 All right, we'll go ahead and get started. Welcome everyone to our glaucoma service rounds this morning. It's great to have everyone here and many attending virtually as well. So, you know, we're just kind of introduce our division a little bit here and then talk about several things today. So in our glaucoma division 2023, we have these eight providers that are full-time providers and then our two fellows, as you know, very well, Paul and Sean, our research fellow, John. And you know, we run a busy service. So just some stats from 2022. Our division saw over 20,000 patients, did 1,900 surgeries, saw 1,900 new patients, had about 350 clinical procedures and about 3,800 clinical tests like visual fields and OCTs. So it's a great service, great group of people. I love working with them. And you know, we all keep pretty busy, which has been really a lot of fun and rewarding. So what we're gonna do today is first, Craig's gonna give us a little tech and research update and then we're gonna have some case presentations and some other information from Paul and Barb and Sean. So we'll just jump right into it and have Craig come first and we'll get started. Oh yeah, there is no CME today, so just FYI. I think, you know, I appreciate it. So I'm gonna be giving our Moran's Glaucoma Service Technology and research update. It's gonna be just really an update on what we have to offer in terms of, in our service line. Okay, great, these are my financial disclosures, which may be relevant to this discussion. As far as diagnostics, we have not a whole lot in terms of new tools available, but I do wanna just mention briefly the Maya instrument. Maya has been used by our macular generation researchers primarily to look at the sensitivity of the macula. But as we know, many of us are using 10-2 periodically to look for early glaucoma in the macular region. And this might be helpful. The advantage of microprimetry is it has gaze tracking, so it's easier for patients to continue with the test rather than having to be looking across and having a lot of fixation losses. So that is one advantage. So it's a research tool. It's easy to update into access if you need to look at those images. But it's not something that we currently have access at every location, mainly here at the Moran as well as our Mid Valley location. As far as other diagnostics, we continue to have our main staples. We have Dr. Harry running our ultrasonography unit as well as ERG testing with Dr. Creel and Henry. In addition, we have other things that we wanna mention. Many of you know that glaucoma is not just one risk factor. We have multiple risk factors that we're addressing. And just a reminder that if you need to order, sleep apnea consultation and a 24 hour blood pressure test, those are all orders within Epic. The 24 hour blood pressure test works as a library card system. The EKG lab has a number of devices to rent out and check out. And those can be picked up. And then I usually just use rule out nocturnal hypotension as the reason and indication to do a 24 hour blood pressure test. As far as medical therapy, nothing's really changed. We continue to have our staples. SLT has really become first line for many of us based on the light trial. We also have Dorista, which is our only injectable medication. It's a Dorista intracamalpomatoprost implant. Surgical care. Plumbers need tools and we have a lot. So I'm just going to break this down in terms of what we have available. As far as trabecular micro bypass stents, we have the iStent inject W and the hydrous. Hopefully later this year we'll have the iStent infinite, which will be three stents loaded on the same injector. For viscodylation, we have two systems, the iTrack micro catheter and the Omni system. For goniatomy, we have KDB, which is the Cahook dual blade. The Tribex Pro, which is similar to the Cahook dual blade, but it has infusion hooked up that you can hook up to your Faco machine to have continuous infusion and aspiration. The Streamline is a unique tool, which is used to create micro goniatomies, as well as viscodylation. And we also have traditional suture or iTrack cat as well. The Zengel stent is still available. We have the first generation Zengel stent. Hopefully in the future, maybe in a couple of years when there's pivotal data here in the United States, we'll have the larger lumen size. But for right now we have the current iteration, which I believe is 45 microns internal lumen. Tribex Electomy, despite all this new technology, we are still doing a ton of Tribex Electomies on our service line. And our fellows this year have been quite busy managing those Tribex Electomies in clinic as well. As far as glaucoma and drainage devices, we have just one new player on that spectrum. The Ahmed Values are only valve device currently. And as far as non-valve devices, we have the Bare Belt, Molotino and the Clear Path. We continue to have cycle photo coagulation options, both endoscopic and transcleral. As far as research, I'm really pleased that the Crandall Center has been busy. We've conducted three rapid studies this year. Thanks to John Musser, who's led all these studies. There have been two tight-tradeable glaucoma drainage devices study with MyraVision, as well as one eczema laser tracheolostomy with LAOS. For the future, we have potentially two to three more studies that are coming online. One will be with the EPTFE, which is Gore-Tex. This device is a plate made out of Gore-Tex. And so we'll be studying that in rabbits first. And then also, Kornit has this glaucoma ischan, which is really a novel glaucoma drainage device because it's draining into the intraconal space, which presumably has less fibrosis activity and may actually be a really great source for refractory cases. As far as basic science work, we have everything ranging from genetics to conventional outflow homeostasis, with Dr. Fionna McDonald, our newest hire. And also therapeutics and no protection with Dr. Curry's lab. As far as other clinical research that's occurring, Brian Stagg has been busy with statistical modeling for personalized glaucoma care, as well as clinical decision support tools, as well as clinical trials are on the forefront. And we have three that are hopefully gonna start here in Q3, the abexterno zen gel stent, which is not really new per