Yes. Yeah. Any question? I didn't ever. What is the, what is the name of the condition here? We look at the eyes. It's fun to pull it out. I was looking for some. Okay. What are the organs affected by this condition? Rain. Hi. Rain. What else? He has a knee. Okay. What else? Or should I ask which chromosome? Autosomal dominant. Yeah. So you, where are you putting here for some reason? The location. I'm sorry. I just didn't know. Kidney, pancreas, liver system. Of course with the brain and eye, right? C, CNS stuff. I'm just looking at like what's going on here. Okay. What's up with our eye? You know, on FAA, this is not as licky here, but for active lesion like this, how will you treat this? Laser to supply. Yeah. Hot laser photo coagulation or this laser. However, you probably want to try, there's a van here, right? So you're going to try not to laser the van because then you would have a clue then you lead to congestion. You only tell us each for 200? A young patient. Sir, daily double. You see this. What is the answer daily double? Answer daily double. Boradic. So no real genetic inheritance pattern. Wyburn-Mason syndrome. You look like worms, right? Can general right now? AVM with Ypsilato AVMs in phase orbit. Manable. That's why the bleeding teeth start bleeding with dental appointment, complication, reticulum occlusion because of thinking and vitreous hemorrhage. Does not leak on FAA. Wyburn-Mason. Let's do diabetic synopathy for 200. In this patient with diabetic synopathy, what is the cause of patient loss? What is shown here, guys? This patient with a normal FAA, this patient has, oh, this is a different image. So if you imagine that, this is some capillary drop out at the foveal area and also temporal to the macular as well. What is roughly an average FAC? Yeah, it varies by the, I would say around 350 ish. That's, yeah. This is my, my meter. And this has been shown to be just some correlation with the degree of retinopathy. So most prominent in PDR. And then on OCT for macular schemia, how would that present on OCT? Central loss of, or attenuation of the ISOS layer. So thin right there for the receptor loss. That's pretty chronic, right? So in large FAC. Yeah. So that's one of the three main cause of vision loss from diabetic run-up to the first one is magladema, magla schema, which you can really see on your exam, right? Because you can't really visualize that unless you get an OCT or an FAA. So we require some imaging to make that diagnosis. So you're saying that ischemia, that's what leads to the ISOS reduction, or a bias? What stage of diabetic retinopathy is seen here? How will you treat this patient? Okay, good job. So this is from one of the clinical trials demonstrating Irma, which stands for intra-retinal microvascular abnormalities. So inherently, this has to be NPD-R, right? Because the definition of PDR, proliferant disease that it had to be astral retinol, so above the retina surface. They should vessel and look squiggly. So on exam, sometimes for me, it's difficult for me as well to distinguish between Irma and NVE. Or only NVE. So Irma was NVE in those patients, I would get an FAA just so I wouldn't know for sure. And there are times where I felt so confident that this is PDR that looks just like NVE, get an FAA and show no leakage. For example, we had that one patient, Mike, at the VA that day, I thought the right eye has severe, yeah, but I didn't FAA that day, because he had to wait around and it would put his pressure to drop down. In the end, we still give him prophylactic laser in the OR because of his history of like, for follow-up and now his other eye has NVG. Yes, yes. Okay. Okay, can you point out where the Irma is? Yes, here. Yeah, this is not, you see right here. Yeah. This is not a great photo. Sorry guys. But this area here. Wait, am I looking at blood vessels? He'd be here too. Okay, I see the bottom one. Yeah, this one here too. Here as well. It's like, yeah, I think that's a really good versus like sometimes they look pretty frondling, but yeah. Yeah. Heart. So just get an FAA. Yeah. I think the black one for a short while. Yeah. Here's the category for 400. I've got to turn it off. That's a lot of dishes. How about you two? Enter, Ailee Dumbled. Enter, Ailee Dumbled. Ailee Dumbled. Harris PDR, right? So what is this here? Greater than what? All right, Harris PDR. I don't like how like they describe here because you know, this is so trivial. Just knowing you had an NVD with the, with or