se, but it's a new delivery style to receive the on-label indication for the abexterno technique. We're really happy that we have now supercoital shunts in the future coming. And we have two that will be starting, hopefully in Q3 this year, the supercoital scleral biostent, which is a biostent made out of banked sclera. So it's a device, but it's technically a biostent and not a hardware polymer of any kind. We also will have the supercoital mini-ject, which is proprietary material known as star. And this material looks like a honeycomb and will hopefully provide a nice drainage channel using the mini-ject device. As far as other research that we have going on, we have a lot of retrospective and outcomes research. Dr. Roscoe's leading our suit exfoliation comorbidity studies, as well as the Nectohemeral-IOP patterns using ICARE home serial to home tenometry. We have a number of other mixed outcome studies looking at abic-hydrous, multi-centered gap, as well as the hydrous positioning, looking at outcomes of how that correlates with hydrous positioning post-operative outcomes. Finally, we have something that I've termed innovation activities or innovation initiatives through the Crannell Center. These are just a smattering of things that we've been involved with in the last year in terms of new technology, things that are coming in the future. One that I'm really particularly pleased about is, I know I hammer most of the trainees about how to hold a Gonioprism, but we now have a hands-free option that will be mounted onto the biome, which will actually provide the ability to stabilize the eye better for certain cases. In addition, we're working on a virtual rally Gonioscopy module with VR Fundamental. That's been slow because of funding, but we hope that that will become something that all educational programs will have in the future. So thank you, but that was our technology and research updates. I'll turn it over to the rest of my colleagues. We're gonna have a little change of order here. Paul and Craig need to go to the OR, so we'll have Dr. Shamil and go next. The being in Utah, I thought stuck between a rock and a hard place, stuck between a soft and a hard place. We have a pretty afro-po title for a Guacoma talk. I have no disclosures. So get right into a patient presentation. This is an 82-year-old female complaining of blurred vision with hypotony in the right eye for two months following a trabeculectomy blood revision. So it's been ongoing since the revision. She's a history of poag in both eyes, also past surgical histories that cataract surgery in both eyes, SLT in both eyes, trabeculectomy in the right eye in 2022, a blood revision a little over a month later, because the sutures were cut, pressure still had not come down. And so, you know, basically went in with the MVR blade, opened up the flap and she's been hypotenuse since then. So that is the etiology of hypotony. The left eye has also had a cataract with an eye stent, trabe and then an expression, sorry, has had an expression, not a trabe and an expression. And then a blood revision and that one also went well, our pressure's been 10, not currently on any drops and no relevant past medical history. On exam, vision in the right eye is 2070, pre-op, before her trabe and revision, she was 2025 in that eye. Left eye is 2030, but that's with a minus three. And her right eye really is her good eye. I'll show you the visual field in a second, left eye is significantly affected by glaucoma. No RAPD of severe glaucoma in both eyes. IOP is two and 10, full motility, shifted visual fields. This is a 10-2 really approaching fixation, but you can see the left eye is worse than the right. So she's very, very bothered by her right eye. And on exam, just significant things here, beautiful from a glaucoma perspective, absolutely perfect blep. Morphology looks good. It's not leaking, diffuse elevated, but the pressure's two. Left eye also good, good blep chamber deep. On DFE, she's significantly cupped a nerve with not just to the inferior rim. Moderate choroidal effusions on the left eye, for the residents especially, kind of think of choroidal effusions mild, is you can just see them out in the periphery. Moderate may be starting to come into the arcades a little bit, but not really affecting macula. And if they're kissing or close over the macula, that's kind of severe. So these are moderate, pretty good size, but still not in central vision. She might notice them sometimes, but not all the time. So next steps, and I warned the PGY-4s ahead of time, but I might be calling on them just because I hate to talk for 15 minutes. So I'm at Cole. Would you mind, what are our options here? What could we do for this patient? Do nothing, that is a great option. And the one, we have actually, at this point, scheduled the patient to go back to the OR, I think three times, and each time, we're saying, okay, we're gonna do an exam the same day, and we've convinced her, let's just give it a little more time. The pressure's gonna come up, it's gonna be fine. So waiting is a great option. We already feel like, I mean, if we're up to us, we'd say, yes, let's just keep waiting. Patient has decided, no, I don't wanna wait any longer. So what else could we do? But in Dr. Saga, I forgot, had you already filled at one point? I don't think I, early on, yeah. Yeah, I was gonna say, I actually did not put that on here, but we had filled multiple times at this point, or yeah, a couple of times. So yeah, watch and wait, revision, and the revisions, I think you mentioned all these, you know, compression sutures, blood patch, open, conch, and close the flap, and you could combine these with drainage of carotidals if you wanted to. Yeah. So if they're macular folds, those can become more chronic and hard to, you know, hard to get rid of. So if she has severe macular folds, then that's gonna push us more towards doing something sooner rather than later, because with high potting too long, those won't necessarily go away. But if her macula is okay, also, you know, kissing carotidals, severe carotidals will push us. And then, you know, this is not quite as like urgent, but just, you know, if this is her functional eye, which is kind of what pushed us to do something at this point, yeah. I will. Right, yeah, a flat AC with, yeah. And you can have a patient with a pressure of seven who has hypotomy even though you've kind of think, why, yeah, but, okay. So we proceeded, and I'm gonna, my laptop died last night, so I wasn't able to link all my videos to this. So let me pull up the video here. This is a video of the first surgery. So these are compression seizures. I show this video just because it's something that's not very common, so just kind of seeing, essentially going at the limbus, and then this is, we had already done a blood patch, so basically just injected her own blood subcontractively. This throw right here, just trying to, it's kind of blind, but you're just grabbing a little bit of sclera, and then really just you're tightening it down. Now these sutures do not come out. You don't actually ever have to take these out. They'll incorporate just kind of like into the blood. I saw one yesterday in clinic that had been done a couple of years ago, and the entire blood are just like over these sutures. You can kind of see them in place, but they just incorporate into the blood completely. This is 10-0 nylon. This is, we did four of those. So this is a compression suture. Okay, we'll go back to the PowerPoint. Okay, so a month later, after this compression, vision is 2060, IOP is two, still with moderate corrodals, and essentially patient is still very bothered, doesn't want to wait any more again, so decide to go for a more aggressive surgery. So the second revision, we opened the conjunctiva, sutured the flap down. Now we were almost expecting the flap to have melted. The flap looked beautiful. It was like perfect edges, the sides were actually sealed down. It was just, there was a tiny bit of flow at the very posterior edge of the flap. Again, we were just like, oh, this is like a perfect bled right now. Why are we doing two? But so we put down five nylon sutures, one on each corner and one on each side, just to really seal that flap down. And we had filled the eye, made a couple of paracentesis, filled the eye with the viscote at the beginning of the case, just to kind of stabilize the eye during the surgery. And we've closed the flap, are irrigating out the viscote just by pressing on the paracentesis, injecting some VSS. And all of a sudden, the eye becomes rock hard, the AC shallows, and the iris comes to both paracentesis, just like milliseconds. So we stop. The patient actually was not in pain. She did not notice anything. She was, you worry, a patient's screaming. She didn't notice anything. It was just, this is something happened. So, Sean, what might your differential be? What are we most concerned about and what else could it be? Okay, great. Oh, yes. Were they anti-coagulants? She was not on anti-coagulants. I don't remember about hypertension. So, perfect. Superecordial hemorrhage, aqueous misdirection, and then this other one, I'll talk about a little bit more areas that stands for acute intraoperative rock heart eye syndrome. I did not actually. Dr. Chia pointed me to that. And I'm gonna talk about that at the end a little bit. So, what do we do at this point? I was talking with Dr. Stag about this. He said, this is the most stressful situation I've ever been in inside the OR, was this case right here. It's just like, there was no loss of red reflex. We could still see. So, we thought, maybe this isn't, hopefully this isn't a superecordial hemorrhage. So, first thing, get out of the eye. Yes. Oh, okay. You plus or minus, if you had a main wound, definitely suture with paracentesis. Iris coming to the wound, we actually did not suture. We would have been suturing Iris anyway. So, we just, we got an indirect looked in the back. There was no loss of the red reflex. The moderate carotidals that were there before surgery were still present. There was no hemorrhage. So, we kind of thought, this is a form of aqueous misdirection. We did not know this nice acute intraoperative rock heart eye syndrome term at the time. But essentially we thought, is this a form of aqueous misdirection? Which, what are the options here? So, we could close, just start Diamox. She wasn't, she didn't have lens K touch. So, we could just watch her and she might deepen. We could do an IZVH. Yeah, that's 630. So, IZVH, the problem with this is this patient has carotidals. So, going even at paris plana, worried about hitting the retina. In this case, because they had carotidals, we do have the option of draining carotidals. The pressure might actually flatten those out and soften the eye. And then this is something I'll talk about in a minute, which we had not thought of at the time, but I'll talk about that in a minute. So, we opted to drain the carotidals. I'll show a brief video of that. It's actually not this case. So, also this case, because it was the last case of the day, was the only case of the day that we did not get recorded. But this is, you know, essentially four millimeters back to the limbis radial incision, just cutting down. And then eventually you will get a gush of fluid. You can see it right there. This is what I did during residency. And this patient had severe carotidals. And it just drains and drains and drains. We did not need to put it in an AC maintainer for the case with Dr. Stagg, because the eye was rock hard. But if you're doing this for just hypotony and carotidals, you'd want to put it in an AC maintainer to keep the flow going and to make sure the eye doesn't flatten, because there's a lot of fluid in that case. No. It was just manual irrigation with, you know, BSS on a cannula to irrigate out the viscoelastic. Yeah, yeah, we had suture down the flap. We were like closing up conch. It was just like, we got to get the viscoe out. So, you know, and it was when that's when it happened. So if it were, you know, aqueous misdirection, if there weren't carotidals, you could do an IZVH, which one last video here, two of these. So, you know, anterior, you make a, you know, anterior PI, and then you can do this just through a stab incision with an MBR blade. This we actually use to port, and then making sure that you can actually see the vitrector coming up through the iris, and you know you've done the full thing. And then just a small, it doesn't have to be a thorough anterior vitrector. You're really just trying to break that high-loid face. Okay. So, and if it were a