without with him and any with him. Yeah. Just two things to remember because otherwise it's just going to try to like, are you going to stay there and measure? Is it one four or one half? Yeah. Well, and if it's less than one fourth, if you don't do anything, it's going to get greater. So. And just know that even though for, so then it would be high, it would be not Harris PDR, right? But just know that in that study is that it doesn't mean that you can't do the laser. You should still offer the patient. It's just that it's not as mandatory. Oh yeah. And then just touch base on the protocol as we talk about it already. And they are risen benefit to each of the two treatment modality, right? With anti-vest Jeff and Dr. Midas, tear, detachment. Oh yeah, TRD or RD. Why? Because of, you know, contraction if they have peripheral NVE that has already regressed, has mind brain there. I can contract rapidly because anti-vest Jeff work really fast, right? You see patient with Florida and via anti-vest Jeff and after they come back 24 hours, less than 24 hours, it's like, whoa, it's like almost gone. So that's why that rapid contraction. You see that. That's what patient when a patient with presented with pro for TRD, but I also had blood. I don't do anti-vest Jeff. I would do as much laser as I could. What was the question? The answer was already on a previous slide. Have you had PRP? You see this. What is the diagnosis? Wait, wait, any bringing the bell? Yeah. What's the answer? I said TRD. Is it TRD? But is it also like the Corridor fusions like that? Or don't you get like Corridor's app? What's your answer? Pick one. Or it could be endothelitis or it could be. Why could this be endothelitis? Look. I'm teasing you. I mean, it's a Corridor fusions. Yes, it's a Corridor detachment. So just know that TRD, unless there is a reputational component, it's usually kind of shallow, kind of flat. It's not going to be bougie like this. And also, you know, this, it has to be Corridor because this is the laser spot. That's going to be fusions for 200 years. I do. You. Okay. Okay. The diagnosis of this retinol whitening, hey, on OCT, in which layer is there a demon? How would that take for it to not be visible on OCT? When you have optic nerve there, when patient, that's why the diagnosis of, okay, then after three months, what do you see on OCT in this area? So the diagnosis of the occlusion is very difficult to make on clinical exam. If you don't see it, then you rely on OCT to know that they had this. Hypo-profusion from emboli found in 62% of the case. Look for one. Sometimes you don't see them though. Temporary involved in most of the cases. You know, what is actually the best way to see this emboli is the IR imaging that come along with the OCT macular. Okay. So, you know, they are different kind of emboli. They talk about colon horse plank, which is cholesterol. They also like platelet-fabric emboli and specific emboli. You know, this thing is kind of absolute this day, because this is more relevant in the old day where there is, you know, poor access to systemic workup. You know, echocardiogram versus cardiopulmonary cell, when you have to kind of target and you look at this and which one, which test you want to get, right, to have the highest yield. Now a day, a patient presented with an emboli or CIO, BIO, acutely, you will send that to the ED for stroke workup and they should get all of those tests anyway. So, I wouldn't sit there and try to decide which kind of emboli this patient has. It's more for academic exercise than practical patient care. All right, this is a bonus again. Okay. 46-year-old female presented with headache that worsened and became confused, disoriented and off-balance. Tinnitus and vertigo also developed and made it to neurology for and noted to have vision changes. How do you treat her? How do you treat her? Steroids. God damn it. Yeah. Okay, okay. What is the diagnosis? It's sad. It's sad. So high-dose steroid early on and the other men, the other thing that you mentioned, I'm sure they used to at some point, but the first thing is high-dose steroid. Oh, yeah. They keep sending us pain. It's cute. Forever. They see her once and they're like, this girl has headaches and she didn't hear me once when I came in the room. Consul for Susan X. Triad of encephalopathy is a brain infarct BIO and here and lost to you with oral steroid. Immersive crushing with a thing that Catherine mentioned. Yeah, any other stuff. So that's