supracordal hemorrhage, get out of the eye suture wounds, plus or minus strain and get some religion. So acute intraoperative rock heart eye syndrome was described in this case report. They kind of coined the term, but basically for their cases that they had six cases, and it was during cortex removal, and the thought was essentially just, you know, the irrigation went behind some loose zonules, either hydrated the vitreous or, you know, kind of a collection of fluid just between the posterior capsule edge and the high-loid face. So they actually took a needle at parched plane and just stuck it in, aspirated some fluid in the eye software. And that's how they treated it. Now, I thought this was really cool. So I was reading through, you know, their work cited, but I'm thinking of all the wrong words. Citations, thank you. And it said, you know, the first time something like this was described was in 1994, and I looked up the authors, and it was Dr. Olson, Dr. Crandall, and Dr. Mamillus, back, you know, 26 years ago, or 30 years ago. So I think this is just something to know, you know, rock heart eye, if it's not a suprachroidal hemorrhage, and I was talking about this with Dr. Zabrisky as well. If, as long as the chamber's deep, you know, you can try one of these things to soften it up, but they may just get better with time, because if it is just a mechanical thing with you hydrating the vitreous, just, you know, give it some time and it could improve on its own as well. So any questions? Sorry, I think I might be over right now, but. So Dr. Stagg saw her yesterday. Her vision is 2025. Her pressure is eight, and she is not very happy. Oh, my God. We, one pressure was like 22, and she was, you know, really worried. We were just happy she wasn't blind. We said 22 is okay. No, that's great. So you can do them all this way now, just the exact sequence. So thanks everyone. Thanks Norm. So as many of you know, I've become interested in home tenometry and IOP fluctuation, and I'm also conflicted because I did start a company to try to get the eye care home into the hands of patients. Turns out eye care will not sell directly to patients. So there was no way for patients to get access to this device. So we know that glaucoma is a chronic progressive optic neuropathy. We also know that we only have IOP as our modifiable risk factor. Clinical studies have demonstrated that if we lower the IOP, we slow disease progression. We always ask the patient or look in the chart, what's that maximum IOP? And then we target IOP. We also know IOP has diurnal and nocturnal variability and fluctuation, whether they're sleeping, time of day, cortisol levels, nitric oxide levels in yoga, inverted position, it can affect their IOP. I find this fascinating. We spend a few seconds every three to four months to check a measurement where there's 31 million seconds in a year. It's also known that glaucoma progresses, right? Despite well-managed IOP. It's a chronic disease with variability. So why are we not monitoring it, managing it like we do for diabetes and high blood pressure? With a lot of these chronic diseases, we know that outcomes are better if there's multiple time points. This is a great study, which we always, I've forgotten about this. And it wasn't until Craig actually called my attention to this, but this was the SIDGETS nine-year study. So they randomized roughly 700 patients with advanced glaucoma, either to medications or to a trap. They found that initial surgery had a slower rate of progression, but they also found that greater fluctuation during the day, if patients had greater than or equal to 8.5 millimeters of mercury range at that baseline visit, they had a 96% likelihood of visual field loss. I know, I never asked patients about range of IOP. I've never thought of that as a risk factor, and maybe we should start thinking about it. There's several devices that are available. The trigger fish you may have heard about, it's cleared in Europe. It's also FDA approved. It's a device that's contact lens. It doesn't measure IOP directly, it measures basically corneal rigidity, changes in that rigidity, and then interprets it or converts it to an IOP. It's expensive. I don't know many people that use it. I care and plan data is a intraocular device that's put into the sulcus. There was one paper that was published in IOBS in 2015. And it actually is with, it's not without its safety concerns. So prolonged inflammation, but this could be an option. When I last looked on clinicaltrials.gov, there's no current clinical studies in the US because it's a, what's called a class three device. They would need to do clinical studies in the US to have the FDA clear it. So I don't know where they're at. And then obviously it's the eye care tenometer, which we know. So in 2017, the eye care was cleared as a home device. That's the device, the first device in the lower left. And then they went to the home too, which is much more patient friendly. It's indicated as a prescription device that's intended as an adjunct to routine clinical monitoring of IOP of adult patients. We know rebound tenometry. It's something we use in our clinic. We trust it, right? You know, I'm bugging all my residents and fellows to do aplenation because we have become so comfortable with rebound. The FDA has accepted rebound tenometry for years in preclinical, we all know the tonovet. Well, that's rebound tenometry. It's all based on the same premise. The eye care home has similar IOP measurements as are in office eye care tenometry and it's got good approximation to GAT. It's not perfect. But again, if we're looking at deltas, maybe that doesn't need to be perfect. I personally use it as a diagnostic tool, but also as a monitoring tool. So I'm gonna share some cases with you and some of the data that's actually shown that it actually could really help us understand glaucoma. This was a study that was done by the Wilmer group were actually working with them. They had 107 patients and what they did is they basically gave the eye care home to their patients and they found that at the early waking hours between 430 and 8am, 24% of the days in the span of weeks, in a week, seven days, those patients had a higher IOP than expected. And they found that a lot of these patients were younger, men and obviously did not