good. Can we get in for 300? The question to play your career in this condition. Lydia said that in her presentation. Thank you. Let me know both time. Sorry. In the crib before I'm playing in the nose. In the crib. In the crib. Okay. I don't think we should get that one. In the crib. I'm giving points to us. Yeah. NBI is occurring. It's typically sent a patient in ischemic CIO within three to five months. Ischemic CIO is defined as, you know, more than just that this diameter of ischemia on FA that was mentioned in Lydia presentation. How come we don't see this as often clinically that? What do you guys think we don't see as common? This is a really high prevalence, right? But how come clinically we don't see it as much? We're saying start them right away. Yes, because we treat them not because of, you know, not to not to prevent NBI, but because they almost always in CIO have sent to Magalema, right? So then you treat them with anti-vascular and that just mask. That just mask the ischemic load. No, I don't think so. What I meant that mask is that it mask the non, the non perfusion. So unless you get an FA, you won't know how much theology that they really have. And then this patient lots of follow up. They come back after COVID and then they have a lot of complication. Yeah. Okay. So that's why I say, you know, for patient who are getting injection, you're not going to do a gonoscopy, right? Looking for NBI and VA, but let's say for patient who does and they are rare, rarely this happened, but there are some patients, maybe a handful of patients who don't have Magalema that requires treatment. So this patient, you have to be more diligent in doing maybe I don't know if we actually do like for the first month NBI gonoscopy every month and then every after that every six months will do the gonoscopy. If they don't need treatment, but if they are getting anti-vascular frequently, then you don't have to be as diligent. Wait, did you take it far? Yes, I did. 60 year old female who is setting lots of vision. What is the diagnosis? Got it? Got it? She's silly over it. No, I agree with you. Wrong, wrong, wrong, wrong. She's sparing, sparing, sparing, sparing. Yeah, this is big. What's the 60 year old? 60 years old, right? Yeah, she's living. So you're doing minus points. This is a beautiful picture. Look at random whining anywhere. No, I don't know why. Airings, airing is dripping the Magalena that corresponds to the area of retent confusion. I said the wrong thing too. Yeah. And that is the RNNL infarct edema, right, on the OCT. These have to be acute. These have to be within the first two weeks. And then this is the classic chair rest spot in central retina or occlusion that without a celeriac sparing, right? The previous one has some sparing. Okay, retina ischemia. I call that RNNL edema, but it's just a schema that's rolling up. Yeah. Do not miss. Why does this mean like you shouldn't have 60 year old? That was a bonus one. I didn't miss. I don't, I'm like, yeah. Do you have to? So in, when they present like acutely, you do send them to the ED for ESR, CRP and stroke workup, but if they present to you like. Yeah, like two weeks later. Two weeks later. Just do routine outpatient. Ask her to come to the next slide. Let's go on. Yeah, that's going to conclusions for 400. I think that we didn't do vascular. This is for 200. No, we haven't. No, those do that. Oh, no. I was, I was letting you know. I understand. No more risk factor for this condition. Yes. This is BRBO glaucoma is one of them. Age, hypertension, smoking, hypercoagulability, not diabetes, which is a risk factor for CRBO in clinical practice. I still screen patient for diabetes. Oh, yeah. This bonus question will mention in Lydia's presentation as well. Number one, where are the occlusion in BRBO typically occur? And number two, in which quadrant are BRBO most commonly located? Yeah. Crossings of arterioles and veins. Tell you remember in the VA clinic the other day, the patient because of retina for consultation for macladema and we didn't ask for an FAA, FAA staff left. But when you look at the IR imaging, you can clearly see the kinking of the, the nicking of the arterial and vein and that's, it's like a type of cycle. Brents are an event inclusion and you don't have to get an FAA really to start treatment. Why is this super temporal? Yeah, I don't know. Gravity. Gravity. Now, here's a question. I think that's right. It's good. For both, okay, patient present to you and before you see the patient, you already see the image, you look at the OCT, the color photo and you know your diagnosis. What should you do next? Right away. This is a cue. Okay, what was the question? Check your blood pressure. Yeah. Check the blood pressure. And I wouldn't necessarily even, I wouldn't start treatment in the clinic. I would send the patient to the, if their blood pressure is really high, I would send the patient to the ED and delay treatment because you know, just the high, just some association with like stroke, heart attack and especially if they present to you with acute venucleus, high blood pressure that is considered like a crisis. Just send it to the ED. Come back later for interveje. You don't want to cause a complication with your treatment. Which one of the medication has been in some of the old study most commonly associated with those two stemming risk factor? Lucentus. Moving on. I see our occlusion's 400. FA on the last patient, review this. How would you treat this, please? Okay. I think I missed some information here. Actually, no, just keep it that way. There's nothing, by the way, there's no NVI, there's no just hemorrhage. So this FA show a lot of ischemia, however, did not demonstrate NV. So according to the AAO recommendation, you don't treat ischemia in venucleus. You treat NVI, NVE, NVD, PRP only. And the reason for that is whether they did another study. When you do prophylactic PRP in this patient, 30% of them still get NV anyway. And also there's no different in the outcome for patients who get prophylactic treatment and who did not. Make sure, kind of make you want to treat that, right? I think if this is a VA patient or someone with his or her follow-up, I probably would just do some sectoral laser, just to be on the safe side. There's so much. Because they don't have vision there anyway. It's just asking for it. It would be obvious. There's one more that you have mentioned that is basically... Tyler wants it. What I was looking for. This one. Hyperhoboxidinemia. But everything that you mentioned, yes. I didn't include all of them here. Soko-Lupus, all the new vascular stuff. But yes, part of V-Lyden, 5-Lyden, and antifasculate with syndrome. What is strong. All those check out. Because it's not included. You like him so much. 75 year old with sick day. He's with tube vision lot. Vision 2040. What is diagnosis? PAM. Right. Yeah. So the hyperreflectivity. Hyperreflectivity is set up in the retinal fibro-layer as you see in our inclusion. This is more of in the inner layer of the retinal but not in the RNFL. And then this actually is a pretty nice IR image that kind of visualizes these changes down on the IR as a hyporeflectivity. Female with a history of hypertension. The variability in the different layers where the lesion are. And it has to do with poor perfusion to either the decapillaries layer versus the middle layer. It's the same spectrum of the same disease. Most commonly associated with high blood pressure. This is Guatoma. Can get better but a lot of time. Most of the time in my experience stay for a long time. A few months at least. I don't know if in a year or two years they get better but they tend to be persistent. And then you don't really see this on your clinical exam. It's very hard to see. So the IR and the OCT visualize that much better. Same thing along the same thing here. Move on here. That's AMN. PAM, PAM, AMN. Same pathology. This is Kimia, right? Of the capillaries. Where do you think? Okay. So beside RAM, brain disease can cause hemorrhage in all layer. N-A-T. N-A-T. N-A-T. Trauma. Trauma. It's good. Not the R. Diabetes is intramural. Wet AMD. So CNBM that break through. Most commonly seen in what? PCV. And then one more. Rare. Melanoma. So Tertian syndrome. RAM. CNBM classically in PCV. More commonly in PCV than in AMD. But we do see in AMD, right? Melanoma and trauma. Non-accidental abuse. So those are the few things that can cause bleeding in all layers of the retina. Yeah. Okay. Yeah, he had multiple layers. Observe. Laser, efflux, and the macular. Where do these commonly occur? This lesion? So where? Yeah. Just in term of the anatomy. Within the first three order of atrial bifurcation. Atrial bifurcation. Within first three order of atrial bifurcation. Okay. So you don't have to look far out, right? Yeah. Vecobatosis for 300. Input decision. I'm going to laser. Haman-Gioma. No treatment indicated unless Cosmetrist Hamerich. Laser photocoagulation or