have filtering surgery. So their conclusion was that self-tenometry provides IOP data that can supplement in clinic tenometry. This is one of their patients. And you can see that over the course of a week that patient had higher IOPs in those early AM hours. I refer to it as early waking hours, but technically they're not really awake. And then their IOP dropped during the day. This really gave us confidence that maybe only a week is needed to really measure the IOPs. This is a paper that was published out of Symorei's group in Ohio. She's been very active actually doing an NIH study with early onset glaucoma using the eye care home. And this is somebody, he's a 72 year old surgeon. I would doubt he was non-compliant. I'd like to believe that he was compliant with his medications, but you could see again, he's controlled during the day in the clinic. His pressures are in the teens, maybe low 20s, and he's spiking to 48 in that right eye. They gave him, changed his medications, they gave him Natarsidil. That's something I don't know. I don't know if Craig has experience with this, but I've been finding that the Rocklattan, the Natarsidil, the Repressa, actually seems to help with that early morning spike. Again, just as we think about what is the underlying etiology. This is a VA patient. And actually it's a patient that our neuro op team had seen. So this is the 74 year old gentleman who was diagnosed with questionable neuro tension glaucoma. This was several years back. He developed a visual field defect in his right eye. He had a full normal tension glaucoma workup. He had a brain MRI, Doppler, sleep apnea. He comes back to see us recently and I thought, you know what? I wonder if he's spiking. So we got the, for all our VA patients actually, we get them the eye care home for free. I'm trying to work with the VA to actually get them devices that they can actually give to their patients. So anyway, he has an APD in his right eye. This is on medication. So we really don't know what his pressure is without medication. And I just raised the possibility that maybe he was spiking earlier with a greater range in that right eye and that's why he had that visual defect. So maybe as we think about these patients, maybe we can save them some of the additional tests and maybe this could be an early first thing that we do. This is a Moran patient. This I find fascinating. So this is a patient I've chaired with Rachel. So I have had numerous colleagues look at this patient and there was no clear reason for the asymmetry in his glaucoma. No exfoliation, no trauma, no pigmentary go on and on and on. He's got much more advanced disease in his right eye. Very little disease in his left eye. He owns the eye care home. These numbers are fascinating. He doesn't spike in that left eye. So again, is it that range? Is that the reason why his glaucoma is worse in his right eye? I don't know, I don't have the answer but I think it bakes the question. This is a gentleman, 67 year old with controlled normal tension. He'd been followed at Mass Eye Near for years and he actually purchased the eye care home with a lot of difficulty back in 2020. And again, this was sort of the reason why we realized that other patients could benefit from it. So he was spiking into the low 20s. These are his visual fields. The question came up, what do you do with a pressure of low 20s with this visual field? And it was occurring in the early waking hours. And some of the discussions were, well, maybe it's okay to have a pressure in the low 20s with these fields if that spike is early in the morning. My take was, if you came to my office with these fields and your pressure was low 20s, on maximum medication in my clinic, I would tell you you needed surgery. So we ended up having surgery. And again, he owns this. So this device and it's, he ended up doing an abic hydro, it's actually Craig did this work. And you can see that the hydros in the abic really didn't do much to lower his pressure and lower those spikes. He was still going up into the 20s. It wasn't until he had the pressure flow in that right eye and has a beautiful blood and we bypassed the whole outflow system that he actually got more under control. So right now in that right eye, he's off medications as pressures are good. And his left eye, the question is, is whether or not to do a pressure flow. This interesting case, again, a little bit different because this is a young person. UVA to glaucoma complaints of intermittent headaches. This is a case out of Wilmer again, that was published. And with the eye care home, they found that he was spiking to 45. They did a gap on him. Now he responded beautifully. So is there a difference between our glaucoma patients? Perhaps all of his resistance because of the steroids was really at the tebecula mesh work and Schlem's canal. And once you unroofed that resistance, the distal outflow system was working beautifully. Another Moran patient, this is one of our SLT patients. Full visual fields. She's a woman in her 60s. And every time she comes into the office, her left eye is a little bit higher than the right. She has exfoliation. We tried her on prostaglandins. She really didn't like them. And all she has is a little bit of temple thinning on her OCT. So she opted to try an SLT. We went back and forth. Do we treat you, not treat you? She did the eye care home and saw that in fact she was spiking to 32. And she was not comfortable with that. She said, I wanna be treated. This is a beautiful response with an SLT. So she's part of our study. So I ask then, the light study, six years they came out and they showed that perhaps SLT is a safe treat. Well, we know it's a safe treatment, but perhaps it's a better option to slowing down progression. They found that more eyes in the drop arm with equal IOP exhibited disease progression had a higher rate of traps and also had a higher rate of cataract surgery versus those patients in the SLT. Now granted, these were ocular hypertension, mild glaucoma treatment naive. But I'm wondering is the SLT actually working and preventing progression because it's doing a better job of actually flattening that curve. So again, is it that range? Is it that variability that perhaps in some patients is more detrimental? So in conclusion, I found a lot of value. I've been intrigued by this from a research perspective by an underlying physiology perspective. I still don't have a good answer. I've started measuring cortisol levels on some of my patients. Haven't found anything. Craig and I were talking about rent and aldosterone levels. Haven't found anything. I think it's a great way to look at response to surgery, to lasers, also to lack of medication responses. And then in a lot of our patients too, we found that it's useful to follow them after they've had the dorista because they don't need to come to the office to tell you if the pressure's increasing. So I can manage patients more from a virtual manner. So next steps, we're actually working. A group of us are trying to work with payers and insurance companies to basically get this reimbursed. I did have one patient who was able to get this covered by Blue Cross Blue Shield of Illinois. Because again, why should it not be covered? I mean, I think this is game changing for some patients. I have a lot of questions. Who progresses with fluctuation? What numbers are, what's the delta? What's good? What's bad? Is normal tension glaucoma real? The other thing too, if these high spikes are occurring in the early waking hours, is that also responsible for ischemic events that we see in the retina? We have two open INDs. Anybody that would like to enroll patients, please contact George or Cole. We have the SLT study that we're doing where we're looking at patients pre-SLT and then post-SLT. There's no cost to them. And that's in collaboration with Prism and Ike's group. And then we're also collecting all our cases between Moran and Wilmer. And then also hoping to get more cases from source. I think, again, the more patients we get, the more we understand the characteristics. I think we'll learn a lot about this disease. A lot of thank yous. I know Demperz in the room could not have done this without her and her team. And then our entire glaucoma team, obviously, Susan, Rachel, Norm, Brian, Craig, everybody that sent me patients. And then obviously our residents and medical students. Did I stay under 15 minutes? Great, thanks. No, they just submitted it. Yeah, they submitted it as a, as a device. If Blue Cross Blue Shield, what we needed for documentation, they submitted it. And I know we just gave them a documentation saying that it was this much money for a rental and they paid 150 bucks to the patient. And then they actually sent my eyes and said, we're so glad that we can actually help you take care of our patients. Yes. Just, this is awesome work, I think, and super important, super exciting. You know, one of the things that bothers me the most about glaucoma is there's so much we just don't know or don't understand. And I feel like this is starting to look at this a little bit. I just think like just looking at it, I think we need like cohort data on like all patients with glaucoma and follow a group of them for a while and see what these fluctuations mean and see, you know, how this correlates with disease progression. I just think that's super important. And we're in a good spot to do that here. So super exciting. I agree, Brian, 100%. Thank you. And then with that, I'll just give you one last tidbit that I didn't present talking about who progresses. Just quickly, six-year-old woman, myopic, tilted optic nerves, thick corneas, normal visual fields, little bit of thinning on OCT, but she's got tilted nerves, ocular hypertensive followed her for years, gave her the eye care home. She's very data-driven. She's a PhD. She doesn't fluctuate. She goes between 22 and 24. So are those people less likely to progress? I don't know. Thank you. Anybody else? Sorry, any other questions? Thank you. Thanks very much for both of you. Yeah, just unlimited potential on that. I mean, not only for treating patients, but for helping us understand this disease. It's just really remarkable. Okay, we will go to Sean. Okay, thanks, Dr. DuVirsky. So I'm gonna present a couple of cases to illustrate the many ugged moments we have on the glaucoma service. And then I'm curious to get people's current practice patterns in the audience for how they manage this complex and disease that presents in with a wide spectrum of symptoms. So I have no financial disclosures. So first case is a referral for a right eye single-piece IOL that was in the sulcus nasally. This patient had cataract surgery done at an outside hospital back in 2019. So no case mystery here. I've given you the diagnosis already. This is a visual acuity was 2040. The IOP was still under control on no medications. There was two plus endopigment and the iris showed a large nasal iris transillumination defect. They were suspected that the single-piece acrylic lens was in the sulcus nasally. So this patient had assisted macular edema shown on their OST macula, probably the cause of their vision finding to be down to 2040. And then we had a UBM done which showed the inch chakra lens implant was tilted nasally. And it does appear that it is in the sulcus nasally. So I'll present a quick 20 second video. I can press play here. So here we are going in intraoperatively using iris 6 to expand the pupil and get a better appreciation of this lens. We're using a twist and out technique to explain the old single-piece acrylic lens. And here we are doing a Umani technique using a 30 gauge TSK thin wall needle. And that's the end of the case. The purpose of this presentation is to go over surgical videos. That was just a quick demonstration of. What's that? Haptic couldn't be dunked back in the bag and this, I probably didn't show a good view of it, but the capsule Rexis was quite large. So it's a three-piece inch chakra lens implant wasn't, couldn't safely be placed in the sulcus without to capture. There wasn't enough capture support and there was an open posterior capsule. So case number two is a referral for right eye recurrent hyphaeema. This is a more interesting presentation as this patient was managed medically for five to six months at an outside institution for this recurrent hyphaeema. So this patient had cataract surgery done 25 years ago without any issue until this past year. And this patient presented on prednisolone and cosopt for management of the hyphaeema and their pressure. So this patient's vision was down to 2050. Their pressure