cryo. Looks like grapes. It looks like there was hemorrhage. The media was not there. Was there? No. No. No hemorrhage. It is a diagnosis. Proschlorosis. What is the name of this lesion? Lesion. Astrosatoma. Astrosatoma. Astrosatoma. Astrosatoma. Astrosatoma. Astrosatoma. This finding and what syndrome can this be associated with? NF2. Block fluorescence with telangiphthalic vessel. That's the hardest one, I think, of all the picomastauts. Good job. Is that NF2? Yeah. Yes. I don't think I... I know that that's, like, in my notes, but I don't know... Yeah. I haven't seen it. It's just the pictures. Does it? The pictures of it? Of most things. Does it? Yes. I've never seen a picture of it. I mean, I must have. It's your last year of life. Yes. So we move on. I think it's a cold team. I got that. Yeah, you just go up to the park. Okay. Okay. 45-year-old female who received a sort of beam radiation toy. Come on. There's a point of two. What is the diagnosis? Grief. So in radiation retinopathy, more often than not, you see more convulsed part, versus... I'm pretty sure it's movebarks. Convulsed part. There you go. It's fine. Never at least one cause for this fighting. I'm pretty sure it is. Yeah. God, I got it. It's working really well. Fat-hebalism. Acupunctitis. Childbirth. Because of like, amnesia from the amniotic fluid. And vasculitis disease. I did? Yeah, we showed you the picture. And you're like, it looks like purchase. Okay. What is the question here? It's alright. Fibrillator. Randolph capillary bed. I think we missed this. We did this one already. We did? Yeah, the 501. I don't think so. I don't think so. What was it? Oh shoot, no. 501. This is the tertiary. 56 year old woman with recent trauma and stuff. I don't know. Hemorrhage. What is the diagnosis? Bubble jeopardy. Tertiary. Oh shesh. Yeah, you got it. Yeah, those are our points. So here you see that. I, you know, you can see there's blood underneath sub- sub- sub-renal. Cause you can see the vessel over of it, right? This is sub- sub-renal. This is dark blood. This is more like intra-renal here. And this has to be sub-ILM because, you know, cut out both shapes. The ILM is still kind of like preventing it from coming. And this is actually, I think these are also still sub-ILM. It hasn't gotten to the vitreous yet. Yeah. That's why you have nice clear view. Sub-ILM. Yeah. Are you going to score update before the final? What's the treatment? Watch. The trisongerous. Oh, for this patient. Safe lungs and drugs. Oh, hugs and drugs. Observe if it's not affecting the vision, but, you know, if it's vitreous hemorrhage, not clearing or I don't see how it's going to like burst on itself. Unless the patient develop a PVD. But even with the PVD, the ILM is going to stay behind. Yeah. So then we have a case. It's not from Tersian, but the patient has sub-ILM hemorrhage from probably combination about Valsalva and diabetic astrolabe for her. Because she was pregnant. And Dr. Valkenberg, yak. Yak this. It was in the macula. Holy. Yes. What did they have to go about? Yak. He tried to burst, break through that ILM to a lead, blood escape. And hopefully that would resolve. But the thing is like, it just give her, you know, a giant vitreous hemorrhage, and that doesn't clear. Later on develop RTI. Anyway. Don't yak it. Too risky, I think. I think we did this one here. Because I accidentally click it. Okay. Go back. Is there a final jeopardy? Yes. So, you know, my final jeopardy question is really lame. That's okay. Okay. So we just do it? We just do it. Yeah, yeah. Okay. So if you, if a team buzzed in and answered. All right. This is very nitpicky. Just a second. We're not ready. We have to wait. Yeah. So our team is 2500. Your team is 2100. Did you give us our thousand for that last one? No. It was double jeopardy for 500. Everything's double jeopardy. We haven't been doing double jeopardy. Yeah. There was more other double jeopardy. I don't think everything was double jeopardy. No, there was a whole bunch of stuff though. Oh, yeah. We want to recount. So, stop this deal. Oh, what is it? This is a hard one because I know. Maricopa County. It's not super hard. We should know this, but I noticed that a lot of us don't pay attention to this. Oh, no. Oh, no. Ready? No, no. We have to wait for first. We're not buzzing. You just answer, right? Yeah, you just answer after this. You answer. You like write this. Which eyes are this? What? Write down what you're waiting for. Well, it's a secret. I