was 20 on the cosopt. They had one plus cell and they had nasal translimination defects from three to six o'clock. This patient had was pseudophagic with a mild IOL tilt and pseudophagodinesis. So this patient had a UBM done again, which did show a single piece lens that did appear to be in the bag. However, there it looks like there was a large L-shtink pearl or proliferation of lens epithelial cells that was in contact with the iris and likely the cause of the Ogg syndrome for this patient. Here's another view potentially showing some IOL tilt as well. So this is the surgery that was done for this patient, which again, use iris hooks to expand the pupil. Here we can see large sombrings ring material which is pretty consistent with the UBM we saw. And here we are prolapsing the intragal lens into the AC, IOL scissors were used. And now it was used to cut about 90% of the way through the optic which is then expanded from the eye. This elastic is used to burp out the remaining sombrings ring of material. There was vitreous notice so anterior vitrectomy was performed and AC maintainer was placed and again, three piece intragal lenses placed sclerophyxation using a Yomani technique again here. And here we are pulling the haptic out, we planned it and then here's the end of the case. So this patient did not have CMA. So unfortunately that wasn't the end of the story for this patient. Two months later, this patient then represented where they had the IOL optic which was reversed captured by the iris into the AC. Their peripheral iridotomy was patent, their intragal pressure was fine. So you can see in this photo basically the entire optic is captured by the iris within the anterior chamber. So 30 gauge needle was used at the slant lamp to dunk the optic back posterior to the iris. The patient was started on pylocarpean to kind of bring down the pupil, hopefully keep the lens optic posterior to the iris. Patient was also started on moxivoxicin and pranislone. So the next day the patient returned and the lens was in good position just for good measure to try to keep the aqueous outflow and a good dynamic and not have the potentially, hopefully reduce the likelihood of the optic to come back anteriorly. A second PI was placed with the YAG laser. Unfortunately, this patient then returned to the home state, presented to their home eye clinic complaining of changing the refractive air and blurred vision. And the IOL optic had again been partially captured by the iris. So at this point, given it already happened once we already had to push the optic back. Second, the PI was already performed. The decision was made that surgical intervention was warranted. So a couple of options that were discussed with the patient and were considered. One was intraocular lens repositioning using a basket basket technique to just to try to hold the lens optic back and keep it posterior to the iris. That the decision was made that that probably wasn't gonna be enough for the patient. If you actually saw this patient at the slit lamp or were involved in their first surgery, the iris was extremely floppy. Likely from all those recurrent episodes of high FEMA and just that chronic chafing of that L-Stick pearl material and the lens and the IOL itself at the iris. So IOL repositioning using a basket back technique was not thought to be sufficient to protect the patient and keep the lens optic back. So the decision was made to proceed with the pupillary circlodge. Yeah, I'll quickly show another quick video. We're using tenoprolene on a CIF4 needle and using micro-graspers to kind of place the iris around the suture needle. That's done with one quadrant there. You can use a OBD cannula or another cannula of some sort to take out the suture needle. And basically you just continue this process. Here's Dr. Chamberlain masterfully using the micro-graspers to thread the iris over and over and over again around the tenoprolene on a CIF4 needle. Here the suture knot is being thrown which is then pulled into the eye and the patient was left with round pupil is potentially a pupil a little bit on the smaller side but definitely protective against that lens optic coming forward again after the surgery. So quickly I'll just go over what is UGG and potential takeaways. And I'm curious to get the audience some impression about how they currently manage UGG. So what is UGG? So UGG is Intracker Lens Chafing Causing a Spectrum of Findings. It was first described in 1978 describing UVitis, glaucoma and hyphaema. But as we know, there's lots of other exam findings that can be noted Translumination Defects, IOL tilt, refractive error, CME, Vitreous Hemorrhage and then floppy iris and iris hypotonia. So I wanted to highlight the last two as big pieces of the last case I presented. Most people do not talk about floppy iris or iris hypotonia being a consequence of this disease process. But as we can see from the last case, just that repeated process of UGG if we only go with medical management can really worsen that iris tone and predispose the patient to worsen iris tone and floppy iris. So UGG causes, so it was first described in 1978 secondary to ACIOLs. However, it's subsequently being associated with essentially all types of IOL placement. It can be associated with iris fixated IOLs, piggyback IOLs, single-piece IOLs is our big culprit a lot of the times. Secondary IOLs and even IOLs within the capsular bag as we saw with that last case, weak zonules or lenticular epithelial cell proliferation causing somers ring material or allicinic pearl formation can contribute to that disease. So this is a review paper I found that basically said a couple of sentences that I wanted to highlight that I thought were interesting. It says the majority of cases cause minimal symptoms and even go undiagnosed. Majority of cases will also be transient and will resolve with topical steroids and anti-clockwise medications the first line of treatment. We suggest that IOL repositioning or exchange may be considered for medical refractory UGG to reduce or eliminate the effect between contact in the IOL and the UVL tissue. So I wanted to just bring this back to a discussion about when is a good time to intervene? So as we know, there's not really rates like universal recommendations that we can all follow for this disease process