know. We'll write it down. You guys did the scoring. I mean, we don't trust it. I lost your deal. Yeah. I was like, every time we answered something correctly, I was like, we're starting out with a negative five. Yeah, we start with a negative five. I'll type it. Where are you writing it down? On this spreadsheet. It's right here. Okay, so if you're typing, then we're typing. Miranda's not competitive at all for anyone looking at this. It's a nurturing environment. Ready? We're ready. We're ready. Are you writing this down? No. So last year, I think the question was like, which country has a national hero, right? So mine is still relevant to this entire lecture. So it's not as fun. Oh, I want it to be random. But I was having a hard time thinking about one hundred and seventy-seven times. What does that mean? Answer any number. Answer any number. That's right. Answer any number. Are you guys ready? Answer any number. Okay. Every now and then. Answer any number. Answer any number. Answer any number. Indication. Answer any number. Answer any number. Answer any number. It's useful, right? And it's for that better mark like Dima. Decided for what AMD, CMS signature better collusion and myopic CNDM. That's why we do point three. So for insurance purpose, we do point three. Insurance purpose, because that's what is, you know, approved and indicated for. There is another study that says no different between point three and point five and that's how we come to the conclusion of using point three is just as good and it's cheaper. So why didn't they do that for our video? Yeah, I saw that you guys did that too and I have to look back and why they chose that but the bottom line is in clinical practice 0.3 for diabetic myocardema 0.5 for everything else. Yeah, also they did 0.5 for PDR. That's why it's tricky. I think the hoggam is right. They did 0.5 for PDR. Oh, so actually, you're right, but the indication I listed by the company is still for, so for number four, so it's still point three. It's still point three for diabetic monopathy with DME. Okay. But knee vascularization. Yeah. It's still point three. For any kind of diabetic stuff? Oh. It's still point three. I think it's, I mean like in our study for protocol S they used point five but the asterisk that we deleted off our slide was that point three wasn't FDA approved yet so I guess later it was FDA approved but that's what we based our I never paid attention to that. Does that actually happen here? Yes, so like when we, when we do the prior authorization you have to put in a diagnosis right, and you have to put in diabetic matadema or blah blah blah but that's why it's tricky so you guys don't do this at the VA. Is it a cost thing where we don't get to send this to the VA or just like a contract? It's a cost in contract that's 30, right? Yeah. You, Avastin, Lucentis and Alia, right? And you may see a benefit with Alia for patient with worse vision like 2050, right? Let's just do a lot of Alia for this patient. But the cost between Avastin and Alia is like $50 versus 1,000 something but the cost between Lucent and Alia is like 800 versus 1,000. Right, which is why I wonder why we don't have Alia and Lucentis. But that's the reason why we have Alia and not Lucentis because the benefit of Alia and the cost difference is much more versus like, but we still do Avastin because the cost is so much lower. Right, I guess I don't know why we don't have Avastin and Lucentis instead of Avastin and Alia or whatever. Oh. That must have to do with the contract but if we were to choose medication for patient based on cost alone, right? If you are going to make a big jump in cost you might as well go for Alia because at least the one that is proven to be better for the outcome for patient with worse vision. Not Lucentis, right? So if you're going to make a big jump a couple of dollars you're going to make that jump for Alia and not for Lucentis. But I think your question has probably more to do with the contract. So you win. You don't win, you didn't get it. Okay, I'm saying you got it wrong. Oh, well you guys got it right. Oh, we're trying that you guys got it more right. Yeah, you seem more right. So you win. Sorry. I thought that was a joke and then I rose, you're serious. We want the pudding stuff. What kind of pudding is it? It's our mango flavor because I think mango flavor is the best but there are 12 of them here so I'm sure there's enough. What if they want to share? It's their prize. We do.