because the presentation can be so variable and each case is so case specific depending on the presentation. So for the first case, there was kind of those obvious findings, the CME and UBM confirmed that the IOL was placed in the sulcus there. So that's a good pretty obvious case to go ahead and surgically intervene. The second case, this patient are already presented to you with five to six episodes of recurrent hyphemia. And that was also a case where it was pretty obvious to intervene. But what about if you backtrack like maybe five episodes before that? The patient's first episode of hyphemia, maybe it's kind of unexplained. You only see a trace TID. How would you go about managing that situation and would you try, how long is a good time to try medical management for it? Does anybody have any thoughts, Dr. Petty? So first episode of hyphemia, would you try medical management or would you move forward to surgery? Dr. Zabriski, did you have a thought? Yeah, I'm just gonna say certainly, so CME I think is a super important driver towards fixing it. The statement that was made by the authors there that there are some that are very subtle and seem to be like a single episode. I mean, I agree with that. So I think there is some room to watch it and like you've got a few cells in the AC and you think it might be ugg but otherwise the patient's pretty symptom-free. So there's some wiggle room there, I think, to kind of watch a little bit. But again, recurrence, multiple hyphemias, consistently elevated intraocular pressure. Of course, those are the things that are gonna drive you for sure to do something like Jeff's saying to fix the underlying problem. And it might require fixing the IOL as well as doing something else, or maybe glaucoma-wise or something. So it's a, you know, there's a lot of art and to the treatment of ugg, you know, based on symptoms, based on recurrence, severity, those kinds of things. You know, it's interesting too as we always talk about ugg with IOLs and we've seen a few cases now as we put more hardware in the eye for glaucoma cases. With the VA, we've called it ugg, it was with a hydrus. So the tip of it was chafing against the iris and then we've also had some cases with tubes, right? So always think about anything else that's in the eye as well to the resonance. It's that iris chafing, no matter what it is, whether it's an IOL or not. Let's bring up the point, you know, you mentioned about the floppy iris. I mean, is that causative or a consequence? I think sometimes there's just a floppy iris that's banging into whatever might be there, IOL and tube. So I think sometimes a floppy iris can be causative. I know cases that I've done where you have to go in and replace an IOL or do these things that you're doing, it's almost always the iris is nuts, you know? And so you wonder if that's part of the etiology as opposed to a consequence. That's a good point. So this point, we already kind of went over what exam findings such as CME or Recurrent High Femal would tip you over to ugg sooner. How would you advise patients? So let's say you're going for the medical managed route after our first episode, there's maybe a trace TID. How would you advise patients on the likelihood of their ugg to progress? Austin, if you can speak, you can go ahead. Hello, can you hear me? Hello? Yes, we can hear you. Okay, great. Sorry, I'm trying to make a comment for a bit. I'm sorry, I got to rush real quick, but I just want to make a couple of comments real quick before I go. I obviously get a fair number of these from a lot of you all. Thank you all for sending them. We see a lot of the VA as well. And obviously there's a huge spectrum in terms of what is ugg and what is not. But it's true that the symptoms can range from very severe CME, super high pressures, a lot of blood and hemorrhage to just a little, almost like a mild bit of cell and patients just notice that things are kind of a little bit different. And a lot of times the only way we find out these things is if we go and intervene and do something about it and then it gets better. And I just want to make two examples, although there's many, though I had one case of a Yamane fixed IOL that was apparently causing some form of ugg. I went in there and it seemed like the Yamane was in perfectly, was in perfect position and was actually far enough from the Linnus. But I said, well, I mean, I'm in here. I got to do something. So I took it out and I basically moved the haptics maybe like a couple of millimeters away in terms of clock hours and a little bit more nasal temporal. And then I also pushed it back maybe about 0.5 millimeters from the Linnus. And that patient has never had problems since with CME or any of these other symptoms. Another thing is a point that's made by a lot of Yamane surgeons who do this quite frequently is that this can happen. And I'm talking specifically UGG after Yamane and a number of PIs typically have to be made before and surgical intervention should be made. And I discovered this myself because I had a patient who had a very similar situation to the one that you presented. In fact, it might be the same patient anyway. And we kept pushing it back with a 30 gauge needle and pushed him out of capture and he would capture like a few seconds later. So I went ahead and did a PI. He already had one nasal, I did one temporal and inferior. And during one of those PIs that I did, it immediately came out of capture as soon as I did that PI. And this was the second or third PI that was done. So typically think about making more than one PI before you intervene surgically. The last thing I wanna say is that this can actually happen more frequently than people think with a IOL that's in the bag as well. And the thought in that case is it might have to do with some floppy iris in conjunction with weak zongles as well. So anyway, I could talk a lot more about this subject but I just wanna make those points clear before I kinda run off. Thanks. Yeah, sounds good. Here are some takeaways. Importance of UBM as an imaging modality. Consider intervening earlier in the disease process. Take a thorough history request prior op notes when considering again the differential diagnosis. And if you can, it's also ideal to consider the patient satisfaction with their existing IOL. Thanks a lot.